Environmental health

Olympic Games Monitoring acute diseases during the Sydney 2000 Olympic and Paralympic Games Sarah V Thackway, Valerie C Delpech, Louisa R Jorm, Jeremy M McAnulty and Maria Visotina MJA 2000; 173: 318-321 Abstract - Morbidity and mass gatherings - Public health services in Sydney during the XXVII Olympiad - The NSW Health Olympic Surveillance System - The role of general practitioners during the Games - Surveillance system constraints - Public health response - Acknowledgements - References - Authors' details - - More articles on Public and environmental health Abstract The Sydney 2000 Olympic Games (the XXVII Olympiad) will be the biggest peacetime event ever held in Australia. During the Games, all public health decisions will be centralised, with daily briefing sessions held to review emerging public health issues and facilitate responses. Infectious diseases will be monitored and reported through the Olympic Surveillance System, with particular attention to foodborne diseases and conditions spread via the respiratory route. This system relies heavily on the cooperation of key notifiers such as emergency departments, laboratories and general practitioners. The lessons learned during the Games, and the new and enhanced systems and linkages that have been developed to support it, will strengthen future disease surveillance in NSW. The Sydney 2000 Olympic Games (the XXVII Olympiad) will be the biggest peacetime event ever held in Australia, attracting over 10 000 athletes and about 5100 officials from 200 countries, around 15 000 media people and 300 000 domestic and international visitors. The Games period will extend for 60 days; it commenced with the opening of the Olympic Athletes' Village on 2 September and ends with the closure of the Paralympic Athletes' Village on 1 November. During this period, there will be a succession of mass gatherings, including the opening and closing ceremonies and many Olympic-related activities in the city. An estimated 150 000 extra people a day will be in central Sydney between noon and 10 pm. On the night of the closing ceremony, 750 000 people will gravitate to the city centre to attend festivities, and up to 500 000 are expected on Sydney Harbour's foreshores for a fireworks spectacular. Mass gatherings, such as sporting events and outdoor celebrations, require public health and medical services to be provided for the large numbers of people who attend.1-4 Protecting the health of the Olympic "family" (athletes and officials), visitors and residents during the Sydney Olympic Games presents unique challenges. Public health planning commenced shortly after the 1993 announcement that Sydney was to host the 2000 Games. It covers counterdisaster planning,5 environmental hazard monitoring, and food safety strategies. Here, we describe selected public health issues associated with large mass gatherings and outline enhancements made to disease surveillance in Sydney prior to the Games. Morbidity and mass gatherings Injuries and death Although relatively rare, mass gatherings have been associated with significant morbidity and death. Examples include crowd crushes at Hillsborough Stadium in the United Kingdom,6 and more recently at a rock concert in Copenhagen; the collapse of a pedestrian bridge at the 1997 Maccabiah Games in Israel, which led to the deaths of four Australians and injuries to almost 60 other athletes; and terrorist activities resulted in 11 deaths at the Munich (1972) and one death at the Atlanta (1996) Olympic Games.7 Infectious agents Infectious disease outbreaks at mass gatherings are also uncommon. Between 1966 and 1993, a review article identified 38 reports of disease outbreaks or "other instances of transmission" of disease associated with competitive sports.8 In 24 of these outbreaks the disease was transmitted by person-to-person spread associated with contact sports (such as wrestling and rugby); the most common infectious agent identified was herpes simplex virus (12 reports). Other agents implicated in person-to-person spread have included enteroviruses (cocksackieviruses and echoviruses), with many reports indicating that infection was spread through shared water sources and drinking containers.8Infections transmitted through the air or by droplets (or both) have also been reported. This year, the largest recorded outbreak of serogroup W-935 meningococcal disease was reported to the World Health Organization.9 It involved 384 reported cases of meningococcal disease diagnosed in pilgrims from 12 countries who contracted the disease while attending the hajj in Mecca; 71 died.10 In 1991, there was an outbreak of measles in the United States at the International Special Olympic Games,10 a competition launched in 1968 to increase quality of life for people with intellectual disabilities.11 Sixteen US athletes, spectators and volunteers from seven different States were initially affected, followed by another nine (there was no follow-up among international delegations).12 The primary case was identified as a track and field athlete from Argentina, and transmission occurred during the opening ceremony (held in a domed stadium), during track and field events and at first aid stations. This outbreak is an example of the way an international sporting event can provide the means of transmission of measles even in a country where the disease is relatively uncommon. There are a number of particular considerations for the Sydney Olympic and Paralympic Games. The first is that nine cruise ships will be berthed in Sydney Harbour, acting as floating hotels for up to 32 000 guests. Outbreaks of disease, including gastroenteritis, Legionnaires' disease, influenza, and tuberculosis are well documented aboard cruise ships,13-18 and a number of gastroenteritis and influenza outbreaks have occurred on ships visiting Sydney.19-20 The closed environment and controlled ventilation systems aboard ships create the potential for disease outbreaks to affect large numbers of individuals. Secondly, with increased international travel, a range of communicable diseases could be imported. For example, in 1996 tourists travelling in countries where yellow fever is endemic unknowingly imported the disease into the US and Switzerland.21 The same year saw approximately 10 000 reported cases of malaria imported into the European Community.21 Measles is now rare in New South Wales, and people with recent infections have acquired the disease overseas; if measles is encountered during the Games period, it is likely to be an imported strain. Thirdly, the Sydney Olympic and Paralympic Games will be held during spring, which, in our temperate climate, is a time generally associated with increased incidence of diseases like meningococcal infection and pertussis. Finally, an estimated 1.8 million meals will be served to athletes and officials and another one million to staff (John Shields, Food Safety Adviser, Olympic Planning Unit, personal communication), amplifying the potential for foodborne disease outbreaks. Public health services in Sydney during the XXVII Olympiad Public health issues associated with Olympic Games have been recognised and reported since the XIX Olympiad in Mexico City in 1968.22 Public health preparations and surveillance during the Sydney 2000 Olympic Games are based on the experience of previous Olympic Games (Box 1), particularly Atlanta. Routine surveillance of public health conditions in NSW is conducted through 17 Public Health Units in Area Health Services and a centralised Public Health Division within the NSW Health Department (NSW Health). Under the NSW Public Health Act (1991), medical practitioners, hospital chief executives (or general managers), pathology laboratories, directors of childcare centres and school principals are required to notify certain medical conditions to the local public health unit. These data are entered into the NSW Notifiable Diseases Database (NDD) and used to track the incidence of communicable diseases across the State and monitor risks and trends to enable direct intervention to control transmission. The NDD has been effectively used to detect, confirm and monitor outbreaks in NSW. Recent examples include hepatitis A associated with the consumption of oysters,27 hepatitis A among drug users in Kings Cross28 and a cluster of cases of haemolytic-uraemic syndrome.29 The NSW Health Olympic Surveillance System Existing NSW Health structures will be enhanced during the Games and strategic public health decisions facilitated through a centralised NSW Health Olympic Coordination Centre, which will review emerging public health issues daily. The NSW Health Olympic Surveillance System (OSS) will be used to monitor acute disease outbreaks and potentially preventable injuries. This system integrates multiple data sources described in Box 2. It enhances existing mechanisms and includes new surveillance systems, giving particular attention to injury, food-borne diseases, conditions spread via the respiratory route and the need for rapid detection of clusters. Detecting unusual patterns of disease presents a particular challenge. At the Health Olympic Coordination Centre, a team of public health experts will examine the Emergency Department Olympic Surveillance System (EDOSS), food safety, environmental inspection and cruise ship trend data. Three-day moving averages will be used to assist in detecting unusual patterns of disease incidence. Detection of aberrations in the NDD data will be enhanced by using a statistical method to compute a normal confidence theory interval.30 This method can detect significant differences in incidence by comparing the current situation with historical data while adjusting for reporting delays and seasonality. The role of general practitioners during the Games Currently, in NSW, general practitioners should routinely report clusters of disease and notify scheduled medical conditions to the local public health unit (Box 3). During the Games, this role remains vital in the early detection of unusual patterns of disease. Many conditions are notifiable on clinical suspicion rather than waiting for confirmation of the diagnosis to allow early detection of disease and timely public health intervention. GPs should be particularly aware of reporting two or more related cases of gastroenteritis or foodborne illness. Infectious diseases uncommonly encountered in Sydney (such as malaria, dengue, cholera and typhoid) should be considered among travellers with unusual presentations. Surveillance system constraints All surveillance systems have limitations.31 The ability of the Olympic Surveillance System to detect unusual patterns of disease depends on: timely reporting of notifiable conditions by all concerned; presentation of "target cases" at emergency departments; and maintenance of electronic systems for data collection and transfer, and back-up options. To ensure the valididty of newly established data collections, a range of measures were undertaken. For example, EDOSS has been trialled at mass gatherings in Sydney over the past year (eg, Olympic Test Events [September 1999], New Year's Eve 1999-2000] and the Sydney Gay and Lesbian Mardi Gras [March 2000]). In May 2000, a full trial of the system was successfully undertaken in all participating hospitals. A validation of EDOSS test data assessed how many true target cases were missed (sensitivity) and how many of those cases identified failed to fulfil the target case criteria (specificity). EDOSS performed well on both measures, with sensitivity and specificity rates around 85%. Problems with identifying target cases were addressed in subsequent training sessions. Although the surveillance system is designed to detect disease clusters, small localised clusters of some diseases and injuries may not be identified because they are obscured by "background" levels. Measures such as enhanced reporting by laboratories and general practitioners may help overcome this. The notification of suspected clusters on clinical grounds by general practitioners is very important. Public health response In the event of a small disease cluster, public health units, in close collaboration with the Health Olympic Coordination Centre, will implement existing outbreak management plans.32 If unusual patterns of injury are detected, the geographical location will be provided by NSW Health to the relevant authorities, such as police or the Olympic Road and Traffic Authority. In the event of a major public health incident, investigations will be elevated to the State level. To assist any large-scale investigations, the telephone call-room used by the NSW Health Survey Program will be on stand-by to conduct interviews or provide information to the public. Also, public health investigation teams located in public health units on the periphery of metropolitan Sydney are on stand-by, to be deployed in the event of major public health incident. In the event that an emergency is declared, the coordination and control arrangements for any investigations will come under the provisions of the NSW Healthplan,33 which provides detailed procedures to coordinate all health services and resources within the State. Acknowledgements We acknowledge the contribution of Ross O'Donoghue, Tim Churches, John Kaldor, Sue Campbell-Lloyd, Rob Menzies, Mark Bartlett, Kerry Chant, Michael Hills, Peter Waples, Pam Albany, Michael Flynn, Karen Banwell, the staff at public health units and the sentinel hospitals: Auburn, Blacktown, Concord, Liverpool, Nepean, Prince of Wales, Royal Prince Alfred, St Vincent's, Sydney, Royal North Shore, Ryde, Sydney Children's, St George, The New Children's, and Westmead. References Stiel D, Trethowan P, Vance N. Medical planning for the Sydney 2000 Olympic and Paralympic Games. Med J Aust 1997; 167: 593-594. Green GB, Burnham G. Health care at mass gatherings. JAMA 1998; 279: 1485-1486. Leonard RB. Medical support for mass gatherings. Emerg Med Clin North Am 1996; 14: 383-397. Thompson JM, Savoia G, Powell G, et al. Level of medical care required for mass gatherings: the XV Winter Olympic Games in Calgary, Canada. Ann Emerg Med 1991; 20: 385-390. Evangeli A. Disaster planning: bioterrorism and the Olympics. Medicine Today July 2000: 148-153. Wardrope J, Ryan F, Clark G, et al. The Hillsborough tragedy. BMJ 1991; 303: 1381-1385. Meehan P, Toomey KE, Drinnon J, et al. Public Health Response for the 1996 Olympic Games. JAMA 1998; 279: 1469-1473. Goodman RA, Thacker SB, Solomon SL, et al. Infectious diseases in competitive sports. JAMA 1994; 271: 862-867. Centers for Disease Control. Serogroup W-135 meningococcal disease among travellers returning from Saudi Arabia-United States, 2000. MMWR Morb Mortal Wkly Rep 2000; 46: 345-346. World Health Organization. Disease outbreaks reported. 12 May 2000. Meningococcal disease, serogroup W135 -- update. 12 May 2000 <http://www.who.int/disease-outbreak-news/n2000/may/12may2000.html> (accessed August 2000). Feldman CA, Giniger M, Sanders M, et al. Special Olympics, special smiles: assessing the feasibility of epidemiologic data collection. J Am Dent Assoc 1997; 128: 1687-1696. Ehresmann KR, Hedberg CW, Grimm MB, et al. An outbreak of measles at an international sporting event with airborne transmission in a domed stadium. J Infect Dis 1995; 171: 679-683. Jernigan DB, Hofmann J, Cetron MS, Genese CA. Outbreak of Legionnaires' disease among cruise ship passengers exposed to a contaminated whirlpool spa. Lancet 1996; 347: 494-499. Distasio AJ II, Trump DH. The investigation of a tuberculosis outbreak in the closed environment of a US Navy ship, 1987. Military Med 1990; 155: 347-351. Christenson B, Lidin-Janson G, Kallings I. Outbreak of respiratory illness on board a ship cruising to ports in southern Europe and northern Africa. J Infection 1987; 14: 247-254. O'Mahony M, Noah ND, Evans B, Harper D. An outbreak of gastroenteritis on a passenger cruise ship. J Hyg (Lond) 1986; 97: 229-236. Waterman SH, Demarcus TA, Wells JG, Blake PA. Staphylococcal food poisoning on a cruise ship. Epidemiol Infect 1987; 99: 349-353. Rowbotham TJ. Legionellosis associated with ships: 1977 to 1997. Commun Dis Public Health 1998; 1: 146-151. Gupta L, Towler B, Frommer M. Investigation of an outbreak of gastroenteritis on a container ship returning from Asia. NSW Public Health Bull 1994; 5: 61-62 . Ferson MJ, Paraskevopoulos P, Hatzi S, et al. Presumptive summer influenza A: an outbreak on a trans-Tasman cruise. Commun Dis Intell 2000; 24: 45-47. World Health Organization. Global infectious disease surveillance. Fact sheet No. 200. June 1998. <http://www.who.int/inf-fs/en/fact200.html> (accessed August 2000). Thomas CL. Public health problems in the Olympic Games setting. JAMA 1968; 205: 130-132. Panella H, Plascenia A, Sanz M, et al. Evaluation of epidemiologic surveillance system for infectious diseases in the Barcelona Olympic Games 1992. Gaceta Sanitaria 1995; 47: 84-90. Wetterhall SF, Coulombier DM, Herndon JM, et al. Medical care delivery at 1996 Olympic Games. JAMA 1998; 279: 1463-1468. Weiss BP, Mascola L, Fannin SL. Public health at the 1984 Summer Olympics: the Los Angeles County experience. Am J Public Health 1988; 78: 686-688. Keim ME, Williams D. Hospital use by Olympic athletes during the 1996 Atlanta Olympic Games. Med J Aust 1997; 167: 603-605. Conaty S, Bird P, Bell G, et al. Hepatitis A in New South Wales, Australia from consumption of oysters: the first reported outbreak. Epidemiol Infect 2000; 124: 121-130. Delpech V, Thackway S, Young L, et al. Outbreak of Hepatitis A among illicit drug users in South Eastern Sydney [letter]. Med J Aust 1999; 175: 633. Bartlett M, McAnulty J, Rutherford A, et al. Haemolytic uraemic syndrome: a cluster of cases in early 1999. NSW Public Health Bull 1999; 10: 109-112. Stroup DF, Williamson D, Herndon J. Detection of aberrations in the occurrence of notifiable diseases surveillance data. Stat Med 1989; 8: 323-329. Teutsch SM, Churchill RE. Principles and practice in public health surveillance. Oxford: Oxford University Press, 1994. NSW Health Department. Notifiable diseases manual. 5th ed. Sydney: NSW Health, 2000. NSW Health Department. NSW Healthplan. Sydney: NSW Health, 1997. Authors' details NSW Health Department, Sydney, NSW. Sarah V Thackway, MPH, Manager, Olympic Surveillance, Olympic Planning Unit; Valerie C Delpech, FAFPHM, Medical Epidemiologist, Communicable Disease Surveillance and Control Unit; Louisa R Jorm, PhD, Director, Epidemiology and Surveillance Branch; Jeremy M McAnulty, FAFPHM, Manager, Communicable Disease Surveillance and Control Unit; Maria Visotina, MAdmin, Manager, Olympic Planning Unit. Reprints will not be available from the authors. Correspondence: Ms S Thackway, Olympic Planning Unit, NSW Health, Locked Mail Bag 961, North Sydney, NSW 2059. SATHAATdoh.health.nsw.gov.au Make a comment 1: Lessons from previous Olympic Games In most instances, existing surveillance systems were enhanced to monitor infectious disease outbreaks.7,23-26 During the 1992 Barcelona Games enhanced reporting for hepatitis, meningococcal disease, Legionnaires' disease and foodborne disease23 identified no increases in disease compared with the same period in previous years. However, there was an increase in reports of foodborne illness - particularly domestic foodborne illness - by emergency departments. At the 1996 Atlanta Games, enhanced surveillance of infectious diseases in eight sentinel hospitals and public health laboratories detected: No increase in emergency department presentations; No outbreaks of disease at Olympic venues despite increased reporting of gastrointestinal symptoms during the first week; and Management of 106 people at 11 emergency departments for injuries associated with the Olympic Park bombing (including 21 admissions and one death).7 Back to text 2: The NSW Health Olympic survellance System The Notifiable Diseases Database (NDD) reporting of all notifiable conditions has been enhanced in two ways. Firstly, laboratories will be contacted daily by metropolitan public health units to ensure timely reporting of notifiable diseases. Secondly, notification data from public health units will be transferred to a centralised location at NSW Health three times a day. The Emergency Department Olympic Surveillance System (EDOSS) has been implemented in 15 Sydney metropolitan hospital emergency departments to monitor cases of food-related illness, Legionnaires' disease, meningococcal disease, influenza, hepatitis A, pertussis and measles. Approximately 40 hospital staff will collect specific patient data on target cases upon arrival. Data will be entered into a database locally and sent electronically to the Health Olympic Coordination Centre at 8am daily for collation and analysis, thus making EDOSS an early warning system. EDOSS will operate from three weeks before the Games until after the closure of the Olympic Village. National and global epidemic surveillance: National trends in infectious diseases will be regularly reviewed through the Communicable Disease Network of Australia and New Zealand. Data from the World Health Organization and ProMed (a resource of the International Society for Infectious Diseases for Monitoring Emerging Diseases) will be reviewed to provide information on global trends. The Vessel Inspection Program has been modelled on the American Vessel Sanitation Program operated by the United States Centers for Disease Control and Prevention. Cruise ship medical staff are required to report notifiable conditions and complete daily reports outlining the number of passengers on board, the number of medical consultations, hospitalisations, deaths and cases of influenza-like illness, suspected pneumonia and gastroenteritis. Influenza surveillance: Trends in influenza will continue to be monitored by combining reports from major laboratories and clinical data from general practitioners in the Australian Sentinel Practice Research Network. Food safety monitoring: Since early 1999, metropolitan public health units and local councils have enhanced food hygiene surveillance for food premises. This program will play an important role in minimising the occurrence of foodborne illness outside Olympic venues. In addition, NSW Health and local government officers will inspect food premises inside Olympic venues and delivery and distribution outlets to ensure compliance with food hygiene standards. Summary inspection reports will be relayed daily to NSW Health. Environmental inspection program: Priority has been given to minimising risk associated with Cryptosporidium in pools and Legionnaires' disease in water cooling towers. All water-cooling systems, clinical waste management services, toilet hygiene and general public health safety matters at Olympic and Paralympic venues will be inspected before sporting events commence. Waste and toilet services will be routinely inspected and summary inspection reports relayed daily to NSW Health. Back to text 3: Conditions notifiable by doctors under the NSW Public Health Act (1991) Acute viral hepatitis Adverse event following vaccination AIDS Foodborne illness in two or more related cases Gastroenteritis in two or more related cases Leprosy Measles Pertussis (whooping cough) Syphilis Tuberculosis Back to text

Sarah V Thackway · Valerie C Delpech · Louisa R Jorm · Jeremy M McAnulty · Maria Visotina

Personal Perspective The New South Wales Drug Summit: a view from a local foreign observer Jeffrey H Samet MJA 2000; 173: 264-265 1. "The Drug Summit was just a political exhibition" - 2. "All agree on one thing" - 3. "I hope that this forum does not end up as some sort of factionalised debate" - Acknowledgements - References - Authors' details - - More articles on Drugs and alcohol In December 1998, on sabbatical leave from Boston University School of Medicine, I spent time at the University of Sydney's Faculty of Medicine, because I thought that the Australian experience had something special to teach those of us in the United States working on the "drug problem". The timing was remarkable -- illicit drug policy became a captivating major news topic, culminating in the Drug Summit in Sydney in May 1999.1 Drug abuse, despite its importance from personal, public health, public safety and economic perspectives, has not received comparable concerted public attention within the United States in a generation or more. The dynamics of the Australian discussion were fascinating, but certain opinions expressed seemed in need of reconsideration. 1. "The Drug Summit was just a political exhibition -- nothing useful will come of it." This point of view, prevalent before and during much of the Drug Summit, was extremely cynical and not constructive. Not acknowledging the existence of a problem is a very well known practice in the world of drugs and alcohol. In fact, the first goal in the treatment of patients who misuse drugs is getting them to acknowledge that a problem exists.2No one expects to fix the problem the first few times it is addressed. The same perspective should frame the discussion about activities that recently took place in the New South Wales Parliament. Firstly, it was significant that the drug issue was widely acknowledged as a major societal problem. Secondly, it was remarkable that politicians joined together with the most experienced professionals and affected individuals to search for understanding and common ground on how to address the issue. This phenomenon should be recognised for what it was: major progress. The summit enabled politicians to gain, at minimum, a basic understanding of the issues of addiction and substance misuse. Politicians will in future be better able to assess drug policy proposals. The extensive media coverage educated Australia's citizens, both adults and young people, about the realities of falling victim to mind-altering substances. It reminded members of society that drug abuse is a scourge and the reality of drug addiction is painful and sad. History teaches us that this lesson is all too quickly forgotten, and such refresher lessons play a valuable role.3 The Drug Summit's very existence was a very important and useful event. Cynicism was inappropriate. 2. "All agree on one thing, nothing in the past has been successful." One early conclusion, announced after the first day of the Summit, was a condemnation of past efforts. Australian newspaper headlines echoed the theme of past failures. This summary critique was not an appropriate keynote to an Australian drug summit. Absence of either a cure or a recipe for prevention does not equate with a past record of failure. Clearly, the drug problem is huge and ever in need of innovative approaches to combat it; nonetheless, Australia has much about which to be proud in its approach to illicit drug use. One in four injecting drug users in the United States are infected with HIV.4 As a consequence, the individual suffering, high costs of medical care, and transmission to non-injecting partners and newborns are immense burdens on society. This scenario has been largely avoided in Australia, where fewer than 3 in 100 injecting drug users are infected with HIV.5,6 This is success, incredible success, and hopefully not ephemeral success. The existence of a treatment system in which thousands of individuals each year in Australia get help in their struggle to deal with their addiction is progress. Of course, striving to expand and improve the quality of those services and the institution of trials to find innovative new approaches are required, but there has been unequivocal progress in this field. Research successes are also notable. The best data in the world on heroin overdose have been collected and analysed by the Australian National Drug and Alcohol Research Centre.7,8 As a result, approaches to intervention have been developed and this "silent epidemic" is no longer silent in Australia. HIV prevention, extensive treatment (even if insufficient), and innovative practical research are recognised Australian successes in this field. 3. "I hope that this forum does not end up as some sort of factionalised debate ... -- a war on drugs versus legalisation; zero tolerance versus harm reduction." The discourse at the Drug Summit covered important issues, but the terms used in the illicit drug policy discussion often got confused. Consequently, some messages were at risk of misinterpretation. "Harm reduction" is not synonymous with "legalisation". The goals are different. The message is different. Equating these terms does injustice to both issues. There are data to support the effectiveness of some harm reduction efforts and there is a desire to collect data for other proposed harm reduction efforts.9,10 This situation is quite different from a theoretical discussion of the harms and benefits of legalisation of certain aspects of illicit drug use. The latter is a public policy question with enormous potential consequences unlikely to be subjected to the rigours of scientific testing to assess efficacy. On the other hand, it is very useful to subject novel approaches to harm reduction to the careful scrutiny of clinical trials before broader dissemination. The inappropriate equating of these terms is detrimental and should be strongly resisted. It is important to realise that drug problems are an area where agreement on desirable outcomes is possible. The path to those outcomes has been hampered by a disturbing and remarkable amount of factional debate. In this most useful public health discussion, absence of cynicism, recognition of past success, and clarity of terms will serve to remove impediments from a struggle that will continue long after the wonderfully focused efforts of the NSW Drug Summit have become a fading memory. We in the United States can learn from Australia's willingness to publicly confront these issues. Acknowledgements I am indebted to Drs James Rankin, Paul Haber, Alex Wodak and Wayne Hall, who were so kind to me during my sabbatical term in Australia and who provided feedback about this manuscript. Without their openness and generosity of spirit I would not have had the opportunity to see what I saw or write what I wrote. References Swan N. Drug doings down under. JAMA 1999; 281: 1782-1783. Samet JH, Rollnick S, Barnes H. Beyond CAGE: a brief clinical approach after detection of substance abuse. Arch Intern Med 1996; 156: 2287-2293. Musto D. The American disease: origins of narcotic control. New York: Oxford University Press, 1987. Centers for Disease Control and Prevention. HIV/AIDS surveillance report. 1997; 9(2): 1-44. Kaldor JM, Elford J, Wodak AD, et al. HIV prevalence among IDUs in Australia: a methodological review. Drug Alcohol Rev 1993; 12: 175-184. MacDonald M, Wodak AD, Ali R, et al. HIV prevalence and risk behaviour in needle exchange attenders: a national study. Med J Aust 1997; 166: 237-240. Darke S, Ross J, Hall W. Overdose among heroin users in Sydney, Australia I. Prevalence and correlates of non-fatal overdose. Addiction 1996; 91: 405-411. Darke S, Ross J, Hall W. Overdose among heroin users in Sydney, Australia I. Responses to overdose. Addiction 1996; 91: 413-417. Hurley SF, Jolley DJ, Kaldor JM. Effectiveness of needle-exchange programmes for prevention of HIV infection. Lancet 1997; 349: 1797-1800. Drucker E, Lurie P, Wodak A, Alcabes P. Measuring harm reduction: the effects of needle and syringe exchange programs and methadone maintenance on the ecology of HIV. AIDS 1998; 12(Suppl A): S217-S230. Authors' details Section of General Internal Medicine and the Clinical Addiction Research and Education (CARE) Unit, Departments of Medicine and Social and Behavioral Sciences, Boston University Schools of Medicine and Public Health, Boston, MA. Jeffrey H Samet, MD, MPH, Associate Professor of Medicine and Public Health. Reprints: Associate Professor J H Samet, Section of General Internal Medicine, Research Unit, 91 East Concord Street, Suite 200, Boston Medical Center, Boston, Massachusetts, 02118 USA. jsametATbu.edu Make a comment

Jeffrey H Samet

Editorial SIDS: facts and controversies We need to promote the established risk-reducing behaviours, which are based on strong scientific evidence MJA 2000; 173: 173-174 Over the period 1982-1986, Australian Bureau of Statistics figures show that there were an average of 457 deaths per year from sudden infant death syndrome (SIDS) in Australia (1.89 deaths/1000 live births).1 Ten years later, over the period 1992-1996, SIDS mortality had plummeted to 210 deaths per year (0.81 deaths/1000 live births).1In spite of this dramatic decrease, SIDS still causes more deaths than traffic injuries, congenital anomalies and cancer combined in the 1-4 years age group.1 Here, I briefly discuss the established risk factors for SIDS and current areas of controversy. Sleeping position: Studies dating back to the 1960s, but mostly in the 1980s, had suggested that prone sleeping position was associated with SIDS, but it was not until SIDS prevention campaigns had been successfully run in the Netherlands and New Zealand that the potential for reducing SIDS mortality by modifying this risk factor was recognised.2 In 1991, Australia launched its "Reducing the Risk" campaign, driven by SIDS organisations and supported by Red Nose Day funds. In New Zealand, we observed a close temporal relationship between Red Nose Day education campaigns and reduction in the prevalence of placing infants in the prone sleeping position.3 This illustrates the powerful synergy that can be created when professional and voluntary/parent groups work together. The fall in SIDS mortality can be attributed almost entirely to a change in the prevalence of placing infants in the prone sleeping position,4 supporting the contention that prone sleeping is part of the causal pathway and is a cause of SIDS. Recent evidence suggests that sleeping on the side doubles the risk of SIDS compared with sleeping in a supine position, probably because of infants turning to the prone position ("secondary prone").5 Infants who usually sleep supine but are placed prone (ie, are unaccustomed to the prone position) are at very high risk of SIDS.6,7 Smoking: Maternal smoking is the other major non-controversial risk factor for SIDS.8 Since the reduction in the prevalence of prone sleeping position, there have been eight studies examining maternal smoking and SIDS. The pooled unadjusted (not adjusted for confounders) relative risk (RR) determined from these studies is 4.7, which suggests that infants of mothers who smoke are at an almost fivefold greater risk of SIDS than infants of mothers who do not smoke. Evidence for the effect of environmental tobacco smoke exposure can be obtained by examining the risk of SIDS from paternal smoking where the mother is a non-smoker. There have been six such studies. The pooled unadjusted RR for these studies was 1.4. The increased risk of SIDS with tobacco smoke is probably predominantly due to an in-utero effect of tobacco smoke rather than postnatal environmental tobacco smoke.8 Bedding and clothing: Excess bedding and clothing have been shown to increase the risk of SIDS in infants sleeping prone, but not for infants sleeping on their side or back. As few infants in Australia sleep prone,4advice on the amount of bedding and clothing could be dropped. Some 15%-20% of infants who die of SIDS are found with their head covered by bedding.9 Covering of the head might cause death by forcing an infant to rebreathe expired gases or by creating thermal stress. There have been several suggestions as to how to avoid covering of the head, including tucking bedding in firmly, removing bedding, placing infants at the foot of the cot, using the Dutch sleeping sack, and avoiding the use of duvets. The evidence to support these recommendations is limited. Bed sharing: It is well established that infants who share a bed with mothers who smoked during the pregnancy are at increased risk of SIDS.5 Whether or not there is an increased risk for infants sharing a bed with mothers who were non-smokers has not been firmly established. If there is an increased risk it is likely to be quite small (pooled unadjusted RR, 1.4). Complicating the picture is the fact that in some cultures bed sharing is an established practice. Furthermore, others have advocated bed sharing to improve breastfeeding rates.10 Breastfeeding: Most studies have shown that the incidence of SIDS is lower in breastfed infants. However, breastfeeding in most developed countries is associated with socioeconomic advantage, and, when adjustment is made for socioeconomic factors, the protective effect of breastfeeding is less apparent.11,12 Some have concluded there is no decreased risk from breastfeeding,12 whereas others have argued that breastfeeding has a protective effect.11 Use of pacifier: An unexpected finding of several studies has been that pacifiers are associated with a reduced risk of SIDS.13 However, this benefit needs to be balanced against possible detrimental effects of pacifiers, such as a reduction in breastfeeding and increased incidence of otitis media.14 Vaccinations: In the past there was concern that vaccinations might cause SIDS, as the peak age for SIDS is 2-4 months, which coincides with the age for vaccinations. However, studies have shown that vaccinations are not associated with an increased risk of SIDS -- indeed, some studies have shown a reduced risk of SIDS at the time of vaccinations.15 Despite this, the media from time to time revive this old chestnut. "Toxic gas": The "toxic gas" theory has received considerable media attention in the United Kingdom and New Zealand, but has not been substantiated.16 According to this theory, toxic gases are produced by the fungus Scopulariopsis brevicaulis as it metabolises chemicals containing arsenic, antimony and phosphorus in cot mattresses. Proponents of the theory recommend wrapping cot mattresses in polythene, but this is potentially dangerous advice in view of the evidence that plastic sheeting in a baby's sleeping environment can cause death through suffocation.17 Despite the success of the "Reducing the Risk" campaign, SIDS mortality remains unacceptably high among Indigenous Australians (mortality rates for the period 1992-1996, aggregated for South Australia, Western Australia and the Northern Territory, were 30 deaths per year among Indigenous Australians [5.29 deaths/1000 population] compared with 61 deaths/year among non-Indigenous Australians [0.81 deaths/1000 population]). The cause or causes of SIDS remain largely unknown, although the most likely mechanisms include airway obstruction, rebreathing of expired gases, thermal stress and an "arousal defect" (reduced ability to respond to hypoxia or hypercapnoea by arousing or waking up). There is now little support for the (central) apnoea hypothesis, which was the major mechanism postulated in the 1970s and 1980s. Physiologists need to show how the established risk factors might operate, and researchers need to explore the reasons for the high rate of SIDS in disadvantaged and Indigenous communities. We must also continue to promote the established risk-reducing behaviours, which are based on strong scientific evidence, and ensure that all new mothers receive this information. We need to devise and evaluate innovative methods for delivering these messages and changing behaviour among disadvantaged and Indigenous groups. New theories should be examined, and discredited ideas buried. The media have an important responsibility, as they are in a position either to create controversy and confusion about SIDS or to serve as a powerful force for producing change. Ed A Mitchell Associate Professor in Paediatrics Department of Paediatrics University of Auckland, New Zealand. e.mitchellATauckland.ac.nz Acknowledgement: I am grateful to the Australian Bureau of Statistics for supplying mortality data. Australian Bureau of Statistics website <http://www.abs.gov.au> Engelberts AC, de Jonge GA. Choice of sleeping position for infants: possible association with cot death. Arch Dis Child 1990; 65: 462-467. Mitchell EA, Tonkin S. Publicity and infants' sleeping position. BMJ 1993; 306: 858. Dwyer T, Ponsonby AL, Blizzard CL, et al. The contribution of changes in the prevalence of prone sleeping position to the decline in SIDS in Tasmania. JAMA 1995; 273: 783-789. Scragg RKR, Mitchell EA. Side sleeping position and bed sharing in the sudden infant death syndrome. Ann Med 1998; 30: 345-349. L'Hoir MP, Engelberts AC, van Well GT, et al. Risk and preventive factors for cot death in The Netherlands, a low-incidence country. Eur J Pediatr 1998; 157: 681-688. Mitchell EA, Thach BT, Thompson JMD, Williams S. Changing infants' sleep position increases risk of sudden infant death syndrome. Arch Pediatr Adolesc Med 1999; 153: 1136-1141. Mitchell EA, Milerad J. Smoking and sudden infant death syndrome. In: International consultation on environmental tobacco smoke (ETS) and child health. Geneva: World Health Organization, 1999: 105-129. Beal SM, Byard RW. Accidental death or sudden infant death syndrome? J Paediatr Child Health 1994; 30: 144-150. McKenna JJ, Mosko SS, Richard CA. Bedsharing promotes breastfeeding. Pediatrics 1997; 100: 214-219. Ford RP, Taylor BJ, Mitchell EA, et al. Breastfeeding and the risk of sudden infant death syndrome. Int J Epidemiol 1993; 22: 885-890. Fleming PJ, Blair PS, Bacon C, et al. Environment of infants during sleep and risk of the sudden infant death syndrome: results of 1993-5 case-control study for confidential inquiry into stillbirths and deaths in infancy. Confidential Enquiry into Stillbirths and Deaths Regional Coordinators and Researchers. BMJ 1996; 313: 191-195. Fleming PJ, Blair PS, Pollard K, et al. Pacifier use and sudden infant death syndrome: results from the CEDI/SUDI case control study. Arch Dis Child 1999; 81: 112-116. Hunt L, Fleming P, Golding J. Does the supine sleeping position have any adverse effects on the child? I. Health in the first six months. The ALSPAC Study Team. Pediatrics 1997; 100: E11. Hoffman HJ, Hunter JC, Damus K, et al. Diphtheria-tetanus-pertussis immunization and sudden infant death: results of the National Institute of Child Health and Human Development Cooperative Epidemiological Study of sudden infant death risk factors. Pediatrics 1987; 79: 598-611. Expert Group to Investigate Cot Death Theories: toxic gas hypothesis. Chairman, Lady Limerick. Final report. London: Department of Health. May 1998. Kraus JF. Effectiveness of measures to prevent unintentional deaths of infants and children from suffocation and strangulation. Public Health Rep 1985; 100: 231-240. Make a comment

Ed A Mitchell

In December 1998, a 37-year-old Queensland woman died from a rabies-like illness, 27 months after being bitten by a flying fox (fruit bat). Molecular techniques enabled diagnosis of infection with Australian bat lyssavirus (ABL), the second human case to be recognised and the first to be acquired from a flying fox. It must be assumed that any bat in Australia could transmit ABL; anyone bitten or scratched by a bat should immediately wash the wounds thoroughly with soap and water and promptly seek medical advice. The Australian bat lyssavirus (ABL) was first recognised in June 1996.1 It was subsequently shown not only to belong to a new genotype within the Lyssavirus genus, but also to be more closely related to classic rabies virus than any of the other five genotypes of lyssavirus.2 The first recognised human infection with ABL was in November 19961,3 (Box 1). The patient died from a rabies-like illness 20 days after first becoming unwell. She had apparently been bitten by a yellow-bellied sheathtail bat (Saccolaimus flaviventris; an insectivorous bat) about 4.5 weeks before onset of the illness (R Taylor, Public Health Physician, Rockhampton, QLD, personal communication). We describe here the features of the second recognised human infection with ABL, which had a much longer incubation period and was transmitted by a flying fox (fruit bat; Pteropus sp.). Clinical record A 37-year-old woman was admitted to Mackay Base Hospital in late November 1998 with a five-day history of fever, vomiting, anorexia, pain about the left shoulder girdle, paraesthesiae about the dorsum of her left hand and sore throat with difficulty swallowing. On examination she was acutely ill but well oriented. She was unable to fully open her mouth, was drooling saliva and had difficulty speaking. She was febrile (38 degrees C) but normotensive. Muscle tone was increased, and examination occasionally provoked painful spasms. Examination of the throat provoked spasmodic attempts to swallow. Apart from neutrophilia (12.0 x 109/L; reference range, 2.0-8.0 x 109/L), routine haematological and biochemical tests gave normal results. Twelve hours later her condition had deteriorated considerably, with increased agitation, dysphagia and dysphonia, and the muscular spasms had become more frequent and severe. She was paralysed and ventilated. At about this time, a history of a bat bite was elicited, and a diagnosis of ABL infection was considered. Cerebrospinal fluid (CSF), serum and saliva were submitted for testing. An attempt on Day 2 of hospitalisation to cease artificial ventilation was unsuccessful; when the sedative dose was reduced, she was no longer able to communicate and did not appear to understand verbal commands. Thereafter, she remained ventilator-dependent; whenever the dose of muscle relaxants was reduced, purposeless movements, such as facial grimacing and rolling eye movements, and muscular spasms, such as arching of the back, became evident. Another prominent feature of the illness was marked fluctuations of body temperature and blood pressure. On Day 4 of hospitalisation, the reference laboratory reported that a polymerase chain reaction (PCR) had detected what appeared to be a specific ABL product in the saliva. Nursing and medical staff were informed of the probable diagnosis of ABL infection, and appropriate precautions were implemented.4 The diagnosis of ABL infection was confirmed four days later. On Day 14 of hospitalisation, the patient ceased spontaneous movements and respiratory effort. Ventilator support was withdrawn; she died 19 days after onset of the illness. Post-exposure treatment (PET) was provided to seven healthcare workers because of possible percutaneous or mucous membrane exposure to the patient's saliva.4,5 The patient had attended an evening barbecue in late August 1996, 27 months before onset of the illness (Box 1). At the function, a flying fox had suddenly landed on the back of a young child. In the course of removing it, the patient was bitten at the base of her fifth left finger. Two days later, she presented to her general practitioner and was given tetanus toxoid and appropriate antibiotics. Six months later, in early March, she returned to the GP, asking about a blood test for the "bat virus". She was advised that she should instead receive PET because of a potential exposure to ABL, but decided against this. As soon as the diagnosis of ABL infection was confirmed, PET was administered to the child and to four other people exposed to the flying fox at the barbecue. Diagnostic studies No antibodies to Japanese encephalitis (JE), Murray Valley encephalitis, Kunjin or rabies viruses were detected by enzyme immunoassay tests of serum and CSF collected on Day 2 of hospitalisation. Attempts were made to culture virus by inoculating serum, CSF and saliva onto monolayers of C636, BHK-21, Vero and mouse neuroblastoma cells, but no viruses were isolated. Serum, CSF and saliva were examined for RNA of JE virus, Hendra virus (formerly known as equine morbillivirus) by in-house reverse transcriptase PCR, and for RNA of ABL by heminested reverse transcriptase PCR.6 No viral RNA was detected in serum or CSF, and neither JE nor Hendra virus RNA was detected in saliva. However, the heminested PCR for ABL in saliva produced amplicons of the expected size6 in both first- and second-round reactions (600 and 586 base pairs, respectively). Nucleotide sequencing showed that the amplicon was a lyssavirus-specific product that differed from any other ABL held at the reference laboratory. Concurrently, products from the amplification were separated electrophoretically, transferred onto a nylon membrane7 and hybridised with a digoxigenin-labelled ABL-specific probe. The probe hybridised with the control virus and with amplicons generated from the saliva, indicating that the amplicons were indeed lyssavirus-specific products. Postmortem studies Light microscopy revealed widespread and severe encephalitis affecting all parts of the brain other than the cerebellum. Inflammation and necrosis were particularly severe in the brainstem and hippocampi, where most neurones had either completely disappeared or were necrotic. There was perivascular cuffing by lymphocytes and diffuse infiltration of grey matter neuropile by microglia and lipid-laden macrophages. Occasional neurones showed neuronophagia. A few cytoplasmic inclusion bodies were seen, particularly in the hypothalamus. Light microscopy also revealed diffuse pancarditis with focal myocyte destruction and infiltration of epicardial nerve branches with mononuclear cells. There was no evidence of viral inclusions in acinar or ductal epithelial cells of the parotid and submandibular glands, but nerve bundles in each were infiltrated by mononuclear cells. Spinal cord, brainstem, cerebellum, midbrain and both cerebral hemispheres were examined by immunofluorescent antibody staining. Intense fluorescence was observed in all impression smears, indicating the widespread presence of ABL (Box 2). RNA extracted from these brain samples, as well as salivary and adrenal glands, was tested for ABL by heminested PCR; all samples were strongly positive. Portions of each tissue section were cultured with mouse neuroblastoma cells. PCR indicated successful virus isolation from brain and spinal cord after the first blind passage (Day 7 after inoculation), while specific immunofluorescent antibody staining of cells, indicating presence of ABL, was evident after the second blind passage (Day 14). Sequencing of the PCR product from the cell cultures confirmed that the isolate was the flying-fox variant of ABL. Public health responses As soon as the patient's diagnosis was announced in the media, requests for PET increased markedly throughout Queensland. Many requests were for exposures that had occurred many months, sometimes years, previously. Five hundred and eighteen courses were requested between December 1998 and February 1999 (inclusive), compared with 24 courses in the same three months the previous year, and 59 courses in the preceding three months (Box 3). Discussion The clinical presentation, duration and course of the patient's illness were virtually indistinguishable from those seen in rabies. A short, non-specific prodrome was followed by inexorable progression through distinct stages, culminating, after a relatively short illness, in coma and death. Pain and paraesthesiae about the site of the bite and signs of autonomic instability, such as hypersalivation and labile blood pressure, are also commonly seen in rabies.8 The histological features in the brain were similar to those seen in rabies, including the pathognomonic Negri-like inclusion bodies.8 Findings similar to those seen in the heart and salivary glands have been described in patients who died of rabies.9 Monoclonal antibody and molecular sequencing studies have shown distinct variants of rabies virus, each associated with a dominant mammalian reservoir.10 The first reported patient with ABL infection was infected with the virus variant associated with yellow-bellied sheathtail bats (A Gould, Senior Principal Research Officer, Australian Animal Health Laboratory, Geelong, Vic, personal communication), and, as expected, our patient was infected with the flying-fox variant. ABL has been found in all four Australian flying fox species, and, to date, all ABL-infected bats have been either unwell or dead at the time of collection.11 An extraordinary feature of the patient's illness was the very long (27 months) incubation period. The usual incubation period for rabies is 20-90 days, and 95% of cases occur within a year of exposure.8 Although rare, prolonged incubation periods have been reported,12,13 but the reason for the prolongation has not been established. Even if the patient had accepted the recommended PET, it is uncertain whether the illness would have been prevented. This is because the guidelines at the time recommended vaccine only, without rabies immunoglobulin, as treatment after a bat exposure more than three months previously.5 Rabies that occurred because PET was either delayed or did not include rabies immunoglobulin has been reported.14 The guidelines were subsequently changed to recommend rabies immunoglobulin for all bat exposures,15 but most public health authorities do not include this immunoglobulin if the potential exposure to ABL was more than 12 months previously. Media reporting of the patient's diagnosis was initially restrained but changed on her death, with some reports becoming blatantly alarmist. This media attention and the inherent concern about rabies contributed to intense public demand for PET from Queensland public health units. Although the cost of this PET was considerable, it was predominantly for "catch-up" treatments for those with historical exposures and therefore probably represents a "one-off" expense. This case reminds that ABL infection, although rare, is lethal. Any bat in Australia must be assumed to have the potential to transmit the virus, and members of the public should therefore avoid handling bats. Anyone either bitten or scratched by a bat should immediately wash the wounds thoroughly with soap and water and promptly seek medical advice, regardless of the site or severity of the exposure. Acknowledgements Many people were involved in the management of the patient and in the public health responses. We wish to thank the nursing staff of the Intensive Care Unit, Mackay Base Hospital, and the Public Health Nurses, in particular Mrs Dorothy Symons, of the Tropical Public Health Unit Network. We also thank Ms Judy Northill and Mr Alan Westacott (Queensland Health Scientific Services) and Mr David Gould (Communicable Diseases Unit, Queensland Health). References

Jeffrey N Hanna · Ian K Carney · Greg A Smith · Joseph E Deverill · John A Botha · Ina L Serafin · Bruce J Harrower · Peter F Fitzpatrick · Jeffrey W Searle

Abstract Objectives: To compare rates of mortality from coronary heart disease (CHD) between populations living within and outside Australian capital city statistical divisions. Design and setting: Descriptive epidemiological study based on data for all residents of Australia aged 30-69 years who died between 1986 and 1996 in all States and Territories of Australia. Main outcome measures: Standardised mortality rates from all causes and coronary heart disease as coded by the Australian Bureau of Statistics, and estimated excess deaths in populations living outside capital city statistical divisions. Results: Between 1986 and 1996, mortality from CHD declined by 46% in men and 51% in women, and accounted for 61% of the decline in mortality from all causes in men and 48% in women. More deaths than expected from acute myocardial infarction resulted in mortality rates from CHD up to 30% higher in men and 21% higher in women living outside the capital city statistical divisions, and accounted for an overall estimated excess of 3835 deaths from CHD in men (32% of excess deaths from all causes), and 1385 deaths from CHD in women (27% of excess deaths from all causes) over the 11-year study period. Conclusions: Although there were impressive declines in coronary mortality in all Australian States and Territories from 1986 to 1996, populations living outside capital cities continue to have higher death rates from CHD. These differences in mortality rates indicate a need for further research into factors which may influence mortality rates for CHD in rural and remote areas, and immediate measures to ensure optimal treatment of coronary risk factors and acute coronary events in such populations. Coronary heart disease (CHD) remains the largest single cause of death in Australia.1 Although there has been a steady decline in the death rate associated with CHD over the past 30 years, rates of decline have not been equal throughout Australia.2,3 A study of coronary mortality in Tasmania showed higher rates of mortality outside the capital city region.4 We examined official data for Australian men and women aged 30-69 years between 1986 and 1996 for evidence of differences in rates of death from CHD between capital city and regional populations. Methods The Australian Bureau of Statistics (ABS) collects and disseminates social, demographic and economic statistics for 66 Statistical Divisions based on an Australian Standard Geographical Classification (ASGC).5 The boundaries of capital city statistical divisions are determined by the anticipated development of the city for a period of at least 20 years, and delimit an area that is stable for general statistical purposes. Statistical divisions outside a capital city are relatively homogeneous regions characterised by identifiable social and economic links between the inhabitants and between the economic units within the region, under the unifying influence of one or more major towns or cities. We obtained ABS estimates of the size of the Australian population aged 30-69 years, and its distribution between capital city and other statistical divisions for the years 1986 and 1996. We also obtained ABS data for mortality from all causes, and from CHD, acute myocardial infarction (AMI) and subacute and chronic myocardial ischaemia for men and women aged 30-69 years living within and outside capital city statistical divisions for each year from 1986 to 1996. We excluded deaths at 70 or more years because certification of the cause of death in older people may be unreliable.6 We defined mortality from CHD as deaths with an underlying cause classified under rubrics 410, 411, 413 and 414 of the International classification of diseases, ninth revision (ICD-9-CM),7 with mortality from AMI classified under ICD-9-CM rubric 410, and mortality from subacute and chronic myocardial ischaemia classified under rubrics 411, 413, 414. Statistical methods Annual age-standardised rates for mortality from all causes, CHD, AMI and subacute and chronic myocardial ischaemia were calculated as follows: The number of deaths in each age group (30-39, 40-49, 50-59 and 60-69 years), coded to each cause of death category, were summed. Age-specific rates were calculated and then standardised with weightings obtained from Segi's "world population" (World Health Organization standard population).8 The normal approximation for the distribution was used to calculate 95% confidence intervals. For each State and the Northern Territory, we calculated expected numbers of deaths in each age group for populations living outside capital city statistical divisions by applying age-specific mortality rates from populations living within the capital city statistical division. Differences between the actual (observed) number of deaths and the expected number of deaths were then summed across 10-year age strata to give total expected numbers of deaths. Excess deaths were calculated as the difference between the sum of the observed and the sum of the expected number of deaths for all States and the Northern Territory. The population of the Australian Capital Territory living outside the Canberra Statistical Division was less than 0.1% of the total population of the ACT and was not included in the calculation. Results Population size and distribution Unpublished regional population data from the ABS estimated that, in 1986, there were 7 174 246 Australians aged 30-69 years, 64.4% of whom lived in capital city statistical divisions. The sex distribution in capital cities was 49.9% men and 50.1% women, compared with 51.0% men and 49.0% women outside capital cities. By 1996, the estimated population of Australians aged 30-69 years had increased to 8 793 107, 63.5% of whom lived in capital city statistical divisions. The sex distribution in capital cities was 49.8% men and 50.2% women, compared with 50.7% men and 49.3% women outside capital cities. Trends in mortality rates among men Between 1986 and 1996, mortality from all causes in all 30-69-year-old Australian men declined by 23%; this decline within capital city statistical divisions was 25%, compared with 21% among men living outside capital city statistical divisions (Box 1). Mortality from all causes in populations outside the capital cities remained higher than in capital city populations, with the difference increasing from 12% in 1986 to 18% in 1996. Between 1986 and 1996, mortality from CHD in Australian men aged 30-69 years declined by 46% and accounted for 61% of the decline in all-cause mortality. Mortality among men living within capital city statistical divisions declined by 49%, compared with 41% among men living outside capital city statistical divisions (Box 1). Mortality from CHD in populations outside the capital cities remained higher than in capital city populations, with the difference increasing from 13% in 1986 to 30% in 1996. Mortality from AMI among men living within capital city statistical divisions declined by 62%, compared with 50% among men living outside capital city statistical divisions (Box 1). Mortality from AMI in men living outside the capital cities remained higher than in capital city populations, with the difference increasing from 24% in 1986 to 63% in 1996. Excess mortality outside capital city statistical divisions Box 2 shows that, among men, CHD accounts for 32% of the excess deaths from all causes from 1986 to 1996 occurring outside the capital city statistical divisions. Among those deaths coded as CHD, observed deaths from AMI exceeded expected deaths by 5487. The number of excess deaths from CHD is smaller than that from AMI, as there was a higher rate of death from subacute and chronic myocardial ischaemia in capital city populations. Observed deaths from AMI among men aged 30-39 years living outside capital city statistical divisions exceeded expected deaths by 79%; corresponding figures for the remaining age groups were 72% (40-49 years), 51% (50-59 years), and 25% (60-69 years). Trends in mortality rates among women Between 1986 and 1996, mortality from all causes in all 30-69-year-old Australian women declined by 21%; this decline within capital city statistical divisions was 24%, compared with 18% among women living outside capital city statistical divisions (Box 1). Mortality from all causes in populations outside the capital cities remained higher than in capital city populations, with the difference increasing from 6% in 1986 to 15% in 1996. Between 1986 and 1996, mortality from CHD in Australian women aged 30-69 years declined by 51% and accounted for 48% of the decline in all-cause mortality. Mortality among women living within capital city statistical divisions declined by 54%, compared with 50% among women living outside capital city statistical divisions (Box 1). Mortality from CHD in populations outside the capital cities remained higher than in capital city populations, with the difference increasing from 13% in 1986 to 21% in 1996. Mortality from AMI among women living within capital city statistical divisions declined by 59%, compared with 54% among women living outside capital city statistical divisions (Box 1). Mortality from AMI in women living outside the capital cities remained higher than in capital city populations, with the difference increasing from 24% in 1986 to 38% in 1996. Excess mortality outside capital city statistical divisions Box 2 shows that, among women, CHD accounts for 27% of the excess mortality from all causes occurring outside the capital city statistical divisions. Observed deaths from AMI exceeded expected deaths by 1479. Observed deaths from AMI among women aged 30-39 years living outside capital city statistical divisions exceeded expected deaths by 108%; corresponding figures for the remaining age groups were 75% (40-49 years), 44% (50-59 years), and 20% (60-69 years). Overall mortality Box 3 shows that death rates from CHD outside capital cities are consistently higher than within capital cities in all Australian States and the Northern Territory, the only exception being mortality from CHD among women in the Northern Territory in 1986. Discussion The contribution of reduced CHD mortality to the overall decline in all-cause mortality in Australia from 1986 to 1996 was 61% for men and 48% for women. However, our findings show that CHD mortality rates were higher outside capital cities, and that discrepancies increased from 1986 to 1996 and were largest in younger age groups. It is likely that the differences we found in CHD mortality are real, as they are matched by parallel trends in all-cause mortality rates, and at least two studies have confirmed the validity of deaths coded by the ABS to CHD.9,10 While a study based on 1979 data questioned the validity of subcategories of CHD such as rubric 410 (AMI),11 we found consistently higher death rates from AMI in populations outside capital cities in all Australian States and the Northern Territory (data not shown), despite variations in medical certification requirements between States. The apparent higher rates of mortality in capital city populations from subacute and chronic CHD may be the result of a coding anomaly or of deaths occurring in large population centres after patients were moved there for the management of their subacute or chronic CHD. Our study was limited to documenting the difference in CHD mortality between capital cities and other areas. Clearly, an understanding of the factors associated with higher CHD mortality outside capital cities has implications for prevention and improved treatment of CHD. This would require detailed examination of population characteristics to determine which populations outside capital cities, including subpopulations such as Indigenous people, are most at risk of higher mortality. It is also necessary to consider factors such as differences in socioeconomic status, in risk factors for CHD, and in access to medical care. Previous reports showed that the decline in mortality from CHD in NSW was slower in lower income populations, many of which were in rural or regional areas.12,13 Also, sudden cardiac death in Tasmanian men was found to occur twice as frequently in unemployed men compared with employed men.14 While the association between populations with lower socioeconomic status and higher risk for CHD is recognised, the actual factors that influence this association have not been well delineated. Risk factors for CHD clearly have an influence on mortality. Much of the decline in mortality from CHD in Finland from 1972 to 1992 can be explained by changes in the three main coronary risk factors: serum cholesterol level, blood pressure and smoking.15 In Australia, the National Heart Foundation (NHF) Risk Factor Prevalence Surveys found significant declines between 1980 and 1989 in the prevalence of hypertension and cigarette smoking, but no overall favourable trend in lipid levels.16 However, these surveys are limited to capital cities, and it is not known whether regional areas of Australia have seen the same trends in risk factor prevalence. In 1992, a major risk factor prevalence survey based on the 1989 NHF Risk Factor Prevalence Survey was undertaken in two rural regions of Tasmania. The prevalence of major coronary risk factors was consistent with the high rate of mortality from CHD among men in North-West Tasmania, but did not explain variation in rates of mortality in women across the three regions of Tasmania.17 Differences in mortality from CHD may be the result of differential incidences of CHD or differences in case-fatality rates. A detailed study of sudden cardiac death among previously asymptomatic men found that the higher rate of deaths in the two rural regions of Tasmania occurred mostly among men for whom symptomatic CHD could have been diagnosed, implying a higher case-fatality rate for CHD.14 This finding was supported by higher rates of coronary deaths occurring after hospitalisation in the two rural regions of Tasmania from 1986 to 1989,4 and in Newcastle in 1984.18 A higher case-fatality rate may result from differences in risk of death from factors such as previous infarction, delays in reaching medical care, or differences in medical care.19 While the relative geographic isolation of most populations outside the capital cities may be expected to result in delays in reaching secondary and tertiary medical centres, the findings of the MONICA study did not support changes in time to medical care (including ambulance staff) having a significant effect on deaths before hospitalisation in major population centres.18 A significant decline in case fatality after hospitalisation did, however, make an important contribution to the overall decline in coronary deaths in the MONICA centres of Auckland (New Zealand), Newcastle (Australia) and Perth (Australia) from 1984 to1993. Medical management of acute coronary events has changed substantially over the past 20 years. The use of aspirin, thrombolytic therapy and coronary angioplasty as first-line treatments for AMI has resulted in reductions in mortality of up to 43%.20,21 The use of thrombolytic therapy in the MONICA centres increased from being rare in the early 1980s, to being used in approximately 50% of hospitalised patients with non-fatal definite myocardial infarction or coronary death by the early 1990s.22,23 The benefits of such treatments are dependent on them being given soon after the event,24 and it is not clear whether populations living at any distance from secondary or tertiary medical centres experience delays in access to new treatment methods for symptomatic CHD. In southern Tasmania between 1992 and 1996, 849 doses of streptokinase and tissue plasminogen activator were administered for AMI. No thrombolytic therapy was administered outside the capital city of Hobart (Royal Hobart Hospital Pharmacy Supplies Report), despite 15% of the population of the Southern Region living outside the capital city and having mortality rates approximately 40% higher than the capital city population. In conclusion, although there have been impressive declines in mortality from CHD in all Australian States and Territories over the past 30 years, the 35% of the Australian population living outside the capital cities continue to have higher coronary mortality. Our results indicate the need for increased research into factors which may influence mortality rates for CHD in rural and remote areas. Acknowledgements This study was supported by funding from Roche Products Pty Ltd and the Tasmanian branch of the AMA, and by assistance in-kind from the Hobart City Council and Australian Hospital Care Ltd. We are grateful to Chris Sweeney from the Australian Bureau of Statistics and to the Pharmacy Department of the Royal Hobart Hospital. References Tonkin AM, Bennett S. Cardiovascular disease at the turn of the century. Med J Aust 1999; 170: 408-409. Gibberd RW, Dobson AJ, Florey C du Ve, Leeder SR. Differences and comparative declines in ischaemic heart disease mortality among sub-populations of Australia 1969-1978. Int J Epidemiol 1984; 13: 25-31. Sexton PT, Woodward DR, Gilbert N, Jamrozik K. Interstate differences in trends in coronary mortality and risk factors in Australia. Med J Aust 1990; 152: 531-534. Sexton PT, Jamrozik K, Walsh J, et al. Regional variation in coronary mortality within Tasmania. Med J Aust 1992; 157: 449-451. Australian Bureau of Statistics. Australian Standard Geographical Classification. Canberra: ABS, 1998. Christie D. Mortality from cardiovascular disease. Med J Aust 1974; 1: 390-393. National Coding Centre, Faculty of Health Sciences, University of Sydney. Australian version of the international classification of diseases. 9th revision, clinical modification (ICD-9-CM). 2nd ed. Vol.1: Tabular list of diseases. Sydney: NCC, University of Sydney, July 1996. Doll R. Comparison between registers, age-standardised rates. IARC Sci Publ 1976; 3: 453-459. Martin CA, Hobbs MST, Armstrong BK. Estimation of myocardial infarction mortality from routinely collected data in Western Australia. J Chron Dis 1987; 40: 661-669. Sexton PT, Jamrozik K, Walsh J. Death certification and coding for ischaemic heart disease in Tasmania. Aust N Z J Med 1992; 22: 114-118. Dobson AJ, Gibberd RW, Leeder SR. Death certification and coding for ischaemic heart disease in Australia. Am J Epidemiol 1983; 117: 397-405. Burnley IH. Inequalities in the transition of ischaemic heart disease mortality in New South Wales, Australia. Soc Sci Med 1998; 47: 1209-1222. Taylor R, Chey T, Bauman A, Webster I. Socio-economic, migrant and geographic differentials in coronary heart disease occurrence in New South Wales. Aust N Z J Public Health 1999; 23: 20-26. Sexton PT, Jamrozik K, Walsh J. Sudden unexpected cardiac death among Tasmanian men. Med J Aust 1993; 159: 467-470. Vartiainen E, Puska P, Pekkanen J, et al. Changes in risk factors explain changes in mortality from ischaemic heart disease in Finland. BMJ 1994; 309: 23-27. Bennett SA, Magnus P. Trends in cardiovascular risk factors in Australia. Results from the National Heart Foundation's Risk Factor Prevalence Study, 1980-1989. Med J Aust 1994; 161: 519-527. Thomson A, Rundle S, Singh BB, et al. Regional differences in cardiovascular risk factor prevalence in Tasmania: are they consistent with the increased cardiovascular mortality. Aust N Z J Med 1995; 25: 290-296. Beaglehole R, Stewart AW, Jackson R, et al. Declining rates of coronary heart disease in New Zealand and Australia, 1983-1993. Am J Epidemiol 1997; 145: 707-713. Beaglehole R. Medical management and the decline in mortality from coronary heart disease. BMJ 1986; 292: 33-35. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI). Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet 1986; 1: 397-402. Second International Study of Infarct Survival Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17 187 cases of suspected acute myocardial infarction: ISIS-2. Lancet 1988; 2: 349-360. Doggen CJM, van der Palen J, Beaglehole R. Trends in medical management of acute myocardial infarction. N Z Med J 1993; 106: 278-281. Dobson AJ, Jamrozik KD, Hobbs MST, et al. Medical care and case fatality from myocardial infarction and coronary death in Newcastle and Perth. Aust N Z J Med 1993; 23: 12-18. Bett JHN. LATE assessment of thrombolytic efficacy with alteplase (rt-PA) six-24 hours after onset of acute myocardial infarction. Aust N Z J Med 1993; 23: 745-748. (Received 23 Sep 1999, accepted 31 Jan 2000) Authors' details The Hobart Private Hospital, Hobart, TAS. Peter T Sexton, PhD, FAFPHM, Director of Medical Services; Tiina-Liisa H Sexton, BCom, CA, Research Assistant. Reprints: Dr P T Sexton, The Hobart Private Hospital, Cnr Argyle and Collins Streets, Hobart, TAS 7000. 1: Comparison of mortality rates between populations aged 30-69 years living within and outside capital cities in Australia Back to text 2: Estimated excess deaths from all causes, CHD and AMI among men and women living outside capital city statistical divisions from 1986 to 1996 Age group (years) 30-3940-4950-5960-69Total Men Mortality from all causes Observed deaths8599126982622760856108380 Expected deaths736310718216195672596425 Excess deaths123619804608413111955 Mortality from CHD (ICD-9-CM 410, 411, 413, 414) Observed deaths682270372391824128865 Expected deaths493209959021653625030 Excess deaths189604 133717053835 Mortality from AMI (ICD-9-CM 410) Observed deaths470197253341328721063 Expected deaths263114435411062815576 Excess deaths207828 179326595487 Women Mortality from all causes Observed deaths38877021138633146756238 Expected deaths32025998119722991851090 Excess deaths6851023189115495148 Mortality from CHD (ICD-9-CM 410, 411, 413, 414) Observed deaths143537 187869379495 Expected deaths91381 150361358110 Excess deaths52156 3758021385 Mortality from AMI (ICD-9-CM 410) Observed deaths102391 140050736966 Expected deaths49223 97242435487 Excess deaths53168 4288301479 CHD=coronary heart disease. AMI=acute myocardial infarction Back to text 3: Mortality within and outside capital city statistical divisions by Australian States and Territories Men Age-standardised mortality rate per 100000 (95% CI) % changeEstimated excess 1986 1996 per yeardeaths from CHD All causesCHDAll causesCHDfrom CHD1986-1996 New South Wales Capital722 (702-741)223 (212-234)511 (496-527)106 (99-113)-4.8 Balance761 (736-786)232 (218-246)601 (581-622)143 (133-153)-3.51506 Victoria Capital658 (638-678)199 (188-210)487 (470-503)97 (90-105)-4.7 Balance755 (722-789)242 (223-261)583 (556-611)131 (118-144)-4.21015 Queensland Capital691 (657-724)226 (207-245)549 (523-575)122 (109-134)-4.2 Balance754 (723-785)227 (210-245)585 (562-609)136 (125-147)-3.6444 South Australia Capital653 (619-687)213 (194-232)528 (499-557)125 (110-139)-3.8 Balance707 (650-764)234 (201-267)633 (583-683)160 (135-186)-2.9291 Western Australia Capital638 (603-673)183 (164-202)498 (471-525)102 (89-114)-4.0 Balance779 (716-841)249 (214-285)594 (546-642)121 (100-143)-4.7203 Tasmania Capital605 (526-684)141 (103-179)595 (520-669)102 (71-133)-2.5 Balance758 (685-831)276 (232-320)619 (558-680)144 (115-174)-4.3243 Northern Territory Capital640 (463-817)115 (46-185)716 (569-863)97 (36-158)-1.4 Balance1443 (1206-1679)233 (138-329)1030 (862-1199)132 (73-191)-3.9133 Australian Capital Territory 598 (521-675)205 (159-251)428 (372-484) 111 (82-140)-4.2 All of Australia Capital679 (668-690)209 (203-215)510 (501-519)107 (103-111)-4.4 Balance763 (747-778)237 (228-245)602 (590-614)139 (133-145)-3.83835 Women Age-standardised mortality rate per 100000 (95% CI) % changeEstimated excess 1986 1996 per yeardeaths from CHD All causesCHDAll causesCHDfrom CHD1986-1996 New South Wales Capital391 (377-405)82 (76-88)284 (273-296)32 (28-36)-5.5 Balance420 (401-439)89 (80-97)335 (319-350)45 (39-51)-4.5564 Victoria Capital360 (346-375)65 (59-72)274 (262-286)31 (27-35)-4.8 Balance361 (338-384)68 (58-77)307 (287-327)35 (28-41)-4.4277 Queensland Capital371 (347-395)67 (57-78)308 (288-328)39 (32-46)-3.8 Balance378 (355-400)75 (65-85)299 (282-316)36 (30-42)-4.7171 South Australia Capital347 (323-371)69 (58-79)285 (264-306)31 (24-38)-5.0 Balance291 (317-400)83 (64-103)339 (301-377)39 (26-52)-4.8143 Western Australia Capital349 (324-374)59 (49-70)275 (255-295)37 (30-45)-3.4 Balance386 (339-433)78 (296-372)334 (57-99)36 (24-49)-4.9105 Tasmania Capital424 (360-488)68 (42-93)365 (308-422)49 (28-70)22.5 Balance421 (367-475)87 (62-111)385 (336-434)54 (36-72)-3.462 Northern Territory Capital434 (271-597)46 (-10-103)392 (261-523)41 (-3-86)-1.0 Balance911 (702-1120)37 (-6-81)762 (593-932)88 (28-148)+12.563 Australian Capital Territory 380 (319-440)56 (32-80)267 (223-311)41 (23-59)-2.4 All of Australia Capital372 (363-380)71 (68-75)284 (278-291)33 (31-36)-4.9 Balance396 (384-407)80 (75-85)326 (317-335)40 (37-44)24.51385 CHD=coronary heart disease. Capital=within capital city statistical divisions. Balance=outside capital city statistical divisions. Back to Text

Peter T Sexton · Tiina-Liisa H Sexton

Abstract Objective: To describe the epidemiological pattern of newly diagnosed HIV infection and AIDS among Indigenous Australians. Design and setting: National surveillance for newly diagnosed HIV infection and AIDS in Australia. Information on Indigenous status was sought at HIV/AIDS notification in all State/Territory health jurisdictions, except the Australian Capital Territory, and Victoria before June 1998. Main outcome measures: Number of people with newly diagnosed HIV per year and population rate of HIV diagnosis; demographic characteristics of people with HIV and AIDS diagnoses by Indigenous status. Results: From 1992 to 1998, 127 Indigenous Australians were newly diagnosed with HIV infection and 55 were diagnosed with AIDS. The population rate of HIV diagnosis among Indigenous Australians (5.23/100 000 per year) was similar to that among non-Indigenous Australians (5.51/100 000 per year). The annual number of HIV diagnoses among Indigenous people was relatively stable, but among non-Indigenous people it declined steadily over time. A higher proportion of Indigenous people diagnosed with HIV were women (26.8% v 8.9%; P < 0.001). Although male homosexual contact was the predominant source of exposure for both Indigenous (46.7%) and non-Indigenous (75.0%) people with HIV infection, exposure by heterosexual contact (36.7% v 15.3%; P < 0.001) was reported more frequently among Indigenous people. Conclusion: Although HIV incidence was similar among Indigenous and non-Indigenous Australians, the lack of a recent decline in incidence and the higher proportion of Indigenous people exposed to HIV by heterosexual contact indicate the need to intensify interventions to prevent HIV transmission among Indigenous people. Introduction The epidemic of HIV transmission peaked in Australia in the mid 1980s, and there was a subsequent peak in AIDS incidence of nearly 1000 cases in 1994.1 The estimated number of people diagnosed with HIV infection in Australia to the end of 1998 was 16 714, with an estimated 11 800 living with HIV infection. Although the peaks of both the HIV and AIDS epidemics in Australia have passed, HIV infection continues to be transmitted, predominantly through male homosexual contact, at an estimated level of 450 cases per year.1 Despite evidence of a relatively well-controlled HIV epidemic in Australia, evaluation of the Third National HIV/AIDS Strategy noted an increase in the reported number of Indigenous Australians diagnosed with HIV infection in the early 1990s.1 Furthermore, high rates of other sexually transmissible infections in some Indigenous communities indicate the potential for HIV transmission.1 To define the pattern of HIV infection among Indigenous Australians, and to assess time trends in new diagnoses of HIV infection and AIDS, we examined national HIV and AIDS notification data by Indigenous status for the years 1992-1998. National Health and Medical Research Council guidelines on ethical matters in Aboriginal and Torres Strait Islander health research were followed.2 Methods National surveillance procedures Surveillance procedures for newly diagnosed HIV infection and AIDS have been described previously.3,4 Briefly, newly diagnosed HIV infection and AIDS are notifiable conditions in each State or Territory health jurisdiction in Australia. Information sought at national notification of newly diagnosed HIV infection includes the State or Territory of diagnosis, postcode of residence, namecode (based on the first two letters of the family name and the first two letters of the first given name), sex, date of birth, Indigenous status, date of HIV diagnosis, CD4 cell count at HIV diagnosis, evidence of newly acquired HIV infection, and patient-reported source of exposure to HIV. Information sought at AIDS notifications also includes the date of AIDS diagnosis, AIDS-defining illnesses, and use of antiretroviral therapy before AIDS diagnosis. People with newly diagnosed HIV infection with evidence of newly acquired HIV infection (ie, a negative or indeterminate HIV antibody test result or a diagnosis of HIV seroconversion illness within 12 months of HIV diagnosis) were defined as having "newly acquired HIV infection". People with AIDS were classified as having "late HIV diagnosis" if HIV infection was newly diagnosed within three months of AIDS diagnosis. Indigenous status From 1985, information on Indigenous status, obtained through self-identification as Aboriginal or Torres Strait Islander, was routinely sought at notification of HIV infection and AIDS for people newly diagnosed in the Northern Territory, Queensland, South Australia, Tasmania and Western Australia. In New South Wales, Indigenous status has been sought for newly diagnosed cases of HIV infection and AIDS since 1992. Indigenous status was not available for people with HIV infection or AIDS diagnosed in the Australian Capital Territory, or from Victoria before June 1998. Information on Indigenous status has been sought nationally from 1995; available information on Indigenous status for cases diagnosed before 1995 was obtained retrospectively through State or Territory health authorities. Exposure category HIV exposure was classified as male homosexual contact, male homosexual contact plus injecting drug use, injecting drug use, heterosexual contact only, haemophilia/coagulation disorder, receipt of blood or tissue, mother with or at risk for HIV infection, and other or undetermined exposure. Statistical analysis A χ2 or Fisher's exact test and odds ratios were used to test for differences between Indigenous and non-Indigenous cases with respect to demographic characteristics (sex, residence), newly acquired HIV 1infection, late HIV diagnosis, HIV exposure category, and individual AIDS-defining illnesses. Residence was divided into "metropolitan" and "non-metropolitan" on the basis of postcode. "Metropolitan" was defined as capital city (including Canberra), and "non-metropolitan" was defined as other than capital city. In the analyses, cases without information on Indigenous status were grouped with non-Indigenous cases. The population-based rate of HIV diagnosis was calculated by Indigenous status and year (for States and Territories other than Victoria and the ACT) using Australian Bureau of Statistics (ABS) census data for 1996.5 Results Information on Indigenous status was available for 91% of people with newly diagnosed HIV infection. For the period 1992-1998, 5313 cases of newly diagnosed HIV infection were notified to the national HIV surveillance centre, of which 127 (2.4%) were Indigenous cases. For the same period, 3638 AIDS cases were notified, of which 55 (1.5%) were Indigenous cases. The annual number of HIV diagnoses among Indigenous people was relatively stable over this period (Box 1). In contrast, the annual number of HIV diagnoses among non-Indigenous people gradually declined over the years 1992-1998. During this period, the annual HIV diagnosis rate per 100 000 population among Indigenous people (diagnosed in States and Territories other than Victoria and the ACT) (5.23) was similar to that among non-Indigenous people (5.51) (Box 1). A higher proportion of Indigenous people with HIV were female (26.8% v 8.9%; P < 0.001) (Box 2). The median age at HIV diagnosis (30 years v 33 years; P < 0.001) and AIDS diagnosis (32 v 37 years; P < 0.001) was lower among Indigenous cases. The pattern of exposure to HIV reported by Indigenous people was different from that reported by non-Indigenous people both for newly diagnosed HIV infection and AIDS (Box 2). Although male homosexual contact was the predominant source of exposure to HIV for both Indigenous (46.7%) and non-Indigenous (75.0%) people, a history of heterosexual contact only was reported more frequently by Indigenous people (36.7% v 15.3%; P < 0.001). The proportion of Indigenous and non-Indigenous people with AIDS with "late HIV diagnosis" was similar (23.6% and 18.3%; P = 0.42), as was the proportion reporting antiretroviral therapy before AIDS diagnosis (56.4% and 62.2%; P = 0.5). No difference between Indigenous and non-Indigenous cases was observed in the median CD4 cell count at diagnosis of HIV and of AIDS. The spectrum of AIDS-defining illnesses for Indigenous and non-Indigenous people with AIDS is shown in Box 3. Cryptococcal disease (odds ratio [OR], 3.3; 95% CI, 1.4-7.6; P = 0.004), oesophageal candidiasis (OR, 1.8; 95% CI, 0.95-3.38; P = 0.05), and atypical mycobacterium (OR 8.3; 95% CI, 2.4- 25.42; P = 0.002) were more frequent among Indigenous AIDS cases, whereas Kaposi's sarcoma was less frequent (OR, 0.12; 95% CI, 0.01-0.80; P = 0.01). Among people with HIV, there were more Indigenous than non-Indigenous cases in non-metropolitan locations (36% v 16%) (P < 0.01). Similarly, among people with AIDS, there were more Indigenous than non-Indigenous cases in non-metropolitan locations (37% v 19%) (P = 0.002). Discussion The HIV epidemic among Indigenous Australians has been relatively limited to date, with an overall rate of HIV diagnosis comparable with that for non-Indigenous Australians over the years 1992-1998. However, there have been contrasting trends in these rates, with a declining rate of HIV diagnosis among the non-Indigenous population, but a relatively stable rate among Indigenous people. Features that distinguish the Indigenous from the non-Indigenous HIV epidemic are a higher proportion of women affected, a higher proportion with heterosexual exposure to HIV, a younger age at HIV and AIDS diagnosis, and a higher proportion of people with HIV in rural areas. The low proportion of people with "late HIV diagnosis" among both Indigenous and non-Indigenous AIDS cases would suggest that a large pool of undiagnosed HIV infection is not present in Australia. The very low HIV prevalence among prison entrants in all States and Territories, including those where Indigenous Australians constitute a large proportion of prison inmates, is further confirmation that HIV prevalence among Indigenous Australians remains low.6 Our findings also extend those of an earlier study that showed comparable rates of HIV infection in both the Indigenous and the non-Indigenous population in Queensland.7 In interpreting our findings, several limitations to the study methods need to be considered. Firstly, the lack of a uniform reporting system for Indigenous status in all States and Territories may result in under-reporting in some jurisdictions. However, there is evidence that in recent years Indigenous status has been more completely reported, with 91% of HIV notifications in those States/Territories other than the ACT and Victoria currently reporting Indigenous status.1 Secondly, reporting of Indigenous status was based on "self-identification", which may either not be reported correctly by the patient, or not requested by the clinician. If identifying as Indigenous is more likely in a census setting than in clinical practice, our rates of Indigenous HIV diagnosis may be underestimates. Thirdly, reported rates of HIV and AIDS diagnoses are dependent on the level and extent of HIV testing. Poor access to and uptake of confidential testing by some Indigenous people, and fear of possible stigmatisation arising from positive test results, may influence the extent of HIV testing among Indigenous people. The explanation for the apparently limited HIV epidemic among Indigenous Australians is almost certainly multifaceted. The drop in HIV transmission from the mid 1980s has meant that the extent of the Australian HIV epidemic has been limited compared with many other countries.1 Behaviour change among homosexual men was largely responsible for the initial reduction in HIV transmission from the mid 1980s,1 with other measures such as the widespread introduction of harm minimisation programs for injecting drug users,8 and high condom use and low rates of sexually transmissible infections among most sex workers9 contributing to the ongoing relatively low level of HIV transmission. The absence of substantial levels of HIV infection among injecting drug users and female sex workers1 may have limited the spread of HIV into the heterosexual population. Despite the fact that the proportion of HIV diagnoses attributed to heterosexual contact has increased in recent years, homosexual contact remains the exposure category for about 85% of new HIV diagnoses.1 Australia's Indigenous people are not a homogeneous group. There are many hundreds of language groups and a wide diversity of cultural, social, economic and geographical settings within and between Indigenous Australian communities. Most Indigenous Australians suffer a higher burden of illness and die at a younger age than non-Indigenous Australians for almost every type of disease or condition for which information is available.10 Indigenous Australians are more likely to have lower annual incomes, are less likely to have qualifications beyond secondary school,11 and are 15 times more likely to be imprisoned than non-Indigenous Australians.11 These factors, combined with the remote locations in which many Indigenous Australians live and the resulting poor access to health services, contribute to their vulnerability to sexually transmissible infections.12 Associations in other industrialised countries between socioeconomic disadvantage and HIV transmission from heterosexual exposure and injecting drug use13 highlight the need to provide HIV prevention services which reach all sectors of society. The higher proportion of Indigenous people with HIV in rural areas should alert policymakers to the need for access to culturally appropriate health services in these locations. Likewise, the higher proportion of Indigenous people with HIV infection who are women, who report heterosexual exposure only and who inject drugs shows a need for broadly focused HIV prevention programs. This demographic pattern, the relatively stable level of HIV diagnoses in Indigenous people, and the continuing high rates of other sexually transmissible infections among some Indigenous communities,1 highlight the need to strengthen both sexual health and harm-minimisation strategies for Indigenous Australians. Following the recommendations of the Evaluation of the Third National HIV/AIDS Strategy, several measures have been implemented in an attempt to reduce the higher rates of sexually transmissible infections among Indigenous Australians and the associated risk of HIV infection. These include the establishment of an Indigenous Australians' Sexual Health Working Party and the subsequent implementation of the National Indigenous Australians' Sexual Health Strategy 1996-97 to 1998-99, which proposed a comprehensive approach to HIV prevention through a range of strategies considering treatment and care, partnership agreements and a properly resourced workforce.14 In particular, the Strategy emphasises the need for access to primary care services for communities without adequate facilities for diagnosing and treating sexually transmissible infections and the provision of information on reducing the risk of acquisition. Strategies aimed at the underlying causes of low socioeconomic status, low levels of education and low levels of employment must also be employed in order to reduce the risk of transmission of HIV and other sexually transmissible infections in Indigenous Australians. Acknowledgements The National Centre in HIV Epidemiology and Clinical Research (NCHECR) is funded by the Commonwealth Department of Health and Aged Care. We would like to acknowledge the valuable input and feedback received from the National Australian Indigenous Sexual Health Working Party during the drafting of this article. We also thank Ms Yueming Li for statistical analyses, Ms Patty Correll (NCHECR) for her assistance in extracting data, and Ms Suzanne Blogg (National Centre for Epidemiology and Population Health [NCEPH]) for her guidance and assistance. We thank the doctors who reported cases of newly diagnosed HIV infection and AIDS under national surveillance procedures, and the National HIV Surveillance Committee for their collaboration. The National HIV Surveillance Committee comprises Ms Irene Passaris (ACT), Mr Robert Menzies (NSW), Dr Jan Savage (NT), Dr Hugo Ree (QLD), Ms Therese Davey (SA), Mr Neil Cremasco (TAS), Ms Cathy Keenan (VIC), Dr Gary Dowse (WA), Professor John Kaldor (NCHECR), and Ms Ann McDonald (NCHECR). References Commonwealth Department of Human Services and Health. Valuing the past -- investing in the future. Evaluation of the National HIV/AIDS Strategy 1993-94 to 1995-96. Canberra: AIDS/Communicable Diseases Branch, CDHSH, 1995. National Health and medical Research Council. Guidelines on ethical matters in Aboriginal and Torres Strait Islander health research. Canberra: NHMRC, 1991. McDonald AM, Crofts N, Blumer CE, et al. The pattern of diagnosed HIV infection in Australia, 1984-1992. AIDS 1994; 8: 513-519. Kaldor J, McDonald AM, Blumer CE, et al. The acquired immunodeficiency syndrome in Australia: incidence 1982-1992. Med J Aust 1993; 158: 10-17. Australian Bureau of Statistics. Population distribution, Indigenous Australians. Canberra: ABS 1997. (Catalogue No. 4705.0.) McDonald AM, Ryan J, Brown PR, et al. HIV prevalence at reception into Australian prisons, 1991-1997. Med J Aust 1999; 171: 18-21. Neilson G, Hill PS. Human immunodeficiency virus notifications for Aborigines and Torres Strait Islanders in Queensland. Med J Aust 1993; 158: 155-157. MacDonald M, Wodak A, Ali R, et al. HIV prevalence and risk behaviour in needle exchange attenders: a national study. Med J Aust 1997; 166: 237-240. O'Connor CC, Berry G, Rohrsheim R, et al. Sexual health and use of condoms among local and international sex workers in Sydney. Genitourin Med 1996; 72(1): 4-51. Australian Bureau of Statistics. The health and welfare of Australia's Aboriginal and Torres Strait Islander peoples, 1997. Canberra: ABS, 1997. (Catalogue No. 4704.0.) Office of the Aboriginal and Torres Strait Islander Social Justice Commissioner. Indigenous deaths in custody 1989 to 1996. Sydney: Human Rights and Equal Opportunity Commission, October 1996. Fairley CK, Bowden FJ, Gay NJ, et al. Sexually transmitted diseases in disadvantaged Australian communities. JAMA 1997; 278: 117-118. Centers for Disease Control and Prevention. HIV/AIDS Surveillance Report 1998; 10 (No. 2): 1-43. ANCARD Working Party on Indigenous Australians' Sexual Health, Commonwealth Department of Health and Family Services. The National Indigenous Australians' Sexual Health Strategy, 1996-1997 to 1998-1999. Canberra: CDHFS, 1997. Authors' details National Centre in HIV Epidemiology and Clinical Research, Sydney, NSW. Jillian A Guthrie, BA, MAE (Indigenous Health) also at National Centre for Epidemiology and Population Health, Australian National University, Canberra, ACT. Gregory J Dore, FRACP, MPH, Lecturer. Ann M McDonald, MPH, Coordinator, National HIV/AIDS Surveillance. John M Kaldor, PhD, Professor; and Head, Epidemiology Unit. Reprints will not be available from the authors. Correspondence: Professor J M Kaldor, National Centre in HIV Epidemiology and Clinical Research, Level 2, 376 Victoria Street, Darlinghurst, NSW 2010. jkaldorATnchecr.unsw.edu.au 2: Newly diagnosed HIV infection and AIDS, 1992-1998, by Indigenous status and selected characteristicsHIV diagnoses IndigenousNon-IndigenousP Odds ratio (95% CI)Total casesn=127n=5186Males93 (73.2%)4726 (91.1%)<0.0010.27 (0.17-0.41)Median age (years)3033Median CD4 cell count4844000.10Newly acquired HIV*24 (18.9%) 930 (17.9%)0.79Late HIV diagnosis?---HIV exposure categoryn=120?n=4507?Male homosexual contact56 (46.7%)3382 (75.0%) <0.0010.29 (0.20-0.43)Male homosexual contact and injecting drug use 12 (10.0%)191 (4.2%)0.0022.51 (1.29-4.78)Injecting drug use6 (5.0%)176 (3.9%)0.3Heterosexual contact only44 (36.7%)689 (15.3%)<0.0013.21 (2.16-4.77)Receipt of blood/tissue0 (0.0)34 (0.8%)0.4Mother-to-child transmission2 (1.7%)35 (0.8%)0.2Other/Undetermined7679 AIDS diagnoses IndigenousNon-IndigenousPOdds ratio (95% CI)Total casesn=55n=3583Males43 (78.2%)3411 (95.2%)<0.0010.18 (0.09-0.37)Median age (years)3237<0.001Median CD4 cell count90600.71Newly acquired HIV*---Late HIV diagnosis?13 (23.6%)675 (18.8%)0.42HIV exposure catergoryn=52?n=3405?Male homosexual contact26 (50.0%)2783 (81.7%)<0.0010.22 (0.12-0.38)Male homosexual contact and injecting drug use7 (13.5%)167 (4.9%)0.0162.95 (1.20-6.93)Injecting drug use1 (1.9%)127 (3.7%)0.4Heterosexual contact only17 (32.7%)238 (7.0%)<0.0016.28 (3.33-11.75)Receipt of blood/tissues0 (0.0)76 (2.2)0.3Mother-to-child transmission1 (1.9%)15 (0.4%)0.2Other/Undetermined3178 *A negative or indeterminate HIV antibody test result or a diagnosis of HIV seroconversion illness within 12 months of HIV diagnosis. ?HIV infection newly diagnosed within three months of AIDS diagnosis. ?The "other/undetermined" category was excluded from the calculation of the percentage of cases attributed to each HIV exposure category.

Jillian A Guthrie · Gregory J Dore · Ann M McDonald · John M Kaldor

Gene technology is a new form of biotechnology with much greater potential applications. Biotechnology is nothing new. In fact, humanity has been using biotechnology for the preparation and manufacture of food for hundreds of years -- using yeast for making beer and bread, and selecting and breeding plants and animals for higher productivity and nutritive value. Recombinant-DNA (gene) technology is an aspect of modern biotechnology that represents a quantum leap in potential applications. It allows new genes to be introduced into plants and animals -- genes can therefore be moved from one species to another (eg, from bacteria to plants or from non-crop to crop plants), a feat impossible through conventional plant breeding. (For a description of the science behind gene technology and its applications in agriculture, see references 1 and 2.) Gene technology offers enormous potential benefits for world agriculture, including the possibility of producing higher yields of more nutritious food in more environmentally sustainable ways. It offers a powerful new tool to assist plant breeders to introduce resistance to insects and diseases, as well as traits for higher quality and nutritive value. Moreover, the next generation of genetically modified (GM) crop plants promises a significant impact on human health (eg, rice has been engineered with enhanced levels of vitamin A and iron to correct nutrient deficiencies common in the developing world, although more research is needed for a practical outcome). The first commercial applications of gene technology in crop plants have involved modifying the plant for greater disease or insect resistance or a more efficient production system. Introduction of these GM crops has been extremely rapid, particularly in the United States. In 1996, transgenic crops covered 1.7 million hectares worldwide. By 1998, that area had increased 15-fold to almost 28 million hectares.3 In that year, the most common transgenic crops in the world were soybean and corn, with significant areas of cotton, canola and potato. There are now over 50 individual transgenic products, involving 13 separate crops. It has been predicted that, within 20 years, gene technology will touch every type of agricultural crop in the world, although this will depend on a high level of consumer acceptance. In Australia, only one GM crop is currently grown commercially -- insect-resistant (INGARD) cotton. This is now entering its fourth commercial year and currently accounts for 30% of the Australian cotton crop. In the past three years, GM cotton has been sprayed with less than 50% of the insecticides used on the conventional crop -- a reduction of 1.5 million litres of spray per year.4 Although cotton is the only GM crop in Australia, the ready acceptance of GM crops by farmers in the US has resulted in about 50% of the soybean crop and 30% of the corn crop being genetically modified. This has relevance for Australia, as significant quantities of soybean are imported and used in processed food. Food safety The safety issues surrounding foods derived from GM plants are central to their acceptance into the food chain. Consumers seek reassurance about the safety of the food they eat, in terms of both its immediate and long-term health effects. Rigorous scientific assessment of GM food safety is therefore essential to provide a sound scientific basis for future regulation. In dealing with the issue of safety of food and food products from GM plants, regulatory authorities in many parts of the world have relied on the principle of substantial equivalence. Substantial equivalence is established if food products are essentially the same in composition, nutritive value, functional characteristics and organoleptic properties (taste, smell, mouthfeel). When it has been established that the food derived from a GM plant is substantially equivalent to that produced by the conventional crop, then the focus of testing becomes the introduced genes and their specific products. Alternatively, if a food derived from a GM plant differs from that produced by the conventional crop, then it must be assessed for food safety on a case-by-case basis. For example, transgenic rice with enhanced vitamin A would be considered a "new" food and assessed for safety accordingly. The safety implications of new characteristics introduced into GM plants have been evaluated in much the same way as new food additive or agrochemical products such as pesticides (eg, in-vitro and animal-feeding trials). The company or institution applying for registration for use must provide a dossier describing safety tests performed in compliance with the protocols set by regulatory authorities. These data are rigorously assessed before regulatory approval is given. Examples include antibiotic-resistance genes, used as selectable "markers" during the development of the GM plant (Box 1). Herbicide-resistance genes can also be used as markers and give the plant an agronomic advantage. Both these introduced traits have caused considerable controversy, albeit for different reasons, and illustrate the type of assessment undertaken to establish confidence in their safety. Safety implications of antibiotic resistance Among the common types of selectable marker, antibiotic resistance has created most controversy, mainly because of the fear of transfer to the bacterial microflora of humans or animals. By far the most commonly used antibiotic resistance marker is the NPTII gene, which codes for the enzyme neomycin phosphotransferase NPTII, which inactivates neomycin and related antibiotics, including kanamycin. Numerous studies have suggested that the presence of this antibiotic-resistance gene in any crop or crop products will have negligible impact on food safety.5 A concern about use of antibiotic resistance as a selectable marker is its potential to compromise the therapeutic use of antibiotics in humans and animals. The presence of the gene product in food or feed has been considered, as has the possible transfer of this resistance to gut and potentially hazardous microorganisms. Dröge et al clearly demonstrated that such transfer occurs, if at all, at extremely low frequency.6 Most, if not all, of the NPTII gene ingested will be degraded in the human stomach and small intestine. Moreover, the probability of gut microorganisms integrating this exogenous DNA and producing the NPTII protein is extremely low, particularly as the latter would require the bacterial DNA to be rearranged, with replacement of the plant promoter (the DNA sequence that allows RNA polymerase to bind) by a bacterial promoter. Even if the NPTII protein was produced, it would be expected to rapidly degrade, as shown by experiments under simulated gastric conditions.7-9 Therefore, Kärenlampi, in his 1996 report to the Nordic Council (responsible for directing food policy issues in the five Nordic countries), concluded that the overall risk is effectively zero, and that the therapeutic use of antibiotics in humans or animals will not be affected by commercialisation of transgenic crops containing antibiotic-resistance selectable marker genes.5 Nevertheless, the Royal Society's report on GM plants, while conceding that risks were minimal, recommended that antibiotic-resistance marker genes no longer be used in GM food crops.10 Alternative systems to select for genetic modification are now available, and it is possible to delete the marker gene altogether in regeneration of some crops. Safety implications of herbicide resistance The introduction of herbicide-resistance genes into specific target crops is a major objective of plant biotechnology programs, with some 50% of commercial transgenic crops being herbicide resistant. Herbicide-resistant crops can significantly increase production efficiency. In addition, as they increase farmers' options for weed management (eg, by eliminating the need for pre-planting herbicides and allowing flexible timing of herbicide application for maximum efficacy), herbicide-resistant crops can decrease overall herbicide use and lead to the use of more environmentally acceptable herbicides. By far the largest area is planted to crops tolerant of the herbicide glyphosate (Roundup; Monsanto, St Louis, Mo), which is relatively non-toxic and readily deactivated and degraded in the soil. These crops contain a version of the herbicide target enzyme that was derived from bacteria and is naturally tolerant of the herbicide (Box 2). The target enzyme is present in all plant, microbial and fungal food sources and is therefore not novel to the food supply. A comprehensive series of scientific evaluations showed that the genetically modified version of the enzyme behaves like other versions and has no adverse safety effects.4,11 Detailed analysis of nutrients and antinutrients, including fatty acids, amino acids, protein and micronutrients, in glyphosate-tolerant GM soybeans confirmed that they are substantially equivalent to conventional soybeans currently in commercial use.11 Extensive testing of the bacteria-derived enzyme from GM soybeans established that, in simulated gastric and intestinal fluids, it is not toxic or allergenic and is rapidly digested.4,12 Recent developments Of great concern in late 1998 were reports of experiments by Pusztai at the Rowett Research Institute in the United Kingdom. The results were initally published through the media rather than through peer-reviewed scientific journals and caused considerable controversy and public concern, as they suggested that serious health effects could arise from a genetic modification itself rather than from the particular gene that had been inserted. Pusztai's experiments set out to investigate whether GM potatoes that contained a gene encoding snowdrop lectin (a plant protein with potential to increase insect and nematode resistance) affected the health and growth of rats to which they were fed. He concluded that the GM potatoes significantly affected the immune system of the rats, as a result of the genetic modification itself rather than of the particular gene that had been inserted. These claims were so serious and caused such public concern that the Royal Society set up a review of their implications for food safety. After examining all available information on the experiments, six independent reviewers with expertise in statistics, clinical trials, physiology, nutrition, quantitative genetics, growth and development, and immunology, prepared a report.13 This found that the Pusztai experiments were flawed in many aspects of design, execution and analysis, and that no conclusions could be drawn from them. The expert review group found no credible evidence of adverse effects from GM potatoes. Recently, despite the objections of several referees,14 The Lancet published some of Pusztai and colleagues' experiments.15 While The Lancet undoubtedly felt this was justified to promote critical discussion of the data, no definitive conclusion can reasonably be drawn from the published results. Perhaps because of the unfortunate circumstances surrounding the Pusztai experiments, doubts continue to be raised about the longer-term safety of GM foods. As pointed out above, the principle of substantial equivalence relies on comprehensive testing of the introduced new trait in terms of the gene construct and its product -- not testing the whole food which contains that product. As a general rule, food is not tested for safety, other than for contaminants. For example, a new wheat variety containing new genes for disease resistance produced by conventional breeding is considered identical -- substantially equivalent -- to its parent cultivars. Providing the flour produced from this new wheat variety is acceptable to millers and bakers and similar to flour produced from other wheat, it is accepted into the food chain without further food safety evaluation. Therefore, the products of GM crop plants currently in the food chain have been tested far more thoroughly than any conventional food. Regulation in Australia Australia has been well served by the Genetic Manipulation Advisory Committee (GMAC), which has provided a clear, comprehensive, transparent framework for the conduct of research into GM organisms in the laboratory, in glasshouses, and in the field. The protocols developed and used within the GMAC framework in regulating research into GM organisms in Australia have become the model for similar research in other countries, including Malaysia, Thailand and Singapore. While the present protocol through GMAC provides a satisfactory avenue for planned release of GM organisms to the "proof of concept" (precommercialisation) stage, the pathway to commercialisation is far less clear. To correct this deficiency, the Australian government recently allocated funding for the establishment of an Office of the Gene Technology Regulator (OGTR) to ensure an effective, enforceable system of regulation for the biotechnology industry. This office, currently known as the Interim OGTR, will develop an appropriate regulatory regime to cover the development, clearance and labelling of foods and food products derived from the new gene technologies. As such, it needs to meet the dual imperatives of providing consumers with confidence in the safety and regulation of gene technology products and of fostering an environment conducive to industry innovation and commercialisation. The Interim OGTR is currently seeking community views and comment on the Draft Gene Technology Bill 2000 (dated December 1999), which covers the regulation of all aspects of the research, development and use of GM organisms and their products, where no other body has responsibility. The Government has also established a Senior Ministerial Council to manage biotechnology issues across the relevant portfolios of Health, Industry, Environment, Education and Agriculture, as well as a Commonwealth agency within the Department of Industry, Science and Resources, to be known as Biotechnology Australia, to coordinate the Commonwealth's activities in biotechnology. It is clear that the new regulatory system must provide consumers with confidence that the necessary checks and balances are in place to ensure food derived from the new technology is safe and beneficial. Consumer education will remain a major factor in determining the acceptance of the new technology, and it is important that balanced information on the science of the risk and safety assessment of food derived from gene technology is made freely available to the community. Disclosure statement The authors are employed by the Commonwealth Scientific and Industrial Research Organisation (CSIRO), a publicly funded Australian research organisation. CSIRO Plant Industry undertakes research in the plant sciences, including the use of plant molecular biology to develop new and improved crop plants for the benefit and sustainability of Australian agricultural industries. References Larkin P, editor. Genes at work: biotechnology. Canberra: CSIRO, 1994. Commonwealth Scientific and Industrial Research Organisation. <http://genetech.csiro.au> James C. Global review of commercialised transgenic crops. ISAAA Brief No 8. Ithaca, NY: ISAAA, 1998. Fitt GP, Wilson LJ. Genetic engineering in integrated pest management: case study -- Bt plants. In: Emerging technologies in integrated pest management. Sutton T, Kennedy GG, editors. St Paul, Minn: American Phytopathological Society Press. In press. Kärenlampi S. Health effects of marker genes in genetically engineered food plants. Report to the Nordic Council Copenhagen: TemaNord, 1996: 530. Dröge M, Pühler A, Selbitschka W. Horizontal gene transfer as a biosafety issue: A natural phenomenon of public concern. J Biotechnol 1998; 64: 75-90. Redenbaugh K, Hialt W, Martineau B, et al. Aminoglycoside 3'-phosphotransferase II (APH (39) II or NPTII): Review of its safety and use in the production of gentically engineered plants. Food Biotechnol 1994; 8: 137-165. Nap JP, Bijvoet J, Strikena WJ. Biosafety of kanamycin-resistant transgenic plants: an overview. Transgenic Crops 1992; 1: 239-249. Fuchs RL, Ream JE, Hammond BG, et al. Safety assessment of the neomycin phosphotransferase II (NPTII) protein. Bio/Technology 1993; 11: 1543-1547. The Royal Society. Statement 1998: genetically modified plants for food use. London: The Royal Society, 1998. Padgette SR, Taylor NB, Nida DL, et al. The composition of glyphosate-tolerant soybean seeds is equivalent to conventional soybeans. J Nutr 1996; 126: 702-716. Fuchs RL, Re DB, Rogers SG, et al. Safety evaluation of glyphosate-tolerant soybeans. In: Food safety evaluation. Paris: OECD, 1996: 61-70. The Royal Society. Statement 1999: review of data on possible toxicity of GM potatoes. London: The Royal Society, 1999. Horton R. Genetically modified foods: "absurd" concern or welcome dialogue [editorial]? Lancet 1999; 354: 1314-1315. Ewen SWB, Pusztai A. Effect of diets containing genetically modified potatoes expressing Galanthus nivalis lectin on rat small intestine. Lancet 1999; 354: 1353-1354. Authors' Details CSIRO Plant Industry, Canberra, ACT. John L Huppatz, PhD, Deputy Chief. Paula A Fitzgerald, BA (Comm), Public Affairs Manager. Reprints will not be available from the authors. Correspondence: Ms P A Fitzgerald, CSIRO Plant Industry, GPO Box 1600, Canberra, ACT 2601.

John L Huppatz PhD · Paula A Fitzgerald BA (Comm)

We would be wise to hold off until we know more about the health, ecological and economic effects of genetically modified food. Advocates of genetically modified (GM) foods often assert that the processes of laboratory genetic engineering are really no different from those of plant and animal husbandry. This argument is not as convincing as they expect. Those who express concern about the safety of GM food claim that genetic engineering allows humans to do what nature will not -- they worry that scientists cut and paste genes and can now transfer genes between species. This gene transfer raises new safety questions, making the production and marketing of GM foods a matter for consideration by public health authorities. Food safety is a public health issue. Most food is provided by private enterprise, and consumers understand that food advertising, while commercially justifiable, exhibits the qualities of advertising in general: truth is spun and packaged to make the product attractive. Regulatory mechanisms, including surveillance, have been put in place in many countries over many years to ensure food safety and to balance commercial profit with the public good. Increasingly, food manufacturers and retailers understand the critical importance of safety as well as the healthiness of their product for market share. Can we rely on the food industry regulating itself? Not in all times or all places has the public found commercial interest, even in food production, to be trustworthy. When outbreaks of food poisoning occur, long-held public suspicions erupt as rage. Furthermore, a contributing factor to the outbreak of mad cow disease (bovine spongiform encephalopathy, or BSE) in the United Kingdom was a change in the processing of animal feed. Altered rendering practices, introduced in the late 1970s and early 1980s when the feed industry was deregulated, allowed scrapie-like agents to survive.1 This finding shocked the community and shattered trust in commercially driven food enterprises. The change in rendering practices paralleled adoption of the political view that the food industry needed self-regulation only, and the winding back of the public health food surveillance system. Thus, the attitude of some of the UK public to GM food was formed by their experience with BSE. GM technologies, which are profit driven (for manufacturers of GM strains and the farmers who use them), did not impress a community that felt it had been falsely reassured that food safety could be left to the producers. Although GM food safety is clearly a public health issue, in Australia at present the Genetic Manipulation Advisory Committee (GMAC) and the Interim Office of the Gene Technology Regulator (OGTR) comprise individuals who, although highly skilled, can opine only about the laboratory or clinical safety of products. The federal Minister for Health and Human Services, Michael Wooldridge, has agreed to consider appointing to these bodies a professional with extensive skill and experience in public health. Public health concerns about GM food include potential direct ill-effects from consuming the food, or imported allergens in the food, as well as their ecological impact. The histories of medicine and public health contain many examples of substances initially assumed to be safe and later found otherwise. These range from specific drugs, such as the class IC antiarrhythmic agents (eg, flecainide), which turned out to be proarrhythmic in certain circumstances,2 to more general environmental conditions, such as low level air pollution, once thought harmless but now correlated with mortality rates.3 These histories alone should deter GM food manufacturers from prejudicial paternalism in dealing with public concerns. The forms of testing outlined in this issue of the Journal by Huppatz and Fitzgerald, based on establishing substantial equivalence, are necessary but not sufficient to establish public health safety.4 Even here uncertainties remain, because of the lack of adequate benchmarks for cellular safety of non-GM foods. Most public health safety is established only by intervention followed by careful monitoring. The equivalent approach to GM foods would involve developing suitable surveillance systems for adverse events in those eating GM foods and for ecological impact. Thus, there is some justification for the introduction of these foods under surveyed conditions. Advantage could be taken of natural experiments. For example, the production and consumption of GM foods is greater in the United States than in Europe. Observational studies on the health of the two populations and their agricultural environments may at least provide clues to the long-term consequences of GM foods. This would not be easy, and the effects, as with BSE, might not be apparent for years or even decades if the latency were long between the impact of the food and its expression as illness. What are the concerns with GM food? In the UK and elsewhere in Europe, media coverage of GM foods has been intense and often sensational. In Australia, media concern has been obvious, and, while claims of irresponsible sensationalism have been made, in my opinion the quality of much of the reporting and journalistic comment has been fair to good. An investigative series on GM foods by Mark Ragg, health writer for the Sydney Morning Herald, fuelled the debate in Australia.5 Much that has been written has focused on human safety and the arguments for and against GM food labelling, while relatively less has been concerned as yet with environmental impact. In recent issues of the British Medical Journal strenuous efforts have been made by editorial writers, scientific writers and freelance consultants to dampen the European "bioangst" about wayward genes in GM foods.6-8 However, as far as population and ecological safety are concerned, I believe we are at the scientific starting line: we simply don't know whether GM foods are safe, what their environmental impact will be, or how the gains will trade with the losses. In that case, says the British Medical Association, we should wait until we have evidence that GM foods are safe before proceeding. Science has yet to do its work in establishing the safety of these products.9 In a statement earlier this year, the UK's Chief Scientific Adviser, Robert May, concluded: "There can be questions of health and safety associated with some GM foods, particularly if we introduce genes coding for production of toxins against certain kinds of pests."10 May, together with the Chief Medical Officer, Liam Donaldson, also wrote that, although "there is no current evidence to suggest that the GM technologies used to produce food are inherently harmful . . . nothing can be absolutely certain in a field of rapid scientific and technological development".11 Donaldson and May urged the UK government to study the potential effects of GM food technology on health and to develop a research strategy into the technology.12 Antibiotic resistance: A further worry about GM food arises from the practice of using antibiotic resistance, which is easily established, as a marker to measure the success of a genetic modification. Antibiotic resistance is tagged onto the genetic modification, so that cells that contain the new gene are also antibiotic resistant. Were this resistance to spread to pathogenic bacteria via the GM food, it could cause great harm.9 Ecological and economic effects: Doubt about GM food does not stop at the medical boundary. Many scientists sleep easily about the safety of GM foods for human consumption after proper testing and regulation, while having nightmares about the environmental impact of these foods. For example, genes that code for resistance to chemical herbicides could be transferred from GM plants to weeds. Cultivation of GM crops on a large scale may have implications for biodiversity, the balance of nature and wildlife. Third World countries may have the most to benefit from the potentially greater productivity of GM crops, but, if the price is increasing debt to the multinationals that produce GM seed, it will simply increase the north-south wealth disparity which lies at the heart of so much appalling public ill-health.9 As Jeffrey Sachs, Director of the Centre for International Development and Professor of International Trade at Harvard University, wrote in The Economist: Just as knowledge is becoming the undisputed centrepiece of global prosperity (and lack of it, the core of human impoverishment), the global regime on intellectual property rights requires a new look . . . now transnational corporations and rich-country institutions are patenting everything from the human genome to rainforest biodiversity. The poor will be ripped off unless some sense and equity are introduced into this runaway process.13 Concerns about the terminator gene, which prevents plants being propagated and requires farmers to repurchase fertile stock seed from the manufacturer at each planting, have drawn widespread criticism for much the same reason. This especially unpleasant commercial ploy has major implications for Third World countries. Monsanto has recently been forced to rethink its GM food strategy, with company head Bob Shapiro conceding: We have irritated and antagonised more people than we have persuaded. Our confidence in biotechnology has been widely seen as arrogance and condescension because we thought it was our job to persuade. But too often we forgot to listen.14 In the meantime, a healthy scepticism about the massive commercial interests in GM food is warranted. The moratorium called by the British Medical Association has much to commend it, especially for those who believe that human progress is best served when we listen to the guidance of science -- even when it says "I don't know".9 Disclosure statement No conflicts of interest. References Department of Health, MAFF. Report of the Working Party on Bovine Spongiform Encephalopathy (the "Southwood report"). London: DOH, 1989. Echt DS, Liebson PR, Mitchell B, et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo: the Cardiac Arrhythmia Suppression Trial. N Engl J Med 1991; 324: 781-788. Dockery DW, Pope CA III, Xu X, et al. An association between air pollution and mortality in six US cities. N Engl J Med 1993; 329: 1753-1759. Huppatz JL, Fitzgerald PA. Genetically modified foods -- safety and regulatory issues. Med J Aust 2000; 172: 170-173. Ragg M. Genetic food: you're eating it. Sydney Morning Herald 1999 Jul 24; 1 (col 1), 10. Dixon B. The paradoxes of genetically modified foods. BMJ 1999; 318: 547-548. Berger A. Hot potato. BMJ 1999; 318: 611. Jones L. Genetically modified foods. BMJ 1999; 318: 581-584. Leeder S. Frankenstein and the hot potato. Aust N Z J Public Health 1999; 23: 227-228. May R. Genetically modified foods: facts, worries, policies, and public confidence. London: Office of Science and Technology, 1999. Donaldson L, May R. Health implications of genetically modified foods. London: Department of Health, 1999. Horton R. Genetically modified foods: "absurd" concern or welcome dialogue? Lancet 1999; 354: 1314. Sachs J. Helping the world's poorest. The Economist 1999 Aug 14: 17-20. Vidal J. GM company chief takes blame for public relations failures and pledges to answer safety concerns. Guardian 1999 Oct 7. Authors' Details Faculty of Medicine, University of Sydney, Sydney, NSW. Stephen R Leeder, FRACP, FAFPHM, FFPHM, Dean. Reprints will not be available from the author. Correspondence: Professor S R Leeder, Faculty of Medicine, University of Sydney, NSW 2006. steveATmedicine.usyd.edu.au

Stephen R Leeder FRACP, FAFPHM, FFPHM

Editorials Measles in an era of measles control As measles becomes rare in Australia, clinical diagnosis becomes increasingly inaccurate MJA 2000; 172: 103-104 It has been a long road to the control of measles in Australia. Live attenuated measles vaccine was licensed in 1968, and included in childhood vaccination schedules in 1971. Even after the first national measles campaign, in 1988, coverage remained too low (85%)1 to achieve herd immunity, as evidenced by major measles outbreaks in many areas in 1993-1994. In 1994, a second dose of measles-mumps-rubella (MMR) vaccine was introduced for all children aged 10-16 years. Although the incidence of measles declined, seroprevalence studies2 indicated that further measles outbreaks were likely. In response to these findings, the Australian Measles Control Campaign (MCC) was launched in July 1998. The centrepiece of this campaign was administration of a dose of MMR vaccine to all primary school children in the second half of 1998. This "catch-up" dose was needed before lowering the recommended age for the second dose of MMR vaccine to four years in 1999. After the MCC, an estimated 96% of children aged five to 12 years had received two doses of MMR vaccine.3 As a result of this campaign and the continuing efforts to eradicate measles, it is hoped that Australia will soon be shown to have joined other countries, such as the United States,4 the United Kingdom5 and Finland,6 where indigenous measles transmission has been interrupted. The better the control of measles, the lower the probability that someone presenting with fever and rash will have measles, and the poorer the positive predictive value (PPV) of a clinical diagnosis. Even in 1990-1993, before any major measles control measures, a study of 58 people notified with measles in eastern Sydney found that only 49% of cases were serologically confirmed.7 A case definition of morbilliform rash, cough and fever at rash onset had a PPV of 69%.7 In this issue of the Journal, there is a report of a larger study of enhanced measles surveillance in Victoria from July 1997 to December 1998 (ie, primarily conducted before the MCC) which showed a much lower level of confirmation.8 Only 8% of the 248 notified cases that could be classified on the basis of serological results were confirmed as measles. The PPV of the National Health and Medical Research Council (NHMRC) clinical case definition for considering public health action9 was as low as 5% when secondary cases from clusters were excluded.8 Since the MCC, the proportion of serologically confirmed cases is likely to have fallen even further. In the UK, after a similar school-based MMR program in 1994,5 and in Finland 12 years after high coverage with a two-dose MMR schedule,6 only about 1% of suspected cases were shown to be measles. These developments necessitate major changes in the approach of medical practitioners to suspected measles, especially in general practice where most cases will be seen. The latest draft of the revised NHMRC guidelines for measles control emphasise that confirmation by detection of measles IgM in a serum specimen is essential when measles is clinically suspected.10 This policy is also recommended by the authors of the Victorian study and by the National Measles Surveillance Strategy.11 Confirmation is particularly important in sporadic cases, where the prior probability of measles is especially low, and should also be obtained from at least two cases during an outbreak. The high level of laboratory testing achieved in Victoria is encouraging. However, overall, only 44% of the 428 cases accepted as measles notifications in Australia between January 1998 and June 1999 were laboratory confirmed (personal communications from State and Territory health departments). It may be possible to improve this percentage -- although teams of venepuncturists are impractical for many areas of Australia, arrangements to bleed patients can usually be made in consultation with local public health authorities. Considerable interest has also focused on non-invasive diagnostic methods, such as salivary testing. This method has been used in the UK but has technical difficulties,11 making timely testing more difficult than for serological testing. Even when serological testing is done, as measles becomes rare the likelihood of a falsely positive measles IgM will rise, as found in Victoria and elsewhere.4 A positive measles IgM test should therefore be confirmed by a reference laboratory, especially in sporadic cases. Clinicians should be aware that many viral infections in children may resemble measles clinically, and that measles is more likely in older children and young adults than in infants. After control of measles in Finland,6 37% of 993 children with suspected measles had serological evidence of infection caused by parvovirus, enteroviruses, adenovirus or human herpesvirus type 6 (HHV-6).12 The most common serological diagnoses were parvovirus infection, in children aged four to 15 years, and enterovirus and HHV-6 infection, in children aged under four years. In Sydney, in 1990-1993, the mean age of patients with confirmed measles was 11.3 years,7 and, in Victoria in 1997-1998, more than half (53%) the patients with confirmed measles were aged at least 10 years.8 An outbreak of measles in Victoria in 1999, after the MCC, indicates the likely future pattern of measles in Australia -- 84% of patients were aged 18-30 years and all patients aged one to eight years were unvaccinated.13 Sustained measles control will require further efforts in young adults as well as continued high coverage with two doses of measles vaccine in children. Young adults, especially those attending tertiary institutions or planning travel to areas where measles remains endemic, should be encouraged to have a second dose of MMR or serological confirmation of measles immunity. Peter B McIntyre Deputy Director Heather F Gidding Epidemiologist National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases, Royal Alexandra Hospital for Children and University of Sydney, Sydney, NSW Gwendolyn L Gilbert Director, Centre for Infectious Diseases and Microbiology and University of Sydney, Sydney, NSW Australian Bureau of Statistics. National health survey. Children's immunisation, Australia, 1989-90. Canberra: ABS, 1992. (Catalogue no. 4379.0.) Gilbert GL, Chan S-W, Escott R, et al. Seroepidemiology of measles in New South Wales, 1997. Report to the National Centre for Disease Control, Commonwealth Department of Health and Aged Care, 1998 (available from the Department). National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases. Australian measles control campaign 1998. Evaluation report. Sydney: University of Sydney, Royal Alexandra Hospital for Children, 1999. Watson JC, Redd SC, Rhodes PH, Hadler SC. The interruption of transmission of indigenous measles in the United States during 1993. Pediatr Infect Dis J 1998; 17: 363-366. Gay N, Ramsay M, Cohen B, et al. The epidemiology of measles in England and Wales since the 1994 vaccination campaign. Commun Dis Rep CDR Rev 1997; 7: R17-R21. Peltola H, Hienonen OP, Valle M, et al. The elimination of indigenous measles, mumps, and rubella from Finland by a 12-year, two-dose vaccination program. N Engl J Med 1994; 331: 1397-1402. Ferson MJ, Young LC, Robertson PW, Whybin LR. Difficulties in clinical diagnosis of measles: proposal for modified clinical case definition. Med J Aust 1995; 163: 364-366. Lambert SB, Kelly HA, Andrews RM, et al. Enhanced measles surveillance during an interepidemic period in Victoria. Med J Aust 2000; 172: 114-118. National Health and Medical Research Council. Measles: guidelines for the control of outbreaks in Australia. Canberra: NHMRC, 1996. National Health and Medical Research Council. Measles: guidelines for the control of outbreaks in Australia [draft]. Canberra: NHMRC, 2000. Heath T, Burgess M, McIntyre P, Catton M. The national measles surveillance strategy. Commun Dis Intell 1999; 23: 41-49. Davidkin I, Valle M, Peltola H, et al. Etiology of measles and rubella-like illness in measles, mumps, and rubella-vaccinated children. J Infect Dis 1998; 178: 1567-1570. Lambert S, Lynch P, Morgan M, Gercovich D. Measles outbreak -- young adults at high risk. Victorian Infect Dis Bull 1999; 2: 21-22. Make a comment

Peter B McIntyre · Heather F Gidding · Gwendolyn L Gilbert

Public Health Enhanced measles surveillance during an interepidemic period in Victoria Stephen B Lambert, Heath A Kelly, Ross M Andrews, Mike C Catton, Pauline A Lynch, Jennie A Leydon, Debbie K Gercovich, Geoffrey G Hogg, Melissa L Morgan and Rosemary A Lester MJA 2000; 172: 114-118 For related article see McIntyre et al Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Infectious diseases and parasitology Abstract Objective: To describe results of the first two years of enhanced measles surveillance in Victoria. Design: Case series identified through enhanced measles surveillance. Participants and setting: All measles cases notified to the Disease Control Section, Department of Human Services, Victoria, in 1997 and 1998. Main outcome measures: Proportion of notified cases laboratory confirmed as measles, rubella, or human parvovirus infection; identification of clusters (two or more linked cases of measles); and utility of the National Health and Medical Research Council clinical case definition for suspected measles. Results: Rates of laboratory testing of notified cases improved after introduction of a paediatric phlebotomy service in July 1997, from 21 of 90 notified patients (23%) in the preceding six months, to 258 of 317 notified patients (81%) between July 1997 and December 1998. Of the 317, only 19 (6%) were laboratory confirmed with measles, while a further 26 (8%) were laboratory confirmed with human parvovirus infection (18) or rubella (8). Three clusters of measles, involving 11 cases, were identified during 1998. Use of the NHMRC case definition did not greatly improve the positive predictive value for diagnosis of measles above that of notification alone (14% versus 8%). Conclusions: Circulation of measles virus in Victoria in 1997 and 1998 appeared minimal. In this interepidemic period most notified cases of measles were not measles; to identify true cases, surveillance during an interepidemic period must include laboratory testing of notified cases. Cases of classical measles are uncommon in countries with successful measles control programs, making clincal diagnosis less reliable. To ensure the validity of clinical notifications, it is increasingly important to confirm the diagnosis in every sporadic case of measles and in at least one case in every chain of transmission in such countries.1 Australia suffered a nationwide outbreak of measles in 1993-1994.2 Since 1994, a two-dose measles-mumps-rubella (MMR) vaccination program has been implemented,3 and in 1998 a national campaign targeting primary school-aged children was conducted.4 The country was free of any substantial outbreak until early 1999, when importation of the disease from Bali resulted in measles cases, mainly among young adults in Victoria.5 To monitor the success of the measles control program, the State of Victoria began a state-based enhanced surveillance program in 1997. This program concentrates on confirming the diagnosis of measles for all notifications received by the Disease Control Section of the Victorian Department of Human Services.6 We report the results of the first two (interepidemic) years of this enhanced measles surveillance program and make recommendations for the investigation of notified cases of measles. Methods The enhanced measles surveillance strategy adopted by Victoria has been reported elsewhere.6 In brief, all notifications to the Department of Human Services in 1997 and 1998 were followed up by a structured telephone interview with the patient or, if the patient was a child, with the parent or guardian. Demographic data, clinical symptoms, and measles vaccination history were recorded. The parent/guardian was asked to read the date of vaccination from the personal vaccination record when available. We attempted to identify a possible source of infection, as well as contacts who required advice about immunoglobulin or MMR vaccination. Suspected preceding or subsequent cases were followed up in a similar manner to identify clusters of infection (defined as two or more epidemiologically linked cases7). A sporadic case was one that could not be linked to another case. Serological testing A serum specimen was sought from each notified patient for laboratory confirmation of the clinical diagnosis. From July 1997, this specimen was obtained by a paediatric phlebotomist in the patient's home. Some patients provided a combined throat and nose swab and a urine specimen for viral culture or isolation of genetic material by polymerase chain reaction, and subsequent virus genotyping.8Sera were tested for measles IgM and IgG at the Victorian Infectious Diseases Reference Laboratory (VIDRL) or, if original testing was performed elsewhere, the testing laboratory was asked to forward remaining sera from measles IgM-positive specimens to VIDRL for confirmatory testing. Testing at VIDRL used a commercial enzyme immunoassay (Dade Behring Enzygnost, Marburg, Germany). The manufacturer reports the measles IgM assay as having a sensitivity of 100% and specificity of 98%. Sera that were negative for measles IgM at VIDRL were assayed for human parvovirus IgM and IgG (Biotrin Parvovirus B19 Enzyme Immunoassay, Dublin, Ireland), rubella IgM (DiaSorin ETI-RUBEK-M reverse PLUS, Saluggia, Italy) and rubella IgG (Panbio Rubella IgG ELISA Test, Brisbane, Australia). Analyses Using a defined algorithm,6 each notified case was classified as confirmed measles or otherwise according to the criteria in Box 1. These included serological and other results, as well as concordance with the clinical case definition for suspected measles11 recommended by the National Health and Medical Research Council (NHMRC) -- morbilliform rash, fever present at rash onset, and cough.12Analysis was performed using Epi Info version 6.04.13 Significance of differences between categorical data was tested by the Fisher's exact or χ2 test. Results In the first six months of surveillance (January to June 1997), sera were collected from 21 of 90 notified patients (23%). After employment of a paediatric phlebotomist to collect samples in the patient's home, collection rates improved progressively -- sera were collected from 258 of 317 notified patients (81%) between July 1997 and December 1998, including from 107/120 (89%) in the second half of 1998.6Because of the lower rate of specimen collection in the first six months of surveillance, we analysed data for July 1997 to December 1998 only. In this period, only 19/317 notifications (6%) were classified as laboratory confirmed (Box 2). The remainder were laboratory rejected (229; 72%), clinically compatible (12; 4%), not clinically compatible (41; 13%) and not classifiable (16; 5%). All epidemiologically linked cases were able to be laboratory confirmed. Of the 229 cases that were laboratory rejected as measles, 18 had human parvovirus infection (8%), and eight had rubella (3%). Box 3 shows serological results by age group. Serum collection rates did not differ significantly between age groups (P = 0.4), but laboratory confirmation was significantly more likely among patients aged 10 years or over than among younger children (P = 0.0002). Clusters of measles Three clusters of measles, involving 11 patients, were identified, all in 1998. The first, involving four people, began in January 1998. A 19-year-old man from New South Wales visited Melbourne soon after illness onset on 10 January. Three other people were infected: his 22-year-old brother (onset, 18 January), six-month-old nephew (onset, 1 February), and a 23-year-old male household contact (onset, 3 February). None of the Victorian patients in this cluster reported previous measles vaccination; all required hospital admission. In the second cluster, the index patient was a two-year-old girl (onset, 1 February). Although she lived within a kilometre of the household of the first cluster, no clear epidemiological link could be established with any of the earlier cases. Three other children, aged 10 months to three years, and an 18-year-old woman were infected (onset, 12 February-13 March); all attended the same small church group as the index patient. The index patient's parent reported she had been vaccinated against measles in New Zealand at the age of one year, but did not have a record to confirm this. No other patients in the cluster had been vaccinated against measles. In the third cluster, the index patient was an 18-year-old woman who had returned from Bali on 4 December and became ill seven days later. Her brother developed prodromal symptoms 12 days later. Neither had been vaccinated against measles. Measles vaccination history Vaccination histories of the 317 notified patients are shown in Box 4. More than half those notified (55%) reported having been vaccinated, more than half of whom provided a vaccination date from a personal vaccination record. Reported measles vaccination status was compared with the presence of measles IgG for those with serological results available. Only 7% of those who reported prior vaccination lacked measles IgG. In contrast, 67% of patients who were aged over one year (and therefore eligible for vaccination) and did not report being vaccinated lacked measles IgG (P < 0.001). Among patients who reported vaccination, those who provided a vaccination date were no more likely to have measles IgG detected than those who did not provide a date (P = 0.76). Prior measles vaccination was reported by 141 patients (62%) who were classified as laboratory rejected, compared with six (32%) who were classified as laboratory confirmed (P = 0.01). Among patients with laboratory-confirmed measles, sporadic cases were more likely to give a history of vaccination (5/8) than those who were part of a cluster (1/11) (Fisher's exact test, P = 0.04). Reference laboratory testing Of the 19 patients classified with laboratory-confirmed measles, 16 were positive for measles IgM on testing at VIDRL, two after initial positive results elsewhere. The 16 comprised all 11 cluster cases and five sporadic cases. Another three sporadic cases were positive for measles IgM on testing at other laboratories but had insufficient serum available for retesting at VIDRL. These cases were still classified as "laboratory confirmed". A further three patients were positive for measles IgM on testing at other laboratories but were negative on retesting at VIDRL and were classified as "laboratory rejected". Evaluation of NHMRC clinical case definition for suspected measles There was sufficient clinical information to classify 275 notified patients (87%) according to the NHMRC clinical case definition for suspected measles: 92 (33%) met the definition, and 183 (67%) did not. To examine the utility of the NHMRC case definition, we analysed cases that were able to be classified both in this way and according to serological results -- either laboratory confirmed (18) or rejected (202) as measles. Results are shown in Box 5. Sensitivity of the NHMRC case definition was 61% and specificity was 66%, while positive and negative predictive values were 14% and 95%, respectively. When non-index cases from clusters were excluded (to test the utility of the definition in identifying cases with no epidemiological link to a confirmed measles case), sensitivity and positive predictive value fell to 40% and 5%, respectively, while specificity and negative predictive value remained almost unchanged. Cases from clusters were more likely than sporadic cases to satisfy the NHMRC case definition (10/11 [91%] versus 1/7 [14%]; Fisher's exact test, P = 0.002). The relationship between notification and laboratory measles diagnosis was also examined: the positive predictive value of notification was 8% (18/220), dropping to 5% (10/212) when non-index cases were excluded. Discussion We found that, during the interepidemic period of July 1997 to December 1998 in Victoria, a clinical diagnosis of measles had a low positive predictive value. Despite an 81% rate of serological testing, only 6% of all measles notifications were laboratory confirmed (8% of those that could be classified on the basis of serological results). Laboratory diagnoses of human parvovirus or rubella infections accounted for a further 8% of measles notifications, similar to experience in other countries that have conducted enhanced surveillance.14These results highlight the critical importance of laboratory confirmation as part of enhanced measles surveillance. They also highlight the low utility of the NHMRC clinical case definition for suspected measles. As only 33% of notified cases met this definition, it does not seem widely used as the basis for notification. Furthermore, it was neither sensitive (40%) nor highly predictive of true measles (5%) during this interepidemic period. Therefore, rather than the NHMRC clinical case definition for suspected measles, we advocate a definition similar to that used by the Pan American Health Organization of all cases in which a health worker suspects measles.15 Our findings do not mean that those responsible for measles surveillance, investigation and control can ignore measles notifications. The Disease Control Section now relies on urgent serological testing performed by VIDRL to inform public health action and improve the quality of the surveillance dataset. In Victoria, clinical specimens can often be collected within 24 hours of notification, with a laboratory result available on the next testing day.6 During the interepidemic period, when measles was rare, if public health action were to involve excluding contacts of a notified case from a school or childcare centre, we attempted to arrange urgent serological testing. No action was taken until the result was available. If serological testing was not possible, we treated the case as though it were measles regardless of whether it met the NHMRC case definition. Based on our experience, and drawing on elements from the National Measles Surveillance Strategy,7 we have refined recommendations for follow-up of measles notifications in a region with good disease control during an interepidemic period (Box 6). We believe these recommendations will allow identification of clusters of disease and minimise unnecessary public health action. We have maximised the sensitivity of the passive surveillance system by following up notifications from any source. By using laboratory testing to identify cases that are not measles, we have minimised the likelihood that our surveillance dataset will consist largely of false-positive notifications. Because no IgM antibody test is 100% specific, even laboratory-confirmed cases may not be measles. We found that three of five laboratory diagnoses of measles made in non-reference laboratories could not be confirmed at VIDRL. Sporadic cases were less likely to be confirmed at VIDRL than cluster cases and were also less likely to meet the NHMRC case definition, but were more likely to report prior measles vaccination. As prior measles vaccination correlates well with measles immunity, we believe that at least some of the sporadic cases classified as laboratory confirmed were not true measles. This reinforces the important role of reference laboratories as we approach national measles elimination and global eradication.7 We suggest that local transmission of measles within Victoria during this interepidemic period was minimal. We base this belief on the small number of sporadic cases identified, along with the possibility that some of these cases were not true measles, and the fact that identified clusters of infection involved few people and were self-limiting. Specimen collection for genotyping is already under way and will provide further evidence of the interruption of indigenous transmission in Victoria.16,17 The findings of the enhanced surveillance program, along with those from investigation of the 1999 measles outbreak in Victoria,5 lead us to believe that the two-dose MMR vaccination policy and the 1998 measles control campaign have dramatically reduced circulation of measles virus in the targeted age groups. We have demonstrated that, when measles is rare, enhanced surveillance relying on laboratory confirmation is essential to identify true cases of measles promptly and to ensure that surveillance datasets do not largely comprise false positive notifications. Acknowledgements The Victorian Enhanced Measles Surveillance Working Party appreciates the cooperation of the patients who agreed to be interviewed and provided serum samples for enhanced surveillance. We also gratefully acknowledge the nursing staff, clinicians, and pathology collection centres who collected serum specimens during the study period. Enhanced surveillance and public health intervention would not be possible without notification of cases by clinicians and laboratories. References World Health Organization. Expanded programme on immunization (EPI). Meeting on advances in measles elimination: conclusions and recommendations. Wkly Epidemiol Rec 1996; 71: 305-309. Lambert S. Measles in Victoria 1992 to 1996: the importance of laboratory confirmation. Comm Dis Intell 1998; 22: 17-22. National Health and Medical Research Council. The Australian immunisation handbook. Canberra: AGPS, 1997. National Centre for Disease Control. Immunise Australia program: measles control campaign. Comm Dis Intell 1998; 22: 156. Lambert S, Lynch P, Morgan M, et al. Measles outbreak -- young adults at high risk. Victorian Infectious Diseases Bulletin 1999; 2: 21-22. The Enhanced Measles Surveillance Working Party. Implementing a system of enhanced surveillance for measles in Victoria. Commun Dis Intell 1999; 23: 51-54. Heath T, Burgess M, McIntyre P, Catton M. A national measles surveillance strategy. Commun Dis Intell 1999; 23: 41-49. Jenkin GA, Chibo D, Kelly HA, et al. What is the cause of a rash after measles-mumps-rubella vaccination? Med J Aust 1999; 171: 194-195. Centers for Disease Control and Prevention. Measles, mumps, and rubella -- vaccine use and strategies for elimination of measles, rubella, and congenital rubella syndrome and control of mumps: recommendations of the Advisory Committee on Immunisation Practices (ACIP). MMWR Morb Mortal Wkly Rep 1998; 47 (RR-8): 1-58. Helfand R, Heath J, Anderson L, et al. Diagnosis of measles with an IgM capture EIA: the optimal timing of specimen collection after rash onset. J Infect Dis 1997; 175: 195-199. Ferson M, Young L, Robertson P, Whybin L. Difficulties in clinical diagnosis of measles: proposal for modified clinical case definition. Med J Aust 1995; 163: 364-366. National Health and Medical Research Council. Measles: guidelines for the control of outbreaks in Australia. Canberra: AGPS, 1996. Dean A, Dean J, Coulombier D, et al. Epi Info, version 6: a word processing database, and statistics program for public health on IBM-compatible microcomputers. Atlanta, Ga: Centers for Disease Control and Prevention, 1995. Brown D, Ramsay M, Richards A, Miller E. Salivary diagnosis of measles: a study of notified cases in the United Kingdom, 1991-3. BMJ 1994; 308: 1015-1017. Centers for Disease Control and Prevention. Measles eradication: recommendations from a meeting cosponsored by the World Health Organization, the Pan American Health Organization, and CDC. MMWR Morb Mortal Wkly Rep 1997; 46 (RR-11): 1-20. Rota JS, Heath JL, Rota PA, et al. Molecular epidemiology of measles virus: identification of pathways of transmission and implications for measles elimination. J Infect Dis 1996; 173: 32-37. Chibo D, Birch C, Rota P, Catton M. Genetic characterisation of measles viruses isolated in Victoria, Australia 1973-1998. Immunisation beyond 2000. 6th National Public Health Association Immunisation Conference; 1998 Nov 4-5; Melbourne. Canberra: Public Health Association of Australia, 1998. (Received 30 Jun, accepted 27 Oct, 1999) Authors' details Department of Human Services, Melbourne, VIC Stephen B Lambert, FAFPHM, Public Health Physician; Ross M Andrews, MPH, MAppEpid, Epidemiologist; Pauline A Lynch, Public Health Nurse; Debbie K Gercovich, Paediatric Phlebotomist; Melissa A Morgan, MB BS, Immunisation Coordinator; Rosemary A Lester, FAFPHM, Public Health Physician. Victorian Infectious Diseases Reference Laboratory, Melbourne, VIC Heath A Kelly, FAFPHM, Head, Epidemiology Division; Mike C Catton, FRCPA, Head, Virology Division; Jennie A Leydon, BAppSci, Senior Scientist. Microbiological Diagnostic Unit, University of Melbourne, Melbourne, VIC. Geoffrey G Hogg, FRACP, FRCPA, Director. Reprints will not be available from the authors. Correspondence: Dr H A Kelly, Victorian Infectious Diseases Reference Laboratory, Locked Bag 815, Carlton South, VIC 3053. heath.kellyATnwhcn.org.au Make a comment Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> 1: Classification of notified measles cases by the Victorian Enhanced Measles Surveillance Program 1. Laboratory confirmed Serum is positive for measles IgM,* and patient had not received the first dose of a measles vaccine within 45 days of specimen collection9 OR Diagnostic rise in measles antibody titres in paired sera OR Wild-type measles virus isolated from a clinical specimen OR A clinical specimen is PCR-positive for wild-type measles virus 2. Laboratory rejected Serum is negative for measles IgM with sample collected at least three days after rash onset10 OR Serum is negative for measles IgM but positive for measles IgG OR Serum is positive for rubella IgM OR Serum is positive for human parvovirus IgM 3. Epidemiologically linked to a laboratory-confirmed case Neither 1 nor 2 above AND An epidemiologic link to a laboratory-confirmed case has been established7 4. Clinically compatible Neither 1, 2 nor 3 AND The case satisfies the NHMRC clinical case definition † for suspected measles 5. Not clinically compatible Neither 1, 2 nor 3 AND The case does not satisfy the NHMRC clinical case definition for suspected measles 6. Not classifiable Neither 1, 2 nor 3 AND There are insufficient clinical data available to allow classification as clinically compatible (4) or not clinically compatible (5). NHMRC=National Health and Medical Research Council. PCR=polymerase chain reaction. *Sera that gave IgM-positive results at laboratories other than the Victorian Infectious Diseases Reference Laboratory (VIDRL) were retested at VIDRL and classified accordingly. If serum was not available for retesting, then the case was classified as laboratory confirmed to maximise sensitivity, rather than positive predictive value, of the system. †Morbilliform rash, fever present at rash onset, and cough. Back to text Back to text 3: Serological results for patients notified with measles in Victoria, July 1997 to December 1998 Age group (years)Number (% of notifications) Serologically tested (% of age group) Serologically confirmed (% of tested)<190 (28%)69 (77%)2 (3%)1-4122 (38%)100 (82%)7 (7%)5-963 (20%)55 (87%)010-1927 (9%)22 (81%)5 (23%)>2015 (5%)12 (80%)5 (42%)Total317258 (81%)19 (7%) Back to text 4: Measles vaccination and immunity for 317 notified cases in Victoria, July 1997 to December 1998 Reported vaccination statusNumber (% of notifications)Serologically tested (% of vaccination group)IgG-negative (% of tested)Vaccinated174 (55%)152 (87%)11 (7%)Date provided9987 (88%)7 (8%)No date provided7565 (87%)4 (6%)Not vaccinated124 (39%)92 (74%)83 (90%)Age <1 year9068 (76%)67 (99%)Age ≥1 year3424 (71%)16 (67%)No information19 (6%)14 (74%)2 (14%) Back to text 5: Utility of the National Health and Medical Research Council clinical case definition for suspected measles in Victoria, July 1997 to December 1998 Predictive value SensitivitySpecificityPositiveNegativeAll cases11/18 (61%)133/202 (66%)11/80 (14%)133/140 (95%)Excluding non-index cases4/10 (40%)133/202 (66%)4/73 (5%)133/139 (96%)Back to text 6: Recommendations for follow-up of measles notifications in an interepidemic period Cases of measles should be notified on suspicion, regardless of whether they satisfy the NHMRC clinical case definition for suspected measles. A serum specimen should be obtained for all sporadic notified cases of measles, and from at least two cases in an outbreak. All IgM positive serological results should be confirmed at a reference laboratory. If public health action during an interepidemic period is to involve excluding contacts, this action should be postponed if rapid serological testing is available. If a serum specimen cannot be obtained from a notified case, or rapid serological testing is not available, it should be assumed the case is measles, regardless of whether the case meets the NHMRC clinical case definition for suspected measles, and public health action should be taken immediately. Back to text

Stephen B Lambert · Heath A Kelly · Ross M Andrews · Mike C Catton · Pauline A Lynch · Jennie A Leydon · Debbie K Gercovich · Geoffrey G Hogg · Melissa L Morgan · Rosemary A Lester

Water Hazards Patterns of drowning in Australia, 1992-1997 Ian J Mackie MJA 1999; 171: 587-590 For editorial comment, see Walker Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Public and environmental health Abstract Objective: To determine patterns of victims, circumstances and locations of drownings in Australia in 1992-1997, inclusive. Methods: Population figures and available details of all drownings were obtained from the Australian Bureau of Statistics. Accidental non-boating drownings (ICD E910), boating incidents (E830-832), homicide (E964), suicide (E954), and other deaths without a drowning E code but "flagged" because drowning was involved (although not the primary cause of death) were included. Results: The overall accidental non-boating drowning rate was 1.44/100 000 population/year. The commonest sites for non-boating drowning were ocean or estuary (22%), private swimming pools (17%), non-tidal lakes and lagoons (17%), surfing beach (10%) and bathtub (7%). 22% of victims were aged under 5 years; this group had a drowning rate of 4.6/100 000 population/year. Very few young children drowned in the ocean or in boating incidents. The rate of boating drownings was 0.29/100 000 population/year. Overseas tourists comprised 4.7% of all non-boating drownings, 18% of surf and ocean drownings, and 25% of all scuba drownings. Indigenous people had a much higher drowning rate than the general population. Conclusions: Drownings in children aged less than 5 years continue to be the greatest challenge for water safety organisations and legislators. Drownings in the Indigenous community and among tourists requires more detailed study and action. To assist in developing preventive strategies, the National Water Safety Council will need to clarify the categories described as "ocean/estuary" and " lake, lagoon, dam and waterhole". Introduction Accidental drowning is a largely preventable cause of death. Water safety organisations, the general public and legislators need adequate information about the circumstances of drowning to target preventive action effectively. While the 1993 National Drowning Study concluded that the risk of accidental drowning in Australia and other countries has steadily decreased since 1920,1 that study and a later report2 did not provide detailed national information on where drownings occurred. Although the Australian Bureau of Statistics (ABS) has provided figures on accidental drownings in Australia dating from 1920, it has only reported the locations of accidental drownings since 1992. Currently, drowning is classified under the International Classification of Diseases (ICD) Supplementary classification of external causes of injury and poisoning codes.3 The relevant "E" codes and brief descriptions are shown in Box 1. In addition to the E codes, in 1992 the ABS introduced a nationally consistent system of "flags" for all drownings and other conditions where drowning is cited as one of two or more causes of death, but not the primary cause. These flags form the basis of specialised drowning tables in which flags 1-36 are for non-boating drownings and flags 37-53 are for various boating deaths. In this study, I examined both the international E codes and the ABS flag system4 to present new data which may help target those most at risk in the different locations where drownings occur. Methods Figures on accidental drownings in Australia from 1992-1997, inclusive, were obtained from the ABS. Accidental non-boating drownings (ICD E910: "Accidental drowning and submersion") were divided into locations and activities, which were then examined separately for age and sex distribution. Boating incidents (E830-832), homicide (E964), suicide (E954), and other deaths without a drowning E code but with the drowning flag applied were also studied. Implementation issues in 1992 and 1993 resulted in very slight discrepancies in drowning figures between the "E" code and "flag" systems. Five groups were subjected to detailed analysis. These were children aged under five years, people aged over 65 years, Indigenous people, overseas tourists, and those who drowned in the bathtub. Results Overall, 2673 people drowned in Australia in 1992-1997. These included 1551 non-boating drownings (E910; see Box 2), 292 drownings in boating incidents (E830-832; see Box 3), 390 suicides in the water (E954), and 28 homicides (E964), as well as several accidental drownings that appeared under a "drowning flag" rather than an E code (46 people with epilepsy who drowned, 13 who drowned because they had a heart attack or stroke while in the water, and 86 who drowned in motor vehicles accidents in the water). The remaining 267 deaths were "incidental" drownings -- generally those for which the coroner could not decide on a classification. The distributions of locations of all Australian accidental non-boating drownings and for selected groups are shown in Box 4, as is a summary of features of drowning deaths for children aged under five years, people aged 65 or more years, Indigenous people and overseas tourists. The age and sex distribution and detailed findings for bathtub drownings are shown in Box 5. Discussion Overall, this study shows that children aged under five years are most vulnerable to drowning in Australia. It also shows, with data not previously presented, that a considerable number of overseas tourists drown in our waters, and that the frequency of drownings of Indigenous people is disproportionately high, with an unusual number of drownings in young men. Twenty-two per cent of all drowning victims are in the 0-4-years age group, although this group comprises only 7% of the population. The rate of drownings in this age group (4.6 per 100 000 population per year) for 1992-1997 has changed little from that for 1986-1990 (4.7 per 100 000 population per year).1 It is thus clear that the high frequency of drowning in very young children is not improving. The figures provide strong backing for the recommendations of Nixon and colleagues,2 which were compilation of better coronial information, better police investigation of toddler drownings to include information on fencing and other vital details, detailed study of adolescent drownings, investigation of surveillance methods, support for advocacy of fencing of swimming pools, community education on the dangers of mixing alcohol with aquatic activities, and making first aid training mandatory for all pool owners. In particular, legislation on fencing for private pools is inadequate -- it varies from State to State, and local government areas have their own rules which are not always enforced. There is a real need for uniform national legislation for pool fencing that complies with the recommendations of the Australian Standards Association to help arrest this high rate of drowning in very young children. Details of drownings involving overseas tourists have not previously been published, and this is clearly an area in which government must work through the Water Safety Council to reduce the risk. Tourists and new migrants must be provided with suitable information and perhaps increased supervision when near the ocean. The ocean and recreational snorkelling or scuba diving present the greatest risks for tourists. Drowning in Aboriginal and Torres Strait Islander people also requires urgent government action through the appropriate established organisations. Differences in drowning incidence in different racial groups have been previously documented.6-8 The pattern of drownings in the Australian Indigenous population (Box 4) is quite different from that of the population as a whole, with a very high incidence in children under five years and in the 25 to 34 years age group. Further, ABS advice indicates that "death data for indigenous persons is undernumerated. While indigenous status is now a question on all State and Territory death forms, the ABS only regards data for South Australia, Western Australia and Northern Territory as having sufficient coverage to be of publishable standard" (ABS, personal communication). Bathtub drownings are disturbingly common on a national basis and preventive approaches need to vary for different age groups. The frequency of infant and toddler bathtub deaths has been documented in State reports for two decades,1 but this is the first national survey. The bathtub is the only site where female deaths predominate. This has been reported in previous studies,1 but the reasons for this phenomenon are not apparent. Most bathtub deaths require much more careful forensic scrutiny than they have received to date in most countries. Carbon monoxide, epilepsy, drugs and alcohol, cardiac arrest, suicide, homicide and child abuse have all been implicated, and there is little doubt that death in the bathtub at any age should be investigated carefully to determine whether the cause was natural or deliberate. Confirmation of true accidental drowning in bathtubs may be less common with such an approach. The quality of the information available needs to be improved to help target preventive action. For example, as pointed out previously,4 reliance solely on E codes would result in many drownings remaining unidentified. There were 80 drownings in motor vehicle accidents and a large number of suicides (390, making suicide more common than drowning in boating accidents [292]), and others, such as deaths from myocardial infarction, stroke and spinal injuries, where the involvement of drowning was only obvious from the ABS flag system. Further, there is a lack of detailed information on drownings listed within the E codes. "Lake, lagoon, dam and waterhole" and ocean/estuary drownings cover many different locations requiring different preventive measures -- this needs further investigation by the recently formed National Water Safety Council in conjunction with coroners, police and the National Injury Surveillance Unit. The most comprehensive review of measures to prevent drowning in Australia was published in 1995 by the Commonwealth Department of Human Services and Health, and contains most of the references of importance up to that time.2 The data for 1992-1997 in this study will provide the new National Water Safety Council with added information to assist more informed targeting of individual risk groups in specific areas. Acknowledgements I received great assistance from the officers of the Australian Bureau of Statistics, the executive officers of the Royal Life Saving Society Australia and Dr George Stathers. Purchase of the statistical computer disk with relevant data was funded by the Royal Life Saving Society Australia. References Mackie I, Tebb N, Eady T. National drowning study, Parts 1 to 4. Sydney: Royal Lifesaving Society Australia, 1993. Nixon J, Pearn J, Oldenburg B, Pitt W. Review of countermeasures to reduce drowning, near drowning and spinal injuries fron diving into shallow water. Canberra: Commonwealth Department of Human Services and Health, 1995. Department of Health and Human Services. The international classification of diseases, 9th revision, clinical modification (ICD-9-CM). 5th ed. Vol. 1: Diseases tabular list, October 1994. Bethesda, Md: United States DHHS (Publication No. PHS 94-1260). Smith G, Langley J. Drowning surveillance: how well do E codes identify submersion fatalities. Injury Prevention 1998; 4: 135-139. Australian Bureau of Statistics. Population by age and sex. Canberra: ABS, 1997. (Catalogue no. 3201.0.) Dietz P, Baker S. Drowning: epidemiology and prevention. Am J Public Health 1974; 64: 303-312. Branche C. Who drowns in the United States? Proceedings of International Medical-Rescue Conference. San Diego: International Lifesaving Federation, 1997. Mael F. Staying afloat: within-group swimming proficiency for whites and blacks. J Appl Psychol 1995; 80: 479-490. (Received 5 May, accepted 28 Oct, 1999) Authors' details Royal Life Saving Society Australia, Sydney, NSW. Ian J Mackie, AM, FRACP, National Medical Adviser. Reprints: Dr I J Mackie, PO Box 280, Cronulla, NSW 2230. ianmackieATmsn.com.au 1: International Classification of Diseases (ICD) Supplementary classification of external causes of injury and poisoning codes relating to drowning*E830Accident to watercraft causing submersionE832Other accidental submersion or drowning in water transport accidentE910Accidental drowning and submersionE954Suicide and self-inflicted injury by submersion (drowning)E964Assault by submersion (drowning)E984Submersion (drowning) undetermined whether accidentally or purposefully inflicted.*Drowning is defined by the Medical Commission of the International Lifesaving Federation as death resulting from suffocation within 24 hours of submersion in a liquid medium. Back to text2: Accidental non-boating drownings in Australia in 1992-1997 (E910) Overall There were 1551 drownings, a national rate of 1.44 per 100000 population per year (based on 1996 population data5) 77% of victims were male. Of 1096 victims aged over 14 years, the presence of drugs including alcohol was recorded in 148 (14%); 117 of these were male. The highest prevalence was in the 0-4 years age group Males made up 64% of the 0-4 years age group and 62% of people aged over 64 years who drowned. Locations of drownings Most non-boating drownings (22%) occurred in ocean/estuary (tidal) sites. - 90% of the victims were male and very few were aged under 15 years. 17% of drownings occurred in private swimming pools. - 64% involved children aged under four years, two-thirds of whom were male. - Of all those aged over 34 years who drowned in private pools, 63% were female. - Only 3% of accidental drownings occurred in public and "other" pools (28 drownings in public pools [20 males] and 18 in "other" pools [11 males]). 17% of drownings occurred in non-tidal lagoons and lakes. - 82% of victims were male, and there was a high frequency of drownings in 0-4-year-olds. 10% of drownings (162) occurred at surfing beaches. - 144 victims (89%) were male. - No one aged less than 5 years and few aged 5-14 years drowned at a surfing beach. 5.8% of drownings occurred while victims were fishing. - They comprised 54 victims (one female), all aged over 15 years, who were washed from rocks, and another 36 people (35 male) who drowned in tidal water. - The only female was 10 years of age, one male was four years old; there were no drownings in males aged 5-14 years, then deaths were relatively evenly distributed for age, with the greatest number, eight, in the over 65 years age group. 3.6% of the 1551 people drowned while using scuba equipment. - 44 (79%) were male, 15 (27%) were overseas tourists. - 36% of scuba deaths occurred in Queensland, 21% in Western Australia and 18% in New South Wales. 15 people drowned while snorkelling (11 males, 3 overseas tourists). 36 people (34 males) drowned while attempting rescues; 12 in surf, one in a public pool and 23 at other sites. Back to text 3: Drowning in boating incidents in Australia in 1992-1997 (E830, E832) There were 292 boating drownings, an average of 52 per year and a rate of 0.29 per 100000 population per year 94% of victims were male. The presence of a drug was reported in 7% of victims, all aged between 35 and 54 years (alcohol in 19, and a different drug in two others). Back to text 4: Drownings in selected groups Children aged <5 years There were 353 drownings in this group (64% boys), a rate of 4.6 per 100000 population/year. - In addition to the locations shown, 6% of toddlers drowned in an object such as a bucket and 2% drowned in an irrigation canal. - 37 infants (22 boys) drowned in their first year of life, 26 in the bathtub, 4 in a private pool, 3 in an object such as a bucket, 2 in a lake, 1 in the ocean and 1 in an irrigation canal. People aged 65+ years 12% of all accidental drowning victims were in this group (38% were women), a rate of 1.5 per 100000 population/year. - More women than men drowned in pools (22 v.11) and bathtubs (18 v. 4). Indigenous people The 63 non-boating drownings of Aboriginals and Torres Strait Islanders represent 4.2% of the national total, while they constitute only 1.8% of the population. - 30% of all Indigenous drownings were in the 25-34 years age group (95% of these male). - Only 7 Indigenous people drowned in boating incidents. All victims except one were in motorised craft; all were male. Overseas tourists 88 tourists from 12 countries drowned in Australia during 1992-1997 (age range, 3-78 years; 16 female) - 73 drowned in non-boating incidents, 5 in boating incidents and 10 in unspecified circumstances. - 38 tourists came from Europe (15 from the United Kingdom, 10 from Germany), 35 from Asia (17 from Japan), 7 from the United States and 8 from other countries. - 89% of tourists drowned in the ocean and 11% drowned in fresh water. 61% drowned at surfing beaches or elsewhere in the "ocean" and a further 24% drowned while scuba diving or snorkelling. Tourist drownings comprised 4.7% of non-boating drownings, 18% of surf and ocean drownings, 25% of scuba and snorkelling drownings and 1.6% of boating drownings. Back to text 5: Bathtub drownings in Australia, 1992-1997 There were 112 bathtub drownings (64 female [57%]). Bathtub drownings comprise 7% of all drownings. 47% of victims were aged <5 years. 20% of victims were aged over 64 years. Alcohol was present in 14% of victims aged over 15 years. Of these, all except one were aged over 60 years. An unspecified drug (but no alcohol) was detected in three younger people who drowned in the bathtub. Back to text

Ian J Mackie

Bites and Stings Funnel-web spider (Hadronyche infensa) envenomations in coastal south-east Queensland Five patients with confirmed funnel-web spider bites (Hadronyche infensa) presented to Nambour General Hospital, in south-east Queensland, between 1992 and 1998. Two patients required antivenom; low doses of antivenom were effective. Patients were bitten in spring and early summer. In areas such as this, where funnel-web spider bites are reported less frequently than in New South Wales, clinicians and the community should be aware of the risks and immediate management of these bites. Anthony P Harrington, Robert J Raven, Paul C Bowe, Gabrielle M Hawdon and Kenneth D Winkel MJA 1999; 171: 651-653 Introduction - Clinical record - Discussion - Acknowledgements - References - Authors' details - - More articles on Insects, bites and stings

Anthony P Harrington · Robert J Raven · Paul C Bowe · Gabrielle M Hawdon · Kenneth D Winkel

Bites and Sting Exotic myiasis with Lund's fly (Cordylobia rodhaini) After a four-week holiday in East Africa, a woman was diagnosed with furuncular myiasis: a third-instar larva of the fly Cordylobia rodhaini (Lund's fly) was found in a skin lesion. This is the first report of exotic myiasis and importation of this species of fly into Australia, and reflects the increasing risk of introducing exotic flies of public health and veterinary importance to Australia. Merilyn J Geary, Bernard J Hudson, Richard C Russell and Andrew Hardy MJA 1999; 171: 654-655 Introduction - Clinical record - Discussion - Acknowledgements - References - Authors' details - - More articles on Insects, bites and stings Introduction Myiasis is the invasion of living tissue by the larval stage (maggot) of flies.1 Australia has some species of flies that produce facultative and accidental myiasis in humans,2 but in other countries, particularly in Africa and South America, there are flies with zoonotic obligate myiasis that infest humans. With more frequent international travel, there is an increasing risk of infestations of these species being brought into Australia. Clinical record A 57-year-old woman presented to her general practitioner (A H) with a painful, discharging lesion on the outer aspect of her right thigh three days after returning to Australia from a safari vacation in East Africa. She was referred to a specialist (B J H), who diagnosed furuncular myiasis after seeing "something moving" at the base of the lesion. After occlusion with petroleum jelly, a fly larva protruded from the lesion and was removed with forceps (Figure 1a). The lesion healed uneventfully over the following two weeks. The patient had left Australia one month earlier and spent most of the safari trip camping. She travelled in four countries -- Kenya, Tanzania, Uganda and Zimbabwe (see Map). For the final 10 days she stayed at a private residence on a ranch between Bulawayo and Victoria Falls in Zimbabwe. She noticed the lesion two days after arriving at the ranch. It gradually developed over the next 10 days, becoming moderately painful and discharging. Although it was not possible to determine exactly where the infestation was acquired, from the species involved and the time required for its stage of development the contact probably occurred shortly before or shortly after arrival at the ranch in Zimbabwe. Discussion Genus Cordylobia The genus Cordylobia contains three species, C. anthropophaga, C. rodhaini and C. ruandae.1 Larvae of these flies are parasites of various mammals, particularly rodents. C. anthropophaga (the Tumbu fly of sub-Saharan Africa), and occasionally C. rodhaini, also parasitise humans.3,4Cordylobia is confined to the African continent, with C. rodhaini associated with tropical Africa, especially areas of rainforest from Senegal, through Central Africa, to Angola and Zimbabwe (see area marked on Map). The adult flies of C. rodhaini are large and robust, with a non-metallic red-brown to black abdomen and yellow coloration on the thorax and head. Adult flies feed on rotting fruits, vegetables and faeces, and are more abundant throughout the wet season, and most active in the early morning and evening. The life cycle of C. rodhaini is shown in Figure 2. Public health concerns Although importation of exotic myiasis-causing flies into Australia is not common, several species of obligatory fly parasites enter this country each year in the skin of overseas travellers (unpublished data).2,5-10 The most common exotic species of myiasis fly imported to Australia in humans is the human botfly (Dermatobia hominis) (Figure 1b), found in travellers returning from South and Central America (unpublished data). Others include the Tumbu fly (C. anthropophaga) (Africa), and the New World screw-worm fly (Cochliomyia hominivorax) (Central and South America). All are of medical and public health concern, and some, such as Chrysomya bezziana from Africa, South-East Asia and Papua New Guinea, and C. hominivorax, are of critical veterinary importance,8,11 and threaten local livestock industries. Travellers to the tropics and general practitioners in Australia should be aware of the potential for skin infestation by fly larvae, and local health professionals can assist quarantine, agriculture and other interested bodies to monitor the importation of these medically important insects. Acknowledgements The photographs were taken by Mr Stephen Doggett of the Department of Medical Entomology, Institute of Clinical Pathology and Medical Research (ICPMR), Westmead Hospital. References Zumpt F. Myiasis in man and animals in the old world. London: Butterworths, 1965: xi-xii, 75-77. Lee DJ. Human myiasis in Australia. Med J Aust 1968; 1: 170-173. Bertram DS. A note upon myiasis due to the larvae of Cordylobia Rodhaini Gedoelst. Ann Trop Med Parasitol 1938; 32: 431-435. Scholten ThH, Hicks RJ. Myiasis by Cordylobia rodhaini contracted in Africa and diagnosed in Canada. Can J Public Health 1973; 64: 488-489. Field AS. Myiasis in an Australian abroad. Med J Aust 1981; 1: 581-582. Moorehouse DE. Exotic parasitic infections in Australia [editorial]. Med J Aust 1983; 2: 592-593. Prociv P. The risk from exotic myiasis in Australia [letter]. Med J Aust 1989; 150: 722-723. Searson J, Sanders L, Davis G, et al. Screw-worm fly myiasis in an overseas traveller -- case report. Commun Dis Intell 1992; 16: 239-240. Rubel DM, Walder BR, Jopp-McKay A, Rosen R. Dermal myiasis in an Australian traveller. Australas J Dermatol 1993; 34: 45-47. Levot G. Interception of larvae of an exotic fly pest in skin lesions on Australian travellers. Commun Dis Intell 1994; 18: 229-230. Norris KR. Myiasis in humans. Med J Aust 1989; 150: 235-237. (Received 17 Jun, accepted 27 Oct, 1999) Authors' details Department of Medical Entomology, University of Sydney, and Institute of Clinical Pathology and Medical Research, Westmead Hospital, Westmead, NSW. Merilyn J Geary, DipAppSc, Senior Technical Officer. Richard C Russell, MSc, PhD, Director. Microbiology Department, Royal North Shore Hospital, Sydney, NSW. Bernard J Hudson, FRACP, FRCPA, Staff Specialist. Manning Medical Practice, Woollahra, NSW. Andrew Hardy, MB BS, General Practitioner. Correspondence: Professor R C Russell, Department of Medical Entomology, Westmead Hospital, Westmead, NSW 2145. RichardRATicpmr.wsahs.nsw.gov.au Make a comment Back to text 1a 1b Back to textBack to textFigure 1a: A third-instar larva of Cordylobia rodhaini (size about 20mm, bar=1mm), infecting a woman just returned from East Africa. Myiasis caused by this species has not previously been recorded in a patient in Australia. The third instar of C. rodhaini is readily recognisable, with a scattered covering of spines, longer than those of the related fly larva C. anthropophaga and not organised in rows as in that species.1,3 Figure 1b: A third-instar larva of Dermatobia hominis (bar=1mm), which occurs in Central and South America, and is the myiasis fly species that most commonly infects travellers returning to Australia. Figure 2: Description of lesion: At the site of penetration, a red papule forms and gradually enlarges. At first the host may experience only intermittent, slight itching, but pain develops and increases in frequency and intensity as the lesion develops into a furuncle. The furuncle's aperture opens, permitting fluids containing blood and waste products of the maggot to drain. Back to text

Merilyn J Geary · Bernard J Hudson · Richard C Russell · Andrew Hardy

Clinical Practice Health online: the future isn't what it used to be Over the next 10 years, the healthcare system will change to focus more on preventive medicine and healthcare in the home, with fewer doctors and a new class of home healthcare providers. Healthcare professionals need to debate how best to manage these changes. Peter M Yellowlees and Peter M Brooks MJA 1999; 171: 522-525 Introduction - Changing information presentation - The effects - The solutions - References - Authors' details - - More articles on Informatics and computers Introduction Over the past 30 years the framework in which doctors and other healthcare professionals practise has changed relatively little in comparison with the enormous changes seen in transport, manufacturing and telecommunications. While many doctors and health service managers prefer to ignore the extraordinary changes outside of the health system, they do so at their peril. Healthcare will be very different by 2010; the focus will be on the patient at home rather than the provider in the institution. There are three major drivers for this change.1 The first is the economic imperative to restrain healthcare costs in a setting of an ageing community and escalating costs of institutional care and technology. Our present model of care primarily focused on institutions, be these hospitals or related step-down facilities and nursing homes, is not sustainable. In Australia, we already spend more than $21 billion per year on institutional (hospital and nursing home) care. We have to explore ways of reducing this cost. The second is increasing consumerism, and the evolution of the "informed patient". As the "baby boomer" generation ages it will be increasingly concerned about its own welfare and will focus more and more on health. Every social issue that this generation has touched has changed radically, and there is no reason why healthcare should be exempt. The dynamic, yet often self-centred, approach by the baby-boomers is likely to be translated into a much stronger push for home healthcare. The third is the extraordinary changes in communication technology, and the evolution of the Internet. Knowledge has never been as important and as accessible as it is today -- it is now one of the economic cornerstones of our society. The distribution of knowledge is occurring at a remarkable pace via the Internet, as well as through multiple other media outlets. For some years, clinical care has been increasingly delivered electronically via telemedicine, as well as telephonically. Australia is at the leading edge of these developments.2,3 Changing information presentation Before we can benefit from the new technologies (see Box), we have to solve the problems of information quality and information overload, especially on the Internet.9 A variety of sites are being developed as quality health information portals, such as the National Library of Medicine in the United States,10 HealthInsite in Australia,11 and Omni in the United Kingdom.12 In addition, approaches are being developed to allow clinicians and patients to better assess the reliability and validity of health information.13 A more comprehensive Internet classification and coding system using metadata, as well as the development of sophisticated search engines, needs to emerge as a long term solution for this important problem.9 Only then will doctors be able to effectively obtain good quality decision support information within the time and process of a typical consultation. Within the health industry there have been enormous strides in the past five years in the development of electronic patient records, many using Internet protocols. The health system is, unfortunately and inevitably, still replete with many different types of information systems, most of which have been focused on financial and administrative applications. The challenge in the future will be to get all of these "legacy" systems to talk to the new Internet-based systems. Fortunately, Australia is well placed in this respect with the recent funding by the Federal Government of the Cooperative Research Centre for Distributed Systems Technology,14 which has a long term research program with the Centre for Online Health at the University of Queensland.15 There are many related activities at Monash University,16 the University of New South Wales,17 and in private industry. The national approach taken by the Collaborative Health Informatics Centre18 is greatly assisting the integration of the health and information technology industries. The effects We have a good idea of the illnesses and diseases that will be most prevalent and will cause the greatest disease burden by 2020.19 These are chronic cardiac, respiratory and psychiatric diseases, as well as road traffic accidents. The cardiac, respiratory and psychiatric diseases are all highly amenable to the provision of long term home care, while clearly a much more active approach to prevention and education is required to reduce the impact of road traffic accidents. A changing paradigm If we assume that by 2010 health information will be available in the homes of most Australians, and certainly on every health professional's desktop, then what will be the effects? The health system is already moving away from supporting episodic care to supporting continuity of care, and from a service-provider focus to an informed-patient focus. Increasingly, our past individual approach to treatment will be overtaken by the need for team approaches, underpinned by evidence and outcomes, clinical pathways, and guidelines. "Wellness promotion" will be seen as being more important than illness treatment. There will be a move away from institutional care to community care and to the development of the shared, distributed electronic patient record. Hospitals and health departments will make the shift from being autonomous, slowly-growing empires to becoming fluid and rapidly changing enterprises, as has occurred in industry. Therefore, there will be a need, quite simply, for fewer hospitals and more home care and community support services. Figure 1 shows a mock-up of how a patient's Web browser might look during an online consultation with a general practitioner. This patient-accessible electronic home care record system would allow instant contact with a range of healthcare professionals, information sources and other health services in an electronic distributed environment. The system will involve telemetry, monitoring, video links and automatic ordering systems, all delivered via Internet2. The entire health system will be focused on the patient at home (Figure 2) rather than on providers and institutions. If we can reduce institutional care by just 10%, over $2 billion per year will be made available for redistribution. The traditional doctor-patient relationship will alter, being driven much more intensively by patients. The doctor's role will become more advisory, analytic and interventionist. Doctors will need to be experts in assessing information from many different sources and in clinical reasoning, particularly for patients requiring more than a guidelines-and-pathways approach to care. Healthcare education will also be radically different. Medical schools and other health education institutions need to be thinking today about educating clinicians to work within a distributed, primary care focused environment.20,21 If we are correct in our predictions, there will be a need for fewer doctors beyond 2010. Not only will so much of our present-day medical content, knowledge and expertise be less important, but a group of highly skilled home healthcare professionals will exist, probably evolved from today's nurse practitioners. These healthcare providers will have prescribing and other treatment roles for patients being treated within pathway and guideline protocols. The changes will not stop there. There will also be massive opportunities, particularly for Australia, as it may be possible for Australian physicians to provide very much cheaper electronic healthcare into the US than is available locally within that country, if only because of differences in the cost of living and the strength of the dollar. It is more likely, however, that electronic healthcare will be provided in three main time zones (Figure 3), as it is highly unlikely that a doctor in, say, Australia will be prepared to consistently get up in the middle of the night to treat a patient in, for instance, Saudi Arabia or Brazil. The introduction of global electronic physicians and virtual healthcare systems will raise many important cultural, ethical, legal and legislative issues. These include, for example, the need for international medical registration and medical defence systems, the development of global information and security standards for the Internet, more flexibility in drug licensing across countries, and the need to integrate Eastern and Western styles of medicine when working across cultural boundaries. The solutions What are the implications of these changes for the present Australian healthcare sector? What should be done to prepare for this scenario? The following are suggestions. Cultural and political understanding and attitudes: There is a need for increased awareness of the importance of communications technologies in healthcare. Most global companies assume that 5%-10% of their budget will be spent on communication and information technologies. Research into distributed healthcare, both clinical models and technical solutions, is likely to be just as important as biotechnology in improving our national health profile. The clinical and information management issues are more important than, and have to drive, the technological changes. Once government makes a commitment to the changes looming in the near future, there will be the opportunity to create the necessary cultural and social changes required nationally to enable us to move to a future where information technology underpins healthcare delivery. The healthcare environment: There is a need for urgent, widespread debate about the future of healthcare, about the respective roles of doctors, patients, and other healthcare professionals, and about how best to transform a hospital-focused health system to one centred on patients and home care. If change is not guided from within the health system, it will certainly be enforced by external global and national factors. Technological requirements: There is a need to link the many existing computing systems into an Internet-based future. The necessary technological and information-based research and development programs must be focused on the development of user-friendly interfaces for patients of all ages, as well as for clinicians, and will involve the development of electronic clinical care protocols, whether these be delivered in real time, or by "store-and-forward" email, video mail, video conferencing, telephony or other methods. Specific projects need to be developed in home care, in wireless and collaborative environments, and in the development of improved electronic records. Australia needs closer links to the Internet2 consortium and to the exciting opportunities occurring in other countries, such as the Multi Media Super Corridor in Malaysia.22 Henry Ford, around the start of the 20th century, was quoted as saying that "history is bunk". While we believe strongly that history is of great importance, we also have to be well aware that the range and variety of changes confronting the world at present are greater, and are occurring more rapidly, than has ever been the case in the history of mankind. To quote Dr Rick Satava, an eminent surgeon with NASA: "The future isn't what it used to be."23 References Yellowlees P. Therapy online. Kansas: Telemedicine Today, 1999. Queensland Telemedicine Network. Queensland Health. <http://www.health. qld.gov.au/qtn/home.htm>. Accessed 18 October 1999. Yellowlees PM, Kennedy C. Telemedicine: here to stay. Med J Aust 1997; 166: 262-265. University Corporation for Advanced Internet Development. The Internet2 Project. <http://www.internet2.edu/>. Accessed 18 October 1999. Cairncross F. The death of distance. How the communications revolution will change our lives. Boston: Harvard Business School Publishing, 1997. Virtual Collaborative Clinic. <http://www.nren.nasa.gov/vdoc.html>. Accessed 5 October 1999. Graphics Visualisation and Usability Center, College of Computing, Georgia Tech. Virtual Reality Exposure Therapy. <http://www.cc.gatech.edu/gvu/virtual/Phobia/>. Accessed 5 October 1999. Van Houweling D. Distributed Education. 1998. Telecon '98 Conference, Anaheim, California. Appleyard R. Enhancing internet medical document retrieval with 'medical core metadata'. Health Information on the Internet 1999; 10: 6-8. United States National Library of Medicine. <http://www.nlm.nih.gov/>. Accessed 18 October 1999. HealthInsite. Commonwealth Department of Health and Aged Care. <http://www.healthinsite.gov.au/>. Accessed 18 October 1999. OMNI: Organising Medical Networked Information. <http://omni.ac.uk/>. Accessed 5 October 1999. Discern Online. <http://www.discern.org.uk/>. Accessed 12 October 1999. Distributed Systems Technology Centre. <http://www.dstc.edu.au/>. Accessed 5 October 1999. Centre for Online Health. University of Queensland. <http://www.coh.uq.edu.au/>. Accessed 5 October 1999. Centre of Medical Informatics. Monash University. <http://www.monash.edu.au/informatics/>. Accessed 5 October 1999. Biomedical Systems Laboratory. University of New South Wales. <http://www.bsl.unsw.edu.au/>. Accessed 5 October 1999. Collaborative Health Informatics Centre. <http://www.chic.org.au/main.html>. Accessed 5 October 1999. Murray CJ, Lopez AD, editors. The global burden of disease: a comprehensive assessment of mortality and disability from diseases, injuries, and risk factors in 1990 and projected to 2020. Harvard School of Public Health, 1996. Carlile S, Sefton AJ. Healthcare and the information age: implications for medical education. Med J Aust 1998; 168: 340-343. Coiera E. Medical informatics meets medical education. Med J Aust 1998; 168: 319-320. Mohan J. Malaysia's Telemedicine Vision and Initiatives. 1997. Telemed Asia '97 Conference, Kuala Lumpur, Malaysia. Satava RM. Telemedicine and virtual reality. American Telemedicine Association Annual Meeting, Salt Lake City. 17-21 April 1999. Authors' details Faculty of Health Sciences, University of Queensland, Brisbane, QLD. Peter M Yellowlees, MD, FRANZCP, Professor of Psychiatry, and Director, Centre for Online Health; Peter M Brooks, MD (Monash), FRACP, Professor, and Executive Dean. Reprints will not be available from the authors. Correspondence: Professor P M Yellowlees, Department of Psychiatry, University of Queensland, K Floor, Mental Health Centre, Royal Brisbane Hospital, Brisbane, QLD. P. YellowleesATmailbox.uq.edu.au http://www.coh.uq.edu.au Changing information technologies The technical ability to obtain high quality health information in the home or on the doctor's desktop depends on two things: bandwidth and accessibility. Both are on the point of being transformed to make massive amounts of information easily available to the clinician. The bandwidth issue relates to the development of Internet2 by a consortium of about 200 partners, mainly in North America, and including over 130 universities and more than 40 commercial concerns. Internet2 is expected to be between 100 and 1000 times more powerful than the present Internet. It will use much more efficient methods of information packaging to send more information down an equivalent-sized channel in a given time. This will enable a whole new generation of applications and has the potential to transform our lives in ways we cannot yet imagine.4 The issue of accessibility to information is also being resolved within First World countries, although it is crucial to note that in 1999 two-thirds of the world's population still do not even have access to a telephone.5 There are already over half a million kilometres of fibreoptic cable connecting cities and countries around the world. This will double within the next five years. By the end of 2000, it is expected that the latest of many intercontinental data links, a massively powerful fibreoptic cable weaving from Germany through the Mediterranean, across south-east Asia and on to Japan and Korea, will be installed. Simultaneously, greatly improved interactive satellites are being launched. There are now more than 200 such satellites in low earth orbit, acting like mobile phone towers or repeaters above the earth. Within five years, it is likely there will be more than 1000 such satellites, providing accessible global coverage. Improved bandwidth and accessibility will provide the opportunity to radically change the way we work and conduct business. We will be able to develop fully digitised libraries that include comprehensive video and audio collections, as well as develop cyberclinics such as the NASA-sponsored Virtual Collaborative Clinic.6 There will also be collaborative virtual research laboratories enabling "tele-immersion" - the ability to move inside space, inside the human body and into virtual reality situations. Virtual reality scenarios, where the patients move into a virtual world as part of their treatment process, are already being used to treat patients with specific phobias of heights and spiders.7 Scenarios also exist to allow surgeons to immerse themselves within a virtual middle ear, and teach the anatomy, pathology and surgery of the ear from within that organ.8 Glossary Bandwidth: The data transfer rate of an electronic communications system. Internet: An electronic communications network that connects computer networks and organisational computer facilities around the world. Internet protocol: The communications methods used for the Internet. Metadata: Data about data, such as what field the data relate to, who compiled the dataset, or how the data are formatted. Telemetry: Measurement of data and transmission to another site for storage or analysis. Virtual reality: An artificial environment which is experienced through sensory stimuli (as sights and sounds) provided by a computer and in which one's actions partially determine what happens in the environment. Back to textBack to textBack to textBack to text

Peter M Yellowlees · Peter M Brooks

Editorial Preventing stroke: what is the real progress? At last, stroke prevention is high on the political and public health agenda MJA 1999; 171: 285-286 National Stroke Awareness Week (27 September - 3 October) is a pertinent time to review recent progress in stroke prevention and awareness in the past few years. In Australia, stroke continues to be a major public health issue.1 More than 40 000 Australians each year experience a stroke, nearly a third of which are fatal.1,2 Another third of stroke sufferers become disabled, and stroke victims make up nearly one in four of Australia's chronic disabled population.1 The annual total cost of caring for stroke victims is at least $1.67 billion,2 a figure which will continue to rise with ageing of Australia's population. It is estimated that there will be at least 70 000 new stroke patients each year by 2016.2Nevertheless, real progress has been made in the past few years in several areas: The emergence, and application in clinical practice, of sound evidence for the effectiveness of several stroke-prevention strategies in people at high risk; A decline in stroke incidence due to effective prevention measures; and A willingness of Federal, State and Territory governments to take a more active role in stroke prevention. Strategies for reducing the social and economic burden of stroke are summarised in the Box. The effectiveness of primary stroke prevention in the entire population is difficult to ascertain. Mortality statistics are the only routinely collected data for measuring and monitoring the burden of stroke nationally, and between 1986 and 1997 the stroke mortality rate for Australian men and women fell by 3.2% and 3.5% per year, respectively. Since 1970 there has been a 68% overall reduction in stroke mortality.1,3 The recent Perth Community Stroke Study (PCSS)4 found that the decline in stroke mortality was due to a reduced incidence of stroke rather than an improvement in survival or a change in casemix (eg, a reduced proportion of lethal intracerebral haemorrhages). This fall in stroke incidence is likely to be due to a decline in the prevalence of important causal and modifiable risk factors. The PCSS identified several of these risk factors, many of which are well established, and some of which require confirmation in future studies.5 These include previous stroke or transient ischaemic attack, cigarette smoking, excess alcohol intake (> 60 g daily), a history of hypertension, diabetes mellitus, meat consumption (more than four times weekly), and adding salt to food. Over the past one to two decades, the Australian Institute of Health and Welfare (AIHW) has documented a significant decline in the population prevalence of many of these risk factors (ie, hypertension, smoking, total dietary fat intake, and saturated fat as a proportion of total energy intake).1 Although it is not possible to prove that health promotion programs, government legislation and the decline in prevalence and mean level of risk factors have been directly responsible for the reduction in stroke incidence in Australia, I believe the above data endorse the concept and power of the population approach to stroke prevention. It might be argued that the population approach impinges on all for the benefit of relatively few.3 However, most of us are prepared to adopt lifestyle behaviours (eg, wearing of seatbelts, application of sunscreen lotion) which reduce harm to the population as a whole, and stroke prevention measures would be similar in principle. Moreover, given that the risk of stroke in the next 40 years for a 45-year-old is one in four for men and one in five for women,1 there is also a reasonable chance of individual benefit in adopting lifestyle changes aimed at reducing the risk of stroke. The push for greater stroke awareness in our society has received a considerable boost in recent years from a greater involvement of governments in promoting awareness of stroke and facilitating educational programs aimed at reducing the risk of stroke. The involvement is exemplified by: Establishment of the National Stroke Foundation, which published a National Stroke Strategy and Victorian Stroke Strategy in 1997;9 Establishment by the New South Wales Health Department of the NSW Stroke Project;10 Endorsement by Australian health ministers of heart, stroke and vascular disease as one of the five National Health Priority Areas (NHPAs). The recent NHPA report, Cardiovascular Health 1998,11 highlights the strategies that are in place (and to be developed) to prevent stroke by improving awareness, lifestyle behaviours, and risk factor profiles of Australians, and improving outcomes for those with symptomatic disease through optimal diagnosis, management, rehabilitation, and community care.11 It also emphasises the ongoing role of the AIHW in operating a national system to monitor stroke incidence, pathology, risk factors, treatments, care, outcome (for patients and carers) and costs. At last, stroke is high on the political and public health agenda, but it is crucial that the commitment be maintained to measuring, monitoring and reducing the burden of stroke by widespread adoption of evidence-based practices and other strategies outlined in the NHPA report.11 Otherwise, we will soon experience a needless epidemic of stroke, with its legacy of death, disability and mounting cost. Graeme J Hankey Consultant Neurologist, and Head of Stroke Unit, Royal Perth Hospital Clinical Associate Professor, Department of Medicine, University of Western Australia, Perth, WA Email: gjhankeyATcyllene.uwa.edu.au Australian Institute of Health and Welfare (AIHW). Heart, stroke and vascular diseases, Australian facts. Canberra: AIHW/Heart Foundation of Australia, 1999. (AIHW Catalogue No. CVD 7; Cardiovascular Disease Series No. 10.) National Health and Medical Reseach Council (NHMRC). Clinical Practice Guidelines. Prevention of stroke: the role of anticoagulants, antiplatelet agents and carotid endarterectomy. Canberra: NHMRC/Australian Government Publishing Service, 1997: 3-4. Rose G. The strategy of preventive medicine. Oxford: Oxford University Press, 1992: 29-52, 64-106. Jamrozik K, Broadhurst R, Lai N, et al. Trends in the incidence, severity and short-term outcome of stroke in Perth, Western Australia. Stroke 1999. In press. Jamrozik K, Broadhurst RJ, Anderson CS, Stewart-Wynne EG. The role of lifestyle factors in the etiology of stroke. A population-based case-control study in Perth, Western Australia. Stroke 1994; 25: 51-59. Hankey GJ. Stroke: how large a public health problem, and how can the neurologist help? Arch Neurol 1999; 56: 748-754. Hankey GJ, Warlow CP. Treatment and secondary prevention of stroke: evidence, cost, and effects on individuals and populations. Lancet 1999. In press. Gorelick PB, Sacco RL, Smith DB, et al. Prevention of a first stroke. A review of guidelines and a multidisciplinary consensus statement from the National Stroke Association. JAMA 1999; 281: 1112-1120. National Stroke Strategy. Melbourne: National Stroke Foundation, 1997. Stroke in NSW. Priorities and strategies for better care. Sydney: NSW Health Department, 1997. Commonwealth Department of Health and Aged Care and Australian Institute of Health and Welfare. National Health Priority Area Report: Cardiovascular Health 1998. Canberra: Australian Institute of Health and Welfare, 1999. (Catalogue No. PHE9.) Strategies for reducing the burden of stroke and stroke recurrence (in increasing order of potential impact)6,7 Effective treatment of acute stroke6,7 Organised care in a stroke unit by a multidisciplinary team Aspirin 300 mg for acute ischaemic stroke tPA (may be effective, but possibly hazardous, and therefore is not currently registered in Australia or Europe for stroke treatment6) Secondary prevention of recurrent stroke in patients with transient ischaemic attacks (TIAs) and stroke (in decreasing order of cost-effectiveness)7* Treatment of high blood pressure with a diuretic or β-blocker Aspirin, aspirin + dipyridamole, or clopidogrel for patients in sinus rhythm Anticoagulation with warfarin for patients with atrial fibrillation Carotid endarterectomy for patients with severe stenosis of the internal carotid artery on the symptomatic side Primary prevention of stroke among people at high risk of stroke (eg, those with severe hypertension or atrial fibrillation)3,8 Treatment of high blood pressure with a diuretic or β-blocker "Statins" to lower serum cholesterol levels in patients with symptomatic coronary artery disease or hypercholesterolaemia Anticoagulation with warfarin for patients with atrial fibrillation and specific risk factors (age > 65 years, diabetes, hypertension, TIA or stroke), or patients with recent myocardial infarction who have atrial fibrillation, decreased left ventricular ejection fraction, or left ventricular thrombus Primary prevention of stroke in the general population by reducing risk factors3,6Reducing consumption of meat, salt, saturated fat and alcohol Reducing prevalence of smoking Reducing prevalence of obesity Increasing physical activity Controlling hypertension and hypercholesterolaemia Controlling diabetes mellitus *Randomised trials of the effect of smoking cessation, other antihypertensive agents, and 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) reductase inhibitors ("statins") in secondary stroke prevention are either still in progress or yet to be undertaken. 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Graeme J Hankey

Editorial The health of Australia's mothers and babies Improvements in the collection of perinatal statistics are needed to fill the gaps MJA 1996; 164: 198-199 Childbirth in Australia is relatively safe, as measured by the traditional outcomes of maternal and perinatal mortality. About 1 in 8000 mothers die from all direct, indirect and incidental causes associated with pregnancy and childbirth.1 The perinatal death rate, which includes fetal deaths and neonatal deaths up to 28 days of infants weighing at least 500 g, declined to 8.2 per 1000 births in 1993,2 the lowest level yet achieved. During the last two decades, all States and Territories have developed perinatal data systems that provide valuable information on maternal risk factors and complications and the outcomes of mothers and infants. This information, collected by midwives and medical practitioners, is increasingly being used for research and policy development and discussion about issues relating to pregnancy and childbirth. The 1992 report on Australian mothers and babies drew attention to births to teenage mothers, mothers born overseas and Australian Aboriginals and Torres Strait Islanders, and to factors associated with caesarean births.3 Teenage births. Births to teenage mothers in Australia, of just over 20 per 1000 in the early 1990s, were well below the peak of 55.5 per 1000 in 1971.4 However, these figures give an incomplete picture of teenage pregnancy because only South Australia and the Northern Territory have population-based data about induced abortions. Analysing trends in birthrates fails to indicate the total extent of teenage pregnancy. In 1992, 14 396 teenage mothers gave birth in Australia: 4115 were aged under 18 years (2503 were aged 17; 1133 were aged 16; 357 were aged 15; and 122 were under 15 years). The South Australian data showed that for every 100 births to teenage mothers, there were 82 induced abortions.5 Extrapolating from these data, the estimate of teenage pregnancies nationally in 1992 was in excess of 26 000. Based on these annual figures, about one in five teenagers will become pregnant at some stage between the ages of 15 and 19 years, and one in 10 will give birth. Women born overseas. Of all the women who gave birth in Australia in 1992, more than one in five (22.7%) were born overseas, and 6.3% of all mothers were born in Asia. Of those born in Asia, 3605 women (1.4% of all births) were from Vietnam, 2660 (1%) from the Philippines, 1881 (0.7%) from China, 1365 (0.5%) from Malaysia, 1164 (0.5%) from India and 1046 (0.4%) from Hong Kong. Perinatal outcome did not seem to differ greatly from that of infants of Australian-born mothers,6 but further research is needed to determine the effects of maternal risk factors on outcomes such as birthweight and perinatal mortality. The recent substantial increase in births to Asian-born mothers, notably Vietnamese and Chinese women, places extra demands on health services to ensure that their special needs are met, particularly in Sydney and Melbourne, where disproportionate numbers of people from non-English-speaking backgrounds live. These women often have vastly different cultural beliefs and practices associated with pregnancy and childbirth. Bicultural health workers are increasingly being recognised as having an important role in establishing support networks for these women, familiarising them with the Australian health system, and assisting them in overcoming language and attitudinal barriers. Australian Aboriginals and Torres Strait Islanders. Many aspects of caring for overseas-born women are also pertinent to health services for Australian Aboriginals and Torres Strait Islanders. In 1991, 7027 Aboriginal and Torres Strait Islander women gave birth, and 7257 did so in 1992, accounting for 2.9% of all mothers in both years. Many of these women travel long distances from remote communities to hospitals in larger centres, and thus frequently give birth in an unfamiliar environment. In 1992, one in four births in this group were to teenage mothers and almost one in three of these teenagers had had at least one other child. The average birthweight (3150 g) of babies born to Aboriginal Australians and Torres Strait Islanders was 206 g less than that of all Australian babies, and the proportion of babies that were of low birthweight (< 2500 g) was 12.9%, more than double the rate of 6.3% for all births. Caesarean births. The seemingly inexorable rise in deliveries by caesarean section in Australia continues unabated, with a peak at 18.3% of total deliveries in 1992. South Australia (22.1%) and Queensland (20.9%) consistently have the highest caesarean rates and Tasmania (16.1%) usually the lowest. The caesarean rate of 22.4% for women with private health insurance was more than 40% higher than the rate of 15.8% for women without insurance (partly attributable to more older women in the insured group). Caesarean rates for women with insurance having their first baby increased with maternal age, from 21.9% at 25-29 years to 28.1% at 30-34 years, 37.4% at 35-39 years, and 47.4% at 40-44 years. High caesarean rates were also associated with multiple births (39.2% for twins and 85.3% for triplets, compared with 18% for singleton births), with breech presentation in singleton births (73.8%), and with very low birthweight babies (53.8% for singleton babies weighing 1000-1499 g). Relatively simple measures, such as more detailed recording of the indications for caesarean section and obtaining an opinion from another obstetrician about whether operative intervention is indicated, have proved effective in reducing caesarean rates.7The Royal Australian College of Obstetricians and Gynaecologists should address the issue of high caesarean rates in Australia by requiring regular audits of hospitals and medical practitioners. The quality and usefulness of information about perinatal health can be enhanced in several ways. Firstly, it should be recognised that analysis of trends in teenage pregnancy and the formulation of preventive strategies require data about induced abortions as well as data about births. Secondly, by linking registrations of perinatal and infant deaths to information for all births from the perinatal data systems in every State and Territory, the association between maternal risk factors and outcomes can be better evaluated.8,9 Thirdly, while the patterns of risk factors, type of care and outcomes are remarkably consistent from year to year, shortening the interval between the year of birth and the publication of State and national reports is an important goal. Paul A L Lancaster Director, Australian Institute of Health and Welfare National Perinatal Statistics Unit, University of Sydney, NSW National Health and Medical Research Council. Report on maternal deaths in Australia 1988-90. Canberra: AGPS, 1993. Australian Bureau of Statistics. Perinatal deaths, Australia 1993. Canberra: ABS, 1994. (Catalogue No. 3304.0.) Lancaster P, Huang J, Pedisich E. Australia's mothers and babies 1992. Sydney: AIHW National Perinatal Statistics Unit, 1995. Australian Bureau of Statistics. Births, Australia 1993. Canberra: ABS, 1994. (Catalogue No. 3301.0.) Chan A, Scott J, McCaul K, Keane R. Pregnancy outcome in South Australia 1992. Adelaide: South Australian Health Commission, 1993. Guevara V, Taylor L. The health of mothers born in non-English-speaking countries and their babies, NSW 1990-1993. New South Wales Public Health Bull 1995; 6 Suppl S2: 1-52. Myers SA, Gleicher N. A successful program to lower cesarean section rates. N Engl J Med 1988; 319: 1511-1516. Perinatal Data Collection Unit. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity. Births in Victoria 1983-1992. Melbourne: Department of Health and Community Services, 1994. Gee V. Perinatal statistics in Western Australia. Tenth annual report of the Western Australian Midwives Notification System, 1992. Perth: Health Department of Western Australia, 1993.

The vilest deeds, like poison weeds, Bloom well in prison air; Oscar Wilde, "The Ballad of Reading Gaol", 1896 More than two years ago, an editorial in this Journal stated: "Prison authorities and governments must realise that the responsibility for the infection of a prisoner with a bloodborne virus, because means for prevention were not available within the prison, rests with them."1 Sadly, there is little improvement to report. Bleach, for cleaning injecting equipment, has been made available since 1995 in most custodial systems. Condoms and dental dams were first introduced into New South Wales prisons in 1997, but are currently provided to prison inmates in only three jurisdictions. The methadone maintenance program began in New South Wales in 1986 and will soon expand through trials in Queensland and South Australian prisons. Methadone withdrawal regimens are provided in Victorian prisons. Three articles in this issue of the Journal highlight some of the continuing health risks faced by inmates in Australian prisons.2-4 These reports raise concerns that inmates are still placed at unnecessary risk by not being offered opportunities to minimise infection with bloodborne viruses, and complement reports of transmission of a wide range of contagious diseases from custodial systems in other countries.5,6 McDonald et al report that control of HIV transmission in the community has protected prisoners, with sustained low levels of identified HIV-antibody-positive individuals entering Australian prisons.2 The evidence for transmission in prison of HIV presented by Dolan and Wodak3 and of hepatitis C by Haber et al4 indicate that custodial authorities' commitment to zero tolerance would be better applied to the transmission of these viruses rather than to illicit drugs and injecting equipment within prison. Despite universal support for zero tolerance among Australian custodial authorities, drug use continues after reception into prison. In New South Wales, in 1996, 21% of men and 32% of women reported that they had injected drugs in prison; 18% of men and 11% of women did so in the week before interview. Of those who had injected in prison, 69% of men and 64% of women reported that they had shared needles.7 Zero tolerance is not protecting the lives of prison inmates. Between 1980 and 1998, there were 86 deaths in custody in Australian prisons that were classified as accidents -- overwhelmingly drug related.8 The fear of having illicit drugs confiscated leads to "binge" use. Irregular use and inexperience in assessing dosage and drug purity readily lead to overdosing. Needles and syringes have a higher probability of being infectious in the prison environment, as the prevalence of bloodborne viruses is so high. An environment that inadvertently encourages sharing of equipment actually promotes transmission of bloodborne viruses. Consider the ability of zero tolerance in providing prison workers with a safe work environment. It might be argued that the restrictions on needles and syringes make prisons a safer workplace, but the evidence for this is not compelling. The malicious stabbing of a prison officer with a syringe filled with HIV-contaminated blood in 1990 occurred when needles and syringes were prohibited items. The principle of harm minimisation guides public health efforts to control bloodborne viruses in the community. Why should this not also be applied in the prison environment? No measures should be spared to provide a safer environment for prison inmates, and health and custodial staff. A full range of options need to be available for custodial and health authorities to offer inmates, including drug-free prisons, methadone maintenance and consideration of therapeutic prescription of injectable drugs. With controlled heroin prescribing and provision of syringes and needles, the trafficking of contaminated equipment should decrease. In Switzerland and Germany, programs for therapeutic heroin prescription in a few prisons are currently being evaluated.9 These initiatives will require strong advocates for the health of prison inmates and the general community. For this to occur, prison health services must be brought into the mainstream of clinical medicine and public health.10 This can be accomplished by granting autonomy to prison health authorities, by fostering ties between correctional health programs and academic and public health departments, and by funding research that addresses public policy questions peculiar to the prison environment.11 To accelerate the uniform introduction of health protective measures throughout Australian prison systems, correctional health programs need standards against which their performance can be monitored. Australian prison authorities have devised uniform guidelines of operation, but they are not health standards, and they are not enforceable.12 There are currently over 19 000 inmates in Australian prisons, and the number is increasing by more than 7% each year.13 The importance of the health of prisoners and its impact on the general community can only grow. Since March 1999, the Australian Red Cross has identified imprisonment in the previous 12 months as an unacceptable risk factor for blood donation.14 Two years have been squandered. The evidence mounts that prisons pose a health risk to inmates, to workers within prisons, and to the general community. The statement by Crofts bears repeating: "Prison authorities and governments must realise that the responsibility . . . rests with them."1 Michael H Levy Director, Population Health, Corrections Health Service Matraville, NSW, and Department of Public Health and Community Medicine University of Sydney Crofts N. A cruel and unusual punishment. Med J Aust 1997; 166: 116. McDonald AM, Ryan J, Brown PR, et al. HIV prevalence at reception into Australian prisons, 1991-1997. Med J Aust 1999; 171: 18-21. Dolan K, Wodak A. HIV transmission in a prison system in an Australian State. Med J Aust 1999; 171: 14-17. Haber PS, Parsons SJ, Harper SE, et al. Transmission of hepatitis C within Australian prisons. Med J Aust 1999; 171: 31-33. Taylor A, Goldberg D, Emslie J, et al. Outbreak of HIV infection in a Scottish prison. BMJ 1995; 310: 289-292. Valway SE, Richards SB, Kovacovich J, et al. Outbreak of multi-drug-resistant tuberculosis in a New York State prison, 1991. Am J Epidemiol 1994; 140: 113-122. Preliminary findings of the Inmate Health Survey. Sydney: Corrections Health Service, 1997. Dalton V. Prison homicide in Australia: 1980 to 1998. Trends and issues in crime and criminal justice. No. 103. Canberra: Australian Institute of Criminology, 1999. Vumbuca G. Finding a better way. Canberra: The Winston Churchill Memorial Trust of Australia, 1999. Prisoners: an end to second class health care? BMJ 1999; 318: 954-955. Correction of attitudes to prison medicine [editorial]. Lancet 1998; 351: 1371. Standard Guidelines for Corrections in Australia 1996. The Corrective Services Ministers' Conference. 1995. Australian Bureau of Statistics. Corrective Services, Australia. Canberra: ABS, 1998. (Catalogue no. 4512.0.) Australian Red Cross Blood Service. Donor Questionnaire. March 1999.

Michael H Levy

Abstract Objective: To investigate possible HIV transmission among prison inmates. Setting: A prison system in an Australian State. Participants: 13 ex-prisoners and their prison contacts. Methods: Ex-prisoners who claimed to have been infected with HIV in prison and their prison contacts were interviewed about HIV risk behaviour. Entries in prison and community medical records were used by a three-member expert panel to establish the likelihood of primary HIV infection and its possible timing and location. Main outcome measures: Determination of whether HIV infection probably occurred in prison. Results: There was a very high probability that at least four of 13 ex-prisoners investigated acquired HIV in prison from shared injection equipment. Another two ex-prisoners most probably acquired HIV infection outside prison. The location of infection for the remaining seven could not be determined. Conclusions: HIV transmission in prison has substantial public health implications as most drug-using prisoners soon return to the community. HIV prevention strategies known to be effective in community settings, such as methadone maintenance treatment and syringe exchange schemes, should be considered for prisoners. Introduction HIV transmission in prison has been reported in the United States,1 Scotland2 and Australia.3 The infrequency of these reports has led to a belief that HIV transmission occurs rarely among inmates. A more likely explanation is that confirmation of HIV transmission is more difficult in prisons than community settings.4 Multiple and powerful factors conducive to high HIV incidence are found in prisons. These include that: HIV prevalence is generally several times higher in prisons than in surrounding communities because of the considerable over-representation of injecting drug users (IDUs) among prisoners;5 reports of syringe sharing with multiple injectors are still common in prisons but now rare in community settings;6 HIV infection has been associated with imprisonment in France7 and Spain;8 and incidence of hepatitis C among IDUs incarcerated twice within a 12-month period was double that among IDUs who remained at liberty.9 Furthermore, HIV prevention measures, such as provision of sterile injecting equipment, condoms and methadone maintenance, are uncommon in prisons.10 Although several estimates of HIV prevalence have been conducted in correctional institutions,1,11,12 assessing the incidence of HIV transmission within a prison system poses considerably greater challenges.4 Most drug users serve short, repeated sentences. This hampers the investigation of infection outbreaks and identification of transmission location. In an earlier Australian study,13 several IDUs claimed to have become infected with HIV in prison. Some reported symptoms indicative of primary HIV infection while incarcerated. The aim of this study was to assess, using epidemiological data, whether these IDUs or their contacts had become infected in prison. A similar approach has been used to investigate an HIV outbreak in a Scottish prison.2 Methods Index cases The investigation took place between 1993 and 1994. Seven IDUs from an earlier study13 who claimed to have acquired HIV infection in prison were recontacted. In the earlier study, respondents who had injected drugs and had recently been released from prison were recruited from methadone units, hostels for ex-prisoners or drug injectors, probation offices, syringe exchange schemes, local media advertisements, AIDS organisations and via street networking.13 Prison contacts We traced prison contacts nominated by these seven people through the state methadone registry, AIDS services, drug users' organisations, HIV physicians and the State Registry of Deaths. The contacts were inmates with whom the seven index inmates had engaged in syringe sharing, anal sex or tattooing while in prison. Assessment of HIV infection HIV infection was assessed by an expert panel of three HIV physicians. The experts were provided with dates of entry to and exit from prison, HIV test results, symptoms recorded at the time the prisoner believed infection occurred, self-reported symptoms and self-reported risk behaviour. All dates were referenced in months from the year before the first detected case had last tested HIV negative. Each expert independently assessed whether the recorded symptoms indicated an HIV seroconversion illness and whether the infection occurred in prison, in the community, or if the location was indeterminate. We then accepted the majority decision in each assessment. Ethical approval Relevant ethics committees approved the study on condition that study participants' contacts in the community following their release from prison were not traced. We were also required to alert potential study participants to the possibility of legal or other consequences of admitting drug use in prison or transmitting HIV to another person. Participation in the study required signed, informed consent. Information which would identify the exact time and location of these possible infections has not been included, in accordance with requirements of one ethics committee. Results Contact tracing Between 1993 and 1994, seven male IDUs described in a previous study13 were recontacted (subjects A, B, C, D, E, F, G). They identified 20 prison contacts: six of these contacts could not be located, six had died of AIDS (according to death certificates), and two declined to participate for fear of repercussions for transmitting HIV. The six remaining contacts (H, I, J, K, L, M) plus the seven index cases made a total of 13 ex-prisoners available for investigation (Figure). Prison clusters Prison records revealed two clusters (C1, C2) of six subjects in one or two prison wings. Subjects B, E, I, K and M were held in Prison 1 (population about 250 inmates) in months 22 and 23, during which time index subject B seroconverted. Subjects B, D, I, K and M were held in Prison 2 (population about 300 inmates) in months 29 and 30, during which time contact subject K seroconverted. Index participant A was not part of either cluster, but another participant reported sharing syringes with him. Of the six deceased potential respondents, two had been part of C1 and another two had been part of C2. According to death certificates, two deceased potential respondents became infected with HIV in the year when they were held with the clusters. Cluster analysis was not possible because of the lack of records being kept on the total number of inmates held in the prison wings during the crucial times. Self-reported risk behaviour Eleven participants (A, B, C, E, I, K, M, D, F, G, L) reported syringe sharing in prison, with the first seven nominating another person in this series as a sharing partner. Contact participants I and M also reported receiving a tattoo in prison, and index subject C reported unprotected anal sex. All six deceased prison contacts wereidentified by one or more participants as having shared syringes with them around the crucial periods of months 22 and 23 and months 29 and 30. Assessment of HIV infection Medical file entries for 10 subjects (A, B, C, E, F, G, I, K, L, M) were reviewed by the expert panel. The experts concluded that five participants (A, B, C, G, K) had experienced primary HIV infection and that the most likely location of transmission for individuals A, B and C was in prison (Box 1). Overall, it was concluded that infection occurred in prison for four subjects and in the community for two (Box 2). Discussion The epidemiological evidence that individual A was infected in prison is beyond doubt: he tested negative and then positive for HIV infection after years of confinement in prison. There was strong epidemiological evidence that individuals B, C and J were also infected in prison. Individuals D and G were infected with HIV in the community. The location of infection for the remaining seven subjects (and the six deceased potential respondents) could not be determined. Thus, on epidemiological grounds, at least four of the 13 people investigated were infected with HIV while in an Australian prison system. The most likely route of HIV transmission was shared injection equipment. These are both conservative and probabilistic assessments. It is likely that a prospective investigation of these 13 people, or even a retrospective investigation closer to the events, would have yielded a larger number of confirmed HIV transmissions in prison. However, the strength of evidence for this network and the multitude of factors conducive to HIV infection in prisons suggest that the extent of HIV transmission occurring in prisons through shared injection equipment is underestimated. A mathematical model of HIV transmission in an Australian prison system14 using values derived from empirical studies also suggests that transmission is occurring within correctional centres. This study illustrates some of the difficulties of confirming HIV transmission in prison. We became aware of a possible outbreak by chance. Obtaining ethical approval for the study was an extremely protracted process requiring the assistance of a legal expert. Inmates were understandably wary of admitting risk behaviour because of the potentially serious consequences (as outlined in the consent form). Apart from the logistical and ethical problems of this type of research, the incubation period for HIV infection is almost as long as the average duration of a prison sentence served for drug-related offences in Australia. Consequently, many HIV infections occurring in prisons will not be detected by conventional surveillance. These factors may help to explain why so few cases of HIV transmission among inmates have been reported. Our study differed from previous reports10 in the extent of transmission detected and the type of prisoners studied. Previous studies have investigated long term, high security prisoners, who have less opportunity to associate with other inmates and visitors to obtain drugs and consequently become infected with HIV.15 Our study found a relatively large number of incident cases considering the small sample size, the extremely low prevalence of HIV infection in the Australian prison population16 and the rapid turnover of inmates. All these factors militate against detection of HIV transmission in prison. A limitation of the study was reliance on self-reported risk behaviour. However, we accepted self-reported data only if corroborated by another external source. Moreover, symptoms reported by informants coincided closely with medical records, supporting the validity of self-reported data. We were precluded by ethics committee requirements from determining whether any sexual partners (and their children) were infected with HIV by participants following release from prison. This restriction prevented investigation of possible HIV transmission beyond prison to the community. However, medical files indicated that four subjects had each had an HIV-positive female sexual partner following release from prison. Two of these women, and an additional HIV-negative partner, became pregnant, with at least two pregnancies reaching full term. Medical files also indicated that at the time of the investigation two former inmates had been engaging in unprotected sex with two HIV-negative women, against the advice of their counsellors. Existing evidence of HIV transmission among prisoners has persuaded prison authorities in few countries to implement effective prevention strategies for inmates. Confirmation of HIV infection from prison to the community may be more persuasive for authorities. Syringe exchange, methadone and bleach programs reduce the spread of HIV in community settings,16-18 and preliminary results from these programs in prison appear promising.19-21 The paucity of data confirming HIV transmission in prison should not be regarded as adequate justification for the lack of effective HIV prevention measures within prisons. There is already sufficient information on HIV transmission between prisoners to justify rapid implementation in correctional institutions of prevention measures shown to be effective in community settings. Improved methods of monitoring the spread of HIV within prisons and from inmates to community members following release are required urgently. Acknowledgements We are grateful to the NSW Department of Health for funding this study. We also wish to thank David Buchanan, Andrew Carr, Ying Chun Ge, David Cooper, Anthony Cunningham, Basil Donovan, John Dwyer, Tania Sorrell and Dominic Dwyer. Results of tracing 20 prison contacts of seven index cases for recruitment into the study. References Brewer TF, Vlahov D, Taylor E, et al. Transmission of HIV-1 within a statewide prison system. AIDS 1988; 2: 363-367. Taylor A, Goldberg D, Emslie J, et al. Outbreak of HIV infection in a Scottish prison. BMJ 1995; 310: 289-292. Dolan K. AIDS, drugs and risk behaviour in prison: state of the art. Int J Drug Policy 1997; 8: 5-17. Dolan K. Why is there conflicting evidence of HIV transmission in prison? In: O'Brien O, editor. Report of the 3rd European Conference on Drug and HIV/AIDS Services in Prison. London: Cranstoun Drug Services, 1997; 19-21. Gaughwin MD, Douglas RM, Wodak AD. Behind bars -- risk behaviours for HIV transmission in prisons, a review. In: Norberry J, Gerull SA, Gaughwin MD, editors. HIV/AIDS and prisons conference proceedings. Canberra: Australian Institute of Criminology, 1991; 89-107. Crofts N, Webb-Pullman J, Dolan K. An analysis of trends over time in social and behavioural factors related to the transmission of HIV among IDUs and prison inmates. Evaluation of the National HIV/AIDS Strategy. Technical Appendix 4. Canberra: AGPS, 1996. Richardson C, Ancelle-Park R, Papaevangelou G. Factors associated with HIV seropositivity in European injecting drug users. AIDS 1993; 7: 1485-1491. Granados A, Miranda MJ, Martin L. HIV seropositivity in Spanish prisons. Presented at the VIth International AIDS Conference, San Francisco. Abstract no Th. D.116, 1990. Crofts N, Stewart T, Hearne P, et al. Spread of blood-borne viruses among Australian prison entrants. BMJ 1995; 310: 285-288. Dolan K, Wodak A, Penny R. AIDS behind bars: preventing HIV spread among incarcerated drug injectors. AIDS 1995; 9: 825-832. Vlahov D, Brewer TF, Castro KG, et al. Prevalence of antibody to HIV-1 among entrants to US correctional facilities. JAMA 1991; 265: 1129-1132. Bird AG, Gore SM, Jolliffe DW, Burns SM. Anonymous HIV surveillance in Saughton Prison, Edinburgh. AIDS 1992; 6: 725-733. Dolan K, Wodak A, Hall W, et al. Risk behaviour of IDUs before, during and after imprisonment. Addict Res 1996; 4: 151-160. Dolan K, Wodak A, Hall W, Kaplan E. A mathematical model of HIV transmission in NSW prisons. Drug Alcohol Depend 1998; 50: 197-202. Dye S, Isaacs C. Intravenous drug misuse among prison inmates: implications for spread of HIV. BMJ 1991; 302: 1506. Feachem R. Valuing the past . . . investing in the future. Evaluation of the National HIV/AIDS Strategy. 1993-94 to 1995-96. Canberra: AGPS, 1996. Ward J, Mattick R, Hall W. Methadone maintenance treatment and other opioid replacement therapies. Amsterdam: Harwood Academic Publishers, 1998. Normand J, Vlahov D, Moses LE. Preventing HIV transmission: the role of sterile needles and bleach. Washington: National Academy Press, 1995. Nelles J, Harding T. Preventing HIV transmission in prison: a tale of medical disobedience and Swiss pragmatism. Lancet 1995; 346: 1507-1508. Dolan K, Wodak A, Hall W. Methadone maintenance treatment reduces heroin injection in NSW prisons. Drug Alcohol Rev 1998; 17: 153-158. Dolan K, Wodak A, Hall W. A bleach program for inmates in NSW: an HIV prevention strategy. Aust N Z J Public Health 1998; 22: 838-840. Authors' details National Drug and Alcohol Research Centre, University of New South Wales, Sydney, NSW. Kate A Dolan, BSc, PhD, Research Fellow. Alcohol and Drug Services, St Vincent's Hospital, Sydney, NSW. Alex Wodak, FRACP, FAFPHM, Director. Reprints: Dr K A Dolan, Research Fellow, National Drug and Alcohol Research Centre, University of New South Wales, Sydney, NSW 2052. Email: ndarc8@unsw.edu.au

Kate A Dolan · Alex Wodak

Transmission of hepatitis C within Australian prisons Transmission of hepatitis C virus (HCV) within prisons has long been suspected but has not been satisfactorily documented. We present four cases of HCV infection occurring during periods of continuous imprisonment. Each subject was HCV seronegative on entering prison and on repeat testing after 4-52 months in prison, but subsequently became seropositive. Two subjects gave a history of injecting drug use, and the most likely means of infection in the other two subjects were lacerations from barbers shears and lacerations arising from physical assault. There is an urgent need for detailed study of the incidence of HCV infection and the modes of transmission in prisons. Introduction The prevalence of hepatitis C (HCV) infection in voluntary screening among entrants to Australian and North American prisons is as high as 40%.1-3 It is therefore surprising that HCV transmission within prisons has not been well documented, although it is known that a history of incarceration is an independent risk factor for HCV seroconversion4 and uninfected prisoners are at high risk of seroconversion by the time of a second prison entry.1,3 These observations provide only indirect evidence of transmission within prisons, as infection could have occurred either during the first period of imprisonment or outside prison between release and re-incarceration. This report describes the first published series of well-documented cases of transmission of HCV within a prison. The Research Ethics Committee of the Corrections Health Service of New South Wales approved reporting of these cases. Clinical records Between April 1994 and October 1997, four male prisoners presented with HCV infection appearing a minimum of 11 months after entry to prison (Table). All had had negative HCV antibody tests on entry to prison and again after 4-52 months of continuous incarceration (anti-HCV ELISA version III, Murex Diagnostics, Kyalamani, South Africa; confirmation by Innotest HCV Ab III assay, Innogenetics, Zwijnaarde, Belgium). All bore tattoos, but all four stated that no tattoos had been applied within two years of the last negative HCV antibody test. None had received blood products, or undergone medical or dental procedures, including vaccination, in the year before acquisition of HCV. All four denied any body piercings within two years of the last negative HCV antibody test, or sexual intercourse with another person since entering prison. Case 1 A 23-year-old inmate requested an HCV antibody test after receiving a scalp laceration during a close-shave haircut (performed with electric shears without a plastic guard) in June 1997. There was minimal bleeding and the wound did not require suturing. The patient denied having injected drugs at any time, but admitted to smoking marijuana and snorting cocaine in the past. Indeed, he regarded any injection with abhorrence and feared bloodborne infection. As a result, he had requested HCV antibody tests after numerous low risk events in prison and was repeatedly seronegative. After this latest incident, the patient again requested serological tests for HCV, and seroconversion was documented six weeks later. The patient stated that several of the four preceding inmates on whom the barbers shears were used on the same day were HCV antibody positive and had also received minor lacerations during their haircuts. He also claimed that the electric shears were not disinfected in any way between uses. No further details are available of the barber's list for that day, as no permanent records of these lists are kept. Sterilisation of shears before reuse was not normal practice at the time. One of the other inmates on whom the shears were used was confirmed to be positive for HCV antibody and HCV-RNA by polymerase chain reaction (PCR) analysis (Amplicor HCV detection kit, Roche Diagnostic Systems, Branchburg, NJ, USA). Case 2 A 35-year-old inmate suffering from lassitude and anorexia presented for examination. He had started using intravenous drugs for the first time after being in prison for several years. For a period of six months, he had injected two to three times per week, frequently sharing needles with known HCV-seropositive inmates, but routinely sterilising the injecting apparatus using a recommended bleaching protocol with 5.25% hypochlorite solution.4 Six weeks after ending drug use, he developed the symptoms described, which, in association with raised alanine aminotransferase (ALT) levels, were consistent with viral hepatitis. HCV seroconversion was found to have taken place since his last negative test one year previously. Case 3 A 27-year-old inmate presenting with lassitude was found to have abnormal liver function tests typical of acute viral hepatitis. The patient was an infrequent injecting drug user who had continued his habit intermittently during imprisonment. As he was aware of the risk of transmission of bloodborne pathogens, he used a bleached injecting apparatus for each episode, but shared the mixing spoon in which the drug suspension was prepared. HCV seroconversion was confirmed. Case 4 A 25-year-old inmate presented for examination after being involved in a physical assault with another inmate, during which blood-to-blood contact occurred from abrasions and lacerations. He had sustained no serious injury. The other inmate was a known HCV-positive injecting drug user who later left prison and was lost to follow-up. Blood taken soon after the assault was negative for HCV antibodies, but seroconversion, associated with mild symptoms of hepatitis, was documented three months later. The patient denied injecting drug use. Discussion These cases provide strong evidence that transmission of HCV occurs in prison. Infection during injecting drug use is likely to be a leading mode of HCV transmission in prisoners. Inmates report that injecting apparatus is scarce in the prison system, whereas heroin is readily obtained. These circumstances favour repeated use of a limited number of needles and syringes by many prisoners. The recommended bleach cleansing of the injecting equipment appears ineffective, as our report corroborates previously documented transmission of HCV, but not HIV, after sharing of cleaned injecting apparatus.5 In two of the cases, HCV may have been transmitted by means unrelated to injecting drug use. The high prevalence of HCV among those entering prison, together with the strong likelihood of blood-to-blood contact in the prison environment, may increase the chance of HCV transmission by barbers shears, during physical assault or by other mechanisms.6 However, a limitation of our study is the reliance on self-reporting of risk factors by prison inmates. Inmates' self-reporting is relatively accurate if their status is unlikely to be affected by the content of the report, but may be biased if they perceive that harm or benefit may result.7 Our study provides the strongest evidence to date that transmission of HCV infection occurs within prisons. Two cases of HCV seroconversion among prisoners in Maryland (USA) have been reported:2 of 164 prisoners who tested negative for HCV on entry to prison, two tested positive 18 months later. However, there was not unequivocal evidence that HCV transmission occurred within prison, as the initial negative HCV test may have been carried out during the window phase between infection and seroconversion if viral transmission occurred outside prison shortly before incarceration. In our study, all four subjects were seronegative for HCV after 4-52 months' continuous imprisonment, and remained in continuous full-time custody until seroconversion was documented (Table). Approximately 10 500 imprisonments occur annually in New South Wales, which has a population of 6 300 000. At any one time, the NSW prison population is about 6000. The average sentence is seven months, and there are more than 25 000 transfers between prisons each year. Thus, the prison population has a high turnover and is not isolated from the general community. The extent of HCV transmission may be significant because of the prevalence of high-risk behaviours in prison, and the fact that some harm-reduction measures, such as needle exchange programs, are not available in Australian prisons. Thus, the prison community is a population at significant risk of HCV infection and a potentially important source of subsequent transmission of HCV into the general community. The cases presented here probably represent only a small fraction of inmates acquiring new HCV infection in prison. Firstly, our cases were detected clinically (whereas most primary HCV infections are subclinical) and, secondly, our study did not attempt a systematic search for HCV transmission among inmates. Moreover, there are rare occurrences of HCV infection without detectable HCV antibodies, and such cases depend on HCV-PCR testing for diagnosis.8 This report confirms that HCV is currently being transmitted within NSW prisons. The circumstances for acquisition of serious bloodborne infections during imprisonment should be identified and opportunities for transmission minimised where possible. Accordingly, detailed studies of the incidence of and risk factors for HCV transmission within prisons are urgently needed, followed by development and implementation of control measures. References Crofts N, Stewart T, Hearne P, et al. Spread of bloodborne viruses among Australian prison entrants. BMJ 1995; 310: 285-288. Vlahov D, Nelson KE, Quinn TC, Kendig N. Prevalence and incidence of hepatitis C infection among male prison inmates in Maryland. Eur J Epidemiol 1993; 9: 566-569. Butler TG, Dolan KA, Ferson MJ, et al. Hepatitis B and C in New South Wales prisons: prevalence and risk factors. Med J Aust 1997; 166: 127-130. van Beek I, Dwyer R, Dore GJ, et al. Infection with HIV and hepatitis C virus among injecting drug users in a prevention setting: retrospective cohort study. BMJ 1998, 317: 433-437. Bodsworth NJ, Robertson M, Kaldor J. Transmission of hepatitis C but not human immunodeficiency virus type 1 following sharing of injecting equipment. Genitourin Med 1994; 70: 206-207. Gill ON, Noone A, Heptonstall J. Imprisonment, injecting drug use, and bloodborne viruses: a threat of transmission but an opportunity for prevention. BMJ 1995; 310: 275-276. Darke S. Self-report among injecting drug users: a review. Drug Alcohol Depend 1998; 51: 253-263. Gretch DR. Diagnostic tests for hepatitis C. Hepatology 1997; 26 Suppl 1: 43S-47S. Authors' details Drug and Alcohol Services, Royal Prince Alfred Hospital, Sydney, NSW. Paul S Haber, MD, FRACP, Staff Specialist. Public Health Nursing Unit, Corrections Health Service, Sydney, NSW. Sandra J Parsons, RN, Clinical Nurse Consultant; Susan E Harper, RN, Public Health Nurse. Virology Division, Department of Microbiology, South Eastern Sydney Area Laboratory Services, Sydney, NSW. William D Rawlinson, PhD, FRACP, FRCPA, Division Head. Peter A White, PhD, Research Fellow. School of Pathology, University of New South Wales, Sydney, NSW. Andrew R Lloyd, MD, FRACP, Associate Professor, Inflammation Research Unit.

Paul S Haber · Sandra J Parsons · Susan E Harper · Peter A White · William D Rawlinson · Andrew R Lloyd

Participatory, non-punitive involvement of healthcare practitioners is needed MJA 1999; 170: 8-9 Increasing use of pathology services is a worldwide phenomenon in countries with substantially different healthcare systems.1 In Australia, for almost a decade and a half the annual growth rates of Medicare-funded services have shown that the rates for pathology services have generally exceeded, and often been more than double, those of other medical services.2-4 In the financial year 1997-98, pathology, diagnostic imaging and general practitioner services grew by 4.28%, 3.86% and 0.59%, respectively, compared with the previous 12-month period. In the same period, the Medicare outlays (ie, "benefits") paid by the Health Insurance Commission for total medical services were $6.334 billion, of which 14.59% were for pathology services and 14.81% for diagnostic imaging services. Together with general practitioner services (37.39%), these account for two-thirds of Medicare outlays. By the turn of the century, the Medicare outlays for pathology and diagnostic imaging services will each exceed $1.0 billion per year. Pathology services in the public health sector, or for workers compensation and traffic accident insurance, are largely funded at State level by arrangements distinct from Medicare. The extent of pathology services and outlays in these sectors is largely unknown, but service growth rates at hospital level are not uncommonly of the order of 1%-3% per year. At the National Pathology Forum (Canberra, 1995) the annual public health sector pathology expenditure was estimated to be $450 million to $600 million. What is the explanation for the growth of pathology services? There is no consensus, but many real, speculative, anecdotal and even light-hearted reasons are given:2,5 among these are diagnosis, monitoring, screening and prognosis; availability and accuracy of prior result; pressure from patients, relatives and peers; reassurance; medicolegal issues; profit; fraud; research; insecurity; and habit. Given this list, some services would clearly be unnecessary and wasteful in the clinical setting,2 but these reasons do not obviously explain the increasing use of pathology services in Australia2-4 and similar trends in other countries.1 Other suggestions for consideration include improved technology allowing larger throughput with shorter turnaround of services, cost-shifting from publicly funded to Medicare-funded services, and altered clinical practice, such as the increasing need in general practice to exclude organic disease when faced with non-specific symptoms. The nature of Medicare data does not allow for conclusive evaluation of these possibilities. Do we really know whether the growth in use of pathology services is appropriate or inappropriate? In a recent review of 44 published studies of laboratory test use,1 11 studies used implicit criteria that were not provided, were very broad, or had not been adequately assessed for their reliability as criteria. In the other studies, explicit criteria were based on the appropriateness of test choice, frequency, timing, and the probability of a positive result. Estimates of inappropriate laboratory test use ranged from 4.5% to 95%! The review authors concluded that the criteria used in these studies did not meet methodological standards suggested for audits of therapeutic interventions, and suggested that researchers should develop alternative evidentiary standards for measuring inappropriateness of pathology service use. They also concluded that, while the evidence supporting the explicit criteria was weak by methodological standards, it was strong according to principles of physiology, pharmacology, and probability. Perhaps the real issue is how to modify the use of pathology services rather than to seek a definitive explanation for the growth in services. The Commonwealth government has sought to reduce Medicare outlays for these services by restructuring the relevant sections of the Commonwealth Medical Benefits Schedule, by informing those requesting these services of their patterns of use, by licensing and reducing the number of pathology collection centres, and by limiting the number of pathology services allowed per episode (ie, per patient each day) that attract benefits. A three-year agreement to cap outlays within predetermined limits was reached between the Commonwealth government and pathology services in 1996. At State level, many hospitals are applying the principles of competitive neutrality (which aims to ensure that government businesses do not enjoy competitive advantage simply because of their public ownership) and even market testing6 to their own pathology departments in an attempt to reduce expenditure, if not use. Such measures are effectively cost-cutting activities, and are seen to be imposed by the funders, often without effective incentives for the users or providers to change.7 Passive information and educational material accompanying these activities is usually prepared by the funders, and may be seen by the users as of little relevance or of poor quality. Moreover, such measures may not prevent the development of further distortions in use of services (through, for example, inappropriate use of other clinical procedures or marketing of other pathology services). Are there ways, other than externally imposed cuts in outlays, to modify use of pathology services? In this issue of the Journal, Isouard reports on the impact of a total quality management approach on the appropriateness of pathology service use in acute myocardial infarction.8 His study used a team which included doctors, nurses and pathologists to determine unnecessary variation in ordering of tests. The outcome was an increase from 77.5% to 88.2% in the proportion of clinically indicated tests that were ordered, and an 81.7% reduction in the use of non-clinically indicated tests. This is associated with the potential to reduce expenditure. It would be all too easy to criticise Isouard's article as being overly enthusiastic about total quality management, as research based around modification of human behaviour, and for the difficulty in rigidly controlling such experiments. Further criticisms might include the need to verify such major improvements independently, and the observed reduction in compliance with the guidelines once the interventions ceased. However, the importance of Isouard's report is that it provides an alternative, non-punitive way to modify pathology service use. It focuses on the processes of ordering and using services, it uses the knowledge and expertise of all the healthcare practitioners involved in the processes, it has the potential to eliminate inefficient and redundant process steps, and it is more likely to provide incentives to healthcare practitioners to reduce variation and hence costs. It also allows for re-engineering the processes to maintain or enhance quality. Favourable outcomes have been reported for similar studies with total hip replacement,7 elective surgery,9 and addressing adverse drug events.10 In these difficult times of rapid change, healthcare practitioners face increasing pressures to reduce costs while providing high quality patient care. Reductions in funding and the use of the traditional scientific method, accoutred with reductionism and concepts developed in "wet" laboratory experiments, may prove inadequate as tools to deal with situations such as the growth in use of pathology services. Healthcare practitioners now need to include in their armamentarium quality improvement techniques,7,9 critical pathways analysis,7 process re-engineering,7,9 and other methods such as qualitative research.11 Robert A J Conyers Medical Director, Gribbles Pathology (Vic) Pty Ltd South Yarra, VIC Van Walraven C, Naylor CD. Do we know what inappropriate laboratory utilization is? A systematic review of laboratory clinical audits. JAMA 1998; 280: 550-558. Deeble J, Lewis-Hughes P. Directions for pathology. National Health Strategy Background Paper No 6. July 1991. Health Insurance Commission web site. <http://www.hic.gov.au>. Accessed 23 November 1998. Australian Medical Association Ltd. Medicare volume and expenditure report. Canberra: AMA Federal Council, August 1998. Lundberg GD. Perseveration of laboratory test ordering: a syndrome affecting clinicians. JAMA 1983; 249: 639. Knowles R. "Significant opportunities" for private sector in Victoria's public health services. Healthcover 1997; 7(5): 11-20. Evans J, Hwang Y, Nagarajan NJ. Cost reduction and process re-engineering in hospitals. J Cost Management 1997; May-June: 20-27. Isouard G. A quality management intervention to improve clinical laboratory use in acute myocardial infarction. Med J Aust 1999; 170: 11-14 Caplan GA, Brown A, Crowe PJ, et al. Re-engineering the elective surgical service of a tertiary hospital: a historical controlled trial. Med J Aust 1998; 169: 247-251. Jones BC. Every defect a treasure: learning from adverse events in hospitals. Med J Aust 1997; 166: 484-487. Peat JK, Toelle BG, Nagy SA. Qualitative research: a path to better healthcare. Med J Aust 1998; 169: 327-329.

Protozoa in drinking water: is legislation the best answer? A cooperative approach is a better option to protect public health MJA 1998; 169: 296-297 In late July, Australians were shocked to learn that the water supply in their largest city had been declared unsafe to drink because of protozoal contamination.1 In late August Sydney's water was again declared unsafe. The publicity surrounding these events in Sydney doubtless left most of the public, and perhaps many health professionals, with the impression that swallowing a mouthful of the affected water virtually guaranteed an episode of severe gastroenteritis. However, the magnitude of the risk to public health is far from clear as there are many limitations in our understanding of the biology of these organisms, and in the methods used for their detection in drinking water. Public and political concern has resulted in calls for legislative enforcement of water quality standards for Giardia and Cryptosporidium, but we believe that this approach is both unwise and unworkable at present. Such measures would require the setting of permissible levels for protozoa in drinking water, specification of sampling programs and approved testing methods. Uncertainties in all these aspects make it extremely difficult to define appropriate parameters to protect public health. Human infection: Information on levels of protozoa associated with illness is available from a small number of human experiments and limited data collected from outbreaks. For Giardia lamblia, a study of adult male prison inmates showed as few as 10 cysts could establish infection (determined by cysts in stools). However, none of the 40 subjects reportedly developed symptomatic giardiasis despite ingesting up to one million cysts, although 21 became infected.2 More recent human experiments,3 in which 50 000 Giardia lamblia trophozoites were inoculated into the duodenum, showed that with one strain all 10 subjects became infected and four developed clinical giardiasis. With another strain none of five subjects became infected or showed clinical disease. In human infection experiments with Cryptosporidium parvum, the minimum dose tested was 30 oocysts. Of five seronegative subjects receiving this dose, one became infected (oocysts in stools) but experienced no symptoms. At the next dose level of 100 oocysts, three of eight subjects became infected and developed symptoms.4 Waterborne outbreaks: Information derived from investigation of waterborne outbreaks is limited and difficult to interpret because of the time lag between the contamination event, the onset of symptoms in the exposed population and subsequent investigation to identify the source. For the Milwaukee cryptosporidiosis outbreak, which affected an estimated 400 000 people, the only data on oocyst levels came from samples of stored ice.5 A concentration of 13.2 oocysts per 100 L was found in ice made eight days before the outbreak was recognised. Maximum exposure to cryptosporidia probably occurred three days later (five days before the outbreak was recognised), when water turbidity rose suddenly to about seven times normal levels, signalling a failure of the water filtration plant. The process used to recover oocysts is noted for its variability,6 and this figure may be a substantial underestimate. Swimming pool outbreaks of cryptosporidiosis illustrate that illness can result from ingestion of a small volume of contaminated water, but, again, the time lag between a contamination event and examination of water samples makes it difficult to estimate actual exposure levels.7 Infected people can shed millions of oocysts per gram of faeces, so ingestion of tiny fragments of faecal matter may be sufficient to cause infection in other pool users.8 Safe drinking water: Overall, data presently available are insufficient to allow a "safe" drinking water level to be defined for these protozoa. It is theoretically possible that ingestion of even a single cyst or oocyst may carry a low risk of developing illness, but it is not feasible to test this hypothesis experimentally. Cryptosporidiosis may cause diarrhoeal illness lasting several days in healthy people, but in AIDS patients inability to clear the infection may result in severe and intractable diarrhoea which ultimately contributes to premature death. It is notable that during the Milwaukee outbreak people with HIV were not more likely to become ill than those in the general population.9 This suggests that the infectious dose for Cryptosporidium parvum is similar in both immunocompromised and immunocompetent people, although the consequences of infection are clearly different. There is evidence that the coagulation step used in water treatment to remove particulate matter causes clumping of coliform bacteria and spores, and similar effects may occur with protozoa. This would result in exposure of fewer people to larger numbers of protozoa than would be predicted from assumptions of uniform distribution in drinking water.10 Water testing: The formulation of a meaningful water sampling program is also a problem. Waterborne outbreaks are rare, and are believed to result from short term "spikes" of contamination from increases in protozoa numbers in the source water, or failure in normal water treatment processes, or a combination of both factors. A program based on spot sampling would be unlikely to detect contamination spikes, and could not provide statistically meaningful information on the very low numbers of protozoa which are normally present. Other parameters, such as turbidity or particle counts, may provide warning of abnormalities in water treatment processes (such warnings were unfortunately ignored in Milwaukee), but in some instances outbreaks have occurred without detectable changes in such measures or any identifiable breakdown in operating processes.11 Only Giardia and Cryptosporidium species of mammalian origin are believed to constitute a risk to human health, but current tests do not indicate the type of animal the protozoa originated from or the viability of cysts and oocysts. Several techniques to determine viability and species have recently been developed but are not yet fully validated. Considerable variability exists in the recovery efficiency of concentration techniques for isolating protozoa from water, making it difficult to compare levels between different studies and different laboratories.6 False positive results from algae and other particles of similar size and appearance to protozoa may also be a significant problem.12 Because of uncertainties about testing methods and the public health significance of low levels of protozoa in water, the National Health and Medical Research Council decided not to set guideline levels for protozoa in the 1996 Australian Drinking Water Guidelines, or to recommend testing for these organisms. Considerable progress has been made in detection techniques since then, but many problems are still to be resolved before we can accurately and reliably measure the number of viable protozoa of the relevant species. Nevertheless, major water companies are testing for protozoa with increasingly sensitive methods in an effort to improve the quality of their supplies, but water and health authorities are faced with a dilemma over what to do when positive results are found. Solutions: While legislation may appear to be the answer to this problem, we believe this issue is far too complex to be resolved in this way. The interests of public health would be better served by an open, cooperative approach bringing together the expertise of government, public health and the water industry. Australia would benefit from the development of best-practice programs, appropriate for the circumstances of different water supplies, and covering water quality from source to tap. Such programs are already being implemented in other countries.13 There is also a need to develop consensus protocols for graded responses to contamination incidents, and improved communication with the public and interest groups. Current surveillance mechanisms for communicable diseases are fragmentary, relatively insensitive and slow,14 and should be improved and integrated with water quality data to provide more sensitive and rapid detection of outbreaks. Cooperative research efforts are required to improve water monitoring techniques and confirmatory tests, together with appropriate measures for quality assurance. Only then will we be in a position to assess whether protozoa in drinking water are causing illness in the community, and determine appropriate measures to protect public health. Martha I Sinclair Senior Reseach Fellow Christopher K Fairley Associate Professor Margaret E Hellard NHMRC PhD Scholar Department of Epidemiology and Preventive Medicine and Cooperative Research Centre for Water Quality and Treatment Monash University, Melbourne, VIC Most of Sydney told: boil drinking water. The Sydney Morning Herald, 1998; 30 Jul: 1. Rendtorff RC. The experimental transmission of human intestinal protozoan parasites. II Giardia lamblia cysts given in capsules. Am J Hyg 1954; 59: 209-220. Nash TE, Herrington DA, Losonsky GA, Levine MM. Experimental human infection with Giardia lamblia. J Infect Dis 1987; 156: 974-984. DuPont HL, Chappell CL, Sterling CR, et al. The infectivity of Cryptosporidium parvum in healthy volunteers. N Engl J Med 1995; 332: 855-859. MacKenzie W, Hoxie N, Proctor ME, et al. A massive outbreak in Milwaukee of Cryptosporidium infection transmitted through the public water supply. N Engl J Med 1994; 331: 161-167. LeChevallier MW, Norton WD, Siegel JE, Abbaszadegan M. Evaluation of the immunofluorescence procedure for detection of Giardia cysts and Cryptosporidium oocysts in water. App Environ Microbiol 1995; 61: 690-697. Lemmon JM, McAnulty J, Bawden-Smith J. Outbreak of cryptosporidiosis linked to an indoor swimming pool. Med J Aust 1996; 165: 613-616. Chappell CL, Okhuysen PC, Sterling CR, DuPont HL. Cryptosporidium parvum: intensity of infection and oocyst excretion patterns in healthy volunteers. J Infect Dis 1996; 173: 232-236. Frisby HR, Addiss DG, Reiser WJ, et al. Clinical and epidemiologic features of a massive waterborne outbreak of cryptosporidioisis in persons with HIV infection. J Acquir Immune Defic Syndr Hum Retrovirol 1997; 16: 367-373. Gale P, van Dijk PAH, Stanfield G. Drinking water treatment increases micro- organism clustering; the implications for microbiological risk assessment. J Water Services Res Technol -- Aqua 1997; 46: 117-126. Goldstein ST, Juranek DD, Ravenholt O, et al. Cryptosporidiosis: an outbreak associated with drinking water despite state-of-the-art water treatment. Ann Intern Med 1996; 124: 459-468. Clancy JL, Gollnitz WD, Tabib Z. Commercial labs: how accurate are they? J Am Water Works Assoc 1994; 5: 89-97. The partnership for safe water. American Water Works Association. <URL http://www.awwa.org/partner1.htm> Padiglione AP, Fairley CK. The early detection of outbreaks of waterborne gastroenteritis -- a feasibility study. WaterTECH Conference, Brisbane, April 1998. - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Martha I Sinclair · Christopher K Fairley · Margaret E Hellard

Preventing suicide: what will work and what will not Stephen J Rosenman Population, not individual, approaches to suicide prevention MJA 1998; 169: 100-102 See also Dudley et al Suicide is the second most common cause of death among young men in the Western world.1 The emotional impact of suicide, especially of young people, on the community has produced a "do something, do anything" flurry of preventive activity, directed mostly at identifying and intervening with people at high risk.2,3 Much of the activity is ineffective4 and some may even make things worse.5-7 Here, I argue that focusing on people at "high risk" squanders resources, and that we may have to abandon this approach to suicide prevention as an immediate health target. Can we identify and assist high-risk individuals? Focusing prevention on people at "high risk" of suicide appears efficient because it seems to concentrate on those most likely to benefit. But can we identify high-risk individuals? Dimensional risk factors, such as hypertension or depression, have a linear relationship to mortality; only an arbitrary cut-off separates high risk from low risk.8 For conditions with multiple risk factors, such as coronary heart disease and also suicide, each factor adds a little to the risk, but often only when it interacts with other factors. No single predictor or combination of predictors is present in every individual, and membership of the high-risk group changes from moment to moment. Half a bottle of whisky may create a high suicide risk within an hour. As we learn to specify risk more precisely, the identified high-risk group gets smaller and -- while the individual risk of each member increases -- as a group they contribute a diminishing proportion of all suicides. Many more suicides come from the very much larger low-risk population. In a hypothetical population of 100 000, we may identify 500 people with a high suicide risk of, say, 10% (the 10-year suicide risk in schizophrenia, for example) and the remaining 99 500 with a low risk of, say, 0.1% (the approximate 10-year suicide risk in the population). The high-risk group will produce 50 suicides, while 100 will come from the low-risk group -- prevention targeted at high-risk people will miss most of the suicides. Another problem appears once we identify high-risk individuals. They then need advice and treatment that is effective, available and acceptable to them. How do we measure effectiveness if we can count only the failures? If we look at population suicide rates, agencies such as telephone suicide crisis services seem ineffective.4 Intervention after suicide attempts has not only been of little effect,9 but is also irregular in its availability, and frequently ignored by those it is intended to benefit.10,11 Those deemed at high risk, such as those discharged from hospital after a suicide attempt, already receive intensive follow-up, and further improvements will show diminishing returns of people saved.12 However, the insuperable problem in the high-risk approach arises when we try to use common characteristics of history and personality to identify individuals at risk of events that are uncommon in statistical terms. For events as infrequent as suicide, even highly specific and sensitive predictions will have high error rates.13 Theoretically, suicide predictions with 99% specificity will predict 1000 suicides in a population of 100 000; but the current suicide rate of around 15 per 100 000 population means that, in a year, fewer than 20 will be correct predictions. In the real world, where 85% is "good" specificity, those who will ultimately die are hidden in a haystack of people "at risk". If a high-risk approach is ineffective, is any other strategy better? Newer approaches and paradigms for prevention in public health have not fully penetrated policymaking for mental disorders. William Haddon, a former Director of the United States National Highway Safety Bureau, propounded principles for injury prevention which widened the focus from the victim to the array of environmental interactions amenable to change (see below).14 More radically, Geoffrey Rose, an epidemiologist at the London School of Hygiene, switched the spotlight away from individuals at high risk of suicide and turned it onto whole populations.15 He argued that mortality falls more if we reduce the whole population's exposure to factors related to suicide than if we identify and treat high-risk people. Time to consider a population-based approach? The principle of the "population-based" approach is to apply preventive strategies to the whole population or subpopulation in order to shift the distribution of risk, so that at any time fewer people are over the threshold that leads to completed suicide16 (see Figure). We do not have to identify the individuals within the population to save them. This is demonstrated by the successful reduction in mortality from road trauma and from cardiovascular disease. These successes should now be models for suicide prevention. Road trauma deaths in Australia decreased after the apparently inexorable rise seen in the 1960s,17 and this decline clearly followed the introduction of measures that applied to the whole population. These measures -- seat belts, random breath tests for alcohol, speed-limit enforcement, and improvements to roads and cars -- succeeded where strategies to identify the "high-risk" individual -- the dangerous driver, "the nut holding the steering wheel" -- had failed or aggravated the problem. Each measure, ranging from those most proximate to the crash (seat belts, collapsible steering columns) through the antecedent conditions (alcohol, speed) to the most nebulous antecedents, such as public attitudes to road safety,18 contributed its bit to the sum of prevention, and mortality fell without anyone identifying a high-risk individual or tackling the chain of causes which explain an individual death. Indeed, by 1968, Haddon had already challenged myths of accident prevention: ". . . because drivers cause most accidents [we assume that] programs correspondingly must be concerned with drivers. In the real world there is no basis for making this assumption [which] leads to demonstrably false conclusions."19 The decline in cardiovascular disease mortality is not explained by the vigorous treatment of high-risk people. Established risk habits such as smoking and diet were strikingly resistant to change in high-risk individuals.20 More importantly, most cardiac deaths occur among the large numbers of lower-risk people. Overall cardiovascular mortality fell with the change in community-wide attitudes to cigarettes, diet, inactivity and stress.21 At first sight, suicide prevention in these terms seems much more difficult because the antecedents of suicide appear harder to discern and change. However, if we take what we do know about suicide risk and apply it to the population rather than to defining the individual at risk, reducing suicide may become feasible.4,12 How do we put a population-based approach into practice? Restricting access to the means of suicide (eg, by detoxification of domestic and vehicle exhaust gases, gun regulation, control of dangerous medication) will tackle the most proximate antecedents. Close antecedents susceptible to reduction include drug and alcohol abuse; the population load of mood disturbances, including clinical and subclinical depression;22-24 conduct disorders;22 and media modelling of suicide.25 The more remote antecedents in all age groups include socioeconomic deprivation26 and, to a surprisingly uncertain degree, unemployment.4,27 In younger populations, family breakdown and alienation, relationship losses, school failure and suspension may portend suicide,28 while in older populations loneliness and physical morbidity may do so.29 In Aboriginal populations, suicide is prefigured by substance abuse and high incarceration rates, which are problems for the whole community to address, not just the problems of high-risk individuals.30,31 What to do and where to start? Haddon and Baker14 assert that we should first do those things we can, rather than struggling with things we cannot define or alter. Attacks on access to means of suicide, such as firearms32 and car exhausts,33 are within our present reach. By a large margin, they will have the strongest and most immediate effect in reducing suicide rates,4 even though such measures may not strike at what might seem the most "important" emotional antecedents. The problem with social antecedents, such as alienation or drug abuse, is that they demand difficult social engineering. It is unpromising to try to reconstruct families after they have broken down. Reducing the incidence of family breakdown and other such antecedents in the community may not be easier, but may be more profitable34 in terms of prevention, and for this medical efforts must harmonise with other social and educational initiatives. Of course, these antecedent problems (and others such as mental illness) warrant action on their own merits, not just as targets in suicide prevention initiatives. We cannot comfortably assume that education campaigns will always help, and there are good arguments against tackling prevention through "suicide prevention" or "education" campaigns. In the past, school-based driver education in the United States was associated with unexpectedly higher road accidents and deaths.35 Suicide education campaigns in schools not only miss excluded students, but have also shown complex and possibly harmful effects on attitudes to suicide6,10 and on completed suicide.7 The final analysis Firstly, identifying and treating high-risk individuals is unlikely to result in lower suicide rates. The refinement of individual assessment has passed the point of diminishing returns, and the obsessive study of suicidal individuals will not uncover the Holy Grail of perfect prediction. Clearly, we will not stop doing our best for distressed and suicidal people, even though this will not reduce population suicide rates. But this is not prevention. Secondly, pessimism about suicide may not be justified, despite the rising rates. The turnaround in the rising road toll and in cardiovascular disease teaches what can be done. The lesson is that measures which reduce overall risk in the whole population will reduce the number of people above the fatal threshold, and we do not need to identify the high-risk people individually. Consequently, we may have to abandon the frontal assault on suicide. We cannot justify prevention campaigns driven by the suicidal risk of individuals, despite the intuitive and political appeal of such measures. Indeed, to the degree that they drive resources into ineffective strategies, current approaches to "suicide prevention" may impede suicide prevention. Instead, we must "bite the bullet" in restricting access to means of suicide, the most proximate factor. Beyond that, we need the diligent, unspectacular work in the population which mitigates those factors which lead, among other things, to suicide. For medicine, it is to treat the ill,36 whether or not they are suicidal, and, from a public health pulpit, to address the social ills which produce morbidity, whether or not they lead to suicide. References Pritchard C. New patterns of suicide by age and gender in the United Kingdom and the Western World 1974-1992; an indicator of social change? Soc Psychiatry Psychiatr Epidemiol 1996; 31: 227-234. CDC. From the Centers for Disease Control and Prevention. Suicide among children, adolescents and young adults -- United States 1980-1992. JAMA 1995; 274: 451-452. Commonwealth Department of Health and Family Services (Australia). Youth suicide in Australia: the National Youth Suicide Prevention Strategy. Canberra: Australian Government Printing Service, 1997. Gunnell D, Frankel S. Prevention of suicide: aspirations and evidence. BMJ 1994; 308: 1227-1233. Shaffer D, Garland A, Vieland V, et al. The impact of curriculum-based suicide prevention programs for teenagers. J Am Acad Child Adolesc Psychiatry 1191; 30: 588-596. Hazell P, King R. Arguments for and against teaching suicide prevention in schools. Aust N Z J Psychiatry 1996; 30: 633-642. Lester D. State initiatives in addressing youth suicide: evidence for their effectiveness. Soc Psychiatry Psychiatr Epidemiol 1992; 27: 75-77. Patton GC, Harris R, Carlin JB, et al. Adolescent suicidal behaviours: a population based study of risk. Psychol Med 1997; 27: 715-724. Deykin E, Chung-Chen H, Joshi N. Adolescent suicidal and self-destructive behaviours: results of an intervention study. J Adolesc Health Care 1986; 7: 88-95. Shaffer D, Garland A, Gould MS, et al. Preventing teenage suicide: A critical review. J Am Acad Child Adolesc Psychiatry 1988; 27: 675-687. Goldney RD. Out-patient follow-up of those who have attempted suicide: fact or fantasy? Aust N Z J Psychiatry 1975; 9: 111-113. Lewis G, Hawton K, Jones P. Strategies for preventing suicide. Br J Psychiatry 1997; 171: 351-354. Pokorny AD. Prediction of suicide in psychiatric patients. Arch Gen Psychiatry 1983; 40: 249-257. Haddon W, Baker SP. Injury control. In: Clark DW, McMahon B. Preventive and community medicine. Boston: Little Brown, 1981. Rose G. The strategy of preventive medicine. Oxford: Oxford University Press, 1985. Rose G. Mental disorder and the strategies of prevention. Psychol Med 1993; 23: 553-555. Federal Office of Road Safety (FORS). Trends in road safety. Monograph No 1. Canberra: FORS, 1997. Graham JD. Injuries from traffic accidents: Meeting the challenge. Annu Rev Public Health 1993; 14: 515-543. Haddon W. The changing approach to the epidemiology, prevention and amelioration of trauma: the transition to approaches etiologically rather than descriptively based. Am J Public Health 1968; 58: 1431-1438. Susser M. The tribulations of trials: Intervention in communities [editorial]. Am J Public Health 1995; 85: 156-158. Epstein FH. Cardiovascular disease epidemiology: a journey from the past into the future. Circulation 1996; 93: 1755-1764. Shaffer D, Gould MS, Fisher P, et al. Psychiatric diagnosis in child and adolescent suicide. Arch Gen Psychiatry 1996; 53: 339-348. Depression and suicide: are they preventable [editorial]? Lancet 1992; 340: 700-701. Brent DA, Perper JA, Goldstein CE, et al. Risk factors for adolescent suicide. Arch Gen Psychiatry 1988; 45: 581-585. Phillips DP, Carstensen MS. Clustering of teenage suicides after television news stories about suicide. New Engl J Med 1986; 315: 685-689. Gunnell DJ, Peters TJ, Kammerling RM, Brooks J. Relation between parasuicide, suicide psychiatric admissions and socioeconomic deprivation. BMJ 1995; 311: 226-230. Platt S. Unemployment and suicidal behaviour: a review of the literature. Soc Sci Med 1984: 19; 93-115. Gould MS, Fisher P, Parides M, et al. Psychosocial risk factors of child and adolescent completed suicide. Arch Gen Psychiatry 1996; 53: 1155-1162. Draper BM. Prevention of suicide in old age. Med J Aust 1995; 162: 533-534. Royal Commission into Aboriginal Deaths in Custody. National Report. Canberra: Australian Government Publishing Service, 1991. Hunter E. An examination of recent suicides in remote Australia: Further information from the Kimberley. Aust N Z J Psychiatry 1991; 25: 197-202. Kellerman AL, Rivara F, Somes G, et al. Suicide in the home in relation to gun ownership. New Engl J Med 1992; 327: 467-472. Rosenman SJ. Car exhaust suicide. Med J Aust 1997; 166: 288-289. Zigler EF, Taussig C, Black K. Early childhood intervention: a promising preventative for juvenile delinquency. Am J Psychol 1992; 47: 997-1006. Robertson LS. Crash involvement of teenaged drivers when driver education is eliminated from high school. Am J Public Health 1980; 70: 599-603. Wilkinson G. Can suicide be prevented? Better treatment of mental illness is more appropriate aim. BMJ 1994; 309: 860-861. Authors' details Canberra Psychiatry Group, and National Health and Medical Research Council Psychiatric Epidemiology Research Centre, Canberra, ACT Stephen J Rosenman, MD, FRANZCP, Psychiatrist. Reprints: Dr Stephen J Rosenman, GPO Box 610, Canberra, ACT 2601. E-mail: sjrATatrax.net.au - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Stephen J Rosenman

Children are currently being denied vaccines for inappropriate reasons The most recent edition of the National Health and Medical Research Council's Australian immunisation handbook gives very clear guidelines about the contraindications to vaccination with pertussis vaccine and measles-mumps-rubella vaccine (MMR).1 This was necessary because many children have been denied these vaccines for inappropriate reasons, such as previous reactions at the injection site, fever or irritability after pertussis vaccine, or a history of egg allergy (for ruling out measles vaccine).2 The guidelines now recommend only two absolute contraindications to pertussis-containing vaccines -- encephalopathy or severe allergic reaction following a previous dose. However, over the past two years the Australian Childhood Immunisation Register has recorded that more than 32 000 doses of combined diphtheria-tetanus vaccine (CDT) have been administered to children in place of diphtheria- tetanus-pertussis vaccine (DTP), suggesting that doctors are not following this advice. In addition, based on substantial local and overseas evidence, the guidelines also recommend that "egg allergy, even anaphylactic egg allergy, is NOT a contraindication to immunisation with measles vaccine or MMR".1,3 The previous concept that egg allergy contraindicated MMR came from the manufacturers' product insert and was based on the incorrect assumption that, as it was cultured in chick fibroblasts, it could contain egg antigens. It is likely that inappropriate caution about vaccinating children with previous reactions to pertussis vaccine has been partly responsible for the re-emergence of pertussis over the past four years.4 There were more than 10 000 notified pertussis cases in Australia in 1997, and nine deaths between October 1996 and November 1997.5 Similarly, unnecessary caution about children with egg allergy may have contributed to our measles outbreaks.6 In this issue of the Journal, Andrews and colleagues show how children with previous severe reactions to pertussis vaccine (convulsions, apnoea, hypotonic-hyporesponsive episodes, high fever and persistent screaming) were safely vaccinated in a special clinic at The Canberra Hospital.7 This clinic was the first of a number of similar services now operating or about to begin operating in other centres, including Sydney, Melbourne, and Adelaide. Information about these services is available from State and Territory health departments, which have encouraged their establishment. These clinics plan to collaborate and share expertise nationally. What does this mean for the doctors and nurses who provide routine vaccinations? It means that they should be confident about the guidelines in the Immunisation handbook.1 Children with previous mild to moderate non-anaphylactic reactions (including persistent screaming and high fever) can be vaccinated (with routine precautions) by their usual vaccine provider. Paracetamol should be given prophylactically (15 mg/kg body weight for each oral dose1) to reduce the rate of local and systemic reactions to vaccines containing the whole-cell pertussis component. Children who have had severe reactions (prolonged hypotonic-hyporesponsive episodes and seizures, each seen about once every 2000 doses of whole-cell pertussis vaccine) can also be vaccinated safely,8,9 but may need to be assessed and vaccinated at (or, for rural families, in consultation with) a special clinic. The few children with a history of anaphylaxis following vaccination -- said to occur in about 1/50 000 doses of DTPw (diphtheria-tetanus-whole-cell pertussis vaccine)10 -- and children with underlying medical conditions who may be at special risk (eg, severe neurological disorders) should also be referred for assessment and advice. A new vaccine containing acellular pertussis components (DTPa -- diphtheria-tetanus-acellular-pertussis) is now approved in Australia for use in infants and children. It is funded nationally for the doses given to children aged 18 months and 4 to 5 years, and by some States and Territories (at present South Australia and the Northern Territory) for the three infant doses. Acellular vaccines are associated with a significantly lower rate of reactions at the injection site, hypotonic-hyporesponsive episodes, convulsions and screaming.11 For this reason they are recommended for infants who have had a previous severe reaction to DTPw. Acellular vaccines were not available when The Canberra Hospital clinic was established, so DTPw was used and found satisfactory. Since the use of acellular vaccines for the fourth and fifth doses (at 18 months and 4 to 5 years) in the United States, the rate of serious side effects after vaccination has been reduced by 60% to 70%.12 The availability of acellular pertussis vaccine should remove any need for general practitioners to use CDT vaccine. In Australia, as in many other countries, the States and Territories have established a formal reporting system for vaccine adverse events. Providers report vaccine reactions either to their local public health units or to central disease control units of State or Territory health departments. This information is then supplied to the national Serious Adverse Events Following Vaccination Surveillance Scheme (SAEFVSS), which commenced in March 1995 and is run by the National Centre for Disease Control in Canberra.13 Many vaccine providers do not realise that they should be reporting serious reactions -- so, for example, the number of hypotonic-hyporesponsive episodes being reported is less than would be expected from vaccine trials in which there is active follow-up.11 Other forms of adverse event surveillance should now be used to supplement the SAEFVSS. This would include transmission of data to the SAEFVSS from the special clinics and from hospital admissions, or active surveillance, through such initiatives as the Australian Paediatric Surveillance System, of specific rare serious events. These measures would help make the system more sensitive,14,15 and this would further reassure both providers and the public about the good safety record of the vaccines used in the current childhood immunisation schedule. We must conclude from The Canberra Hospital clinic report that most children with previous severe reactions can be safely vaccinated and that no child should be deprived of pertussis or MMR vaccines without consultation with a specialist advisory service. Margaret A Burgess Director Peter B McIntyre Deputy Director Timothy C Heath Research Fellow National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases, Royal Alexandra Hospital for Children Westmead, and The University of Sydney, Sydney, NSW National Health and Medical Research Council. The Australian immunisation handbook. 6th ed. Canberra: AGPS, 1997. MacIntyre CR, Nolan T. Attitudes of Victorian immunisation providers to pertussis vaccine. Med J Aust 1994; 161: 293-294. Aickin R, Hill D, Kemp A. Measles immunisation in children with allergy to egg. BMJ 1994; 309: 223-225. Burgess MA, McIntyre PB, Heath TC. Pertussis re-emerging: who is responsible? Aust N Z J Public Health 1998; 22: 9-10. Communicable Diseases Surveillance. Pertussis epidemic continues. Commun Dis Intell 1997; 21: 359-360. Communicable Diseases Surveillance. Measles. Commun Dis Intell 1995; 19: 562-563. Andrews RM, Kempe AE, Sinn KK, Herceg A. Vaccinating children with a history of serious reactions after vaccination or of egg allergy. Med J Aust 1998; 168:491-494. Miller E. Collapse reactions after whole cell pertussis vaccination. Pertussis remains a bigger risk than collapse after vaccination [editorial]. BMJ 1998; 316: 876-877. Vermeer-de Bondt PE, Labadie J, RŸmke HC. Rate of recurrent collapse after vaccination with whole cell pertussis vaccine: follow up study. BMJ 1998; 316: 902-903. Peter G, editor. Pertussis. In: 1997 Red Book: Report of the Committee on Infectious Diseases. 24th ed. Elk Grove Village, Ill: American Academy of Pediatrics, 1997: 401. Cherry JD. Comparative efficacy of acellular pertussis vaccines: an analysis of recent trials. Pediatr Infect Dis J 1997; 16 (4 suppl): S90-S96. Committee on Infectious Diseases. American Academy of Pediatrics. Acellular pertussis vaccine: recommendation for its use as the initial series in infants and children. Pediatrics 1997; 99: 282-288. Communicable Diseases Surveillance. Surveillance of serious adverse events following vaccination. Commun Dis Intell 1995; 19: 273-274. Farrington P, Pugh S, Colville A, et al. A new method for active surveillance of adverse events from diphtheria/tetanus/pertussis and measles/mumps/rubella vaccines. Lancet 1995; 345: 567-569. Chen RT, Glasser JW, Rhodes PH, et al. Vaccine Safety Datalink Project: a new tool for improving vaccine safety monitoring in the United States. Pediatrics 1997; 99: 765-773. Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia ".

Margaret A Burgess · Peter B McIntyre · Timothy C Heath

Collateral damage from alcohol abuse: the enormous costs to Australia Curtailing the rippling effect of irresponsible drinking MJA 1998; 168: 6-7 Alcohol abuse is a problem that could affect any member of society, including the majority who are abstinent or use alcohol in moderation. Although much has been written about alcohol abuse and its effects on the drinker, there has been less emphasis on the deleterious effects on innocent bystanders, such as the physical, emotional and/or financial loss or damage. The spectrum of this "collateral damage" includes alcohol-related violence, road accidents, family problems, adverse pregnancy outcomes, consequences of alcohol abuse by doctors, and the resultant financial burdens incurred by society. Past studies have found that alcohol abuse plays a significant role in violent crime.1 It is estimated that about 13% of Australians aged 14 years and over (well over one million people) have been physically abused at least once by someone affected by alcohol, while 16% have had their property damaged at least once.2 Alcohol has also been implicated in about one-third of sexual assault cases.3 In 1992, 294 people died from alcohol-related assaults in Australia.1 Drunk drivers put not only their own lives in peril, but also pose a significant risk to other road users. In NSW in 1995, of the 620 people killed in road accidents, 141 (including 37 passengers and pedestrians) died in alcohol-related accidents. In addition, 298 non-drivers were seriously injured.4 Even more dramatic examples of alcohol-related transport accidents have been recorded internationally, such as the tragic Exxon Valdez oil spill in Alaska in 1989. At least 1% of the population (about 180 000 people) have a close family member with a serious alcohol problem. Isolation, neglect, aggression and disruption within the family, particularly spouse abuse, are frequent.5 Sexual and financial problems, stress, verbal and physical abuse, separations and divorce are also common between couples where at least one partner abuses alcohol.6 A Victorian report in 1988 found that alcohol was definitely or possibly involved in 53% of several thousand reported incidents of family violence.7 Children are particularly affected by having an alcoholic parent and they are more likely to become depressed,5 have lower IQ,8 and be alcohol dependent themselves in the future.9 In 1992, there were 226 hospital episodes resulting from alcohol-related child abuse in Australia.1 However, the extent of family problems is probably underestimated because there is underreporting of alcohol-related domestic violence. Maternal alcohol abuse is associated with adverse perinatal outcomes. These include the fetal alcohol syndrome, pseudo-Cushing's syndrome, alcohol withdrawal in the newborn, and increased risk of perinatal mortality.10 The incidence of fetal alcohol syndrome has been estimated to be between one and two per thousand live births, or 250 to 500 new cases per year in Australia.11 Alcohol abuse among doctors may lead to impaired clinical judgement and skills. While it is widely believed that alcohol abuse may be common among medical professionals, it is very difficult to identify doctors with alcohol-related problems. In the 12 months to March 1996, the NSW Medical Board heard 31 matters related to "impaired registrants", of which five were related to alcohol abuse.12 Similar problems may also occur in other health care workers. The costs of this to society include the costs of litigation, as well as the costs of patients' excess morbidity and mortality. The financial burden of alcohol abuse to the Australian community is substantial. In 1992, the costs of alcohol abuse were estimated to be $4.5 billion, or $250 for every man, woman and child in Australia.13 About three-quarters of these costs were tangible, including lower productivity because of lost work days, health care costs, road accident costs and legal and court costs. About 93% of the total tangible costs were borne by business and government. The intangible costs of about $1 billion include the value of loss of life, and pain and suffering of road accident victims.13 The extent of the problems and costs of alcohol abuse is enormous, but they can be reduced or prevented. About 84% of the costs ($3.8 billion) have been deemed avoidable and potentially amenable to public policy initiatives and behaviour changes.13 While health interventions may play a role, by detection and treatment of alcohol misuse, tougher measures need to be taken in other areas to prevent hazardous drinkers from doing harm to themselves and also to others. Such measures might include: alcohol taxation to reflect alcohol content of beverages rather than the cost of manufacture; major aim of liquor law reforms to be reduction of alcohol-related harm; strict enforcement of liquor laws by both police and state licensing authorities; mandatory training in liquor laws of bar staff, managers and licensees; and a truly independent alcohol advertising regulation authority. The NSW Parliament has enacted legislation which requires hotels, clubs and restaurants not to serve alcohol to patrons with certain defined behaviour suggesting intoxication (Liquor and Registered Clubs (Harm Minimisation) Act (NSW) 1997). The fines for drunken patrons who refuse to leave entertainment premises, if requested to do so, have been increased from $2000 to $5000. These measures are a necessary, but only preliminary, step to place the onus of responsibility on alcohol abusers for their actions, to encourage retailers to adopt a strict code of conduct and to protect the public from the consequences of irresponsible drinking. Yen F Tai Medical Student, University of Sydney, NSW John B Saunders Head, Department of Alcohol and Drug Studies University of Queensland, Brisbane, QLD David S Celermajer Associate Professor of Medicine, University of Sydney, NSW English DR, Holman CDJ, Milne E, et al. The quantification of drug caused morbidity and mortality in Australia. Canberra: Commonwealth Department of Human Services and Health, 1995. National Campaign Against Drug Abuse. National Household Drug Survey report. Canberra: AGPS, 1993: 2. Victorian Community Against Violence. A profile of rapes reported to police in Victoria 1987-1990. Melbourne, 1991. Roads and Traffic Authority, New South Wales. Road traffic accidents in NSW -- 1995. Sydney: Roads and Traffic Authority, 1996: 84-86. Orford J. Family coping. In: Proceedings of the International Congress on Alcohol, Other Drugs and the Family; 1988 November 27-30; Sydney: Alcohol and Drug Foundation, 1989: 30-35. Straussner SLA. The impact of alcohol and other drug abuse on the American family. Drug Alcohol Rev 1994; 13: 393-399. Law Reform Commission of Victoria. Homicide. Report No. 40. Melbourne: The Commission. 1991: 149. Ervin C, Little R, Streissguth A, Beck D. Alcoholic fathering and its relation to child's intellectual development: A pilot investigation. Alcohol Clin Exp Res 1984; 8: 362-365. McCaul ME, Turkkan JS, Svikis DS, et al. Alcohol and drug use by college males as a function of family alcoholism history. Alcohol Clin Exp Res 1990; 14: 467-471. Rankin JG, Ashley MJ. Alcohol-related health problems. In: Last J, Wallace R, editors. Public health and preventive medicine. 13th ed. Connecticut: Appleton-Lange, 1992: 741-767. Abel EL, Sokol RJ. Incidence of fetal alcohol syndrome and economic impact of FAS related anomalies. Drug Alcohol Depend 1987; 19: 51-70. New South Wales Medical Board. Annual report for the period ending 31 March 1996. Sydney: The New South Wales Medical Board, 1996. Collins DJ, Lapsley HM. The social costs of drug abuse in Australia in 1988 and 1992. National drug strategy monograph series No. 30. Canberra: Commonwealth Department of Human Services and Health, 1996. ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Yen F Tai · John B Saunders · David S Celermajer

Forty years of plotting for public health The fight to have research results applied to people has as much to do with politics as with science MJA 1997; 167: 587-589 Introduction - Public health and the Anti-Cancer Council of Victoria - The cancer outcomes - Cancer research - Bringing about change -- how it all happened - Conclusion - Author's details - - - ©MJA1997 Introduction Graduating in 1953 introduced me to the fascinating world of 1950s medicine. I spent most of that decade, after very basic training, in the practice of infectious disease, much of the time at Fairfield Hospital -- now defunct. Infectious disease was frightening, if rewarding. Every one of the 150 tracheotomies in which I participated scared me. Infant whooping cough, poliomyelitis, diphtheria, tetanus and meningococcal septicaemia needed urgent management and immaculate nursing. Drama was part of daily life. My research training period in Cleveland (USA) in 1958 and 1959 fortuitously put me in the position of administering the first doses of Ender's measles vaccine given to humans and also of Sabin's type 1 polio vaccine to newborns. I recall follow-up jugular punctures on roughly a thousand black children given Sabin vaccine orally at birth. Visiting these children in their homes in Cleveland required the company of a uniformed nurse, for the safety of my white skin. I greatly enjoyed the experience, the people and my first acquaintance with gospel music on the breakfast program. This period turned out to be one of dramatic progress in the field. By the 1960s we knew we had seen the effective end of polio, diphtheria, scarlet fever, whooping cough, measles, tetanus, and of rubella-affected babies. Pneumococcal pneumonia virtually disappeared; staphylococcal pneumonia and osteomyelitis, which sometimes followed it, became controllable; rheumatic fever and acute nephritis became increasingly rare. Vaccination, antibiotics and sanitation worked quickly, eradicating mortality, morbidity and sometimes the disease itself. I left Fairfield in 1964 for a pleasurable four-year stint at the Royal Children's Hospital and, in 1968, was invited by Bill Keogh to apply for his job as Director of the Anti-Cancer Council of Victoria, as he was finally retiring. He said I would enjoy it and I accepted his manipulation, happy in the conviction that he would never give me bad advice. I was by then well informed about epidemiology and preventive medicine as well as about the treatment of infection. Progress had been rapid but was that not what progress was about? Certainly, I was unprepared for the slow rate of change in the battle against cancer. Public health and the Anti-Cancer Council of Victoria Progress in Victoria and Australia has been both surprising and substantial during my 27-year tenure at the Anti-Cancer Council. My current experience, both as Consultant to the European Institute of Oncology and as President of the International Cancer Union (the global volunteer-based non-government cancer body), tells me that such progress is not uniform, even among rich and developed countries. However, Victoria, like most of Australia, is readily organisable. It has an accessible population of three to four million, prosperous and generous, educated and with good social and physical infrastructure (Melbourne has 150 golf courses -- Milan, where I currently live, has five). It is possible to know or find an approach to almost anyone, and sometimes to see, or meet, the Premier in the main street. The Anti-Cancer Council of Victoria, as a well known charity with over 140 000 donors and a high profile in the press, was particularly well equipped to operate in this favourable environment. The Council played a leading role in the initiation and development of virtually all the Victorian cancer control programs, from the establishment of the cancer registry, the first public education programs, cancer research, the cervical and breast cancer screening programs, sun and skin protection, and -- most difficult of all -- the anti-smoking battle. The Anti-Cancer Council was set up by Act of the Victorian Parliament in the early 1930s as a volunteer-based, non-profit cancer charity. I responded to the Executive Committee, which had most of the powers, and the Finance Committee, both of which were advised by a group of issue-specific volunteer committees staffed by clinicians, research workers, business people, ethnic groups, and many others. I was advised by, and advised, distinguished Chairs of the Executive Committee -- Weary (Sir Edward) Dunlop, Tom Hurley, Max Whiteside and Brian Fleming. David Hume, as Chair of the Finance Committee, tolerated but controlled my preference for programs over financial reserves, and Allan Dick, as President, taught me much about management. Between them these individuals converted my creative opportunism into a series of strategies and, at least sometimes, a proper plan. As the frontispiece, I always had rock solid support and good advice. The cancer outcomes Lung cancer mortality in Australian men has declined by about 15% since the mid 1980s. (Yes, I am still surprised by this one.) This is prevention in its most classical form, working faster than expected on lung cancer but even more strongly on heart disease, for which the cigarette is only one of a galaxy of risk factors. This downturn occurred over three decades after we knew with confidence that most, in fact nearly all, lung cancer was caused by cigarettes. By contrast, the rate in Hungary is double that of Australia, and climbing consistently.1 Cervical cancer mortality is half what it was in the 1960s. The reduction is due to progressively more effective application of the Papanicolaou smear. It took a long time (too long) for the Pap smear to achieve its potential. The quality of the laboratory service was always there, but the mortality reduction owes as much to progressive social organisation over time, aided, in Victoria, by a helpful Parliament. Melanoma in both men and women is relatively curable, but shows a doubling of mortality each decade in most white-skinned populations. Australian mortality has reached a plateau in men and shows a slight downturn in women -- a world first. This is the result of early detection, the achievement of which was apparent in the mid 1980s, when over half the melanomas in the Victorian Cancer Registry were less than 0.75 mm thick. Melanoma mortality will continue to decline in Australia. So, in due course, will the incidence of both this disease and non-melanotic skin cancer as the "Sunsmart" program continues to bite. Although the management of breast cancer has become more patient-friendly, treatment has yet to deliver striking change, although modest improvement is apparent. Mammographic screening offers expectation of a mortality decline (if community practice can be brought to match clinical trials) of 30% or better as the technology improves. Its success is dependent on the participation rate and Victoria already promises to deliver a high one. The social organisation developed for the cervical cancer program, and applied in a very similar way to mammographic screening, is theoretically simple but took years to devise and then to evolve. It is now accepted that a Victorian woman of relevant age will receive through the mail, at appropriate intervals, personalised invitations to visit her doctor and enter a screening program based on the Pap smear and, separately, to visit one of the 40-years-plus mammographic screening centres and enter a breast screening program of similar design, again at appropriate intervals based on her age. I personally regard access to these programs in an affluent society as a human right, much the same as the right to be immunised at birth. Similar rights exist in the United Kingdom and Sweden, but not in Italy, France or Spain, or in the United States. These Victorian programs are of excellent quality. The laboratories and mammographic facilities participate in quality control programs, and the results of cervical and breast screening tests are registered and linked with the Victorian Cancer Registry. Thus, mistakes become apparent, are investigated and further improvements made. Organising such systems is theoretically easy, and can be achieved in Victoria, but nothing is ever as easy as it should be. The ability of the Victorian Electoral Commissioner, at one stage, to withhold the Electoral Register -- which is the only public listing on which invitations can be based -- was an illustrative example of what single-minded obduracy can do. Senior political intervention was necessary, and was available, to circumvent this. Cancer research The Council always spent about half its income on research. It fostered the research establishment and trained many good people, but could not have done so if there had not been good people available to support. Fortunately, since his appointment by Bill Keogh in 1953, we also had Don Metcalf as the jewel in our crown. Appointed as Carden Research Fellow in 1953, our investment in his basic research work on haemopoietic growth factors led to a General Motors Prize, and others, and was never questioned. Had it been, I would have expected a thunderbolt from above fired by my now-deceased predecessor. Clinical research was harder to develop. Stimulated by Max Whiteside, we established the Victorian Co-operative Oncology Group (VCOG) in the late 1970s, and over time it became a force for the conducting of clinical trials, surveys of management and other analyses. Both the Anti-Cancer Council Scientific Committee and the VCOG play important roles in Victorian cancer policy. Bringing about change -- how it all happened I was mildly surprised when David Hill, friend, colleague and Associate Director of the Anti-Cancer Council, accused me at my farewell morning tea of being creative, stylish and farsighted. Farsighted? I saw myself as an opportunistic person but I doubt if my executive committee ever saw me as a long term planner. However it was, and is, important for the Director of Victoria's major non-government cancer body to pick the issues and to know, or to find out, what to do. We never saw it as our job to do everything, but it was our job to bring about change when a public health opportunity in the field of cancer control beckoned. Ignoring a new piece of knowledge was inexcusable. Our broad base of community and scientific support came because people saw us as a way they could contribute to change, and not merely as a source of research funds. The role of opportunism is clearly exemplified by my visit to David White, Minister for Health, in February 1987. The agenda was to tell him the background and basis of mammographic screening, to persuade him that its time had come, and that it should be an organised program, based on a proper pilot project, and that it should not be left happenstance to the private sector alone. He listened and accepted this advice, and said, as we finished, something to the effect that this was a non-election year and it might be possible to do something about tobacco. The easily drafted comprehensive submission branded into my brain over 20 years was soon on his desk, and was read. Thus, opportunistically, began the coalition which was to drive the Victorian Tobacco Act through Parliament on November 17 that year -- one of the most serious political defeats suffered by the tobacco industry. The Victorian tobacco story is long and can only be summarised. Health Warnings, given in 1970 by (Sir) Rupert Hamer over the grumpy opposition of Sir Henry Bolte, converted the Government from being pro-smoking (yes!) to anti-smoking, at least in theory, and saw our views gain their first political respectability. Television commercials voluntarily made by Warren Mitchell (as Alf Garnet), Miriam Karlin and local actor Fred Parslowe were dramatic and effective, particularly when Fred Parslowe's send-up of the Marlboro Country ("Cancer Country") advertisement was censored, as we had planned. We had not planned to have our "respectability" commercial, made by Nobel Prize winner Sir Macfarlane Burnet, censored also, but when it was he was delighted and the headlines were huge. Action then moved to Canberra, where in 1975 Malcolm Fraser gave us a radio and television advertising ban, subverted in the closing minutes of debate by the Country Party with an amendment which was to legitimise sporting advertising and the take-over of sport by the tobacco industry for another 17 years. That simple slick manoeuvre taught us a good lesson. The Victorian Tobacco Act of 1987 banned those forms of advertising susceptible to State control, such as billboards, competitions, giveaways, and applied a hypothecated (earmarked) tobacco tax to Victorian cigarettes. This tax was pioneering legislation, which was quickly copied by South Australia, Western Australia, California, Massachusetts and others. The idea of earmarking tobacco tax for buying back sport had surfaced in my correspondence as early as 1981. This very public non-party-political battle was the single most difficult and testing event of my career, and brought into play all the goodwill, supportive networks and moral courage of the Council's officers, committees and staff. This Victorian campaign started in February 1987 with a detailed plan which involved me meeting weekly or fortnightly with David White. Mark Birrell, a long-time supporter and Liberal Leader of the Upper House (as well as Shadow Minister for Health) was apprised early and planned much of the second half of the campaign. It was understood at the beginning that the hardest hurdle was likely to be the Liberal Shadow Cabinet, in which 11 out of 20 votes were needed in order to carry the party room. The plan required us to persuade Cabinet and the Labor Party by August of the need for a Bill, and for the Bill to be drafted within the Health Department by then. It would then be announced and followed by a 6-10-week public debate, during which time we had to persuade the Liberal Shadow Cabinet and back bench, then generate a vocal lobby as Parliament debated the Bill. The plan was military in style, with set times, targets and marshalled resources. We conducted an opinion poll which showed clearly that tobacco tax increases were popular, that tobacco advertising was not, and that tobacco sponsorship of sport, while less unpopular, could be replaced by a tobacco-tax-funded body (which eventually was the Victorian Health Promotion Fund) without upsetting the voters. This impressed Cabinet and Parliament. The Age , after a visit to the editor (Creighton Burns), published a five-day intensive coverage of tobacco on the requested date (to coincide with a key Cabinet meeting). This gave both sides much publicity and allowed our public health case to be seriously contrasted with the rather ugly and certainly specious case of the tobacco industry. Sir Gus Nossal was hunted down in Japan and agreed, with typical generosity, to accept the Chair of the Victorian Health Promotion Foundation at a critical time. A dramatic television advertisement (entitled "Coroner", and depicting a cigarette packet as cause of death) focused attention and infuriated the tobacco industry, which responded with an advertisement we labelled "Commissar" which painted us, implausibly, as Big Government fascists. Other industry blunders helped. One tobacco company reacted to the announcement of the Bill by asking their large staff to telephone, write or visit their parliamentarians. They blocked the parliamentary switchboard, often leaving the company switchboard as the call-back number, thereby enraging many politicians. Our 140 000 donors were requested to do the same and a large but unknown number did so, somewhat more temperately it seemed, but clearly representing grassroots opinion. We solicited support from innumerable community organisations and were rarely refused. The then Opposition Leader, Jeff Kennett, may or may not have been surprised to receive about 20 calls from senior Liberals, including his Treasurer. They were organised by one phone call to a well connected businessman. Two calls to the Anglican and Catholic Archbishops (men I had never met) triggered contacts from them to five important members of the Shadow Cabinet just before the crucial vote. So the Bill came to Shadow Cabinet, was passed, passed the Liberal Party room, and went to Parliament, where it was the object of a filibuster attempt by the National Party. Mark Birrell merely told them Parliament would sit until the Tobacco Bill had been dealt with. I watched the tobacco industry people leave Parliament about 5:30 pm, visibly angry, and stayed to see the Bill passed by a unanimous Parliament late on the night of November 17, 1987. Afterwards, the tobacco industry took their money away, at least temporarily, from the Liberal Party, and I was mortified to discover it was the equivalent of only about 10 per cent of our research budget. Should we have been spending our money on political party contributions instead of research? In 1990, led by the Democrats, Federal Parliament abolished print advertising after a short but well-designed campaign. In 1992, Federal Parliament provided Australia with exemplary tobacco legislation, although the exemptions for Grand Prix advertising will probably remain until the United States and Europe act on this issue. Conclusion Not all of this was science, but it was public health, and it shows what science has to do if the results of research are to be applied to humanity. While tobacco control is political warfare, mammographic and cervical screening also needed explanation and lobbying, albeit to a sympathetic Parliament. So there will always be a role for an activist mouthpiece for public health which is trusted, supported and advised by the diverse members of the cancer establishment. Why DO research if the results are not used when known? Nigel J Gray European Institute of Oncology, Milan, Italy Peto R, Lopez AD, Boreham J, et al. Mortality from tobacco in developed countries: indirect estimation from national vital statistics. Lancet 1992; 39: 1268-1278. - ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Nigel J Gray