Environmental health

Kristine Macartney,* Peter McIntyre† * Senior Research Fellow, † Director, National Centre for Immunisation Research, The Children’s Hospital at Westmead, Locked Bag 4001, Westmead, NSW 2145. petermATchw.edu.au Comment: Recently published data have added considerably to the evidence about the impact of varicella vaccination programs, and address many of the concerns raised by Mackenzie. First, in the United States where universal varicella vaccination was recommended a decade ago, recent data show that — despite much slower implementation than is expected in Australia — varicella-related disease has declined by up to 90%, and hospitalisation rates and deaths from varicella by more than two-thirds, due to herd immunity.1,2 Second, data have now been published on the incidence of herpes zoster in areas of sentinel surveillance in the US, showing no change in age-specific rates to 2002.3 Along with the success of a recent trial of high-dose varicella vaccine in reducing herpes zoster in older adults,4 these data add to confidence that any increase in herpes zoster — as predicted in some models — will be detected and effectively combated by vaccinating people aged over 60 years. A substantial allowance for surveillance of both varicella and herpes zoster was included in the 2005 federal budget, to accompany the introduction of universal varicella vaccination in Australia. Mackenzie is correct that varicella is perceived by some as a mild illness, but it is important for general practitioners to emphasise to patients that this is incorrect.5 Each year in Australia, varicella causes around seven to eight deaths and more than 1500 hospitalisations,6 many associated with serious complications, such as invasive bacterial infection, pneumonia, and encephalitis. Although complications are more likely in adults and immunocompromised patients, 42% of hospitalisations are in children aged 0–4 years,6 most of whom are otherwise healthy.7 Patients can also be reassured about the safety of varicella vaccines, as clinical trials now date back 30 years, and more than 40 million doses of vaccine have been distributed in the US. Mackenzie suggests alternatives to universal childhood varicella vaccination, such as vaccination of “high risk” patients and their families, or of adolescents alone. However, these programs would not prevent morbidity among otherwise healthy young children and older age groups, as they would be insufficient to generate herd immunity. Moreover, age-based vaccination strategies have been shown to be easier to implement than more targeted programs. In the absence of a publicly funded universal program, the private market could sustain modest varicella vaccination rates of around 40%–50% in Australia.8 This would increase the number of adolescents and adults susceptible to varicella, because of reduced exposure to the virus and lack of vaccination; these groups also experience greater morbidity with infection than children. A universal program vaccinating young children and adolescents against varicella offers the best current option to reduce morbidity and mortality from this disease in Australia. Ongoing surveillance of varicella and herpes zoster in Australia and elsewhere will reveal whether there is a need for further interventions, such as a second dose of varicella vaccine in children and high-dose varicella vaccine to prevent herpes zoster in older adults.

Kristine Macartney · Peter McIntyre

Re: the letter “Reliability of parental reports of head lice in their children”, by Megan L Counahan, Ross M Andrews and Rick Speare, in the 7 February issue of the Journal (Med J Aust 2005; 182: 137-138). There was an error in Box 2, Sensitivity and specificity of parental report versus screening. The specificity given as 94.0% (969/1030) should have been 98.8% (1018/1030). The html and pdf versions of this article published online were corrected on 5 August 2005.

Megan L Counahan · Ross M Andrews · Rick Speare

Fighting the current epidemic requires intensive education of clinicians and men who have sex with men, as well as targeted screening A research article (page 179)1 and a letter to the editor (page 218)2 in this issue of the Journal should leave you in no doubt that syphilis is back. After falling precipitously with the onset of the HIV epidemic in the early 1980s, syphilis infection rates are rising dramatically in Australia and the developed world among men who have sex with men.3 Why has this occurred, and what can be done about it? Australia’s response will determine if the current syphilis epidemic is remembered as an isolated epidemic or the return of endemic infection. The prevalence of a sexually transmitted infection (STI) is determined by three factors: the probability of transmission per partnership, the rate of partner change, and the duration of infectiousness. The particular importance of the duration of infectiousness is illustrated by the dramatic 100-fold fall in the prevalence of syphilis following the introduction of antibiotics.4 Another example is in situations where access to health care is poor and duration of infectiousness is therefore prolonged, as in isolated Indigenous communities in Australia. In such communities, both syphilis and gonorrhoea are common, despite rates of partner change being similar to those in the rest of Australia.5 In contrast, gonorrhoea or syphilis struggle to exist in communities with adequate access to health care, unless the rate of partner change is high. What then has changed among men who have sex with men to cause this sudden rise in syphilis infections in New South Wales and Victoria? Sexual behaviour has changed, with rates of any unprotected anal intercourse among men who have sex with men having increased by 50% in Australia over the last 10 years — this was also a strong risk factor for incident syphilis in the Health in Men (HIM) study6 mentioned in the research article by Jin et al.1 Oral sex is also transmitting syphilis, despite being considered relatively safe in terms of HIV transmission. Over half of the men in Jin et al’s cases series believed they had contracted syphilis through oral sex,1 and oral sex has been reported as the sole risk factor in up to 50% of cases reported overseas.3 HIV-positive men who have sex with men appear to be at increased risk of syphilis in Australia, representing between 40% and 54% of the cases reported by Jin et al1 and Guy et al.2 In addition, unprotected anal intercourse with an HIV-positive man was a strong risk factor for incident syphilis among HIV-negative men in the HIM Study.1 These findings are consistent with overseas reports that syphilis is more commonly diagnosed in HIV-positive men.3 The critical issue is what can be done now to control this epidemic. Clearly, increasing the use of condoms is important, particularly for anal sex. It is unlikely, however, that condoms will be widely used for oral sex, even though this practice is transmitting syphilis. In addition, reducing the rate of partner change is important, but it has been difficult to demonstrate large effect sizes in controlled studies.7 Substantially reducing the duration of infectiousness may be possible through educational campaigns, increased screening and enhanced contact tracing. Intensive educational campaigns for clinicians and men who have sex with men are fundamental for promoting early diagnosis and treatment, and screening high-risk individuals. Remember, most doctors under the age of 45 have not seen a case of syphilis, and young men are also less likely to be aware of the symptoms and clinical presentation of the infection. Educational campaigns that use the Internet can be relatively cheap and effective. For example, one banner advertisement on gay websites resulted in 32 270 click-throughs to public health websites with syphilis information.8 The cost per “click” varied from $0.05 to $10.8 Increased screening is the only way to detect asymptomatic infection; up to 33% of infections reported by Jin et al in the syphilis case series and the HIM study were asymptomatic.1 Guidelines suggest yearly testing for syphilis for any man who has had sex with another man in the past 12 months.9 This is easily justifiable given the syphilis incidence rate of 0.78 per 100 person years among men in the HIM study, but not necessarily easy to implement because it involves reaching all men who have sex with men, not just those attached to the gay community.1 Screening at every clinic visit for syphilis among HIV-positive homosexually active men may be necessary in view of the higher incidence of syphilis in this group. STI control is most cost effective if programs are focused on core group members who have large numbers of sexual partners. In the syphilis case series, up to two-thirds of the men had attended sex-on-premises venues or saunas where rates of STI infections have been previously reported to be extremely high.1,10 Contact tracing is an essential part of effective STI control but is difficult among men who have sex with men, whose partners are often anonymous. Nevertheless, innovative programs can prove effective. One study found that contact tracing was relatively effective even though the only identifying information available to public health officials were the “screen names” used in internet chat rooms. In this study, 41 of the 97 contacts of men infected with syphilis were traced through their “screen names”.8 Lastly, information about the epidemic, including the typical clinical features, who is affected, and risk factors for infection, is critical to inform intervention, as indeed both Jin et al1 and Guy et al2 have shown. For example, Jin et al provided much needed information about the usual clinical presentation of syphilis, finding that rash was the most common symptom (42%), but an ulcer or sore was also common (40%).1 As the rash of secondary syphilis is extremely infectious, identifying such cases early will significantly improve control. Australia’s response will determine if the current syphilis epidemic is remembered as an isolated epidemic or the return of endemic infection. Endemic syphilis will be expensive; both in human and financial costs, not least because it promotes HIV transmission. We need to learn from Australia’s effective and early response to the HIV epidemic that was characterised by community partnership, bipartisan government support, a commitment to harm minimisation and dynamic, original strategies.

Christopher K Fairley MB BS, PhD, FRACP · Jane S Hocking MPH, MHlthSc, PhD · Nicholas Medland MB BS

This new definition should assist both researchers and clinicians The metabolic syndrome — the clustering of abdominal obesity, dyslipidaemia, hyperglycaemia and hypertension — is a major public health challenge worldwide.1,2 The metabolic syndrome is not benign; it is associated with a substantially elevated risk of type 2 diabetes (5-fold) and of cardiovascular disease (CVD) (2–3-fold),1 and its increasing prevalence could possibly reverse the gains made through recent declining CVD mortality. The metabolic syndrome is not a new condition. It was first described in the 1920s by Kylin, a Swedish physician, as the association of hypertension, hyperglycaemia and gout.3 In the 1940s, attention was drawn to upper body adiposity (android or male-type obesity) as the obesity phenotype commonly associated with type 2 diabetes and CVD.4 This constellation of CVD risk factors has been given a number of names, including “deadly quartet”, “syndrome X”, and “insulin resistance syndrome”,1 but “metabolic syndrome” is likely to hold sway for the foreseeable future. Just as the metabolic syndrome has borne a variety of different names, numerous definitions have also surfaced. The World Health Organization definition,5 and two others, developed by the European Group for the Study of Insulin Resistance6 and the National Cholesterol Education Program — Third Adult Treatment Panel (ATP III),7 have been the main ones in use. Each of these agreed on the core components of obesity, hyperglycaemia, dyslipidaemia and hypertension. However, the definitions differ in the cut-points used for each component, and the way in which the components are combined, leading to considerable confusion.1 The confusion has been particularly apparent in attempts to compare the burden in different populations, where the use of different definitions has seriously hampered the ability to make comparisons between and within communities.1,2 The parameters for assessing obesity have been most problematic, with the current definitions failing to account for ethnic differences for cut-points in waist circumference and body mass index. It was also uncertain which of the definitions best predicted those at risk of CVD and diabetes, although from a clinical perspective, the ATP III definition was probably the most practical for alerting health care professionals to subjects at risk.1,7 Because of the confusion, the International Diabetes Federation (IDF) embarked on the process of developing consensus on a new global definition (Box). The definition recognises the mounting evidence that visceral adiposity is common to each of the components of the metabolic syndrome. Thus, an excessive waist circumference (a good proxy measurement for visceral adiposity) is now a necessary requirement for the metabolic syndrome. Furthermore, as it is clear that the level of obesity at which the risk of other morbidities begins to rise varies between population groups,1,10 ethnic-specific waist circumference cut-points have been incorporated into the definition, so that for South and South-East Asians, 90 cm and 80 cm are the cut-points for men and women, respectively. The cut-points for lipids and blood pressure are unchanged from those used by ATP III, and the glucose cut-point is the value most recently recommended as the upper limit of normal by the American Diabetes Association. As with many previous attempts to define diagnostic criteria for obesity, diabetes, hypertension, and dyslipidaemia, there is always the possibility that new research will force changes, including the possible incorporation of new components such as C-reactive protein and adiponectin. The IDF consensus also includes recommendations for future research into components not currently included in the core definition of the metabolic syndrome. It further highlights strategies for treatment of the metabolic syndrome and its components.8 It addresses both clinical and research needs and: provides a simple entry point for primary care physicians to diagnose the metabolic syndrome; provides an accessible diagnostic tool suitable for worldwide use, taking into account ethnic differences in waist circumference and associated type 2 diabetes and CVD risk; and establishes a comprehensive “platinum standard” list of additional criteria that should be included in epidemiological studies and other research into the metabolic syndrome. Using this new definition, analysis of AusDiab indicates that 29.1% of Australian adults (aged 25 and over) have the metabolic syndrome, compared with 19.3% according to ATP III (P Z Z, J E S, unpublished data). Much recent discussion about the metabolic syndrome has appropriately raised questions about its definition, its clinical role, and even its existence.1,11 At its heart, the syndrome represents the association between a range of factors that appear to be united both in terms of aetiology and consequences. The new IDF definition should provide researchers with a common platform for investigating the metabolic syndrome and its consequences. It should provide a useful practical tool that reminds health care professionals of the metabolic consequences of obesity, and identifies individuals at risk of CVD and type 2 diabetes who are likely to benefit from (lifestyle) interventions. The 2005 International Diabetes Federation definition of the metabolic syndrome8,9 According to the International Diabetes Federation definition, for a person to be defined as having the metabolic syndrome, they must have: Central obesity (defined as waist circumference ≥ 94 cm for Europid men and ≥ 80 cm for Europid women, with ethnicity specific values for other groups*) plus any two of the following four factors: raised serum triglyceride level (≥ 1.7 mmol/L) reduced serum HDL-cholesterol level (< 1.03 mmol/L in males and < 1.29 mmol/L in females), (or specific treatment for these lipid abnormalities) raised blood pressure (systolic blood pressure ≥ 130 mmHg or diastolic blood pressure ≥ 85 mmHg), or treatment of previously diagnosed hypertension impaired fasting glycaemia (fasting plasma glucose [FPG] ≥ 5.6 mmol/L), or previously diagnosed type 2 diabetes * South Asian and South-East Asian men ≥ 90 cm, women ≥ 80 cm; Japanese men ≥ 85 cm, women ≥ 90 cm.

Paul Z Zimmet MD, PhD, FRACP · Jonathan E Shaw MD, MRCP(UK), FRACP · K George M M Alberti FRCP, PhD

Objectives: To describe trends in the notification of infectious syphilis in New South Wales, the characteristics of homosexually active men recently notified with early syphilis, and the seroprevalence and incidence of syphilis, as well as associated risk factors, in a Sydney cohort of HIV-negative homosexually active men.Design, setting and participants: Secondary analysis of New South Wales infectious syphilis surveillance data from 1998 to 2003; a case series of 57 homosexually active men diagnosed with early syphilis in inner Sydney from December 2002 to January 2004; and a prospective cohort study of syphilis among 1333 HIV-negative homosexually active men in Sydney recruited from June 2001 to December 2003.Main outcome measures: Rates of notification of infectious syphilis in New South Wales and in areas of inner Sydney; behavioural and clinical features of men with syphilis in the case series; and incidence of syphilis and hazard ratios (HRs) associated with sexual behaviours in the cohort study.Results: Infectious syphilis notifications in inner Sydney rose more than 10-fold (from 6 in 1999 to 162 in 2003), and the increase was confined to men. Of 57 men with early syphilis in the case series, 54% were HIV-positive and 32% reported no symptoms of syphilis. These 57 men were highly sexually active and likely to report recreational drug use. In the cohort study, 1292 men (97% of participants) consented to syphilis testing; the incidence of syphilis was 0.78 per 100 person-years, and risk factors included reporting unprotected anal intercourse with HIV-positive partners (HR, 5.31; 95% CI, 2.00–184.93) and insertive oral sex (HR, 4.55; 95% CI, 1.14–18.18).Conclusion: Syphilis has been re-established among homosexually active men in Sydney, and HIV-positive men are over-represented. Frequent screening is needed in this population to curb the transmission of both syphilis and HIV.

Fengyi Jin MPH · Garrett P Prestage PhD · John M Kaldor PhD · Andrew E Grulich PhD, FAFPHM · Susan C Kippax PhD · Catherine M Pell MB BS · Basil J Donovan MD, FAChSHM

Objective: To examine the effects of asbestos exposure and tobacco smoking on the level and rate of change of the diffusing capacity of the lung for carbon monoxide (Dlco).Design and participants: A cohort study of 934 people (including both mine workers and town residents) exposed to crocidolite (blue asbestos) at the asbestos mines and in the town of Wittenoom, Western Australia, between 1943 and 1966. Dlco measurements were taken during a follow-up period from 1992 to 2002.Main outcome measures: Baseline levels of Dlco and change in levels over time.Results: 2980 Dlco measurements were done on 934 people (of whom 818 were men and 724 were workers) who underwent a median of 2 (range, 1–17) measurements during the follow-up period. Radiographic asbestosis at baseline and asbestos exposure at a younger age were associated with lower Dlco values. The average rate of decline in Dlco was 0.33 (95% CI, 0.31–0.35) units per year, plus an additional decrement of 0.22 (95% CI, 0.12–0.32) units per year if the participant had radiographic asbestosis at the beginning of the follow-up period. Compared with never-smokers, current smokers and ex-smokers had lower Dlco at baseline, but smoking status did not affect the change in Dlco during the follow-up period.Conclusions: Our results confirm a continuous deleterious effect of crocidolite on Dlco, especially on people with asbestosis. Smoking was associated with lower Dlco levels, but was not a significant predictor of rate of change in Dlco. Smoking status did not affect the relationships between crocidolite exposure and the level or rate of change of Dlco in this population.

Helman S Alfonso PhD · Lin Fritschi PhD · Nicholas H de Klerk PhD · Nola Olsen MSc · Jan Sleith MSc · Arthur (Bill) W Musk PhD, FRACP

Caroline F Finch Director, New South Wales Injury Risk Management Research Centre, University of New South Wales, Level 8, Applied Science Building, Sydney, NSW 2052. c.finchATunsw.edu.au To the Editor: I am prompted to write to you in response to a recent MJA editorial.1 It amazes me that the health sector in Australia, as I think the editorial did, continues to largely ignore the magnitude of the problem of injury in our children. This is despite clear evidence of the excess ill-health burden that injury places on our children, according to the Australian Institute of Health and Welfare (AIHW) report (the subject of the editorial)2 and other reports.3-5 Having said this, the editorial did highlight a very pleasing trend — there has been a steady decline in injury deaths in later childhood. Unfortunately, however, this was the only mention of injury in the editorial, and readers could be forgiven for thinking that this is the end of the story: the injury death rate is declining; therefore, we are doing all we can, and injuries are not a major issue. Nothing could be further from the truth. Our children continue to die from road and drowning accidents and will do so until injury prevention is recognised as paramount. The AIHW report clearly states that the single highest cause of death in children remains injury and poisoning.2 Accordingly, trauma is the single highest contributor to premature mortality and years of potential life lost of any health condition in Australia. If we don’t develop new approaches to reducing the incidence of drownings and road deaths, in particular, we will not see further declines in injury-related death rates, and injury will continue to rate highly as a killer of young people. Importantly, injuries do not only kill young people — they also hospitalise and maim them. The second most common reason for hospitalisation in Australian children is injury.2 Unlike injury deaths, there has been no trend in the rate of hospitalisation for injury. Across age groups, there appears to be a shift from fatalities to an increasing number of people with a high lifetime burden of significant disability, including brain and spinal cord damage. Imagine what this does to the quality of life and life expectancy of a child. How many of these children will be able to lead physically active lives? It is time for the health sector, particularly public health agencies, to properly recognise injury as a critical issue for the ongoing health of Australian children and to formally commit to appropriate preventive actions, commensurate with the priority ranking of childhood injuries.

Caroline F Finch

George C Patton,* Sharon R Goldfeld,† Indrani Pieris-Caldwell,‡ Meredith Bryant,§ Graham V Vimpani¶ * VicHealth Professor of Adolescent Health Research, Centre for Adolescent Health, Murdoch Childrens Research Institute, Flemington Road, Parkville, Melbourne, VIC 3052; † Paediatrician and Research Fellow, Royal Children’s Hospital, Melbourne; ‡ Senior Analyst, § Project Officer, Australian Institute of Health and Welfare, Canberra; ¶ Clinical Chair in Paediatrics, University of Newcastle, NSW. george.pattonATrch.org.au In reply: There is little to disagree with in this excellent summary of injury morbidity and mortality in Australian children. However, the principal point of our editorial1 was to highlight important problems where adequate data are currently unavailable. The Australian Institute of Health and Welfare report was able to give extensive coverage to injuries and accidents in children.2 Indeed, seven indicators specifically addressed aspects of childhood injury, with a range of others (eg, child abuse and neglect, neighbourhood safety) addressing relevant aspects of the family and social context. This emphasis reflected not only the importance of childhood injury, but the extent to which reasonably good data are available. We agree that, despite some favourable mortality trends, the burden of childhood injury remains high, as are associated health care costs. However, childhood injury is an area where advocacy has translated into action.3 One of the reasons for the success of that advocacy has been the availability of sound data, both to make the case and to ensure an appropriate focus in policy responses.4 While there is undeniably much more to do, we can learn much from injury prevention about how to tackle the newly emerging problems of childhood.

George C Patton · Sharon R Goldfeld · Indrani Pieris-Caldwell · Meredith Bryant · Graham V Vimpani

Macrophagic myofasciitis is characterised by sheets of macrophages in striated muscle, a few lymphocytes and inconspicuous muscle fibre damage. It is due to aluminium contained in vaccines, and is localised to the inoculation site. We report the first Australian case, detected incidentally when investigating a raised serum creatine kinase level. Clinical record During investigations for gastroesophageal reflux, a 32-year-old man was noted to have intermittently raised serum creatine kinase levels: 78 U/L in April 2003, 484 U/L in July 2003 and 8846 U/L in August 2003 (reference range, < 196 U/L), with normal troponin levels. He had no neuromuscular symptoms and played sport regularly. A previous serum creatine kinase level of 2000 U/L had been recorded in April 2000, when he had multiple pulmonary emboli after an overseas trip. He had been given inactivated hepatitis A (Havrix) and poliomyelitis vaccines intramuscularly in March 2000, and a booster inoculation for hepatitis A in February 2001. He was taking allopurinol for renal calculi and omeprazole for reflux. His father had died from motor neurone disease and a brother had fasciculations. The patient had no evidence of muscle weakness or wasting, no fasciculations, and the remainder of his neurological examination, as well as needle electromyography, was normal. Muscle biopsy The interstitial connective tissue of the deltoid muscle contained a dense infiltrate of large macrophages (Figure A). Electron microscopy showed spiculated structures within these macrophages (Figure B). When an electron beam hits a sample it releases x-rays of wavelength specific to the elements in the sample. Using this principle, an EDAX x-ray detector revealed an aluminium peak (Kα, 1.48 keV) from the aggregates. A: Deltoid muscle biopsy. Densely packed macrophages with abundant cytoplasm (arrowhead) were seen between muscle fibres (M), together with a few peripheral lymphocytes (thin arrow). No muscle fibre necrosis, regeneration, multinucleate giant cells, Michaelis–Guttmann bodies (found in malakoplakia) or granulomas were present. The macrophages stained positively with acid phosphatase and CD68. The lymphoid population showed a mixture of T and B lymphocytes. Stains for acid-fast bacilli were negative. (Haematoxylin and eosin. Bar = 50 m.) B: Electron micrograph showing electron-dense, randomly orientated, fine spiculated structures (asterisks) within a macrophage (M) (200 nm resin sections on nickel grids examined in a Philips CM120 electron microscope. Osmium and uranyl acetate. Bar = 1 µm.) Macrophagic myofasciitis is characterised by the presence of sheets of macrophages in striated muscle, a few lymphocytes and inconspicuous muscle fibre damage. It is due to the persistence of vaccine-derived aluminium in the muscle at the injection site and the myofasciitis is localised to the injection site. Since macrophagic myofasciitis was first described in 1993,1 more than 200 cases have been identified in France, with only a few cases reported from other countries.2 This is the first case of macrophagic myofasciitis reported in Australia. Aluminium is used as an adjuvant in diphtheria – tetanus –pertus sis, some Haemophilus influenzae type b, pneumococcal, hepatitis A and B, anthrax and rabies vaccines, as well as in tetanus toxoid.3 For example, each millilitre of Havrix contains 0.5 mg of aluminium, as aluminium hydroxide. The mechanism of macrophagic myofasciitis is thought to be secondary to an ongoing local immune reaction to the long-term persistence of this aluminium in the muscle.4 Macrophagic myofasciitis commonly occurs in adulthood, although the age ranges between 1 and 70 years.5,6 The clinical picture is variable, and includes nonspecific symptoms such as myalgia, arthralgia, muscle tenderness, muscle weakness, fever and fatigue. A few patients show raised serum creatine kinase levels and myopathic electromyography.6,7 Neurological manifestations resembling multiple sclerosis have been reported in some patients,8 and rarely it is associated with other diseases such as inclusion body myositis.9 Co-existent autoimmune diseases have been recorded in some patients with macrophagic myofasciitis.10 Steroids, analgesics and antibiotics have been used in attempts to treat this condition.10 Our patient did not have any neuromuscular symptoms and the muscle biopsy was performed because of his raised serum creatine kinase level. There was no correlation between macrophagic myofasciitis and the clinical signs and symptoms in this patient, who was asymptomatic. Therefore, we consider this histological finding to be incidental in a patient with a “CKopathy”. Recently, a genetic predisposition to macrophagic myofasciitis has been suggested to account for the disparity between the low prevalence of this disorder and the widespread use of aluminium-containing vaccines, as well as the variable incidence of this condition in different populations.5 The diagnosis of macrophagic myofasciitis is important to bear in mind, as other diagnoses such as sarcoidosis, connective tissue disease, tuberculosis, Whipple’s disease and malakoplakia may be entertained. The patient could then be subjected to needless further investigations and undue anxiety. We hope this report will help increase awareness of this condition, and predict that more Australian cases will come to light in future deltoid muscle biopsies.

Meena Shingde MB BS, MD · Roger Pamphlett MD, FRACP, FRCPath · James Hughes FRACP · Ross Boadle Dip(MT), MAIMS · Edward J Wills MD, FRCPA

Clinical record 1 Area of necrosis on right shin 2 Areas of necrosis at graft site A 50-year-old woman was referred for surgical consultation after accidental self-inoculation with Gudair ovine Johne’s disease (OJD) sheep vaccine 18 days earlier. The automatic vaccination syringe had been hanging from her neck by a plastic delivery tube connected to the vaccine pack when a sheep had bumped the syringe. This resulted in a needle-stick injury to her right shin. Within hours, the area became red, and 3 days later she consulted her general practitioner. Tetanus toxoid was administered, and she commenced a course of dicloxacillin. The inflammation failed to resolve and had progressed to a 2 cm-diameter area of skin necrosis by the time of presentation (Box 1). The necrotic skin and subcutaneous fat were then debrided. Despite careful wound packing, a tender nodule developed in the overhanging edge of the ulcer. On Day 15 after presentation, soft granulation tissue extending down to the deep fascia and the overhanging skin were debrided. A week later, a split skin graft was applied. Although the graft was successful when seen about 7 weeks after initial presentation, two red, tender areas had appeared about 5 mm from the edge of the graft. Within a further 9 days, the inferolateral area had proceeded to necrosis. At the patient’s request, further surgery was delayed until 2 months later (Box 2), when two necrotic areas and associated granulation tissue (arrows A and B) were curetted. No obviously oily material was detected (mineral oil is a component of the vaccine). The uppermost red tender area (arrow C), had settled, but subsequently flared up and discharged a little serous fluid. All three areas of necrosis had finally healed when the patient was seen 6 weeks later, and there was no evidence of inguinal lymphadenopathy, although the patient reported continuing fatigue and nausea. During the course of treatment of the leg, she developed recurrent urinary tract infections due to Proteus mirabilis. Histopathological observations on all occasions showed necrosis with adjacent marked oedema and granulation tissue, with polymorphs and occasional acid-fast bacilli (at the time of the first and second operation) but no microcavities suggestive of oil implantation. No stains are available to help differentiate human oil from mineral oil. No pathogens were cultured. For the past year, the patient has been free of systemic symptoms and her leg remains healed. Ovine Johne’s disease (OJD) is a chronic wasting disease of sheep caused by the “S” strain of Mycobacterium avium subsp. paratuberculosis. It has spread widely through Australian sheep flocks, causing significant economic loss since it was first detected in New South Wales in 1980. A national vaccination program to control OJD is currently in progress using Gudair vaccine (CZ Veterinaria, Porriño, Spain),1 which is distributed by Pfizer Animal Health. (The Gudair vaccine has been available in Australia since late 1999 for experimental use in about 50 approved flocks. This research work led to registration of the product in April 2002.) Vaccination of sheep against OJD is now widespread in Australia: over 7 million vaccinations have been performed — primarily in the central and southern tablelands and south-west slopes of New South Wales, across Victoria and on Kangaroo Island (SA), and to a lesser extent in the northern tablelands and western areas of NSW, mainland South Australia, Tasmania and Western Australia. Each 1 mL dose of Gudair contains killed (heat-inactivated) Mycobacterium paratuberculosis organisms and mineral oil, with thiomersal as a preservative. The oil forms a depot at the injection site to act as a potent adjuvant, stimulating a cell-mediated immune response to the mycobacteria. In humans, accidental injection or exposure of the skin surface or mucous membrane may cause a severe local reaction and, uncommonly, a systemic reaction. Despite education of vaccinators, there have recently been seven documented cases of accidental self-inoculation in Australia resulting in prolonged morbidity.2,3 Wider use of the vaccine has increased the risk of self-inoculation injuries. There is a need to improve safety for farmers during vaccination and to bring the potential for serious complications of self-inoculation to the attention of doctors in rural areas. Accidental self-injection may occur because of inadequate animal restraint, poor inoculation technique or carelessness, facilitated by hanging the automatic vaccinating syringe from the neck (Box 3) or shoulder.3 Although self-inoculation in this patient did not appear to penetrate the deep fascia, there was nonetheless severe long-term morbidity. The volume of injected material that is sufficient to cause necrosis is unknown. It is postulated that the adjuvant mineral oil combined with killed mycobacterial cell-wall components is responsible for provoking the necrotic response.3 This explains why antibiotics do not prevent necrosis and why surgical debridement of the inflammatory vaccine material is the preferred therapeutic approach. Mycobacterial cell-wall antigens have been traditionally added to oil-emulsion adjuvants (Freund’s complete adjuvant) to enhance the efficacy of experimental vaccines in stimulating cell-mediated immune responses. Such oil-based adjuvants, although generally considered too reactive for routine use in human vaccines, are considered acceptable for use in animals. Research in heavily OJD-infected Australian merino sheep flocks has shown that OJD vaccine injection-site lesions are common, but usually cause minimal untoward sequelae when administered subcutaneously at the recommended site (ie, high on the neck behind the ear).4 Necrosis similar to that seen in human case reports is usually only observed in a small proportion of vaccinated sheep. The vaccine product label clearly states that users should seek medical attention immediately if accidental self-administration occurs. Further information is contained in a fact sheet provided to farmers that emphasises the importance of avoiding exposure to the vaccine and outlines the procedure to follow if exposure occurs.5 A more detailed fact sheet prepared for medical practitioners, based on reports in the medical and veterinary literature,6,7 outlines a graded medical and surgical approach to intervention after clinical assessment of the patient’s condition.8 Box 4 presents a summary of our recommendations for treatment of accidental self-inoculation with OJD vaccine. These are based on the manufacturer’s recommendations, together with preliminary evidence from the case described here and a series of six similar cases.3 Accidental self-inoculation with Gudair vaccine has major occupational health and safety implications, and it is essential that medical practitioners be aware of the emerging use of oil-based OJD vaccine in the sheep industry and the potential seriousness of accidental self-inoculation. Further information is available from the Poisons Information Centre (tel: 13 11 26) or Pfizer Animal Health Veterinary Services (tel: 1800 814 883). Lessons from practice Accidental injection of the skin or exposure of the skin surface or a mucous membrane to an oil-based animal vaccine may cause a severe local, or occasionally systemic, reaction. Redness after exposure to vaccine material may indicate a granulomatous reaction with associated necrosis, rather than infection. Necrosis or apparent abscess requires early surgery to remove necrotic tissue and any remnants of the vaccine material. Despite debridement, prolonged morbidity may occur. 3 Administration of sheep vaccine for ovine Johne’s disease Note vaccine and syringe slung from neck. ◆ 4 Recommended treatment following accidental self-inoculation with ovine Johne’s disease vaccine Category 1 injury (superficial skin exposure). Simply wash the contaminated area. If vaccine material is splashed onto mucosal surfaces (eg, eyes), there is greater risk of a local adverse reaction, and topical corticosteroids should be considered. Category 2 injury (simple needle-stick injuries without injection). Treat symptomatically (eg, wash skin, ensure appropriate tetanus cover, prescribe topical corticosteroids and oral antibiotics to prevent opportunistic infection). Category 3 injury (injection of vaccine material). Acute pain and inflammation are usually evident within 24 hours. Perform early surgery and drainage to remove the oil-based vaccine material before it spreads or elicits a severe granulomatous reaction. Category 4 injury (lesion that has progressed to necrosis or granulomatous ulceration). Perform surgical debridement to remove any residual vaccine material. Skin grafting may ultimately be required.

Graeme D Richardson MB BS, FRACS, FRCS · Ian I Links BVSc, DipBact · Peter A Windsor BVSc, PhD

Objective: To estimate the short-term benefits of a reduction in smoking on acute myocardial infarction (AMI) and stroke hospitalisations and costs.Design and setting: Epidemiological study which applied functions describing reductions over time in risk of AMI and stroke in people quitting smoking to hospitalisation rates and costs for Australia.Main outcome measures: The numbers of AMI and stroke hospitalisations in 35–64-year-olds and the associated costs that could have been avoided over a 7-year period from 2001–02 if smoking prevalence had decreased by 1% in the first year (Scenario 1) or by 1% per annum for 5 consecutive years (Scenario 2).Results: Under Scenario 1, almost 1000 hospitalisations for AMI and about 350 hospitalisations for stroke would have been avoided over 7 years, saving about $20.4 million in health care costs. Under Scenario 2, over 3000 AMI hospitalisations and over 1000 stroke hospitalisations would be avoided, and health care costs could be reduced by $61.6 million (2.75% of costs for AMI and stroke over the period).Conclusions: This study provides further support for the proposition that modest and achievable reductions in smoking rates can substantially improve health outcomes and reduce health care costs, even in the short term.

Susan F Hurley MPharm, MS(Biostatistics), PhD

My career in Indigenous health was first ignited in my teenage years as part of an overall desire to “work among my own people”. At that point in my life, I never really felt “Aboriginal”, owing, in part, to my being of “mixed descent”, light-skinned and having been raised in a predominantly white neighbourhood in an urban area. My claim to Aboriginality somehow felt a little inauthentic in light of the public imaginings of Aboriginality that I had been exposed to growing up. My perception of the “real” Aboriginal people were those who possessed dark skin, occupied the remotest parts of our country, and had retained a “pure” and “uncontaminated” Aboriginal culture. Rather naively, I had imagined that I would graduate from university and work with those people, sharing my expert wisdom of health knowledge and, in return, finding a connection with my “true” self — my Aboriginality. Funnily enough, I did achieve my goal of finding myself and my sense of Aboriginality. It was just not in the place, and not in the form, that I had first anticipated several years earlier. Commitment to family and community among Indigenous people (quotes from a study by Brough et al4) “My wife’s cousin rings up from Cairns, said, oh some fellas come down for hospital and they want a place to stay. . . . They all say [name’s] daughter, down there in Brisbane, you go stay with her anytime. Because dad was always taking in the homeless up in Cairns.” “To me, being involved in the community is something that, if you identify as being Aboriginal, then that’s part and parcel of what you give back to it by being involved in your community.” “Weddings, sporting events, NAIDOC Week. Sometimes it can be as little as a performing arts thing. People will turn up . . . especially if it’s got some Indigenous input in there . . . they’ll turn up to those events. They’re good events because usually people are feeling high in spirit because it’s something that . . . because there’s an Indigenous input (might be Indigenous actors), so they feel proud and good about themselves. This person put on a good play and there’s lots of white people there too, so that this white person can see black fellows from a different side and it makes black fellows proud and feel good.” NAIDOC = National Aboriginal and Islander Day Observance Committee. The chronicling of this journey is not meant to be a purely narcissistic endeavour. It revolves around two plights — one personal and one professional — which together describe the disjuncture between the lived experience of being an Aboriginal person and the described experience of Aboriginality that is manifest within public health practices and hampers our ability, as health professionals, to have a meaningful and positive impact on Indigenous health. It was upon undertaking a degree in Indigenous health that my romanticised ideas of a noble people quickly came crashing down. I soon learnt that Aboriginal communities were fraught with appalling levels of ill health, disease, despair and dysfunction, a situation that would invoke moral indignation from even the most casual and distant observer. Spurred on by the desire to “save my people”, I successfully obtained a rural health scholarship, which (I imagined) would see me stationed within a rural or remote Aboriginal community upon graduation from university. As it turned out, my placement was in a large rural community just 3 hours west of Brisbane. I was initially a little discouraged, as I didn’t view that placement as capable of providing me with the personal and professional prestige of having proven myself in a more “authentic” Aboriginal community in some far-flung region of the state. Nonetheless, I still found myself in a place with a sizeable Aboriginal population and a sense of community that I thought had eluded me in all my years growing up in Brisbane. Upon starting there, I threw myself into the role of Aboriginal health worker, conducting hospital visits to clients, assisting the community medical centre, liaising with non-Indigenous health providers in a cultural brokerage role, and uncritically, week after week, churning out the employer-sanctioned Aboriginal and Torres Strait Islander cultural awareness program. As each workshop went by, I began to notice that there were increasing numbers of local Indigenous community members in attendance, who were interested not so much in teaching others about specific Aboriginal cultural practices and protocols as in learning, sharing and reflecting upon their own experiences as Aboriginal people. Ironically, the task of educating white health professionals about the local Aboriginal community was inadvertently replaced by an ever more important task of connecting local Indigenous people with their own experiences, their own histories and their own cultures. Similarly, most community members appeared less interested in engaging in the traditional health education campaign of our health service, and instead were much more enthused about cultural revival in the form of NAIDOC Week* celebrations, cultural programs for young people, and sharing their own stories of strength and survival. At the time, I was a little troubled by this because, as a health worker, I was meant to be talking up health, not culture. The two seemed to lie in opposition to each other. My supervisor — a non-Indigenous nurse who had never engaged with the local Aboriginal community outside of a nurse–patient relationship at the local hospital — appeared annoyed and concerned about my inability to persuade the community to engage in the “real” health work. Rather than reflect upon the failings of our health service, she, and many of my non-Indigenous colleagues, saw this predicament as just further “evidence” of the passivity, dependency, and non-compliant nature of our mob, which in turn could be explained away as the “real” cause of our ill health. Any efforts on my part to celebrate Aboriginal culture and community were considered a contradiction within our health service, because of the assumed unhealthiness of the Aboriginal experience. I began to reflect upon the reasons for the Indigenous community’s disengagement with health education and started to question the way in which our communities had been constructed within this practice. Within the health care system, no value or worth was attached to being Aboriginal, as the success of the system was measured solely by its ability to bring the health of Indigenous people up to the same level as that experienced by non-Indigenous Australians. Underlying the quest to reduce health inequalities lay first the assignment of inferior status to Aboriginal people within health education programs. Is it actually any wonder, then, that we’d have to beg “Aunty” to come along to a presentation where she was depicted as nothing more than a subset of problems and unhealthy afflictions that could be remedied by simply telling her to eat better and exercise more? I remember feeling shame about having enticed community members to a workshop for a free feed, only to have them subjected to the paternalism of visiting health professionals, who, by virtue of their occupation alone, assumed they could completely disregard cultural and community protocols and that they were instantaneously authorised to speak to our old people as a parent would to a child. As time went by, I began to feel that health promotion in the form of health education was not empowering, but rather disempowering, to our mob. Under this system, we are seen as nothing more than a group of people who just don’t know what is good for us. And herein lay a strong contradiction between what I had been taught as a health professional and what I had learnt and experienced as an Aboriginal person. Health promotion was, I thought as a health professional, meant to empower people.1 Aboriginality, I thought as an Aboriginal person, was about pride, strength, determination and survival — survival of our people, our communities and our cultures. Why then does Indigenous health discursively reverberate around the inadequacies, impairment and hopelessness of our people, families and communities? Yes, sure, the status of Indigenous health is “appalling”. We have countless reports, studies, investigations and inquiries to remind us and reinforce the nature and breadth of these problems.2,3 But my question remains — so then what? What is left of us that we can draw from to make some improvement to our lot in life? I find it hard to just passively accept, as both an Indigenous person and as a health professional, that Indigenous communities have nothing to bring to the table in efforts to improve our own health. A few years after I began my rural placement, on returning home to Brisbane, I continued working in the field of Indigenous health, this time in the role of project officer for an urban Indigenous health promotion project that critically challenged these assumptions. It was through this project that I was able to realise how health promotion could equate to more than just health education. Here I was able to work in a manner that sought to uncover and support the true assets of our communities. Perhaps one of the most conspicuous strengths, which community members continually spoke of, was strength in identity — the persistence of Aboriginality within ourselves, our families and our communities.4 Here identity was not simply a label or name, a series of health issues, or even a stereotypical depiction, but a very complex, dynamic and fluid entity that provided a resource for everyday living. For instance, a vast number of social resources were derived from large family and community networks, and the values attributed to one’s Aboriginal identity produced a reciprocal exchange whereby individuals felt a strong sense of commitment to their community (Box). The result of this participation, such as community organisations and community events, was a source of strength and pride for many of the respondents. It should hardly be surprising, however, that there is something resourceful about Aboriginal identity, given that it has endured over 200 years of active attempts to remove, deny and delegitimise it. It was here that I made my connection. What resonated most with me was the persistence and diversity of our Aboriginality, which I had witnessed and experienced myself as an Aboriginal person, having lived and worked in both rural and urban Aboriginal communities. All this time, I had been seeking a version of Aboriginality that was simply not mine. So, exactly whose version of Aboriginality was it? My search for answers has led me to undertake a PhD in Indigenous health, to examine how the concept of Aboriginality has been constructed within public health practice. As I’ve reflected on my own culture as an Aboriginal person, I’ve been forced to examine the professional culture of public health that I am also a part of. In so doing, I have realised that my own naive and romanticised understanding of the “authentic Aboriginal” was not unique to me. In fact, I have found that these very images are supported and reproduced within much of Indigenous public health practice. For instance, there has to be some explanation for why the epidemiological gaze in Indigenous health research still disproportionately focuses on rural and remote Aboriginal communities,5 when the majority of Aboriginal people reside in urban centres.6 One must also question the practice of continually highlighting the health inequalities facing Aboriginal people without explaining the precise causal pathways — thus perpetuating assumptions about “innate characteristics related to ‘ethnic’ or ‘racial’ difference”.7 The perception of Aboriginality as nothing more than a label, a health risk, and predicator of unhealthy behaviours within Indigenous public health practice reinforces stereotypical ideas of Aboriginality, demonises those who possess it, and disconnects Aboriginal people from their own identities in a manner similar to past oppressive policies of colonisation, assimilation, segregation and integration. Critically examining such practices is not just a matter of “political correctness”, but a vital step that will have profound and meaningful implications for the health of Aboriginal people. Such depictions fuel the very racism that creates and compounds health inequality,8-10 and may also result in Aboriginal people internalising such negative depictions.11 Internalised racism has been linked to increased drug use, behavioural problems,12 increased rates of depression and obesity, and lower academic aspirations.13 Numerous studies have also demonstrated the association between social status and health inequality,14 the relationship between community integration and health,15 and the influence of factors such as social exclusion, support, isolation, participation and autonomy.16 It has been argued that notions of identity and culture are an important resource for empowering minority or marginalised communities — a goal that accords with the broader global health promotion agenda.17 It is not the quantification or authentication of culture by the dominant group, but rather the process of enabling such communities to define, express and represent themselves that is empowering and conducive to better health outcomes. Bearing this in mind, I have sought to develop my research agenda around examining and validating the way in which Aboriginal people define themselves, without the distraction of a predetermined health agenda guiding or hijacking every activity that I engage in. Importantly, despite my apparent rejection of the way public health is practised and health care delivered to Indigenous people, I do not view my current journey as contradictory to the overall goal of public health practice — which is to improve the health and wellbeing of Aboriginal people. All that differs is the construction of meanings around our own notions of health and Aboriginality. Public health and medicine are themselves cultural practices that have been influenced heavily by the politics of colonialism.18 Rather than claiming to be neutral, objective observers of the cultural domain occupied by Aboriginal people, we, as health professionals, need to be prepared to place our own cultural practices under the microscope and examine their effect on the health of Aboriginal people. For Aboriginal people, health is “not just the physical well being of the individual, but the social, emotional and cultural well being of the whole community . . . [and] a matter of determining all aspects of their life, including control over their physical environment, of dignity, of community self esteem and of justice. It is not merely a matter of the provision of doctors, hospitals, medicines or the absence of disease and incapacity.19 I am currently conducting my fieldwork, the chosen site of which is itself somewhat poignant. It is not in some far-off exotic location, but just a few suburbs over from where I grew up. Through my journey so far, I have found the strength in my identity as an Aboriginal person, in all of its “inauthenticity”, and the strength in my community, in all of its unhealthiness, to see a way forward to improving the health of our people. For me, inherent in the task of improving Indigenous health and in achieving wellbeing as an Indigenous person is providing a space within public health practice and in our own minds that allows us, the “public”, to define and redefine our experiences of our identity.

Chelsea J Bond

To the Editor: The article by Senanayake and Ferson1 on detention for tuberculosis included two case histories. In the case of “Patient 2”, we believe the details published were misleading and unnecessarily disclosed potentially identifying information. This case was presented in sufficient detail to allow identification of “Patient 2” by including date of admission, personal details, city of admission and details regarding his past history of alcohol addiction and attempts to self-discharge. All this information was not necessary and did not take into account all the relevant medical complicating factors. We were surprised that, as the primary treating team involved in this patient’s care over the inpatient stay of 3 months and the following 6-month outpatient follow-up, we were not informed of the authors’ plans for publication, nor requested to comment on the facts of the report. We were also surprised to read details of the article in The Sydney Morning Herald on the day of the article’s publication in the Journal.2 An individual’s right to privacy is a fundamental human right. It is unfortunate that the careful consideration that had been given to his detention was not extended to publishing his case details. As Senanayake and Ferson point out, “Patient 2” recognised that his human rights were being “infringed” because he was being held in a “jail cell”, which was a temporarily modified isolation room in a public hospital under 24-hour guard. In law, information provided to a medical practitioner by a patient becomes subject to a statutory duty to protect the patient’s privacy and a common-law duty of confidence is owed by the treating medical practitioner to the patient. The NHMRC Guidelines approved under Section 95A of the Privacy Act 1998 indicate that, when a patient history is published, an important principle is that a patient may not be identified or held up to ridicule.3 Furthermore, public access to medical journals on the Internet has allowed increased availability of such reports to the general public and increases the chance of family members and others identifying individuals. The principle of protecting patient privacy has previously been respected by the Journal. An article published in 1994 reported a 1979 outbreak of tuberculosis in medical students who attended an autopsy of an immunosuppressed patient with unsuspected active tuberculosis.4 A report of the incident was not published contemporaneously, mainly to protect the privacy of the students involved. As the report by Senanayake and Ferson suggests, our patient was socially disadvantaged, and several aspects of his behaviour were probably attributable to a Jarisch–Herxheimer reaction in conjunction with acute alcohol withdrawal. Although we recognise the need to serve the public interest in health service management activities, this must be balanced against the requirement for patient privacy regardless of social class. We suggest that the publisher has an obligation to ensure that patient consent is obtained, and that the primary treating team has been involved in the review of case details so that misleading and potentially identifying information is not released inappropriately.

Medical Registrar · Respiratory Physician

Ruth M Armstrong,* Martin B Van Der Weyden† * Deputy Editor, † Editor, The Medical Journal of Australia, Locked Bag 3030, Strawberry Hills, NSW 2012. medjaustATampco.com.au In reply: We concur with the principle that patient privacy should be protected in case reports. As recommended by the International Committee of Medical Journal Editors,1 measures in place at the Journal include asking authors to obtain patient permission for publication where possible, and directing authors to remove potentially identifying patient information. The article in question was not a case report. Case details were given to exemplify the circumstances that might lead to detention of a patient for public health reasons in New South Wales, and dates and some details were retained to illustrate the temporal flow of the story. We agree that this may have made the patient identifiable, if not to the general public, to himself or his family. We regret this editorial lapse, and have reworded the patient details in the electronic version of the article.2 Although chastened by our anonymous colleagues’ observations, we are somewhat puzzled as to why, given their concern about their patient’s privacy, they are determined to draw further attention to the exposing details. We assume that, in this case (as in the cases of detaining patients for treatment of tuberculosis), public interest prevails. We also agree that case reports of detailed clinical histories require the input of the primary treating team, but the question of authorship should be determined by the involved parties, not the Journal. Be that as it may, as the article was a public health report (and thus not meant to be a detailed clinical exposition), we do not believe that the input of the treating team was required.

Ruth M Armstrong · Martin B Van Der Weyden

A common-sense approach to reducing exposure to polluted air is required It is an unquestionable fact that regular physical activity is beneficial to health and longevity. Accordingly, it is common practice for physicians and other health care professionals to encourage exercise. However, people exercising in urban regions may be unwittingly at risk because of exposure to concentrated automotive pollution, a known risk factor for cardiovascular and respiratory disease. The physiological changes that occur during exercise probably act to compound the toxic effects of environmental air pollution, and certain patient populations may have increased sensitivity. People should not be deterred from regular exercise, as it is of known benefit, but when prescribing exercise, clinicians should extend appropriate advice to patients to avoid areas with high pollutant concentrations. What, then, is the evidence to support such advice? Automotive exhaust comprises a heterogeneous mixture of suspended particles and gases, the most common gases being sulphur dioxide, nitrogen dioxide, carbon monoxide and ozone. Unburnt fuel emits volatile organic compounds (eg, benzene, toluene) and the fuel combustion process liberates many thousands of chemicals in addition to particulate matter of varying size and composition. Ultrafine particulate matter, with an aerodynamic diameter < 0.1µm, is thought to be particularly harmful to health, as it is readily inhaled and absorbed into the circulation.1 Epidemiological data have identified individual components of air pollution, or pollution collectively, as promoters of cardiovascular and respiratory disease.2,3 Some compounds are also known or suspected carcinogens.4 Harmful effects on the body from pollutants are multifactorial, with acute or chronic exposures increasing the cellular processes associated with atherogenesis (the underlying cause of most cardiovascular disease), impairing pulmonary function, provoking local and systemic inflammation, disrupting cardiac autonomic control and inducing vascular dysfunction. Deleterious health effects may result from exposure to pollutants at concentrations that are lower than recommended air quality standards.5 Indeed, research to date has failed to determine a “threshold” limit for which there is no adverse health effect.6 In general, most large-scale time series analyses of the physiological effects of air pollution find an exposure-dependent relationship that crosses socioeconomic boundaries and poses a significant threat to everyone’s health. Importantly, certain populations may be particularly vulnerable to the effects of polluted air, such as children;7 people with asthma,8 diabetes9 or acute lower respiratory disease; and frail or elderly people with pre-existing heart and lung conditions.10 Why may exercise in polluted areas be particularly hazardous? During aerobic exercise, even at relatively low intensities, inspired air is taken in predominantly through the mouth, and there is a major increase in minute ventilation and diffusion capacity. These factors augment the respiratory uptake of airborne contaminants, with increased penetration to the lower gas-exchange regions of the lung. Indeed, the total amount of ultrafine particulate matter deposited in the respiratory tract of humans during moderate exercise has been shown to be about five times that at rest.11 As would be expected, when the concentration of pollutants increases, so too does the amount of inhaled matter. Thus, habitual exercise in highly polluted localities, such as alongside busy roadways, may increase the overall intensity, duration and frequency of exposure, all of which are relevant to the evaluation of an individual’s risk profile for disease.6 Pulmonary function may markedly decline after inhalation of pollutants during exercise. In one study, when adolescents with asthma were exposed to sulphur dioxide and sodium chloride aerosol during treadmill running, many displayed symptoms of wheezing and shortness of breath.12 Several other studies have shown that poor air quality and acute exposures during exercise may induce symptoms in people with asthma, impair athletic performance in healthy people,13 and contribute to exercise-induced myocardial ischaemia in patients with stable coronary artery disease.14 This information should not be interpreted as a reason for people living in cities to stop exercising. Rather, a common-sense approach to reducing or avoiding exposure to polluted air during exercise is advisable. In summary, there is sound evidence for an exposure-dependent relationship between air pollution, morbidity and mortality, particularly in relation to cardiovascular and respiratory illnesses. Although regular aerobic exercise is recommended for good health, there may be adverse health consequences for people who habitually exercise in areas of high ambient pollution. Despite this, it is not uncommon to see people running or cycling alongside congested roadways, and clinicians should advise patients to exercise on quiet roads or in parks and recreation areas. The best time of day to exercise is early in the morning, before the build-up of traffic and when it is cooler. This is relevant because the combination of sunlight and heat with certain compounds increases ozone production. Importantly, certain groups may be acutely susceptible to the effects of air pollution, and clinicians should advise them accordingly.

James E Sharman BHM(Hons), PhD

Questions of cost-effectiveness, vaccine efficacy and feasibility are yet to be answered In the United States, routine immunisation of all healthy children aged 6–23 months against influenza has recently been introduced. The principal justification for this is the relatively high morbidity and mortality from this disease in very young children.1 The United States is also considering routine influenza immunisation of all children aged over 6 months, in view of the herd protection it would provide to the adult population. Currently, Australian guidelines recommend immunisation of children in groups considered at high risk of severe influenza.2 Should Australia introduce universal childhood immunisation? There is no doubt that children have an extremely high incidence of influenza. It is estimated that, on average, 20%–43% of children are infected during typical influenza seasons.3-5 The incidence is highest in young children less than 2 years old, who are often hospitalised.1,3-5 The mortality due to influenza in infancy is second only to that in the most elderly patients.1 In the severe 2003–04 influenza season, 143 children died from influenza in the United States, of whom 58 (41%) were less than 2 years old and 65 (45%) had no underlying condition.1 These data emphasise the importance of protecting children with annual influenza immunisation, if feasible. Another reason to consider universal childhood influenza immunisation is herd protection. In what turned out to be an illuminating natural experiment, 50%–85% of Japanese schoolchildren were immunised annually against influenza from 1962 to 1987, but there was no routine immunisation of the elderly. When mandatory immunisation of schoolchildren was relaxed in 1987 and repealed in 1994 (because of doubts about safety and effectiveness), influenza immunisation rates dropped to very low levels. A retrospective study comparing excess mortality from pneumonia and influenza in Japan and the United States concluded that the vaccination of Japanese schoolchildren prevented about 37 000 to 49 000 deaths per year, mostly of elderly people. (This represented about one death for every 420 children vaccinated.)6 In considering the feasibility of universal childhood vaccination, vaccine efficacy is one of the factors that needs to be taken into account. In healthy adults under 65 years of age, inactivated influenza vaccine is 70%–90% effective when the match between vaccine and circulating viruses is close.1 However, the same vaccine may be less immunogenic in children. Studies in children aged 6 months to 15 years show a vaccine efficacy of 31%–91% against influenza A and 45% against influenza B.7,8 However, very few of the studies have examined children aged 6–23 months,9,10 the age group currently recommended for routine influenza vaccination in the United States. An alternative form of vaccine administration is on the horizon — live attenuated influenza vaccines. A recent systematic review10 suggested that live vaccines may be more effective than inactivated vaccines in children over 2 years of age (79% versus 65%). Live attenuated influenza vaccines have been licensed in the United States, and might be more acceptable because they are given intranasally.11 However, live vaccines cost a lot more and are not licensed for use in children under 5 years in the United States (because of limited safety data). They are not yet licensed in Australia for use in any age group. The high morbidity of influenza in children and the likely benefits due to herd immunity do make annual childhood influenza immunisation appear economically attractive. However, against this must be weighed the need to immunise with a new influenza vaccine each year, because of antigenic drift in influenza strains, and the need to give two doses of vaccine to children under 9 years in the first year they are immunised.1,2 In addition, the severity of influenza seasons varies unpredictably from mild to severe, and it costs as much to immunise in a mild year as in a severe one. In the United States, indirect costs (mainly days of work lost by parents) dominate economic analyses supporting the use of influenza vaccines in children.12 In Australia, by contrast, the Pharmaceutical Benefits Advisory Committee considers only direct costs of illness, so it is unlikely that a universal, publicly funded childhood immunisation program could be justified using such cost-effectiveness criteria. There may also be practical problems with attempts to introduce routine childhood immunisation. In 2004–05, the uptake of influenza vaccine for children aged 6–23 months in the United States, when the vaccine was recommended universally, was estimated to be only 48%.13 In Ontario, Canada, where all residents aged over 6 months have been offered free annual influenza immunisation since 2000,14 the 2003 uptake in children was only 27%.15 Parents of unimmunised children were more likely to believe that immunisation resulted in a flu-like illness, caused adverse effects more severe than the disease, or weakened the immune system.15 Such immunisation myths are common, although studies have repeatedly shown inactivated influenza vaccine align="right" to be safe, with low rates of adverse events and the benefits clearly outweighing the risks.1,2,9 Another practical issue is the question of how to fit the vaccine into an already crowded childhood vaccination schedule. In general, annual immunisation against influenza is recommended in autumn at the start of the influenza season; there is no fixed age of administration of vaccine. Implementing universal influenza vaccination would place a substantial extra burden on primary care practices.16 Considering all the available information, I believe that there is currently insufficient reason for introducing universal childhood vaccination for this disease in Australia. There are too many unanswered questions about the cost-effectiveness, efficacy and feasibility of universal immunisation of healthy children, whether infants or school-aged. For the time being, we should maintain a watching brief. Future data emanating from Ontario and the United States may provide us with a clearer answer as to whether large-scale programs of routine childhood influenza immunisation are feasible and effective. Further, if the US experience with live vaccines shows consistent immunogenicity and improved ease and acceptability of administration, live vaccines may yet prove to be a cost-effective way to implement universal childhood influenza immunisation in Australia. One thing is clear: influenza vaccination is most cost-effective for children considered at high risk of severe influenza, such as those with chronic cardiopulmonary and other chronic illness. These children should clearly be vaccinated annually against influenza.1,2 Yet vaccine coverage of high-risk groups aged 2–17 years is only 35% in the United States,13 and probably lower in Australia, although we lack age-specific data. Australian immunisation providers should redouble their efforts to ensure that children at high risk are immunised annually.2 Also, it should be remembered that the Australian immunisation handbook2 does not preclude vaccinating others who are not at high risk. It states that “influenza vaccine should be administered to any person who wishes to reduce the likelihood of becoming ill”.

David Isaacs MD, FRACP, FRCPCH

Objective: To assess the prevalence and causes of vision loss in Australia and to project these data into the future.Design: Synthesis of data from two cross-sectional population-based cohort studies — the Melbourne Visual Impairment Project and the Blue Mountains Eye Study — and extrapolation to the entire Australian population.Setting and participants: 8376 community and 533 nursing home residents recruited between 1992 and 1996 in urban and rural Victoria and New South Wales.Main outcome measures: Age-standardised prevalence of low vision (visual acuity < 6/12) and blindness (visual acuity < 6/60) (both measured in the best eye, with spectacles if usually worn for distance vision), and their causes for the Australian population for 2000 to 2024, projected from Australian Bureau of Statistics population data.Results: In 2004, 480 300 Australians were estimated to have low vision, including 50 600 with blindness. The most common causes of low vision were undercorrected refractive error (62%), cataract (14%) and age-related macular degeneration (10%). The latter was responsible for almost half of all cases of blindness. The numbers of people with low vision and blindness are projected to almost double by 2024.Conclusions: Vision loss in Australia is a much bigger problem than is usually recognised; 76% of low vision is caused by uncorrected refractive error or cataract, both readily treatable. However, the prevention and treatment of macular degeneration poses a major challenge.

Hugh R Taylor AC, MD · Jill E Keeffe PhD · Hien T V Vu PhD · Jie Jin Wang MMed, PhD · Elena Rochtchina MApplStat · Paul Mitchell MD, PhD · M Lynne Pezzullo BEc

We report on an elderly couple who presented with a syndrome that included severe generalised tremor and incoordination after eating soup from a damaged can. Black mould contaminating the can was subcultured and the fungus Penicillium crustosum was identified. This fungus usually produces a potent neurotoxin called penitrem A. The couple displayed symptoms consistent with penitrem A ingestion, all of which resolved fully. Penitrem A intoxication has been well documented in animals, but not in humans. Clinical recordsAn elderly couple was admitted to hospital after sudden onset of severe muscle tremors. The husband (aged 89) and wife (aged 84) described an uneventful morning. At about 12:00, they had shared a can of soup and toast, followed by chocolate cake, before catching a bus to the local shopping centre. They noticed the soup had a bitter taste, but dismissed the finding because it was a new brand and type to them. There had been no recent changes to their medications, and no recent exposure to garden sprays, insecticides or pesticides. Patient 1The man was first to develop symptoms. He reported feeling slightly shaky as the bus arrived at the shops at about 13:00. He had difficulty getting off the bus, his legs felt “wobbly” and he had to sit down. He developed uncontrollable shaking throughout the body, and felt sticky and sweaty. Initial assessment by ambulance officers at about 13:10 was that he had severe muscle tremors and was unable to walk, and that it was difficult to understand his speech. He had no nausea or vomiting, and his abdomen was soft. He was diaphoretic, with blood pressure 160/76 mmHg, pulse rate 80 beats/min, respiratory rate 32 breaths/min, and Glasgow Coma Score 15 out of 15. His oxygen saturation level was 85%, improving to 97% with high-flow oxygen. Subsequent assessment in hospital at 13:40 revealed that the patient’s Glasgow Coma Score had fallen to 11. Although his speech was incomprehensible, he was able to obey commands; he also displayed generalised weakness and intention tremor. He remained hypertensive and diaphoretic, but was afebrile. He later recounted (to P R L) that he had thought he was going to die. All symptoms, apart from the intention tremor, had subsided by 16:30. The patient’s medical history included chronic airway limitation, asthma, hypertension, episodic atrial fibrillation, osteoarthritis, a left total hip replacement, and an essential tremor. He had no known allergies. His medications included verapamil, digoxin, aspirin, salbutamol, tiotropium bromide, salmeterol xinafoate, quinine bisulfate prn, paracetamol and rofecoxib prn. His essential tremor remained untreated because of the contraindicated use of β-blockers in asthma. A chest x-ray was unremarkable, but electrocardiography revealed a right bundle branch block. A computed tomography brain scan showed generalised volume loss with no intracranial haemorrhage or early changes of infarction; a small low-density focus present in the right basal ganglia region was consistent with chronic lacunar infarction. The results of haematological and biochemical tests were within normal limits, except for urea (8.7 mmol/L; reference range [RR], 2.5–6.4 mmol/L), white cell count (11.2 × 109/L; RR, 4.0–11.0 × 109/L), and haemoglobin (128 g/L; RR, 130–165 g/L) (red cells were normocytic and normochromic). The patient’s blood glucose level (measured by glucometer) was 7.3 mmol/L (RR, 3.5–8.0 mmol/L). Pseudocholinesterase (13.5 U/mL; RR, 7.0–19.0 U/mL) and serum digoxin (1.5 nmol/L; RR, 1.3–2.6 nmol/L) levels were within normal limits. No urine screen for drugs was carried out. The patient was admitted for observation and investigation. The following day he was lethargic, exhausted, and displayed minimal tremor. He was eventually able to mobilise with the aid of a walking stick, as usual. Patient 2The woman had a similar presentation. She complained of feeling dizzy and shaky, but had no nausea or vomiting. Ambulance officers described her as being anxious, diaphoretic, and with uncontrollable shaking. Her blood pressure was not palpable because of severe shaking, but she was well perfused. She was tachycardic (pulse rate, 110 beats/min, taken from electrocardiographic monitoring), with a respiration rate of 20 breaths/min, temperature 36.5ºC, Glasgow Coma Score of 15, and blood glucose level (measured by glucometer) 7.0 mmol/L (RR, 3.5–8.0 mmol/L). Although she was no longer tachycardic on admission to hospital, she remained anxious and diaphoretic, with a generalised tremor that increased with stimuli (eg, being questioned). Her oxygen saturation level on room air remained above 95%. All symptoms, apart from the intention tremor, subsided by 16:30. The patient’s medical history included a left nephrectomy for calculi, right renal calculi and lithotripsy, chronic airway limitation, asthma, hypertension, and a left-eye cataract. Her medications included hydrochlorothiazide, frusemide, nitrofurantoin, aspirin, trimethoprim, salbutamol prn, beclomethasone dipropionate, quinine bisulfate prn, paracetamol prn, and Macu-Vision tablets (containing ascorbic acid, vitamin E, zinc oxide and cupric oxide). A chest x-ray and electrocardiogram were normal. A computed tomography brain scan showed no abnormality apart from a polypoid density in the inferior maxillary sinus. The results of haematological and biochemical tests were normal, except for urea (9.1 mmol/L; RR, 2.5–6.4 mmol/L) and creatinine (0.13 mmol/L; RR, 0.06–0.12 mmol/L). The level of pseudocholinesterase was within normal limits (18.7 U/mL; RR, 7.0–19.0 U/mL). A urine screen conducted for drugs of abuse (including amphetamines, methamphetamines, benzodiazepines, cocaine, opiates and cannabis) was negative. The patient was admitted for observation, and gradually improved the following day. Follow-upBoth patients were discharged 2 days after admission with a very slight residual intention tremor. When assessed by their general practitioner 2 weeks later, the man had only a mild increase in his usual essential tremor and the woman’s tremor had completely resolved. Identification of mouldThe damaged soup can was retrieved from the couple’s residence on the day of onset of their illness and sent to Food Science Australia for analysis. Examination of the can revealed a dent in the top adjacent to the ring-pull on the lid. There was black mould inside the can at the top near the damaged area, and a small amount on the underside of the lid (Box 1). The mould was subcultured onto three different media suitable for growth of common food spoilage moulds.2 The plates were incubated at 25ºC for 4 days. All plates grew a pure culture of a Penicillium species. The mould was then cultured onto identification media, incubated at 5ºC, 25ºC and 37ºC for 7 days and examined again.2 Both microscopic and colony morphology characteristics identified the mould as Penicillium crustosum. It had typical sporing structures for this species (Box 2), and its colonies on malt extract agar shed spore masses in a manner typical of the species. No mycotoxin analyses were attempted. DiscussionPenicillium crustosum is a common foodborne fungus that causes spoilage in a wide variety of foods, including meat, cereals, nuts, cheese, eggs, fruit, and processed and refrigerated foods. Almost all P. crustosum isolates produce the mycotoxin penitrem A.1-3 Its potent neurotoxic effects have been demonstrated in various laboratory animals,4,5 and naturally acquired intoxication has been reported in sheep, cattle, horses and domestic dogs.4,6-9 In animals, symptoms include ataxia, tremors and severe muscle fasciculations.4-9 Larger doses may cause seizures, massive liver necrosis and death.5 To our knowledge, there has been only one case documented in humans of a tremorgenic syndrome following ingestion of P. crustosum.10 A man who had ingested about 30 mL of beer from a can contaminated with a fungus later identified as P. crustosum developed tremorgenic syndrome. About 4 hours later, he developed headache, vomiting, diplopia, weakness and bloody diarrhoea. After 12 hours he developed a tremor. All symptoms resolved within 30 hours. In this case, the fungus isolated was found to produce the mycotoxin roquefortine, but penitrem A was not reported. The authors acknowledged that the isolate lacked a feature typical of P. crustosum. As isolates of P. crustosum almost always produce penitrem A, it is quite possible that the mould involved in this mycotoxicosis was not actually P. crustosum, but some other closely related species such as P. roqueforti.11,12 Inhalation of mouldy silage was implicated in a similar tremorgenic illness in a 16-year-old male.13 Malaise, fatigue, headache, pyrexia and vomiting occurred within hours, progressing to coarse fasciculations and tremors. Symptoms had resolved by the 7th day. A variety of fungi were isolated from the silage, including Aspergillus and Penicillium, both of which produce tremorgenic mycotoxins. Aspergillus fumigatus, which is particularly common in silage, can produce tremorgenic toxins known as fumitremorgens, but not penitrem A.14 There are strong similarities between the cases we report here and numerous documented cases of penitrem A intoxication in animals. Domestic dogs are at particular risk when they have access to household waste.6-9 P. crustosum also produces the mycotoxin roquefortine,15 whose neurotoxic effects have been implicated concurrently with those of penitrem A in some cases.7-9 However, roquefortine has been found experimentally to be far less toxic than penitrem A.15 The elderly couple experienced a comparatively rapid onset of symptoms, but had no nausea or vomiting. The differential diagnosis included a reaction [from exposure] to either a food toxin or an environmental pollutant such as a pesticide or insecticide. The canned soup was a common source of exposure, and its unusual taste further implicated the can as the toxin source. Although we did not attempt to identify the mycotoxin in the cases reported here, isolates of P. crustosum usually produce penitrem A (in one study, of 308 isolates tested, all produced penitrem A12). The highest levels of penitrem A production by P. crustosum isolates occur in liquid media,11 so the soup can in this case would have provided optimal conditions for mycotoxin synthesis. Unfortunately, none of the implicated soup remained for analysis. Most mycotoxins are heat-resistant and comparatively stable,3 so would have survived the mild cooking process. Visual impairment may have contributed to this illness occurring, in that the elderly couple were not aware that the soup can was damaged and discoloured. Experimentally, penitrem A inoculation has been found to produce a tremorgenic syndrome that leads to convulsions and death when larger doses are given.4,5 Administration of pentobarbitone has been found to be effective in controlling muscle tremors and seizures in animals.7,8 This case study highlights the need to avoid ingesting food from damaged cans. Medical and food-authority personnel should be aware of the possibility of P. crustosum ingestion and its potent neurotoxic effects. Limited reporting of this syndrome in humans suggests that it is either rare or under-reported. 1 Damaged can, showing black mould around lid 2 Sporing structures of Penicillium crustosum* * Scale bar is 10 m in length.

Peter R Lewis MB BS, DipObs, FAFPHM · Michael B Donoghue MB BS, FACEM · Lucy Cook BA(SocSc), RN · Linda V Granger BHSc, MPH · Ailsa D Hocking PhD, FAIFST, FASM

Timothy C Crowe,* David Cameron-Smith† * Lecturer, † Senior Lecturer, School of Exercise and Nutrition Sciences, Deakin University, Burwood, VIC 3125. tcroweATdeakin.edu.au To the Editor: Low-carbohydrate diets have re-emerged into the public spotlight and are enjoying widespread popularity. However, current evidence indicates that low-carbohydrate diets have no significant advantage over more traditional energy-restricted diets for long-term weight loss and maintenance.1-3 While these diets have shown short-term efficacy in modifying some lipid parameters and measures of insulin sensitivity, questions remain about the risk of adverse effects with long-term carbohydrate restriction.4 The scientific literature has not addressed the questions of how the general public perceive these diets, and what dieting approaches they adopt. Dieting perceptions and practices within the community may be far removed from the strictly controlled situation of published research. A national telephone survey of 1200 adults aged 18 years and over was conducted by the private market research company Newspoll from 6 to 8 August 2004. The survey asked about knowledge of and attitudes to carbohydrates and dieting. Telephone numbers were randomly selected, with a quota for capital city and non-capital city areas. Selection of an individual in each household was based on the last birthday. Response rate to the survey was 11%. Sex, age, marital status and working status demographics were representative of the Australian adult population. The main findings are summarised in the Box. Most of those surveyed correctly identified foods such as pasta and bread as “carbohydrate foods”. Only a third of people identified soft drinks and lollies as carbohydrate foods, and 20% incorrectly identified cheese and eggs as carbohydrate foods. Almost 17% of people had either tried, or intended to try, a low-carbohydrate diet, with women more likely to have tried this diet. Half of those surveyed believed that carbohydrate foods should make up a quarter or less of the daily diet (current health recommendations are that about half the diet should comprise carbohydrates). Almost 70% of those surveyed believed they needed to cut back on carbohydrates to lose weight. Based on this survey, low-carbohydrate dieting practices are as widespread in Australia as in the United States.5 Interestingly, the US study noted a greater propensity to use carbohydrate-reduced diets among those who were obese, had diabetes, hypertension or high cholesterol. Our data demonstrated widespread misunderstanding of what constitutes a high-carbohydrate food, which may leave many individuals at risk of choosing a diet that selectively excludes wholegrain foods, fruits and some dairy products. Health professionals should be aware that low-carbohydrate diets remain popular, that the people who are following these diets may represent a more “at risk” population, and that the food choices made by those following this dietary pattern may have adverse long-term health effects. Respondents’ knowledge of and attitudes to carbohydrate foods and low-carbohydrate dieting Question Total (n = 1200) Men (n = 600) Women (n = 600) Which of the following foods, if any, do you regard as carbohydrate foods? Bread 89% 85% 93% Pasta 90% 88% 93% Rice 80% 76% 83% Breakfast cereal 79% 77% 80% Lollies 35% 36% 35% Soft drink 34% 31% 36% Cheese 20% 22% 19% Eggs 18% 20% 16% Have you tried or do you intend to try the Atkins diet, or some other low-carbohydrate diet? 17% 11% 22% Based on official recommended guidelines for a healthy diet, about how much of a person’s diet should be made up of foods such as bread, breakfast cereal, pasta and rice? Less than a quarter 7% 7% 7% About a quarter 43% 34% 51% About half 29% 31% 26% About three quarters 6% 8% 4%

Timothy C Crowe · David Cameron-Smith

Mention the name Alistair Cooke, and his legendary Letter from America immediately springs to mind.1 For 58 years his weekly commentaries on happenings in the United States were beamed by the BBC to many countries around the world, including Australia. Indeed, Cooke’s Letter from America was the catalyst for commissioning a regular short piece on the “goings-on” in health care, the medical profession and academia in the United Kingdom. The opportunity to view these through antipodean eyes was entirely fortuitous. Three prominent Australian academics left our shores some 3 years ago to take up prestigious positions in the “old country”: David Weller moved from Flinders University to Edinburgh, Konrad Jamrozik from the University of Western Australia to London, and Richard Heller from Newcastle University to Manchester. With little ado, our expatriate trio agreed to provide regular comments on medicine in the UK. The commentaries were to be journalistic rather than academic, with a humorous or quirky edge, but were also to reflect the profession’s sensitivities and conservatism. And so the Postcard from the UK was born. But now, almost 2 years on, the Postcard will cease to be delivered, and this issue carries the last one. This unfortunate turn of events is due to the break-up of the Postcard’s triumvirate, with the return of one of its members to Australia. Thus, all parties concerned agreed to “pull the plug” on the Postcards. Since December 2003, various Postcards have amused, amazed and even affronted some of our readers, both in Australia and in the UK. The more memorable Postcards have covered such issues as: UK health inequalities, which still reflect the British class divide;2 the political crusades imploding the National Health Service;3 the dependence of the NHS on “the energy of slaves” — through recruitment of doctors and other health professionals from the former British Empire’s colonies;4 and the Sir Humphrey Appleby approach to the bureaucratic Research Assessment Exercise, which gives the lie to the commitment of UK universities “to profess”.5,6 The final Postcard in this issue of the Journal (page 556) explores the difficulties confronting the NHS in bringing IT systems on stream.7 What, then, is the lasting message of the postcards? The issues involving the UK health system, its medical profession and academia are mirrored in our system, and the solutions seem to come from the same cookbook. Both countries’ bureaucracies are incredibly insular and spawn ill-conceived ideas, reflecting their isolation. But, overall, we are left with an impression of the political impotence of the UK medical profession and its institutions compared with those in Australia, a situation to be expected if most doctors are, in reality, public servants. In the meantime, sincere thanks to the Postcard’s trio and vale to our Postcard from the UK.

Martin B Van Der Weyden MD FRACP FRCPA

Objectives: To evaluate the impact of a community-based, collaborative, shared antenatal care intervention (the Mums and Babies program) for Indigenous women in Townsville.Design and participants: Prospective cohort study of women attending Townsville Aboriginal and Islander Health Service (TAIHS) for shared antenatal care with a singleton Indigenous birth between 1 January 2000 and 31 December 2003 (456 women; the MB group), compared with a historical control group of 84 women who attended TAIHS for antenatal care before the intervention between 1 January 1998 and 30 June1999, and a contemporary control group of 540 women who had a singleton birth at Townsville Hospital between 1 January 2000 and 30 June 2003, but did not attend TAIHS for antenatal care.Intervention: Integration of previously autonomous service providers delivering shared antenatal care from TAIHS.Main outcome measures: Patterns of antenatal visits, proportion of women undertaking key antenatal screening, and perinatal outcomes.Results: The number of Indigenous women who entered the MB program and gave birth at Townsville Hospital rose from 23.8% in 2000 to 61.2% in 2003. The number of antenatal care visits per pregnancy increased from three (interquartile [IQ] range, 2–6) in the historical control group to seven (IQ range, 4–10) in the MB group (P < 0.001). 88% of women in the MB group had at least one ultrasound. About 90% of all women attending for antenatal care were screened for sexually transmitted infections. In the MB group, there was a significant reduction in preterm births compared with the contemporary control group (8.7% v 14.3%, P < 0.01). There was no significant reduction in the prevalence of low birthweight births or perinatal mortality.Conclusion: A community-based collaborative approach to shared antenatal care services increased access to antenatal care and was associated with fewer preterm births among Indigenous women in Townsville. The model may be adaptable in other urban centres with multiple antenatal care providers and significant numbers of Indigenous people across Australia.

Kathryn S Panaretto MB BS, MPH · Heather M Lee HealthWorkerCert3 · Melvina R Mitchell EN · Sarah L Larkins MPH, FRACGP · Vivian Manessis FRACGP · Petra G Buettner PhD · David Watson FRANZCOG

Do we have a clear enough picture to guide rational health and social policy responses? Australia’s economic prosperity has long brought incremental health gains through better living conditions, sanitation, education, medical care and vaccination.1 The effects on child health and mortality have been striking. The latest report from the Australian Institute of Health and Welfare (AIHW), A picture of Australia’s children, documents this continuing trend. Infant and child mortality rates halved again in the past 20 years.2 The fall in deaths from sudden infant death syndrome (SIDS) to a third of 1991 rates is a tribute to outstanding Australian child health research, as well as the work of child and family health nurses and the SIDS Council of Australia.3 A steady decline in deaths from injury in later childhood has also contributed to lower childhood mortality. Judged by these indices, the present generation of Australian children is the healthiest ever. Key findings of A picture of Australia’s children The infant mortality rate in Australia halved over the past two decades, from 9.6 per 1000 livebirths in 1983 to 4.8 in 2003. The Indigenous infant mortality rate also declined by 3.3% per year, but was still 2.5 times that of other Australian infants. Rates of non-communicable health problems, such as obesity and mental disorders, appear to be rising, but lack of up-to-date national data makes it difficult to accurately assess the current rates. Rates of vaccination among children aged 1 and 2 years have increased over time, with the coverage in 2004 being over 90%. Between 1990 and 2000, children’s dental health improved, with a decrease in the mean number of decayed teeth in 6 year olds (from 2.1 to 1.7), and 12 year olds (from 1.4 to < 1). However, since 2000, tooth decay in Australian children seems to be on the increase again. The number of children on care and protection orders has risen almost 50% in the past 6 years, with the rates sixfold higher in Indigenous children. The proportion of children placed in out-of-home care also rose from 3 per 1000 children in 1997 to 5 per 1000 in 2004. Economic progress has also altered the lives of children through changing the social context of development. The transformation of Australian families has been striking. Fewer children, smaller households, older parents, working mothers, and parental separation and divorce, all affect the way in which families provide a nurturing and secure base.4 There are concerns that a greater investment in fewer children, tied with heightened parental anxieties, has produced a “bubble-wrap generation”. The effects of limiting independent exploration, risk taking and physical activity on children’s physical, cognitive and emotional development may be profound.5 Socioeconomic changes have also affected child health in other ways, such as altering material consumption and lifestyle. Industries, ranging from fashion to food and entertainment, now market to children, regarding them not only as the consumers of tomorrow but as major agents of influence on family spending.6 In this changing social context, the AIHW report attempted to capture a broad picture of the health and development of our children (Box). In preparing the report, emerging morbidities, such as childhood obesity, were to be an important focus. Obesity not only poses risks for later cardiovascular disease and diabetes, but also profoundly affects children’s quality of life and self-concept.7 However, the best available national data are 10 years old, from a time when around one in five children were overweight or obese. Moreover, national data are not available on patterns of physical activity or nutrition. Because of longer-term effects on adult health and prosperity, the socioeconomic circumstances of childhood are central in social policy considerations.8 Nowhere are these continuities between childhood circumstances and adult health clearer than in Aboriginal and Torres Strait Islanders. For this reason the report attempted to capture broader data on family functioning, local neighbourhoods, educational attainment, and the welfare of children in contact with health and social services. Some of the trends revealed by the study provide food for thought. The number of children on care and protection orders has increased almost 50% in 6 years, and rates in Indigenous children are over sixfold higher. The proportion of children in out-of-home care (ie, having to live away from their parents) has risen over 60% in the same period. Around one in ten families with children currently report that their neighbourhoods feel unsafe at least some of the time. This experience is three times commoner in poorer families. What effects these trends may be having on the mental health and emotional development of children is uncertain. Again our picture is incomplete, with the best available national data on child mental health now 7 years old.9 Data from this 7-year-old study suggested that, at any point in time, one in eight children had a diagnosable mental or behavioural disorder. These rates were twice as high in sole parent and blended families (ie, families formed by second marriages between parents with children). Thus, in attempting to paint a bigger picture of child health, development and wellbeing, the AIHW report has exposed huge gaps in the information needed for rational health and social policy responses. Perhaps the clearest gaps concern the emerging non-communicable illnesses of childhood. A need for up-to-date national data on the social and geographic distribution of childhood obesity and mental disorders stands out as a priority. What data we have suggest that these problems vary greatly according to geographic location and socioeconomic status and are worsening. If current social changes persist, the worsening trends in obesity and mental disorders seem likely to continue, and the children most affected will be those in disadvantaged and disrupted families. The federally funded Longitudinal Study of Australian Children will address some of the gaps by providing a better understanding of how current social and family contexts affect children.10 However, the study is of two cohorts separated by 4 years and will not be able to adequately capture the continuing and ongoing changes in the social context of childhood that we may expect to see in the coming years. Other gaps relate to our service systems for children and families. The aggregation of service system data to create ongoing national minimum datasets for areas such as juvenile justice, child protection and children’s services is an important first step in understanding how these systems are working. But much more is needed. The development of brief measures of development and social context in early and later childhood11,12 heralds the possibility of efficiently capturing ongoing shifts in the lifestyles, social development and health of our children. The new health problems of childhood are complex in their origins and likely to be complex in their solutions. A clearer picture of our children is needed to guide our responses — whether these be through priority research, informed government policy, better functioning of our service systems or, most importantly, the efforts of Australia’s parents, schools and local communities.

George C Patton MD, FRANZCP · Sharon R Goldfeld FRACP · Indrani Pieris-Caldwell PhD · Meredith Bryant MA · Graham V Vimpani FRACP

Until definitive evidence of the effectiveness of prostate cancer screening is available, most guidelines advocate that men make their own decisions about testing, after being fully informed. A man’s perception of his personal risk is a key element in the decision-making process. In this decision-making, the current routine use of population risk estimates may be misleading. Risk estimates need to be relevant to the man making the choice. In particular, they should be age-specific and, where possible, include adjustments for known risk factors such as family history. As an example, although the population risk of lung cancer mortality is twice that of prostate cancer, for a non-smoking man with a family history of prostate cancer the direction of this comparison would be reversed. A man aged 50 diagnosed with prostate cancer has a greater likelihood (60%) of dying prematurely (before 80 years) from prostate cancer than a man diagnosed when aged 70 (38%). This can be attributed to the longer time available for the prostate cancer to progress, and the increased effect of competing causes of death among older men. This suggests that the oft-used statement “men are more likely to die with prostate cancer than from prostate cancer” is misleading, particularly for men diagnosed in their 50s or 60s. Decisions need to be made by men based on the best possible understanding of their personal vulnerability, and the individualisation of risk provides a more realistic appraisal of potential threat posed by the disease.

Peter D Baade PhD · Suzanne K Steginga PhD · Joanne F Aitken PhD · Carole B Pinnock PhD

Laurelle J Burrell,* Elizabeth A Grabsch,† Alexander A Padiglione,‡ M Lindsay Grayson§ * Infectious Diseases Research Nurse, † Infection Control Scientist, § Director of Infectious Diseases, Austin Hospital, Studley Road, Heidelberg, VIC 3084; ‡ Infectious Diseases Physician, Department of Epidemiology and Preventive Medicine, Monash University (Alfred Hospital), Melbourne, VIC. Lindsay. GraysonATaustin.org.au To the Editor: Patients with end-stage renal failure are a key risk group for colonisation and infection with vancomycin-resistant enterococcus (VRE). Consequently, many renal units in Australia screen these patients regularly for VRE colonisation, to assist with infection control and treatment.1-3 Screening protocols are usually applied equally to inpatients and outpatients, even though the risk of VRE colonisation among outpatients (and therefore the cost–benefit of such screening) has not been clearly defined. To assess the prevalence of faecal VRE colonisation among haemodialysis outpatients, we conducted a cross-sectional survey of outpatients attending 12 Victorian in-centre haemodialysis units — Austin Health (four units), Southern Health (three units) and five regional haemodialysis units (Bendigo, West Gippsland, La Trobe Valley, Central Gippsland and Bairnsdale). Patients attending these units represent about a third of the state’s in-centre haemodialysis population. The study was approved by the ethics committee at each hospital, and written informed consent was obtained from all participants. All patients who attended the units between 1 October 2001 and 3 April 2002 were invited to participate. VRE faecal carriage was assessed by three rectal swabs and one faecal specimen taken on at least three separate occasions. Specimens were inoculated onto Enterococcosel agar (BBL, Sparks, USA) containing 6 μg/mL vancomycin. All cultures were processed by standard methods for VRE identification, as described previously.2,3 Of 345 available haemodialysis patients, 269 (78%) consented to participate in the study (205 [76%] metropolitan, and 64 [86%] regional; participation rate per centre, 70%–91%). The 269 patients represented approximately 30% of Victorian in-centre haemodialysis patients. Overall, 74% of participants had assessment of all three rectal swabs and a faecal specimen. VRE faecal colonisation was found in three of the 269 participants (1.1%) — two were from separate metropolitan hospitals, and one from a regional centre. All isolates were Enterococcus faecium vanB (the most common type of VRE in Australia).3 None of these three patients were known to be previously colonised. This 1.1% prevalence was substantially lower than the 3.0%–4.6% prevalence previously described in renal inpatients in Melbourne,2,3 and the 10% rate reported in the United States (where 33% of dialysis centres have one or more VRE-positive patients).1,4 Statistical comparisons of this study with our previous two Australian studies2,3 should be undertaken cautiously, as screening methods differed in specimen frequency, type and number. Bearing in mind this caveat, the rate of faecal VRE carriage was significantly lower among the haemodialysis outpatients in our current study compared with renal inpatients in a 1997 study by Grayson et al2 (3/269 v 9/194; P = 0.02 by χ2 test), but less definitely so when compared with renal inpatients in the 1998–1999 study of Padiglione et al3 (3/269 v 22/739; P = 0.09, by χ2 test). Since the outpatient study, screening surveys at our hospital have shown intermittent high rates of colonisation in renal inpatients and environmental contamination (unpublished data). Given our findings in outpatients, we believe future VRE screening protocols in Australian hospitals should focus primarily on inpatients, rather than faecally continent outpatients, who have both a low rate of colonisation and low potential risk for VRE transmission or acquisition. Good compliance with practical infection control guidelines remains important to avoid widespread dissemination of VRE in our haemodialysis centres.5

Laurelle J Burrell · Elizabeth A Grabsch · Alexander A Padiglione · M Lindsay Grayson

Fast Facts: Smoking cessation. Robert West and Saul Shiffman. Oxford: Health Press, 2004 (78 pp). ISBN 1 903734 42 8. This is, quite simply, This is, quite simply, a terrific little book. Written by two highly respected figures in the field, it is a fount of evidence-based wisdom. It should be on the bookshelves of every health professional who counsels smoking cessation, or who wants to be well informed. The writing style is very approachable and the synthesis of the material is, for the most part, masterful. It provides a great summary of the main health effects and benefits of quitting. There are figures here that should motivate smokers to think about quitting: half of all long-term smokers who die lose 16 years of life on average; put another way, all smokers lose an average of 8 years of life. In addition, disability sets in 12 years earlier than for non-smokers. I compute this to be, on average, 4 more years of disability-affected life. West and Shiffman also clearly and concisely set out the best path to cessation — behavioural help augmented with pharmacotherapy — with useful hints for helping smokers quit. There is a good explanation of why it is worth health professionals persisting with encouraging cessation, even though, on any one piece of advice, very few clients will eventually quit. The authors also wisely counsel against too much pushing, suggesting annual review (unless a smoker opts to follow up). There were only three things in the book with which I had any serious disagreement. Firstly, I think the authors over estimate the benefits of bans on smoking as a means of encouraging smokers to quit. Secondly, they suggest that the greater incidence of smoking among low socioeconomic groups in many Western societies is due to a deficit of skills. I think it is due partly to less access to compelling information and, for some, the competing priorities of lives out of control or lacking in essential rewards. Finally, they assert that virtually all slip-ups end in relapse. While most do, relapse is far from inevitable, and the danger in assuming relapse will occur is that this may become a self-fulfilling prophecy. However, these quibbles, important as they are, do not distract overly from the utility of the book. Every health worker should have some capacity to help smokers quit, even if only in knowing useful referral sources. This book is a fantastic resource. Ron BorlandNigel Gray Distinguished Fellow in Cancer Prevention, The Cancer Council Victoria, VIC

Ron Borland