Infectious diseases

Graeme H Johnson*, Donna B Mak†; *Acting Public Health Medical Officer; †Former Public Health Medical Officer, Kimberley Population Health Unit, Derby, WA 6728. graeme.johnson@health.wa.gov.au To the Editor: In their study of a SAFE-style trachoma control program (which included Antibiotic treatment, Facial cleanliness, and Environmental improvement, but not Surgery) in a remote Australian community, Ewald et al suggest that no systematic SAFE trachoma control program exists in Australia.1 In the Kimberley region of Western Australia, the Kimberley Public Health Unit (KPHU) has coordinated a trachoma control program since 1989. The World Health Organization SAFE strategy has been implemented since 1996, as described in the Kimberley regional trachoma control guidelines and a peer-reviewed publication.2,3 The trachoma control program in the Kimberley has been delivered by a variety of environmental health, health promotion, community and clinical health professionals employed by State and local governments, and by community-controlled and other non-government organisations. We believe a coordinated regional approach is mandatory, because of the numerous organisations involved in program delivery. The trachoma control program in the Kimberley continues to achieve good results. The prevalences of follicular trachoma during annual screening of school-aged children in the Kimberley have been published annually in the KPHU Bulletin.4 Since 1996, in accordance with the WHO SAFE strategy, communities with trachoma prevalences of less than 5% were not screened in subsequent years and did not contribute to regional prevalence data. Thus, the observed decrease in trachoma prevalence between 1996 and 2001 is likely to be greater than that shown in the Box. We believe the Kimberley region is well placed to achieve the WHO aim of eradicating blinding trachoma by 2020.5 However, it is a concern that other regions of Australia with endemic trachoma infection may not conduct disease control activities in a coordinated manner because of lack of leadership in trachoma control or insufficient resources, or both. The community described by Ewald et al borders the Kimberley region and has strong cultural links with several Kimberley groups. The achievements in trachoma control in the Kimberley cannot be sustained in the long term without a nationally coordinated approach. We believe that it falls within the statutory responsibilities of State and Territory departments of health to ensure that environmental and clinical health services are coordinated to achieve trachoma control in Australia. Trachoma in Kimberley children Point prevalence of follicular trachoma among children in the Kimberley region aged 5–15 years at annual trachoma screening, 1991–2002

Graeme H Johnson · Donna B Mak

Andrew C Laming,* Bart J Currie† * Advisor, Federal Minister for Health and Ageing, Parliament House, MG 48, Canberra, ACT 2600; † Professor in Medicine, Northern Territory Clinical School and Menzies School of Health Research, Darwin, NT. andrew.lamingAThealth.gov.au To the Editor: The important article by Ewald et al shows that offering azithromycin treatment to 70% of a remote community may be inadequate to control hyperendemic trachoma, even when combined with a health promotion campaign.1 Yet, significant short-term gains in similar locations have been achieved with as little as 20% of the population receiving azithromycin, where administration to children with trachoma and their household contacts was directly observed by health staff.2 In that study,2 we reported a 6-month follicle resolution rate in schoolchildren of 72%, followed, however, by a return of trachoma prevalence towards baseline levels over 12 months. The critical factors for short-term success with azithromycin appear to be appropriate selection of cases and contacts, plus, where possible, directly observed therapy to minimise reinfection from untreated cases. Sustainability of initial reduction in trachoma prevalence is problematic, and issues of how extensively and how often to screen and/or treat need to be determined in the Australian context. Similar sustainability considerations have arisen in community scabies programs.3 Ewald et al are correct to identify population mobility as a major issue, with trachoma likely to be reintroduced by untreated children entering a community where a treatment program has occurred. Hence the need for a coordinated regional approach. However, a regional approach to trachoma control does not necessarily mean a uniform approach, and it is vital to tailor programs to suit the capacity of communities and their degree of commitment to labour-intensive treatment and health promotion. Our study suggested that directly observed twice-yearly azithromycin therapy, with a health promotional component, is likely to be preferable to an annual program.2 Mathematical modelling supports this more frequent dosing and, unlike in Africa, the cost of azithromycin should not be a constraining factor in Australia.4 Regardless of the strategy selected, if, after treatment, the prevalence remains hyperendemic (> 20%), then the outcomes from concurrent health promotion are compromised. Appropriately targeted and directly observed azithromycin therapy can help create conditions favourable for health promotion campaigns, which in turn prolong those gains by reducing trachoma transmission.5 Major issues for trachoma control in Australia are (i) who to screen and treat (with directly observed azithromycin therapy); (ii) how often to screen and treat; (iii) how to plan trachoma programs as regional initiatives; and (iv) who will fund, coordinate and implement trachoma programs.

Andrew C Laming · Bart J Currie

Dan P Ewald,* Gillian V Hall,† Christine C Franks‡ * Senior Research Fellow, Centre for Remote Health, Flinders University, PO Box 4066, Alice Springs, NT; † Lecturer, National Centre for Epidemiology and Population Health, Australian National University, Canberra, ACT; ‡ Educator, Health Development, Health and Community Services, Alice Springs, NT. dan.ewaldATflinders.edu.au In reply: These letters reinforce a number of important points about control of trachoma (and other endemic infections) in Australia. The questions of whom and how often to treat need refining through Australian experience. Long-term control needs multifaceted, intersectoral collaboration to alter environmental and behavioural conditions against disease transmission. Strategies should be sustained, regional (large as practicable); acknowledging, and guided by, Aboriginal kinship networks; and recommend observed drug treatment (which was negotiated for the final treatment in our study). A non-uniform approach could include more frequent treatment in hyperendemic communities, probably leading to less net use of antibiotic treatment. Reports from the Kimberley Population Health Unit show a very mixed picture, with wide year-to-year fluctuations in prevalence in many communities. While hyperendemic communities remain in a region, the prevalence of trachoma may increase unnoticed in communities no longer screened because their prevalence has dropped below 5%. If not looked for, it is unlikely to be noticed. Further analysis, such as the graph provided by Johnson and Mak, is to be applauded in the context of a thorough analysis. When this happens, it will greatly strengthen the case for active trachoma control in other regions. For trachoma prevention, and for many other reasons, we believe environmental health interventions are critical. These remain difficult to evaluate given the high mobility of people in Aboriginal communities. Reliable, long-term, regional environmental health and mobility data are needed as part of this broad issue.

Dan P Ewald · Gillian V Hall · Christine C Franks

Tony D Merritt,* Carolyn Herlihy† * Epidemiologist/Biostatistitian, † Environmental Health Officer, Hunter Public Health Unit, Hunter Area Health Service, LMB 119, Wallsend, NSW 2287. tmerrittATdoh.health.nsw.gov.au To the Editor: Travelling animal shows, with animals such as young poultry, rabbits and reptiles, commonly visit childcare centres in Australia. Transmission of Salmonella infection to children from ducklings and chickens is well documented in the United States1,2 and United Kingdom,3 but not in Australia. We investigated a cluster of Salmonella agona cases in children, identified through routine laboratory surveillance. Initial investigations identified a potential association with visits to childcare centres by a single local hatchery. At each show, children saw an egg hatching, watched day-old ducklings swim and had the opportunity to hold a day-old chick or duckling, and to touch an adult chicken. Details of gastrointestinal illness were sought from childcare centres that had hosted visits from the hatchery. This identified laboratory-confirmed cases with onsets between 14 April and 6 May 2002 in seven people. All attended one of four childcare centres; six were children and one was a staff member. Onset of illness occurred 2–12 days after the hatchery visit. A total of 316 children attended shows by the hatchery between 9 April and 8 May. Environmental sampling at the hatchery recovered Salmonella agona from multiple sites over repeated visits. These included the egg incubator, faeces from day-old hatchlings returning from a show with children, faeces from young chicks and ducklings in the brooder cage, duck faeces from their yard, corn meal used in the preparation of feed for all poultry, and rat droppings in the feed preparation and storage areas. No Salmonella were detected in samples collected from the corn meal supplier. New procedures based on guidelines from South Australia4 and the Centers for Disease Control and Prevention5 were introduced for all shows from 8 May. These included supervised handwashing after handling animals, avoiding carpeted areas for the show, adequate cleaning of macroscopic faecal contamination and disposal of the water used by swimming ducklings into the sewerage system. No further cases were identified among the 251 children who attended shows over the subsequent two weeks until the hatchery cancelled all further visits. We conclude that infection was acquired through contact with chicks and ducklings from a single hatchery, and that the outbreak was halted by the introduction of measures emphasising handwashing after animal contact. Contact between young children and young animals, both of whom have naïve immune systems, represents a special ecological niche. Young poultry are particularly vulnerable to salmonella infection and subsequent high level excretion, and young children are similarly vulnerable. As animal visits to childcare centres are highly valued by children and carers, appropriate guidelines should be widely promoted to the childcare sector and the petting zoo industry to reduce the risks these visits pose. The petting zoo guidelines developed in South Australia4 are an excellent resource and NSW Health is currently developing a fact sheet on the topic.

Tony D Merritt · Carolyn Herlihy

Objectives: To determine whether infection with human immunodeficiency virus (HIV), hepatitis B virus (HBV) or hepatitis C virus (HCV) occurred after two potential episodes of exposure through needle- and syringe-sharing in Australian prisons, and to examine use of post-exposure prophylaxis (PEP) against HIV infection in the prison setting.Design: Cohort study of potential contacts of two prisoners infected with HIV, HBV and HCV ...

Belinda G O'Sullivan MPH, GradDipAppEpi · Michael H Levy MB MS, MPH · Sharon G Barton DipApplSc · Kate A Dolan PhD · John M Kaldor PhD · Andrew E Grulich PhD · Jeffrey J Post FRACP · Dominic E Dwyer MD, FRACP, FRCPA

Clinical record At 11: 30 on 8 April 2003, a 64-year-old man presented to the National University Hospital emergency department (ED) complaining of light headedness for 3 days, and dry cough and body aches for 2 days. His general practitioner had recorded a temperature of 37.7°C. On further enquiry in the ED, he described mild dyspnoea and palpitations. For over 40 years, he had smoked 25 cigarettes a day, ...

Dale A Fisher MB BS, FRACP, DTMH · Madeleine H L Chew MB BS · Yean-Teng Lim MRCP, FRCP · Paul A Tambyah MB BS

Re: "The SARS epidemic: lessons for Australia", by Cameron PA, Rainer TH, De Villiers Smit P, in the 2 June 2003 issue of the Journal. The Box with the World Health Organization case definitions of "suspected" and "probable" SARS (severe acute respiratory syndrome) was omitted from the print version of this editorial (Med J Aust 2003; 178: 478-479), but was included with the rapid ...

Peter A Cameron MB BS, FACEM, MD · Timothy H Rainer MB BCh, FHKCEM, MD, FHKAM · Pieter De Villiers Smit MB ChB, FACEM

Forewarned is forearmed Severe Acute Respiratory Syndrome (SARS) is now a global phenomenon, but it remains heavily clustered in mainland China, Hong Kong, Toronto, Singapore and Hanoi.1-5 The world is fearing a global pandemic, but it is not happening as initially predicted. Although there are some uncertainties regarding particular clusters of cases, such as the Amoy Garden Estate in Hong Kong (where about 300 people in one block of flats were affected), the primary mode of spread appears to be by infected droplets, and healthcare staff taking strict barrier precautions appear to be protected. There is some evidence that the virus is present in all body fluids, including faeces and urine, so taking precautions with waste disposal are also recommended. World Health Organization case definitions of severe acute respiratory syndrome (SARS) The WHO case definitions of SARS, revised as of 1 April 2003, for a suspected and a probable case of SARS: 6,7 A "suspected" case of SARS is a person presenting after 1 November 2002, who gives a history of high fever (> 38°C), and cough or breathing difficulty and one or more of the following exposures during the 10 days before the onset of symptoms — close contact with a person suspected of having SARS, or a history of travel to or residing in an affected area. A "probable" case of SARS pneumonia is a suspected case (as defined above), with radiographic evidence of infiltrates on chest x ray consistent with pneumonia or respiratory distress syndrome, or a suspect case with autopsy findings consistent with the pathology of respiratory distress syndrome, but without an identifiable cause. The World Health Organization case definitions of "suspected" and "probable" SARS are given in the Box. The clinical course of the disease follows a 2–16-day incubation period,4,5 with high fevers, chills, rigors and myalgia. In contrast to the WHO definition, respiratory symptoms are not prominent and many cases have presented with diarrhoea, abdominal pain and loss of appetite (unpublished observations). There are very few patients with abnormal findings on chest examination at presentation, but these changes develop in severe cases after admission to hospital.5 Laboratory tests typically show a reduced white cell and lymphocyte count, with a mild increase in the platelet count. Usually after 2–3 days of symptoms, x-ray changes become apparent. Typically, the changes are air-space consolidation, predominantly peripheral and often unifocal initially, but progressing over days to bilateral, multifocal changes. At around 7–10 days, about 20%–30% of cases deteriorate and require admission to an intensive care unit. Of these, about half require assisted ventilation. The overall mortality rate is 3%–5%, but may be higher in elderly people. Treatment has been largely empirical and usually has included an antiviral agent, such as ribavirin, and steroids.5 High-dose steroids have been effective in reducing fever and progression of x-ray changes, with the clinical response and radiological features suggesting bronchiolitis obliterans organising pneumonia as the possible underlying pathology.5,8 It is unclear whether any of these treatments alter the ultimate course of the disease. Intravenous administration of convalescent plasma has also been trialled, in the belief that antibodies may halt the progression of the disease,5 despite a theoretical risk of introducing another viral load. Currently, there are a number of possible aetiological candidates, with corona virus being the most likely;9-11 however, a metapneumovirus from the paramyxovirus group12 has also been suggested. Unfortunately, in our experience, field testing for the viruses has so far been unconvincing. It is unlikely that, in the short term, there will be a reliable diagnostic test or vaccine, although work is progressing at a rapid rate. In Australia, the response to SARS has been dichotomous — varying from panic that SARS will be another pandemic to complacency that this is another region's problem. It is likely that Australia will be less affected than countries with open land borders and crowded cities with poor hygiene control. However, the outbreak in Toronto shows that any Western city may have to manage such an outbreak.3 If this disease spreads in clusters rather than sweeps through communities, then the public-health response must be different. It is clear that hospitals and healthcare workers are particularly at risk. In Hong Kong, in the first weeks of the outbreak, 25% of patients with SARS were healthcare workers.5 The healthcare sector has to be particularly prepared, as this is most likely where a cluster will start. Revision of infection control, with meticulous attention to detail, is important. At the Prince of Wales Hospital, Hong Kong, it took three weeks to bring the secondary infections in staff down to near zero. Despite this experience, other hospitals in the region did not take heed, and many more staff in these hospitals became infected because of suboptimal infection control procedures. It is to be hoped that hospitals in Australia will learn from this experience. Screening potential cases of SARS is particularly difficult, as the signs and symptoms are vague and consistent with virtually any viral illness. Following up patients over a number of days is the only way of ascertaining whether they have SARS. The question of whether to admit all suspected cases to hospital is also an issue. If suspected cases are admitted, they may actually contract the disease in hospital. If they are discharged, they may infect their families and friends. In our recent experience of screening about 1000 people with suspected SARS, we uncovered over 100 confirmed SARS cases. We found that there was no secondary spread among the suspected cases followed at home with strict quarantine instructions. All people with confirmed SARS were admitted to hospital. Guidelines for screening high-risk contact and low-risk non-contact subjects have recently been published, although there are no good studies evaluating their utility or the quality of the supporting evidence.13 SARS will fundamentally change the interaction between primary healthcare workers and patients, in much the same way that AIDS changed the way we handle blood products, with universal precautions to protect ourselves from potential HIV infection. It is likely that, in the future, all healthcare providers in regions where SARS is endemic will use the standard droplet precautions of a mask, goggles, gown and gloves for all patient contact. SARS has the potential to totally disrupt the healthcare system of cities or states. Apart from the potential to use hundreds of general ward beds — a disaster in itself given the bed capacity of most Australian hospitals — the biggest threat is the need for intensive care unit (ICU) beds. If 20%–30% of cases required care in ICU, and a cluster of 200 cases occurred in Melbourne or Sydney, there would be little likelihood of finding 50 ICU beds at short notice. A further problem is that ICU staff are likely to contract the disease (unpublished data). If a number of staff contract the disease in an already overstretched ICU system, this may precipitate a fall in morale and staff departures. Furthermore, many nurses are of child-bearing age, and the antiviral agents and high-dose steroids used in the treatment of SARS are likely to be teratogenic. Health authorities need to think about their ability to provide "surge capacity" — not only in terms of ventilators, but also in terms of trained staff. This might include multiple-skills training for nurses and doctors working in non-intensive-care areas. Some healthcare epidemiologists have suggested that this disease is no more serious than the usual winter influenza outbreaks, and not nearly as serious as a new mutation of the influenza virus would be.14 The difference is that previously we have not seen a healthcare system paralysed for a period of months from the impact of one infectious agent. The annual reported death toll from influenza is mostly due to its impact on elderly people, who may die anyway. SARS puts young healthy people into ICU, and otherwise healthy people die. The death toll from SARS is undoubtedly higher in the elderly, and we have not yet seen what may eventuate if a SARS outbreak occurs in a retirement home. The sensible response of Australian health authorities is to remain on high alert, review infection control procedures within hospitals, develop contingency plans for a possible surge in demand for general and ICU beds, and develop an evidence-based approach to screening and quarantine procedures for potential cases.

Peter A Cameron MB BS, FACEM, MD · Timothy H Rainer MB BCh, FHKCEM, MD, FHKAM · Pieter De Villiers Smit MB ChB, FACEM

A 43-year-old woman taking warfarin for past venous thrombosis presented with 4 days of flu-like symptoms and deterioration in level of consciousness. Computed tomography suggested subarachnoid haemorrhage, and magnetic resonance imaging showed widespread cerebral infarcts. However, these seemed out of proportion to the amount of haemorrhage, and lumbar puncture revealed meningitis caused by Streptococcus pneumoniae. Computed tomography (CT) is a vital investigation in acute medicine, but CT appearances may occasionally be misleading, as illustrated here. Clinical recordPresentation (Day 0): A 43-year-old woman was admitted to the emergency department (ED) in June 2002 with deterioration in her level of consciousness. She had a 4-day history of non-specific flu-like symptoms. On the day of admission, her husband had noted her to be lucid at 09: 00 but found her semi-comatose when he returned home at 14: 30. She had a past history of venous thrombosis, thought to be secondary to the presence of anticardiolipin antibody and lupus inhibitor, for which she took warfarin. She used topical and parenteral corticosteroids to control severe eczema, was a non-smoker and did not take the oral contraceptive pill. On examination, her score on the Glasgow Coma Scale (GCS) was 7/15. Pupils were equal and reactive, and no definite signs of meningism could be elicited. Respiratory rate was 24 breaths/min, with oxygen saturation of 99% on supplemental oxygen, 15 L/min via a Hudson mask. Tympanic temperature was 40.8°C, blood pressure 168/92 mmHg and pulse rate 128 bpm in sinus rhythm. Serum blood glucose level was 7.8 mmol/L (reference range [RR], 3.6–5.8 mmol/L), white cell count was 18.6 x 109/L (RR, 4.2–11.0 x 109/L), with toxic changes on the blood film, and platelet count was 357 x 109/L (RR, 150–460 x 109/L). The international normalised ratio (INR) was 1.8 (RR, 0.8–1.3), with normal values for fibrinogen and fibrin cross degra-dation products, and activated partial thromboplastin time. C-reactive protein level was raised at 402 mg/L (RR, 0–10 mg/L). Other laboratory results, including renal function, were within the reference ranges. In the ED, the patient underwent tracheal intubation because of her low GCS score, and was subsequently sedated with morphine and midazolam. Blood was taken for culture, and intravenous ceftriaxone (2 g daily) was begun. Chest radiography showed segmental right upper-lobe consolidation. Non-contrast CT of the brain was performed during her transfer to the intensive care unit (ICU). This was reported as showing subarachnoid haemorrhage, with increased density in the subarachnoid space, particularly within the basal cisterns (Box A). A neurosurgeon was consulted, and subarachnoid haemorrhage with aspiration pneumonia was diagnosed. The differential diagnosis of meningitis was thought less likely because of the CT appearance. A nimodipine infusion was begun, and cerebral angiography was planned. Her high INR was normalised with 4 units of fresh frozen plasma. Day 1: At 06: 00 the next morning, the patient's pupils became unequal and non-reactive. This was thought secondary to either vasospasm or a re-bleed. Urgent repeat contrast CT at 07: 00 showed a parietal infarct, but no further bleeding or signs of raised intracranial pressure. The hyperdensity in the basal cisterns was less apparent, but there was subtle hyperdensity within the subarachnoid space, around the cerebral sulci near the vertex. On subsequent review, the amount of haemorrhage suggested by the cranial CT scans appeared insufficient to account for the patient's clinical condition. Diffusion-weighted magnetic resonance imaging (MRI) at 13: 30 showed multiple acute cerebral infarcts in the territories of the right middle and posterior cerebral arteries, as well as in the watershed zone between the middle and anterior cerebral arteries (Box B). There was no abnormal enhancement of the leptomeninges to suggest infectious meningitis, and, in particular, no basal leptomeningal enhancement to suggest granulomatous meningitis (Box B). In the absence of abnormal leptomeningeal enhancement, the presence of increased signal within the subarachnoid space was thought to be due to subarachnoid haemorrhage (Box B). Magnetic resonance angiogram and venogram showed no aneurysm or dural venous sinus thrombosis. Appearances were again thought most likely to represent primary subarachnoid haemorrhage, with acute cerebral infarction secondary to vasospasm. However, meningitis with secondary cerebral infarction was raised as a differential diagnosis, and lumbar puncture was recommended. Lumbar puncture was subsequently performed after correction of residual coagulopathy, and revealed an opening pressure > 35 cmH2O, a white blood cell count in cerebrospinal fluid (CSF) of 1510 x 106/L (all polymorphs), red blood cell count of 160 x 106/L (decreasing on subsequent tubes, with xanthochromia not detected), and protein level of 2291 mg/L (RR, 150–450 mg/L). Gram-positive diplococci were visible on Gram stain, and the CSF was positive for pneumococcal antigen. Blood taken on admission subsequently grew Streptococcus pneumoniae. After consultation with the infectious diseases team, we changed the antibiotic regimen to intravenous ceftriaxone (2 g) and vancomycin (1 g) twice daily. The diagnosis was revised to primary pneumococcal pneumonia with secondary pneumococcal meningitis. Course: After 11 days' treatment in the ICU, the patient was transferred to a ward. On Day 13, she developed a large pulmonary embolus confirmed by CT angiogram and was readmitted to the ICU for respiratory support. She recovered and subsequently resumed anticoagulation therapy with heparin and warfarin. She was discharged back to the ward on Day 18. At review a month later: She was undergoing rehabilitation, and was lucid and able to move with a frame, but remained blind in both eyes. DiscussionCranial CT scanning is a vital diagnostic tool in patients presenting with acute alteration in level of consciousness. Our case posed a diagnostic difficulty because of the unusual appearance on initial brain imaging. The initial CT scan showed increased density in the subarachnoid space, which is mostly caused by subarachnoid haemorrhage. Based on the imaging findings alone, the most likely diagnosis was therefore felt to be subarachnoid haemorrhage with secondary vasospasm causing cerebral infarction. However, there seemed to be a disparity between the amount of subarachnoid blood and the patient's clinical condition. This was reinforced by MRI, which showed extensive infarction in different vascular territories. This degree of infarction secondary to vasospasm would be unusual without widespread haemorrhage or thick focal clot, which were not seen. Additionally, vasospasm secondary to subarachnoid haemorrhage tends to peak 4–12 days later, while our patient showed signs of neurological deterioration less than 24 hours after admission. Cerebral infarction has been well reported in bacterial meningitis in both adults2,3 and children,4,5 and is thought to result from an intense inflammatory response in the cerebral vasculature. It is particularly noted in pneumococcal meningitis. Although pneumococcal meningitis was not diagnosed initially in our patient, broad spectrum antimicrobials, to which the organism was fully sensitive, were fortuitously begun on admission. The delay in ascertaining the correct diagnosis created a dilemma about subsequent anticoagulation, which probably could have been recommenced earlier. Increased density in the subarachnoid space on CT has been described in tuberculous meningitis.6-8 However, this was unlikely in our patient — the condition is still uncommon in the Western world, and contrast enhancement of the basal leptomeninges (a sign of granulomatous meningitis) was absent. Increased density in the subarachnoid space has also been reported in anoxic encephalopathy,9 but our patient had no history of hypoxia or prolonged ischaemia. In addition, although the acute infarcts were within regions of the brain susceptible to acute hypoxic injury, they were all within the right cerebral hemisphere. With a global insult such as hypoxia, bilateral lesions would be expected. To our knowledge, there has previously been only one English-language article describing a patient with acute purulent meningitis mimicking subarachnoid haemorrhage on CT scan.10 Presumably this appearance is caused by the high protein concentration of the purulent exudate in pyogenic meningitis, as noted in our case. Although this is uncommon, we present this case to alert both radiologists and clinicians to the presence of this atypical appearance on imaging and to highlight the need for careful evaluation of such patients. The case also illustrates that results of investigations should not be interpreted in isolation from the clinical picture. We suggest that lumbar puncture should be performed if the clinical presentation is atypical or not in keeping with the radiological findings. Brain imaging in a patient with pneumococcal meningitis A: Computed tomography (CT) on Day 0 Non-contrast CT scan, showing increased density within the basal cisterns (arrow A) and along the sylvian fissures bilaterally (arrow B), suggesting subarachnoid haemorrhage. B: Magnetic resonance imaging (MRI) on Day 1 Diffusion-weighted MRI scan showing multiple foci of increased signal intensity in the anterior part of the right thalamus, posterior right temporal lobe and right occipital lobe. Increased signal intensity was also seen in the right frontal and parietal lobes (not shown). This appearance was consistent with multiple acute infarcts in the territories of the right middle and posterior cerebral arteries. Not shown: Multiple small acute infarcts were also seen in the watershed zone in the centrum semi-ovale between the territories of the right middle and anterior cerebral arteries. Gadolinium-enhanced T1-weighted MRI scan showing no abnormal enhancement of the leptomeninges, including the basal leptomeninges. This suggests no evidence of a granulomatous meningitis. Not shown: Increased signal intensity was seen within the subarachnoid space overlying the cerebral sulci of both cerebral hemispheres on the FLAIR sequence (a T2-weighted sequence that nullifies the signal from cerebrospinal fluid [CSF], improving detection of lesions within the subarachnoid space and brain parenchyma1). This is a non-specific finding in a wide range of conditions, principally subarachnoid haemorrhage and meningitis. In our patient, the absence of leptomeningeal enhancement on the post-contrast images favoured a diagnosis of subarachnoid haemorrhage.

Taposh Chatterjee MB BS · John R Gowardman FRACP, FJFICM · Tony D Goh FRANZCR

This is the first time I have felt threatened by the work that I do It begins on Tuesday afternoon, 11 March, with another bothersome call from hospital administration. They want to take over our Emergency Department (ED) observation ward because the Department of Medicine has a couple of doctors who feel ill. They think that this illness may be contagious to other staff and patients, so a ward with a separate entrance and separate air-conditioning would be ideal. I make them aware that this action would severely hamper operations within the ED and that they should manage these doctors the same way we have treated the five ED doctors who, at the moment, have some viral illness: send them home. My answer to their request: no way. A short time later, the Professor of Medicine and the hospital's CEO visit my office — a very unusual event. They say they are very concerned because not just two but up to eight medical staff and a number of nurses are febrile and feel unwell. Being a pragmatic ED doctor, I point out that we have to make sure that this illness isn't just one of the many benign URTIs we see at this time of the year. After all, about 20% of our ED attendances relate to URTIs. So, we all agree to callback 40 medical and nursing staff and have them examined that evening. If it turns out they are suffering from some unusual disease, I will be more than happy to hand over the observation ward. I go home at 7 pm in the certain knowledge that I will have a relaxed evening with my family and will turn up to work tomorrow to greet a red-faced professor, apologising profusely for trying to disrupt our emergency service. But, at 9 pm, I take a call from the medical team: they have screened the first few patients and all have high fevers and pneumonic change on chest x ray. Within hours, 20 staff are patients in the observation ward, not desperately unwell but a little anxious about what will happen next. An over-reaction?The following day, we held a meeting of all the chiefs of clinical services to discuss what we should do next. Among many of the senior people, there was a fair degree of scepticism and more than a suggestion that we were over-reacting to this mystery illness. Could it just be that influenza or mycoplasma infection was affecting a disproportionate number of our staff? An over-reaction to the usual round of spring respiratory infections? We had heard of an outbreak of atypical pneumonia in Guangzhou, but the reports were that this was now under control, although rumours suggested otherwise. Certainly, the features of the illness were typical of the reports of severe acute respiratory syndrome (SARS) in Vietnam. We decided to work on the assumption that all three of the illness clusters were related in some way. The ED staff who had been away from work with a "viral illness" were assumed to have the same disease. Despite their protests that it was just another minor illness, they were forced to come in and be admitted to hospital. More medical and nursing staff became ill, as did patients from the same hospital ward. A number of senior staff refused to come into hospital until they became very ill; this resulted in the spread of the infection to their families. Early scareDespite treatment, the condition of all the patients seemed to deteriorate over the first few days. It was not clear whether anyone was going to improve. Only five days after the illness first became apparent in our hospital, I was facing the real prospect that a member of my own staff would die. One of my residents, gravely sick, now required intensive care; even with 100% oxygen, he could not maintain adequate arterial oxygen saturations. I prepared myself for his death and let my other staff know that it was likely that he would die. Overnight, he was given high-dose steroids; he improved marginally. By some miracle, his condition continued to improve and he survived. However, at this stage of the outbreak, eight other staff from my ED, as well as over 50 other healthcare workers, were still patients in hospital. This illness looked like it could eventually involve all the hospital staff; potentially, any or all of us could end up in the ICU. Empirical experienceMedical treatment was largely empirical because the causative agent responsible for the illness was unknown to us. Patients were initially treated with oseltamivir and broad-spectrum antibiotics to cover all likely known pathogens. Ribavirin and steroids were used, but there was no way of knowing whether this was altering the basic course of the disease. With experience, it became apparent that high-dose steroids had a major impact in halting deterioration late in the illness. Managing an illness that you know little about, under the scrutiny of your colleagues (as your patients), is very difficult. The pressures on all medical units and ancillary staff were enormous. The whole medical department was involved in treating the patients, and the number of staff affected grew steadily to more than 150. After considerable negotiation with the health authorities, normal operations within the hospital were suspended. Fortunately, there was a high degree of altruism and cooperation among the medical staff; all departments contributed to both staffing (in a high-risk situation) and to the overall management of this disaster. There were daily meetings of chiefs of services and forums for regular staff. Daily, factually accurate updates were posted electronically. It was simply incredible to see staff turning up to work each day despite the fact that, in the first two weeks of this experience, each day about four or five more staff members would succumb to the illness. From Day 1, all staff wore masks and gowns but we were still getting breakthrough cases. With meticulous attention to infection control, watched over by infection control "police" in each ward, we were able to reduce this occurrence to near zero. Like a stakeoutAt a personal level, this is the first time I have felt threatened by the work that I do. Perhaps, it's a similar experience to that of a policeman on his first "stakeout", when he realises he might get shot. As a doctor, you know you are potentially vulnerable to the getting of all sorts of illnesses, but rarely a devastating, life-threatening one. I was worried about going home in case I would infect my family. When I did get home, I felt physically exhausted and emotionally drained, and didn't really want to talk to anyone. I would not and could not touch my wife or children for fear of giving them the disease. I slept in a separate bedroom; I ate separately. Clothes and fomites were washed separately and chlorine bleach was everywhere. My youngest boy developed a nervous twitch as he was told tales of the disease and harassed to wash his hands and wear a mask. Some of my colleagues began sleeping in their offices, refusing to go to their homes at all for fear of infecting their families. It wasn't a situation I could go on living with. My wife and I decided it would be easier for all of us if my family returned to Australia. A couple of weeks after they left, I realised how isolated I had become outside of my work setting. No one wanted to come near me for fear of getting the disease; any social encounters became uncomfortable. Even in the carpark, people would skirt around me to avoid close contact. There was little time off work, anyway, because of the constant meetings and service commitments occasioned by the outbreak. By strange coincidence, news of the Iraqi war was being broadcast continuously on television. Disturbing as the images of this war were, I realised that the battle we were fighting here might well have a more long-lasting, devastating impact. Missing the pointWhen I spoke with friends in Australia, I was struck by how little they had heard about the outbreak in the first weeks and how little preparation authorities seemed to have undertaken. Some "armchair experts" were even saying that it was irrelevant to Australia, just another "beat-up". In their minds, influenza was much more important. I tried to remember the last time influenza had put 250 healthcare workers into hospital, with 20% of them in an ICU. I tried to remember the last time all the ICU beds in a city had been filled by influenza cases. As far as I was concerned, these "experts" had clearly missed the point. Also, initially there seemed to be a high degree of misinformation about the symptoms, signs and mode of spread of this disease. In general, the only definite symptom was fever. In the early stages of the illness, cough, rhinitis and other URTI symptoms were actually less prevalent in the SARS group than in other patients. I believe that information being promulgated by WHO and the Centers for Disease Control and Prevention (CDC) was, in some instances, inaccurate and at other times misleading. For example, early enthusiasm surrounding diagnostic tests proved misplaced when we found only a 10% positivity rate. I felt compelled to make time for some radio and television interviews to raise awareness of SARS. Late warningsIn Hong Kong itself, I believe the authorities were initially very keen to keep the public "in the dark". This was followed by an attempt to blame the hospital (and staff) for allowing the disease to spread. Initially, for fear of creating pandemonium, no moves were made to educate the public about preventive measures. We tried, through official channels, to get these messages out; unfortunately, most officials seemed to me to be more concerned with protecting the economy and preventing panic than containing disease. Unfortunately, this response seems to have been the typical one in some other jurisdictions as well. Although the Hong Kong government has since adopted widespread public health measures, at time of writing it still maintains that there is no crisis. I do not agree; there is no obvious end in sight. More and more of the public are becoming infected. There is a high likelihood that more healthcare workers will be struck down. It is distinctly possible that if the numbers of affected patients continue to rise the whole public health system may collapse. The most likely pressure point will be the intensive care setting: with over 100 cases already requiring intensive care, it is inevitable that untrained staff will have to manage critically ill patients. Also, hospitals will have to "triage" patients, allocating intensive care beds and technology to those most likely to benefit before those with a lesser or low chance of survival. Today, despite my concerns for the community, my personal fear has receded. I feel more capable of managing this threat than I did in my first fortnight's experience of it. Although I am not 100% sure of the cause of this illness (despite the confident reports from scientists), I do understand something about its course and how to control its spread, at least within the hospital. I know that most people will survive the disease. However, I remain extremely frustrated that others are not learning the lessons that we have learnt regarding the need for stringent infection control. Most medical staff think they know about infection control and how to manage a crisis, and are unwilling to take advice. As a result of this attitude, and despite direct knowledge of our experience, I believe that about 20 staff at another hospital in Hong Kong have contracted the disease. As a healthcare worker, the likelihood of contracting an infectious disease that will kill you is usually quite small. When a new, mysterious illness smites down a whole hospital and its workers, it hits at the heart of the health system.

Peter A Cameron MB BS, FACEM, MD

To the Editor: We describe six cases of amoebic appendicitis, encountered during a 15-month period in the Pathology Department of the Royal Darwin Hospital. The patients were all Indigenous Australians and four of them came from remote communities. The average age was 24 years and five of the six were men. They all presented with abdominal pain, fever and right iliac fossa tenderness for up to 6 days. The clinical notes did not indicate the presence of pre-existing dysentery, and no faecal examination was undertaken. Recovery following appendicectomy was uneventful in all the cases. No further follow-up is available. The aetiology was established histo-logically, as no distinctive clinical or macroscopic features were noted. The appendices showed extensive coagulative necrosis of the mucosa, submucosa and muscularis propria and invasion of the wall by variable numbers of amoebae with ingested blood cells. Inflammation secondary to perforation was evident in the serosa and the mesoappendix, but no significant inflammation was seen in the inner layers of the wall (Box). Coagulative necrosis of the appendiceal wall was seen in all the cases. In fact, in some of the cases the diagnosis was suspected on seeing this distinctive coagulative necrosis and the amoebae were only found later. Thus, we believe this type of necrosis, which has not been previously emphasised in the literature, to be characteristic of the condition. Amoebiasis is rare in a developed country like Australia. The infection is generally acquired during travel to endemic parts of the world. However, case reports of invasive amoebiasis in Indigenous Australians who have not travelled outside Australia have been previously reported.1,2 Immigration, immunosuppression and poor sanitation are other settings in which amoebiasis can be seen.3 The finding of six cases of amoebic appendicitis in Indigenous Australians in the Northern Territory in a 15-month period is significant, as appendicitis is a very rare manifestation of the disease. McCarthy et al, in a recent MJA article,2 highlight the potential public health significance of endemic invasive amoebiasis because of its high transmissibility in settings where hygiene may be suboptimal. We agree with this and believe in selective screening and appropriate treatment of at-risk contacts of the patients, as prolonged latency between infection and disease is well documented.3 Cross-section of appendix Cross-section of appendix with coagulative mural necrosis and secondary serosal inflammation (haematoxylin and eosin [H&E] original 1×). Numerous amoebae in clear spaces, some with ingested blood cells, are seen in the insert (H&E original 40×).

Ibrahim M Zardawi · Joseph S Kattampallil · Jurgen W Rode

To the Editor: It has been well established that improved compliance in hand washing significantly reduces hospital-acquired infections and cross transmission of methicillin-resistant Staphylococcus aureus.1 Although there have been no reports of infections resulting from cross-contamination via stethoscopes, studies have demonstrated that 80%–100% of these appliances are colonised by bacteria.2-5 However, most of the organisms isolated are considered non-pathogenic. The most common potentially pathogenic organism isolated from stethoscopes is S. aureus, with a prevalence of 4.2%–27.5%.2-5 Cleaning with either 70% isopropyl alcohol or benzalkonium chloride wipes can reduce the bacterial count on stethoscopes by 94%–100%.3,5 We undertook a study to assess the prevalence of S. aureus carriage on stethoscopes and hands of staff of the Canberra Hospital, and to measure the effectiveness of cleaning and hand washing in reducing colonisation. A convenience sample of healthcare workers from various areas of the hospital was obtained over a period of 6 months. The diaphragm of each participant's stethoscope was directly impressed on to mannitol salt agar, before and after being cleaned with a 70% isopropyl alcohol wipe. The dominant hand of each participant was also tested before and after washing with triclosan (1%) antimicrobial handwash and water. S. aureus was identified by standard laboratory methods. There were 134 participants: 69 doctors, 50 nurses, 10 medical and nursing students and five physiotherapists. Most doctors and physiotherapists used their own stethoscopes, whereas most nurses and students used ward stethoscopes. S. aureus was isolated from five stethoscopes before cleaning (4%), but from none after cleaning. The organism was also isolated from the hands of 11 people before hand washing (8%) and of one after hand washing (0.7%). Two people had S. aureus isolated from both sites. There was no statistically significant difference between the prevalence of S. aureus on hands and stethoscopes (P = 0.15, McNemar's test). Hand washing is the best recognised means of preventing cross-contamination in hospitals. However, the simple intervention of cleaning stethoscopes with an alcohol wipe was highly effective, and we believe that this practice should be more widely promoted.

Karina J Kennedy · Dianne E Dreimanis · Wendy D Beckingham · Francis J Bowden

To the Editor: Figures from the Australian Bureau of Statistics show that Australians make about 3.3 million overseas departures each year.1 Few data are published on the extent to which Australian travellers seek pre-travel health advice, what vaccinations they receive, and what risks they are exposed to during travel. A series of surveys of travellers examining these questions has been conducted under the auspices of the Travel Health Advisory Group, a coalition of Australian travel and medical organisations. Surveys were conducted in 1996, 1997, 2000, 2001 and 2002. On each occasion, a market research company telephoned people from mainland capitals using numbers randomly selected from the telephone directory. This process continued until 500 people aged 18 or over who had travelled overseas in the previous two years had been interviewed. In the 2002 survey, about 10 000 calls were made to complete the interviews. The questions on vaccinations focused on hepatitis A and B, two of the most common vaccine-preventable diseases associated with travel.2 Results from the 2002 survey are shown in the Box. A minority of people (31%) reported seeing a doctor or travel clinic for pre-travel health advice. Of those who saw a doctor or travel clinic, 31% did so two weeks or less before departure. Over the series of surveys, there has been an increase in travel to destinations with high- or intermediate-risk for hepatitis A infection, from 40% of travellers in 1996 to 58% in 2002. Despite this increase, only a minority of travellers could recall ever being vaccinated for this illness. Travellers were informed about how they might be exposed to hepatitis A and B and asked if they believed that they could have been at risk during their most recent overseas trip. Substantial numbers recalled a risk (34% and 16% for hepatitis A and B, respectively) and some of these could not recall being vaccinated (18% and 7%, respectively) (Box). These surveys have methodological limitations, including lack of information on the consent rate and potential recall bias. However, the results suggest that substantial numbers of travellers do not seek pre-travel health advice and are at risk of vaccine-preventable diseases during travel. Not only does this have implications for individual travellers, it also creates public health risks, as travellers can introduce hepatitis A and B into their home communities. These results suggest more public education is needed about the importance of pre-travel health advice and appropriate vaccination. Results of 2002 survey of Australian travellers overseas Variable No. of travellers (n = 500) Age (years) 18–29 156 (31%) 30–49 188 (38%) ≥ 50 153 (31%) Not stated 3 (0.6%) Male sex 205 (41%) Hepatitis A risk in country visited* High 226 (45%) Intermediate 62 (12%) Low 212 (42%) Sought pre-travel health advice from doctor or travel clinic Doctor 135 (27%) Travel clinic 20 (4%) No professional advice 345 (69%) Believed could have been at risk of hepatitis on most recent trip Hepatitis A 168 (34%) Hepatitis B 79 (16%) Vaccinated against hepatitis Hepatitis A 195 (39%) Hepatitis B 197 (39%) Believed at risk of hepatitis on most recent trip and not vaccinated or unsure Hepatitis A 91 (18%) Hepatitis B 36 (7%) Hepatitis A risk in country visited* among those not vaccinated for hepatitis A or unsure High 123 (25%) Intermediate 40 (8%) Low 142 (28%) * As defined by the United States Centers for Disease Control and Prevention, 2000.3 Destinations for the cohort of 500 were Asia (45%), northern Europe (28%), southern Europe (14%), North America (15%), Oceania (14%), eastern Europe (3%), Africa (3%), Middle East (2%), South America (1%) and Central America (1%), with some having more than one destination.

Nicholas A Zwar

To the Editor: I note with interest the case study of experimental Ancylostoma caninum infection in a 22-year-old student.1 In his accompanying editorial, Van Der Weyden highlights the courage of these researchers, as well as some of the risks and discomforts associated with their participation,2 including in two studies in which he was a co-author. However, it is also worth highlighting some of the ethical issues associated with such experimentation. Larry Altman, who provided many of the quoted examples of self-experimentation, also reflects on Walter Reed's experiments with yellow fever vectors in Cuba. Although later credited with the use of written consent forms, on an earlier occasion Altman alleges that Reed withdrew at the last moment from inoculation experiments in which one of his colleagues died.3 Although not mentioned in the published work, the A. caninum experiment was initiated and undertaken by Landmann under the supervision of Prociv, who has himself self-experimented with both A. caninum and Necator americanus (human hookworm) in previous work (Juergen Landmann, Student; Paul Prociv, Senior Lecturer, Department of Microbiology and Parasitology, University of Queensland, personal communication). In this case, the study was wholly initiated by the student so consent was not an issue, but other such studies raise the potential problem of consent in situations of an unequal power relationship. Students under supervision constitute a "vulnerable" group in that consent may be given under a form of duress.4 Just as special protection is needed for populations for whom research is combined with care, protection is required for students who may feel obliged to participate in such research. There have been recent calls for a fuller discussion of ethical issues in published experimental studies,5 where ethical justification should be accorded the same weight as statistical considerations. The unusual study by Landmann and Prociv highlights the need for such discussion in potentially controversial research protocols.

Allen C Cheng MB BS, FRACP

Objective: To achieve sustained improvement in use of cefotaxime and ceftriaxone (CEFX) in a major teaching hospital, as measured against national antibiotic guidelines.Design and setting: Pre- and post-intervention survey of CEFX use in the Royal Melbourne Hospital, a tertiary hospital in Melbourne, Victoria.Intervention: Web-based antimicrobial approval system linked to national antibiotic guidelines was developed by a multidisciplinary team and implemented in March 2001.Main outcome measures: Change in rate of CEFX use (defined daily doses [DDDs] per 1000 acute occupied bed days) over 8 months pre- and 15 months post-intervention; concordance of indication for CEFX with national antibiotic guidelines pre- and post-intervention.Results: CEFX use decreased from a mean of 38.3 DDDs/1000 bed days pre-intervention to 15.9, 18.7 and 21.2 DDDs/1000 bed days at 1, 4 and 15 months post-intervention. Concordance with national antibiotic guidelines rose from 25% of courses pre-intervention to 51% within 5 months post-intervention (P < 0.002). Gentamicin use also increased, from a mean of 30.0 to 48.3 DDDs/1000 bed days (P = 0.0001).Conclusion: The web-based antimicrobial approval system achieved a sustained reduction in CEFX use over 15 months as well as increased prescribing concordance with antibiotic guidelines. It has potential for linking to electronic prescribing and for wider use for other drugs, as well as for research into the epidemiology of antibiotic use.

Michael J Richards FRACP · Lyn-Li Lim MB BS · Marion B Robertson BPharm, MSc · Nicholas R Jones BPharm, Grad Dip Clinical Pharmacy · Simone E Taylor PharmD, Grad Cert CRM · Margarida M Duarte BA (CompSci), BEng (partial) · Dale A Kerr BBus (Information Systems) · Graham J Stanton · Peter D Ritchie MPubHlth, FACEM · Jonathan G A Dartnell BPharm, PhD

To the Editor: Methicillin-resistant Staphylococcus aureus (MRSA) with reduced susceptibility to glycopeptides (vancomycin-intermediate S. aureus, or VISA) was initially described in Japan,1 then the United States,2 and subsequently other regions of the world. Recently, Ward and colleagues reported the initial Australian isolate — a heteroresistant VISA (hVISA) strain — in Melbourne, Victoria.3 We report the first isolation of hVISA in Sydney, New South Wales. A 79-year-old man underwent mitral valve annuloplasty in April 2002. Post-operative complications included MRSA bacteraemia, which resolved. He was discharged at the end of July 2002, but 12 days later was admitted to a second hospital with endocarditis caused by Streptococcus viridans. A month later, he developed a third episode of septicaemia, and MRSA was isolated from blood cultures. Despite two weeks' treatment with intravenous vancomycin, blood cultures again yielded MRSA. A transoesophageal echocardiogram confirmed endocarditis. Resistance screening of the MRSA isolate by E test (AB Biodisk, Solna, Sweden)4 gave minimum inhibitory concentrations of 16 mg/L for vancomycin and 32 mg/L for teicoplanin, suggesting resistance to glycopeptides. The patient was then treated with intravenous linezolid and underwent vegetectomy. Subsequent blood cultures were negative for MRSA, but the patient died seven days after surgery from nosocomial pneumonia caused by Escherichia coli. Population analysis of the MRSA isolate showed that it was heterogeneously resistant to vancomycin (hVISA). The emergence of hVISA in Sydney is a sentinel event, with ramifications for clinicians, laboratories and infection control. Routine susceptibility testing will not detect this resistance. Hence, clinicians and laboratories should consider VISA and hVISA if a patient with a proven MRSA infection fails to respond to vancomycin or teicoplanin, or has had several courses of vancomycin/teicoplanin and continuing positive cultures. If alerted that specimens could contain VISA or hVISA, the laboratory should perform glycopeptide resistance screening using E tests or other methods. Isolates that screen positive should be confirmed with population analysis profile testing.4 Treatment of hVISA and VISA infections, particularly bacteraemia and endocarditis, with vancomycin and/or teicoplanin is likely to fail. Alternative antibiotics include linezolid and quinupristin–dalfopristin, which are both very expensive. There is limited information on the success or otherwise of these agents in treating serious staphylococcal infections, especially bacteraemia and endocarditis.5 As a number of outbreaks of VISA and hVISA infection have already been described in other countries, we must ensure that these organisms do not become established in Australian institutions. Strict attention to infection control must be observed, particularly handwashing and use of alcohol hand rubs before and after patient contact. Attention to rational prescribing of antibiotics is required, avoiding broad-spectrum agents whenever possible. Vancomycin and teicoplanin should be used only when necessary: when there is resistance to other agents, and only when infection is present. Colonisation is not an indication to use glycopeptides, nor is minor allergy to β-lactams.

Iain B Gosbell · David H Mitchell · Helen Ziochos · Peter B Ward

Re: "Experimental human infection with the dog hookworm, Ancylostoma caninum", the Research article by Juergen K Landmann and Paul Prociv in the 20 January issue of the Journal (Med J Aust 2003; 178: 69-71). The labels for the second oral infection and cutaneous infection in the Figure in Box 2 were accidentally reversed. The corrected Figure is reproduced here. 2: Peripheral blood eosinophil levels after exposure to infective larvae of Ancylostoma caninum * The three separate experiments were run consecutively over a period of one year.

Juergen K Landmann BSc(Hons) · Paul Prociv MB BS, PhD, FRACP, FRCPA

Aim: To determine effectiveness of treatment for hepatitis C outside clinical trials, by testing the hypothesis that apparent effectiveness and tolerability of interferon alfa-2b/ribavirin combination therapy would be less in a hospital liver clinic setting.Design: Retrospective analysis of all patients in one centre commencing interferon alfa-2b/ribavirin therapy, but not in clinical trials, between 1998 and 2000.Main outcome measures: Effectiveness as sustained virological response (SVR); tolerability as premature discontinuation of treatment.Results: The 121 patients had similar demographic and viral characteristics as those in Australian trials (age, 44 ± 10 years; males, 66%; genotype 1, 44%; genotype 3, 36%), but 38% had advanced fibrosis, including 17% with cirrhosis. Sixty (50%) were previously untreated, 38 (31%) had relapsed after initial response (response relapse) and 23 (19%) were non-responders to interferon monotherapy. Sustained viral response (SVR) was achieved in 53% of patients overall: 47% of patients with genotype 1 HCV, 71% of patients with genotype 3. For patients with genotype 1 HCV, SVR was 43% in those previously untreated, 63% in response relapsers, and 38% in non-responders. Corresponding SVRs for genotype 3 were 65%, 87% and 33%. These results are similar to those obtained in published trials. Only 7% of our patients discontinued treatment because of adverse effects, fewer than reported in most clinical trials. Dose reduction was required in 18% of patients.Conclusions: In a hospital clinic setting the effectiveness of interferon alfa-2b/ribavirin combination therapy appears equivalent to published results from clinical trials.

Dinesh Kumar* MD, DM · Craig Wallington-Beddoe* BSc, MB BS · Jacob George PhD, FRACP · Rita Lin PhD, FRACP · Dev Samarasinghe PhD, FRACP · Chris Liddle PhD, FRACP · Geoffrey C Farrell MD, FRACP

Needle/syringe programs have resulted in enormous savings in both lives and dollars Sixteen years after needle/syringe programs (NSPs) were first introduced in Australia, after a period of civil disobedience and amid intense controversy, the recent report Return on investment in needle and syringe programs in Australia1 has convincingly confirmed the effectiveness of NSPs in reducing HIV and hepatitis C virus (HCV) infection among injecting drug users. The report also draws attention to the program's low cost and high cost-effectiveness. Commissioned by the Commonwealth Department of Health and Ageing, the report summarises 778 years of data from 103 cities around the world. In cities that had ever had NSPs, there had been an average annual decrease in HIV prevalence of 18.6%, compared with an average annual increase of 8.1% in cities without such programs. Australia's NSPs were estimated to have cost Commonwealth and State governments $122 million by 2000, but the return on this investment was the prevention of an estimated 25 000 HIV and 21 000 HCV infections. By 2010, our NSPs will have prevented an estimated 4500 deaths from AIDS and 90 deaths from HCV. The savings to governments for HIV and HCV were estimated to be at least $2.4 billion (allowing for conventional government 5% annual discounting of future costs) or as much as $7.7 billion (without discounting). By any reckoning, this represents an enormous saving in both lives and dollars. In light of these outcomes, opposition to NSPs amounts to public health vandalism and financial recklessness with taxpayers' dollars. However, in spite of these gratifying health outcomes for investments in NSPs, the annual incidence of HCV in Australia continues to rise. Hepatitis C is a very common chronic infection in Australia. At least 80% of infected people have acquired HCV through injecting drug use. A recent report2 estimated that in Australia in 2001 there were about 210 000 people with HCV antibodies, of whom 53 000 had cleared their HCV infection, 151 000 were living with chronic HCV infection and 6500 were living with HCV cirrhosis. Furthermore, according to the report, despite the effectiveness of NSPs in reducing HCV incidence among injecting drug users (IDUs), there were 16 000 people exposed to HCV during 2001, representing a 45% increase on the estimated 11 000 incident HCV infections in 1997.3 The report also projected that the long-term sequelae of HCV infection, such as cirrhosis, liver failure and hepatocellular carcinoma, would all treble by 2020. These two reports1,2 raise several important questions. First, why have NSPs been so successful at limiting HIV infection among IDUs, but less effective in reducing HCV infection? One important reason for the apparent discrepancy is the greater infectiousness of HCV by blood–blood spread compared with HIV, and consequently its heightened transmission among IDUs. Another factor is the higher baseline HCV levels (of the order of 50%–70%) prevalent among IDUs when NSPs were introduced in Australia in the late 1980s.4 At that time, only one in 200 IDUs undergoing treatment in Sydney were infected with HIV.5 HIV appears to have entered IDU populations in Australia in the early 1980s, about 20 years after HCV.6 Second, why has HCV incidence continued to increase so rapidly in Australia throughout the 1980s and 1990s, despite early and vigorous implementation of NSPs? The answer appears to be a combination of the increase in the number of young people who inject drugs7 and the continued high incidence of HCV infection among IDUs, and in particular among young people who have recently started injecting drugs (around 20% of IDUs are infected with HCV within three years of commencing injecting).8 The heroin shortage in Australia beginning in 2000 may have interrupted the increase in the number of IDUs, but whether a shortage will persist is uncertain. It is too early to estimate the net costs and benefits of the heroin shortage, but one benefit has been the 25% drop in deaths from drug overdose between 1999 and 2000.9 Finally, what should be done? Alternative strategies that need to be considered (in combination with NSPs) include medically supervised injecting centres, drug law reform, a trial of medically supervised prescription of illicit drugs for treating refractory drug users, introduction of harm-minimisation strategies into prisons, and education programs to encourage people who do or might inject drugs to consider non-injecting routes of administration. Such strategies must be debated in the community and properly evaluated. As each new HCV infection is estimated to cost healthcare systems more than $10 000,10 such strategies make sound health and financial sense. Many IDUs ultimately abandon injecting illicit drugs — it is in everyone's interests that they are still healthy when they do so, to maximise the likelihood that they will lead normal and useful lives. With the recent confirmation of the effectiveness of NSPs in preventing HIV transmission, it is important that society continues to support these programs. This may appear self-evident, but closing down NSP centres is often politically popular, especially in marginal electorates in tight elections. We must not become complacent just because a feared epidemic of HIV among IDUs has not eventuated. There is no guarantee that it will not happen in the future, as has been seen in some other countries.11 Any loss of resolve in the commitment to NSPs increases the likelihood of an HIV epidemic among IDUs, with potentially disastrous consequences for other at-risk populations (such as female sex workers or Indigenous Australians) and thence for the wider community.

Matthew G Law PhD · Robert G Batey MD FRACP FRCP

1: Clinical definition of adult male or female sexual assault6 a) Penetration of the vulva (beyond the labia majora) and/or anus by a penis or any other object, and/or penetration of the mouth by a penis and b) Without the consent of the person A United States meta-analysis estimates that 13% of women and 3% of men worldwide may be raped at some time during their lives.1 New Zealand and Australian data suggest similar findings,2 ranging from 4.6%3 to 11.3%4 in different populations. Although reliable incidence figures are impossible to estimate given considerable barriers to reporting,4 sexual assault presents, often unexpectedly, to healthcare providers working in diverse areas.5 Practitioners may feel sexual assault is challenging to manage, but it is simple when broken into components — emotional, physical and medicolegal. Here we provide a framework for non-forensic medical management of recent adult sexual assault. Box 1 gives a clinical definition, broader than that used in Australian law. DisclosureVictims are reluctant to disclose that they have been sexually assaulted for many reasons, including fear of police, not being believed or retribution, as well as guilt and a desire to forget the event. However, they may present for medical care because of concerns about pregnancy, sexually transmissible infections (STIs), or injury.7 They may present with post-traumatic stress, depressive symptoms,8 alcohol or substance misuse or self-harm.9 To encourage disclosure it is necessary to ask directly about the possibility of sexual assault. 2: Asking about sexual assault Have you ever been forced to have sex you didn't want? Have you ever had sex forced on you? Have you ever been sexually assaulted? Most victims of reported sexual assault are women; men are also assaulted, but are less likely to disclose.10 Although people of all ages and cultures are vulnerable, prisoners,11 adolescents, injecting drug users, the elderly, those who experienced sexual assault as children, and people with mental or physical disabilities are at particular risk.12 A recent survey of sexual health clinics in Australia and New Zealand found that staff were more likely to ask about sexual assault if their workplace encouraged it.13 It also identified patient distress, time constraints and lack of expertise in managing a positive response as barriers to asking. However, nearly all of the patients in the survey reported they did not mind being asked about sexual assault.13 A recent Sydney survey linked sexual assault firmly with the words "forced" and "non-consent" (L Dayan, Director, Sexual Health Services, Royal North Shore Hospital, Sydney, personal communication). Suggestions on how to ask about sexual assault are shown in Box 2. ManagementWhen responding to a disclosure of sexual assault, it is important to: ensure privacy, safety and adequate time for the victim; acknowledge their courage in speaking out; accept the victim's story in a non-judgemental way — it is the role of police to investigate story veracity; explain that reactions to rape, such as shock, arousal, anxiety and fear are normal, emphasising that the victim is not to blame; and understand that the aim of management is to return control to the victim by enabling them to make choices about reporting, counselling and medical therapy (see Box 3). Further action is defined by whether the victim decides to make a formal complaint. Most jurisdictions require that the first person who hears an allegation of sexual assault must give evidence if the complaint comes to trial, so document the exact words used, even if the victim is referred for forensic management. HistoryAssess any injuries and ongoing safety and support. Emergency accommodation may be needed if the victim's home is not safe. A brief history of when and where the assault took place, who put what where, and contraception or condom use will inform immediate treatment. Ask whether the victim wants to report the assault to the police. Early referral to a sexual assault service assists forensic testing. A forensic assessment involves careful documentation of injuries and testing for the presence of foreign DNA; the findings are compiled in a court medicolegal report. Even if the victim is unsure about wanting to report the assault, if there is any possibility of a complaint being made forensic assessment will preserve evidence in case a formal report is made to police at a later date. Ask about the possibility of drug-assisted rape, which is becoming increasingly common worldwide.14 Early forensic referral may facilitate detection of commonly used drugs (eg, flunitrazepam, ketamine) in the victim's blood or urine. Testing must be performed in a police laboratory to preserve continuity of court evidence. If the patient keeps a spot urine specimen, this can be handed directly to the police. ExaminationA thorough general and genital examination should be performed and any injuries documented. Although most sexual assault services use speculums for examining women, this depends on both the woman (comfort versus her need to know all is normal) and the practitioner (expertise and requirement for testing), and should be discussed with the woman before examination. Similarly, the use of a proctoscope may be required. Victims are often afraid that there has been genital damage which will make it obvious to others that they have been raped. Feedback that everything looks normal, as is usually the case,15 can be very reassuring. InvestigationTests for forensic purposes, sexually transmissible infections and pregnancy are performed according to need. If a woman is being transferred to a sexual assault service for forensic assessment after unprotected vaginal rape, the initial dose of the emergency contraceptive pill should be given first. Forensics: If the victim is willing for the police to be involved, he or she should be referred immediately to an expert sexual assault service for forensic assessment (a list is provided at the end of this article). If a victim is undecided about reporting the assault, forensic specimens may be stored while a formal complaint is considered. DNA evidence left on or in the body of a victim, particularly in moist areas, degrades quickly over 2–10 days.16,17 Therefore, forensic assessments need to be made as soon as possible, but within 10 days of an assault. If proceeding to a forensic assessment, advise victims not to shower (or to clean their teeth or rinse their mouths if the assault was oral), and ensure all clothes worn during the assault remain unwashed. As DNA evidence degrades quickly if moist, ask the victim to store underclothes worn during the assault in paper (not plastic) bags. In remote areas, timely expert forensic assessment is difficult. Most sexual assault services provide 24-hour phone assistance by doctors experienced in forensic medicine to discuss assessment. After discussion, some practitioners in remote areas may decide to perform forensic assessments, but this can be a difficult decision, as the practitioner may later be required to give evidence in court. Sexual assault services in Western Australia suggest a compromise solution that entails wiping the victim's vulval and/or anal area with sterile gauze, air-drying it, putting it into a labelled sterile container and handing it directly to local police for forensic testing before the victim's transfer for forensic assessment.18 Pregnancy risk: Depending on the victim's contraceptive and menstrual history, testing urine or serum might be useful to direct therapy and follow-up. Sexually transmissible infections: Baseline testing of sexual assault victims for sexually transmissible infections (STIs) in Australia varies with local clinical practice. In some Queensland sexual assault services serum is held in case STI testing is requested or required later (M Mobbs, Visiting Medical Officer, Brisbane Sexual Assault Service, personal communication). Baseline testing usually occurs in sexual assault services and communities with known high STI risk. As victims of sexual assault have higher rates of STIs compared with the general population,19 opportunistic screening is worthwhile if follow-up can be organised. Under Australian law, a rape victim's sexual history is inadmissible in court and this includes any history of STI. Thus, possible court prejudice is not a reason to withhold testing. See Box 4 for screening test recommendations. Note PAP smears are not generally included. The HIV/STI status of the perpetrator is usually unknown. In the absence of any better indicators, ethnicity or culture is sometimes used as a proxy for HIV/STI risk. The purpose of this judgement of risk is not to vilify minority groups, but to assess the victim's risk of infection on the basis of often very limited information about the perpetrator. Treatment recommendations alter for victims assaulted by anyone thought to be from a high risk group (see Box 5). The National HIV/AIDS Strategy states that community prevalence of HIV and STIs is higher in certain groups, including African and South-East Asian people, homosexual and bisexual men, and injecting drug users.21 Rates of STI are high in northern Australia, including in Indigenous communities,22,23 while HIV prevalence is higher in inner Sydney than elsewhere in Australia.24 As the risk of sexual transmission of hepatitis C virus (HCV) is low,25 tests are usually only performed in high risk situations (eg, assault with bleeding injuries, or assault by known HCV-positive assailant). Although the risk of HIV from one act of unprotected intercourse is very small, if the assault was penetrative unprotected vaginal or anal rape victims should be advised to use condoms until follow-up testing at three months. Most victims are concerned about HIV risk, even though they may not admit it.7 The vast majority will not require HIV prophylaxis, as the risk of transmission from an HIV-positive assailant is very small (see Box 6) and the chance that the perpetrator was HIV positive far smaller. Specific therapyCounsellingSexual assault is a frightening and sometimes life-threatening violent experience and counselling should be offered to all. Even if victims do not wish to attend counselling, it is important that they know where they can go for help, as memories can surface later (eg, at first childbirth) and can impair future functioning.27 Family and partners may also require counselling, or referral may be needed for domestic violence issues. Safety after rape can require moving house if the rapist lives with the victim, or knows where he or she lives. Emergency housing may be needed, as may other forms of immediate support, such as certificates for absence from work and support letters for school. Emergency contraceptionIf the assault was unprotected vaginal rape, or if there was any possibility that this occurred (eg, victim lost consciousness, was intoxicated or is unsure), then emergency contraception can be offered up to three, and possibly up to five, days after the assault.28 The progesterone-only regimen is recommended over the Yuzpe method because it is more effective with fewer side effects. Give the first dose as soon as possible, as efficacy halves with each 12-hour interval after the assault.29 Progesterone-only method: 750 μg levonorgestrel orally; repeat 12 hours later. A 750 μg tablet (Postinor-2, Schering Pty Ltd) is now available in Australia, or 25 30-μg tablets (Microval, Wyeth Australia Pty Ltd; or Microlut, Schering Pty Ltd) can be used for each dose. Yuzpe method: 100 μg oestradiol orally; repeat 12 hours later. Use two 50-μg oestrogen-containing combined oral contraceptive tablets for each dose. This regimen should only be used if the progesterone-only method is not tolerated or unavailable. Sexually transmitted infectionsFor unprotected vaginal or anal assault, victims are offered single-dose prophylaxis with azithromycin for chlamydia (see Box 5). They are also offered prophylactic hepatitis B vaccine if likely to be non-immune. Treatment varies according to community prevalence of STIs and perceived individual risk. In tropical areas of Australia, or if the perpetrator is considered at high risk of being infected, prophylaxis may also be added for gonorrhoea, occasionally syphilis, and passive vaccination with hepatitis B immune globulin30 may also be given if the recipient is not immune. For victims at high risk of having acquired HIV infection (eg, rape by someone from an area of high HIV prevalence), urgent phone consultation with an infectious diseases or sexual health physician about post-exposure prophylaxis for HIV is recommended (see Box 7). ReviewIt is notoriously difficult to get victims back for follow-up.31 The review program suggested (Box 4) is a guide only and should be tailored to suit individual patients. At the very least, an appointment is recommended at two weeks for discussing test results, further testing (eg, pregnancy), review of coping, and assessment of healing. Follow-up serological tests should be performed at three months for HIV, hepatitis B virus and syphilis. Reviews are a good opportunity to assess the need for counselling if this has not already been organised. Before the victim leaves, give written instructions for taking medications and review appointments, and include counselling service phone numbers. Victims may be intoxicated, shocked or tired and are unlikely to remember verbal medical instructions. SummaryManagement of acute adult sexual assault may appear daunting, but when viewed in its component parts is not difficult. Review by a sympathetic, non-judgemental practitioner can play an important role in helping victims regain control of their lives. Australia-wide resources Websites Comprehensive listing of services available in Australia and New Zealand, both updated 2002. Australia: http://www.acshp.org.au/sexual_health/assault.htm New Zealand: http://www.dsac.org.nz Major State and Territory resource phone numbers for sexual assault services The following lists only one major service for each Australian State or Territory, as these services will refer to other local services as appropriate. Australian Capital Territory Forensic and Medical Sexual Assault Care BH 02 6244 2184/3058 Canberra Rape Crisis Centre 02 6247 2525* Queensland Brisbane Sexual Assault Service 07 3636 5206* Toll free 1800 010 120* Government Medical Office (forensic regional services) 07 3405 5755* Tasmania Sexual Assault Support Service Hobart BH 03 6231 1811 AH 03 6231 1817* New South Wales Eastern and Central Sexual Assault Service, Sydney BH 02 9515 3680 AH 02 9515 6111* (ask for sexual assault counsellor) South Australia http://www.wch.sa.gov.au/yarrow/index.html Yarrow Place, Adelaide BH 08 8226 8777 AH 08 8226 8787* Toll free 1800 817 421 Western Australia Sexual Assault Resource Centre, Perth 08 9340 1820/1830 08 9340 1828* Toll free 1800 199 888* Northern Territory Darwin Sexual Assault Referral Centre 08 8922 7156* Victoria Victorian Institute of Forensic Medicine 03 9684 4444* * Denotes 24-hour contact number. 3: Guide for sexual assault care * Usually includes medical care; check with local service. † See resources section at end of article. ‡ Some rural/remote general practitioners perform forensic assessments after consultation with a sexual assault service. STI = sexually transmitted infection. 4: Baseline screening recommendations for sexually transmitted infections Infection Test Site (take according to history) HIV HIV antibody Blood Hepatitis B Hepatitis B surface antigen (HbsAg), core antibody (anti-HBc) and surface antibody (anti-HBs) Blood Syphilis Rapid plasma reagin (RPR) + treponema pallidum haemagglutination assay (TPHA) Blood Chlamydia Polymerase chain reaction Endocervical swab, first-void urine or high vaginal swab Gonorrhoea Polymerase chain reaction or microscopy, culture and sensitivity (M,C&S) Endocervical swab, first-void urine, rectal swab* or throat swab* Trichomonas Microscopy, culture and sensitivity (M,C&S) High vaginal swab * M,C&S only, as PCR is not validated for these sites. 5: Suggested prophylaxis for sexually transmitted infections (treatment for high risk is bolded) STI Treatment Chlamydia Azithromycin (1 g orally) Hepatitis B Hepatitis B vaccine (1 mL intramuscularly) For high risk add: Hepatitis B immune globulin (400 IU intramuscularly*) Gonorrhoea (only if high risk) Ceftriaxone (250 mg intramuscularly) OR, where local gonococcal sensitivities permit: 20 Ciprofloxacin (500 mg orally) OR Amoxycillin (3 g orally) and probenecid (1 g orally) Syphilis (if high risk) Benzathine penicillin (1.8 g intramuscularly) HIV (if high risk) Phone local infectious diseases or sexual health physician urgently Other STIs Consult local infectious diseases or sexual health physician * Available from Commonwealth Serum Laboratories. STI = Sexually transmitted infection. 6: HIV transmission risk per unprotected act of intercourse with an HIV-positive person*26 Type of intercourse Risk per 1000 acts Receptive anal 1–30 in 1000 Receptive vaginal 1–2 in 1000 Insertive vaginal 1 in 1000 Insertive anal 3–9 in 1000 * For comparison, the risk of acquiring HIV infection from using a shared HIV-contaminated needle is 667 in 1000, and from a needlestick injury to healthcare workers is about 4–8 in 1000. 7: Suggested review program 2–3 days: Assess injury healing if relevant 2 weeks: Test results, pregnancy testing, healing, coping Follow-up testing: Chlamydia, gonorrhoea, trichomonas (depending on local practice and whether previous treatment was given) 3 months: Follow-up serological tests for HIV, hepatitis B virus, syphilis 6 months: Follow-up serological test for hepatitis C virus if a test was performed initially

Jacqueline K Mein,*† MB BS, FACSHP, MAE · Cheryn M Palmer,† BMed, MMed, FACSHP · Meon Carol Shand,* MB ChB, FRNZCGP, FACSHP · David J Templeton,*† MB ChB, DipVen · Vanita Parek,* MB ChB, FACSHP, DRANZCOG, DipVenDFFP · Margaret Mobbs,*† MB ChB, DipVen, Visiting Medical Officer. · Kay Haig,* MB BS, FACSHP · Sarah E Huffam MB BS, FRACP · Lyndall Young MB BS, DFFP

To the Editor: Although liver flukes (genus, Fasciola) are parasites of livestock, human infection is a significant global health problem,1 albeit seldom seen in Australia.2 Infected livestock contaminate waterways with parasite eggs, leading to infection of snails that shed metacercariae on to vegetation, such as watercress.1,3,4 Adult parasites reside in and damage the bile ducts.1,3 Liver flukes could cause disease if introduced into the food chain.1 We report the first case in Australia of liver fluke infection (fasciolosis) in a patient with no history of farm or livestock contact. She probably acquired the disease from eating watercress purchased at a Melbourne market four to five months before symptom onset. Computed tomography of the liver in a woman with fasciolosis Low density lesions (arrowed) following intrahepatic ductal branches in the right lobe of the liver were consistent with Fasciola parasites causing biliary obstruction. A 35-year-old woman presented in August 1998 with fever and right upper quadrant abdominal pain. Blood examination showed eosinophilia (2.5 x 109/L; reference range [RR], < 0.6 x 109/L]). Liver function tests gave normal results apart from elevated serum aspartate aminotransferase levels of 48 U/L (RR < 41 U/L). Abdominal computed tomography showed multiple low density lesions in the right lobe of the liver, with diameter up to 3 cm (Box). A fine needle aspirate showed no evidence of malignancy. Blood tests four weeks later revealed increasing eosinophilia (3.5 x 109/L) and worsening liver function (serum levels: alanine aminotransferase, 163 U/L [RR, 7–56 U/L]; alkaline phosphatase, 126 U/L [RR, 30–120 U/L]; γ-glutamyl transferase, 98 U/L [RR, 5–45 U/L]). A parasitic infection was suspected, but four faecal samples and serological tests for hydatids, Schistosoma, Strongyloides and Entamoeba spp. were negative. Coprological diagnosis of fasciolosis can be problematic, as eggs may be released intermittently and in small numbers, especially in low-intensity infection.1 Enzyme-linked immunosorbent assay (ELISA) using Fasciola hepatica antigen, performed at Westmead Hospital, Sydney, was borderline positive. However, ELISA for IgG4 antibodies against recombinant F. hepatica cathepsin L5 antigen, performed at Monash University, Melbourne, was strongly positive. The patient was treated with two doses of triclabendazole (12 mg/kg body weight per dose) on successive days in October 1998. Abdominal pain subsided within two weeks, her appetite was restored, and eosinophil count and liver function normalised within four weeks. Computed tomography two months after treatment showed a reduction in size of the liver lesions. The patient remained well six months later. This case demonstrates that fasciolosis may present to urban medical practitioners in Australia. Ingestion of watercress is an important clue to the aetiology.2 Serological diagnosis is possible before eggs appear in faeces using a new specific ELISA test that detects the IgG4 response to cathepsin L antigen.5

Andrew J Hughes · Terry W Spithill · Rebecca E Smith · Craig S Boutlis · Paul DR Johnson

To the Editor: Collins and colleagues1 reported a case of bacteraemic community-acquired MRSA (CAMRSA) infection that they believed to be the first reported in Australia. One of us (G N) published a reference to a case of septicaemia and osteomyelitis in Brisbane caused by CAMRSA in 2000.2 This severe case occurred in a previously healthy 16-year-old boy with no risk factors for MRSA infection who, after prolonged ventilatory and inotropic support and vancomycin therapy, required a long period of rehabilitation. A further two cases of septicaemia occurred in Ipswich and will soon be published as part of a study of CAMRSA conducted in 2000–2001.3 We recently encountered another case involving a previously well 23-year-old man who presented to the emergency department with a large abscess on his upper lip and extensive cellulitis of the surrounding face and neck, and with left-sided pleuritic chest pain and associated fevers and rigors. The patient denied previous antibiotic use or contact with healthcare facilities at any time in the past. There was no history of injecting drug use or trauma. Staphylococcus aureus was isolated from blood cultures, and resistance to oxacillin and susceptibility to erythromycin, clindamycin, tetracycline, gentamicin, ciprofloxacin, fusidic acid, rifampicin, and vancomycin was shown. Specimens from operative debridement of the facial abscess yielded S. aureus with the same susceptibility pattern. Chest x-rays showed extensive consolidation of the left lower lobe and an associated loculated pleural effusion. Clinical, radiological, and echocardiographic evaluations did not reveal another focus of infection. The patient was treated with intravenous vancomycin for three weeks followed by oral clindamycin, with complete clinical resolution. It is now clear that CAMRSA infection may result in severe, life-threatening sepsis. The possibility of pneumonia associated with CAMRSA is of particular concern. A 1999 report from Minnesota and North Dakota documented four deaths in children from CAMRSA, including two with necrotising pneumonia.4 A further two fatal cases of necrotising pneumonia caused by CAMRSA were recently reported from France.5 The strains involved in all of these cases carry the gene for Panton-Valentine (P-V) leukocidin, a staphylococcal toxin that has been shown to be strongly associated with cases of severe superficial abscesses and necrotising pneumonia.6 As the strain of CAMRSA most commonly encountered in Eastern Australia also carries the P-V leukocidin gene (Professor J Etienne, Faculty of Medicine, Claude Bernard Lyon 1 University, personal communication), doctors should be aware of the possibility of severe community-acquired pneumonia caused by this organism.

Graeme R Nimmo · E Geoffrey Playford

Despite the risks to unvaccinated children, compulsory vaccination is not the answer In a pluralistic society, there are many views on what constitutes acceptable child-rearing. In Australia and other Western societies, parental discretion is limited primarily by legislation against abuse or neglect. In treatment decisions, the legal starting point is that the united view of both parents is correct in identifying the child's welfare. A court will usually only override the parents' decision if the judge is convinced the child's life is endangered, such as when a child needs transfusion.2 Administration of a vaccine is never immediately life-saving in this sense, except in the case of post-exposure rabies vaccine,3 but vaccination satisfies ethical criteria for preventive interventions in children: it is effective, minimally invasive, and associated with significant societal benefits.3 Indeed, the highly favourable benefit-to-risk ratio of childhood vaccination is so well documented that healthcare professionals are understandably frustrated when faced with what seems to be an irrational decision by parents to refuse vaccination. This is especially so when this decision has resulted in failure to prevent a life-threatening illness, as in the tetanus case presented by Goldwater et al (page 175).4 This case raises issues for both the clinician and society. How do healthcare professionals understand and best respond to a conscious decision not to vaccinate? In a highly immunised population, what is the balance of risks and benefits to individual children and their contacts from refusal to vaccinate? Should a case such as this propel us towards compulsory vaccination? In Australia, vaccination is not compulsory, but various incentives and reminders aim to promote it. First, payment of the maternity allowance at 18 months and the childcare benefit requires up-to-date vaccination according to the Australian Childhood Immunisation Register (ACIR),5 unless a medical practitioner has notified the ACIR of a contraindication or serologically confirmed immunity, or has discussed conscientious objection with a parent. Second, at school entry, documentation of full vaccination is required in most Australian jurisdictions, with children who do not have such documentation or serological proof of immunity to specific diseases, such as measles, able to be excluded from school attendance if suspected cases occur. Although the United States is often quoted as having laws for mandatory vaccination, the practical effect of these laws is also limited to exclusion of unvaccinated children from school during outbreaks, although preschool attendance for such children can be barred altogether.6 Italy is one of a few countries where there is compulsory vaccination, but only for diphtheria, tetanus, polio and hepatitis B. However, this has not been enforced for many years.7 To find examples of truly compulsory vaccination, it is necessary to go back to the 19th century. In England, the Vaccination Act of 1853 made smallpox vaccination compulsory for all infants in the first three months of life, on pain of fine or imprisonment. Its enactment spawned riots in several towns and an active anti-vaccination movement. In 1898, a new Vaccination Act removed these penalties and introduced the concept of "conscientious objector" into English law.8 In present-day Australia, most parents whose children are not fully vaccinated are not conscientious objectors, but rather face practical barriers such as recurrent minor illness, work commitments, large family size or social disadvantage.9,10 Parents who are strongly opposed to vaccination comprise a much smaller group. Of a large sample of 1779 Melbourne children in childcare in 1997, only 13 (0.7%) had not received any vaccines.10 This is similar to the proportion of all children Australia-wide registered with Medicare for whom there is a registered conscientious objection.5 In general, such parents tend to be well educated, older, female and of Anglo-Saxon background.11,12 Qualitative data suggest that conscientious objectors fear possible but unknown, especially long term, adverse effects of vaccines, believe that lifestyle measures to improve general immunity are viable alternatives to protection from vaccines, and often mistrust the motives of healthcare providers.9,12 This limits the ability of healthcare professionals to present pertinent counterarguments. Indeed, there is some evidence that parents philosophically opposed to vaccination may have their objections reinforced by factual information about risks and benefits, because these facts do not accord with their beliefs about health and illness.13 In contrast, parents who are merely doubtful about vaccination are much more likely to be amenable to presentation of relevant factual information.9 Healthcare professionals communicating with such doubtful parents need to have their facts well prepared and be sure that they have ascertained the parents' specific concerns, particularly whether these arise from personal or family experience. This is all potentially achievable within a realistic timeframe for a standard consultation, using readily available material specific to Australia.14 In the current Australian environment of high immunisation rates, does refusal of vaccination pose risks to either the individual or the community? In the case of tetanus, the risk is limited to the individual, as the disease is not transmissible. The risk to the individual is highlighted by the US experience, where, with very high immunisation rates, 15 reported cases of childhood tetanus occurred between 1992 and 2000.15 Children unvaccinated because of their parents' beliefs accounted for 9/11 cases in school-aged children,15 although objecting families represent only 0.6% of families with children attending school in the US.16 For other transmissible vaccine-preventable diseases, such as measles, pertussis and poliomyelitis, the risk goes beyond the individual. In Colorado, schools with a higher percentage of objectors were more likely to have a pertussis outbreak, and at least 11% of vaccinated children in measles outbreaks acquired measles from contact with an unvaccinated child of objecting parents. In addition, there was a 22-fold (measles) and sixfold (pertussis) increased risk for the individual unvaccinated child.16 Similarly, in Germany, almost all cases of Hib meningitis occur in unvaccinated children of objecting parents.17 In closed communities of vaccination objectors, such as certain religious groups, very high levels of morbidity from diseases not present in the general community can occur, such as in polio outbreaks in the Netherlands.18 Although there are few such communities in Australia, there is a tendency for conscientious objectors to cluster in certain geographic areas, so the risk of transmission is amplified. Measles cases in Australia now arise exclusively from imported strains and the unvaccinated children of conscientious objectors have recently been highlighted as at risk.19 Parents should be made aware that a decision not to vaccinate, made on their children's behalf, exposes their child to significant risks, even in 2003. Persuasion, at both the clinical level14 and the societal level,5 is appropriate, but truly compulsory vaccination is not an option, either in Australia or in other comparable countries.6,7

Peter B McIntyre FRACP, FAFPHM · Alison H Williams MB BS, FRACGP · Julie E Leask RM, MPH

Refusal of a parent to have a child vaccinated against tetanus raised ethical issues for the treating clinicians. The clinicians felt their duty to the child was compromised, but recognised that our society leaves the authority for such decisions with the parents. As there was no reason, other than different beliefs about vaccination, to doubt the parent's care for the child, the clinicians limited their response to providing strong recommendations in favour of vaccination. Other issues raised by this case include community protection, and the costs to the community of treating a vaccine-preventable disease.

Paul N Goldwater FRACP, FRCPA · Richard G Power FRACP, MRCP(UK) · Paul H Henning FRACP · Terence G Donald FRACP · Jon N Jureidini PhD, FRANZCP · Christine F Finlay RN, RM · Annette J Braunack-Mayer BMedSci(Hons), PhD · Mike S Gold FRACP, MD

To the Editor: In their article describing an outbreak of Bordetella pertussis infection, Spearing and colleagues report an adult contact who was infected with B. pertussis and was treated with roxithromycin.1 In our experience, this is common practice in Australia, where roxithromycin is a frequently used macrolide antibiotic. We are currently preparing a systematic review (registered with the Cochrane acute infections group) of the effectiveness of antibiotic therapy for treating pertussis. We have found no studies of the effectiveness of roxithromycin for either treatment or contact prophylaxis for pertussis infection. B. pertussis is sensitive in vitro to roxithromycin but 2–4-fold less so than to erythromycin. While relying on the class effect of macrolides in eradicating B. pertussis and using roxithromycin in preference to erythromycin because of its lower side-effect profile may seem logical, there is no evidence to support this practice. In contrast, there is at least one study showing the efficacy of clarithromycin as an alternative to erythromycin for the treatment of pertussis.2

R John Massie · Sultan Altunaji · Renata Kukurozovic · Nigel Curtis