Infectious diseases

We reached the Zambezi escarpment after dark, unable to appreciate the panorama of wilderness that extended 50 or more kilometres to the opposing heights in Zambia, on the other side of the great river that was heading into Mozambique on its way to the Indian Ocean. It was 1972 and we were on our way to collect samples of blood from villagers who shared the Rhodesian (now Zimbabwean) side of the valley with all kinds of wild animals, vectors and parasites. On the top of the escarpment, as we were about to wind our way down into the darkness in our Land Rover, we learned of the return of another violent species to the valley — the freedom fighters from across the border. In what the military wing of the African National Congress of South Africa referred to as the Sipolilo campaign (after a town on the plateau near the escarpment), their soldiers had crossed the river in 1968 in the hope of recruiting villagers for revolution, but they had been discovered by local forces and then dispersed in a process that took lives on both sides, as well as in the hapless middle. As our headlights probed the bush, a camouflaged patrol of Rhodesian infantry appeared and signalled us down. “You should not go any further”, their officer advised, “the terrs are back and the roads might be booby trapped or mined”. I was with Michael Gelfand, Professor of Medicine at the University of Rhodesia, whose lined face, thin body and wispy, grey hair suggested enormous age to my youthful mind, though he was only 60. He was already a legend — son of Lithuanian refugees to South Africa, he had graduated from the University of Cape Town and made his way north to Rhodesia to be fundamental in developing the multiracial medical school in the capital, Salisbury. He was founder and editor of the Central African Journal of Medicine and a prolific writer on tropical diseases. Gelfand was also an observer and recorder of local Shona customs and appeared to be above the racial conflict that was emerging in his country. Though his registrar, I had never spoken to him about race. Perhaps strangely, it had never seemed to be an issue in the “black” Harare hospital in which the University was based. Gelfand, I reflect, set an unspoken standard — he was a kind man, knowledgeable and respectful of local traditions but, above all, absorbed in African medicine with a boyish enthusiasm that simply could not understand preferences for other branches of the profession. When he suggested I join him and the provincial doctor on a research foray, I thought I was made, and although it was a bit of a shock to come across the soldiers and their warning, there was never any question of our turning back. Our lust was up for blood and, I suspect, the old man believed he knew enough about the locals to be able to negotiate any difficulties. Nevertheless, as we descended into the valley in a lighted cocoon of tall grass that bowed before our bumper bar, we knew our wheels would be exerting pressure on the track and whatever might be primed beneath it, and we remained silent. We were going to survey the incidence of the nematode Wuchereria bancrofti by collecting blood samples from villagers. The samples would be examined back in Salisbury for the worm’s larval forms, known as microfilariae (Box 1). First observed by Otto Wucherer in Brazil in 1866, these larvae are released in their thousands from each female adult worm and can be observed wriggling among the blood cells of infected people. The larvae are the width of a white cell but 40–50 times the length. The long (4–10 cm), hair-thin adult worms, discovered by the English physician Joseph Bancroft in Queensland in 1876, live in the lymph vessels of victims, from where the females release the larvae, which make their way to the peripheral blood (Box 2). The adults particularly enjoy the comforts of the lymph vessels in the pelvis and groin, but when these vessels become blocked, the victim’s legs may swell with elephantine disfigurement (Box 3). The blocked vessels can also affect the scrota of the unfortunate, demanding an unusual service from a wheelbarrow. Our hunt was to take place at night because of the still unexplained phenomenon in which the microfilariae appear in the bloodstream after dark to rendezvous with their night-biting mosquito vectors. How they know when to emerge is as much a mystery today as it was in 1877 when first observed by Scottish physician Patrick Manson in China. The allied question of where they go during the day has no better answer than Manson’s original postmortem examinations, which revealed the “majority to be lodged in the blood vessels of the lungs”.1 How they know the time of day and their location, and how they maintain their position in the flow (given that they have no suckers) remains as unanswered as the question of why they feel the need to hide and waste so much energy doing it. The people in our first village had heard us coming long before we had noticed their cooking fires and they surrounded our vehicle with interest when they learned we were doctors and, I suppose, not soldiers. We explained our business and called for volunteers and soon had a long line waiting in the lights of the Land Rover, where we had established our “laboratory”. We took samples and looked for oedema in legs but had concluded that requests to bathe scrota in the limelight might be counterproductive. We did, however, assess the size of spleens as an indication of the prevalence of chronic malaria. All went well for an hour or more, until sudden screeching in the bush around us caused our line to disintegrate in pandemonium. People started yelling and ran to their huts to arm themselves with pots and pans, which they banged together as they disappeared clamorously into the bush. We three doctors were abandoned — immobilised and silhouetted in the lights of the vehicle. “We’re dead”, I thought, “the terrs have arrived”. I looked around for somewhere to run, but Gelfand held his ground. “Settle down. They’re not terrs, they are just elephants who have come after the grain stores in the village”, he explained to the naive Australian. Sure enough, his diagnosis was confirmed by trumpeting and crashing through the undergrowth as the herd surged for the corn. “Stay where you are”, advised the Professor, but the young registrar was consumed by stupidity and went to find an elephant for himself. It did not take long. A huge black shape crashed before his widened eyes. With the villagers in sustained conflict with the marauders, there seemed little prospect of controlled bloodletting, so we decided to pursue our research further down the track. An hour later, we arrived at the next village. The first village had been welcoming. The second was sullen. It was surrounded by a high brush fence and, in the moonless darkness, we heard it before we saw it. We heard the rhythm of drums: a mysterious, exciting, but ominous syncopation; an almost supernatural throbbing bass to the higher pitched cries of birds and monkeys. We drove up to the entrance to the compound and stopped the car, now to be more unnerved by silence. The drumming had stopped and all of nature seemed to be holding its breath. The villagers surrounded us in the darkness and the mood was unpleasant. Gelfand tried to communicate in Shona, but there was little reply. Something was going on in that village. Was it some kind of ancient animistic ritual? Was it some kind of new political ritual? Were there terrs in the village? In the crowd? The Professor was squeezing charm from inner reserves as he slowly backed us to the car. It was plain he was making a retreat, rather than an entreaty for participation in our worthy research, and we wasted no time piling in and waving farewell with ersatz cheer. We were very glad to get away and to be heading for the ranger’s hut on the river bank some kilometres distant, where we were going to spend the night. Relief, however, was limited by the realisation that there was only one track to the one white man’s hut in that direction and it was well known to everyone. The hut was on a grassy clearing about 25 metres back from the Zambezi River, opposite the entrance of the Luangwa River, which rises in northern Zambia. The water was black, wide and fast, but you could not meditate on it in the open. Although the sounds of the nightlife were enticing and the river bewitching, there were lions seeking dinner, hippos waiting to be annoyed and snakes to be insulted, not to mention the mosquito vectors of filariasis and the future prospect of needing a wheelbarrow. We retired to the hut, set up our screens and, in memory of our friends up the track, made sure the doors were locked, for whatever difference that might have made, then tried to go to sleep. We were glad to see the morning. Unanimously, we decided to curtail our field work that week-end and concentrate on our specimens back in the capital, but we did stop at a couple of villages on the top of the escarpment. We looked for clinical signs of filariasis but found none, although previous surveys had confirmed a high prevalence of microfilariae in that area. Relaxed in the open savannah of the plateau, we mused on the disease we had gone to survey. We would have been surprised to know that basic questions would remain unanswered 40 years later, despite an explosion of research of unimagined sophistication.2 Immunology was taking off in those days, and we might have expected an answer to why the microfilariae are able to nullify immune defences to the extent that millions of these motile, burrowing worms can be born, live and die in an infected person’s system for decades without causing much damage. A hundred years earlier, an editorial in the British Medical Journal had wondered that these “swarm(s)” of worms “should produce such a comparatively trivial amount of inconvenience”, but even today we are not much closer to the truth.3 We already knew adult worms had proven resistant to the one hopeful drug, diethylcarbamazine, since its discovery in 1947, but we expected a breakthrough. We would have been disappointed by the lack of any significant challenge to the adult worms in the next 40 years, apart from the extraordinary concept of perhaps being able to affect the adult by damaging bacteria that live symbiotically within it.4 Who would have thought each adult had its own dairy farm? In the 1970s, emphasis was on treatment of individual cases of elephantiasis. How do you manage the grotesque leg? We looked forward to the development of new drugs, but might have done better looking backwards. Considered a “new insight”, it is now believed that “basic hygiene, antibiotics and physiotherapy can slow, prevent, or in some cases reverse elephantiasis”.2 In 1846, however, even before the discovery of the worm, the English surgeon E Bascome had argued that elephantiasis was the result of repeated attacks of erysipelas.5 It now seems that reaction to secondary infection may be more important in blocking the lymph vessels than reaction to the worm. Prevention in the 1970s meant not being bitten by mosquitoes. We could not have foreseen the discovery that semiannual treatment of whole populations with our old friend diethylcarbamazine, and some newer drugs, can so markedly reduce the number of microfilariae that propagation is limited.6 Nor could we have anticipated the ease of diagnosis by measurement of filarial antigen in drops of blood on blotting paper.2 Had we known of these advances, it would have been surprising to know that, despite them, the prevalence of the disease is increasing in some parts of the world, thwarting the concept of eradication. Indeed, the World Health Organization now maintains that over 120 million people are affected worldwide.7 The battle is being lost, not only because of interruption to prevention programs by civil strife but also because of the proliferation of breeding sites resulting from inadequate sewerage in the sprawling suburbs of the developing world. Musing on the complexities of tropical disease, we were enjoying our journey across the plateau on the way back to Salisbury when one of the plateau’s residents invaded our cabin. I had no idea the wasp-like insect was a tsetse fly or I might have better understood Gelfand’s eagerness to dispatch it. Alas, the fly was undeterred by his flailings, and dived on his jaw, provoking a physical response almost as quickly as the emotional. The whole side of the Professor’s face reddened and swelled, from ear to mouth and brow to mandible. Fortunately there were no further anaphylactoid reactions, as we had no medicines, but when the Professor announced it was a tsetse fly I really began to worry. I had driven through Mozambique earlier that year and been intrigued by the Portuguese attempts to limit the spread of the fly by disinfecting vehicles in sheds of corrugated iron. Why? To limit the spread of sleeping sickness. Oh my goodness, there was no effective treatment for that disease either, so I watched the Professor all the way back to Salisbury, hoping his drowsiness was not significant. The Professor recovered, and now that I am almost 10 years older than he was then, I really do understand the physiological rather than pathological attributes of an afternoon nap. As I finish writing this reminiscence in Papua New Guinea as a leader of a team of young postgraduates from James Cook University who are as fascinated as I was by the mysteries of tropical medicine, I remember Michael Gelfand with great fondness. I am sure he enjoyed sharing these mysteries with the young as much as I am doing today. 1 Microfilariae of Wuchereria bancrofti Photo courtesy of Wayne Melrose. 2 Life cycle of Wuchereria bancrofti Reproduced with permission from the Centers for Disease Control and Prevention, Atlanta, Ga, USA. 3 Elephantiasis case from the Western Province of Papua New Guinea Photo courtesy of Wayne Melrose.

John S Whitehall FRACP, MRCP(UK), DCH

We present a case of an older patient who sustained dental trauma during a break-and-enter and assault at his home in Broome, Western Australia. Cruelly nicknamed “Fatso” from a young age, our patient was an 80-year-old gentleman who lived on his own in a care facility, in close proximity to individuals in similar circumstances. Despite weighing 800 kg and being 5 metres tall, the patient was able to mobilise on all four limbs, and was self-caring apart from receiving a daily meal service similar to that of “Meals on Wheels”.1 The assailant sat on top of the patient, who bravely fought back by biting the assailant’s knee. This caused damage to the patient’s teeth. He was unable to mount a more vigorous response, as it was a cool night, which rendered him more lethargic than usual. The patient was a vague historian, but there were no noticeable complaints of pain or any behavioural change. Blood tests were not performed because of the difficulty of penetrating the patient’s extremely tough skin. The patient made a remarkably swift and uncomplicated recovery, restarting his normal high-protein (mostly whole-chicken) diet after a brief period of observation. This was in stark contrast to what followed for his assailant, whose history we also briefly present.2 He was taken into clinical custody, where it was discovered that the patient’s tooth had penetrated his knee joint capsule, as well as causing several deep irregular lacerations. The assailant required a prolonged hospital admission after developing fever and septic arthritis. Despite repeated attempts to culture the assailant’s blood and joint aspirates, the cultures did not grow any organisms. To assist in his treatment, the hospital’s Infectious Diseases Department requested swabs from Fatso’s mouth, teeth and tongue to attempt to identify the likely cause of the infection. This was achieved during a home visit, with specially modified swabs (see Box) and a degree of trepidation. The mouth swabs grew Aeromonas hydrophila and Trichosporon asahii, consistent with the predominantly gram-negative and fungal microorganisms expected. The organisms were found to be sensitive to meropenem, vancomycin and ciprofloxacin. These findings were used to tailor the antibiotic therapy for the assailant. The assailant made a slow and difficult recovery, with ongoing fever and joint inflammation. He was transferred to a metropolitan hospital for further treatment. The patient generously cooperating in helping determine effective treatment for his assailant

Samuel J Fitzpatrick MB BS · Amanda L Thomas MB BS(Hons)

The inaugural Australian Otitis Media (OMOZ) workshop, Darwin, 25–26 May 2010, was well timed. The workshop — held in the same month that the Australian Senate tabled its report, Hear us: inquiry into hearing health in Australia1 — brought together 70 of Australia’s leading otitis media (OM) researchers. The workshop reinforced that OM is a major concern in Australia, identified important research advances, and highlighted future research areas and strategies for long-term interventions. As emphasised in the Senate report, findings from conferences on hearing health should be made publicly available. The purpose of our report, therefore, is to share the main findings from the OMOZ workshop with the broader community of OM researchers, health care professionals and policy leaders. Why otitis media mattersOM, or inflammation of the middle ear, is a prevalent and costly disease. The associated fluid accumulation behind the tympanic membrane can lead to pain, tympanic membrane perforation, and hearing impairment. The prevalence of OM in Australian Indigenous children (about 80% by 12 months of age) is among the highest in the world.2 Tympanic membrane perforation rates among Indigenous children (20%) exceed the threshold of 4% that the World Health Organization considers a “massive public health problem requiring immediate action”.3 Conductive hearing loss in Indigenous Australians has been associated with language and speech development delay, poor educational and employment outcomes, and a heightened risk of criminal activity.1 In 2008, the estimated costs of treating OM in Australia ranged from $100 million to $400 million.4 Clinically important advances in otitis media researchDelegates gained insight into important advances from laboratory-based research, environmental and epidemiological studies, intervention programs and clinical trials. It was highlighted that a multidisciplinary approach is required to better understand, prevent and manage OM. Laboratory-based researchResearchers from the University of Western Australia (UWA) and Telethon Institute for Child Health Research (TICHR), Perth, WA, reported that bacteria (particularly non-typeable Haemophilus influenzae and Streptococcus pneumoniae) and respiratory viruses are more commonly found in the nasopharynx of OM-prone children than in healthy children. They also reported that bacteria persist in the middle ear of OM-prone children, both in biofilms and within cells. Such persistence may contribute to the chronic and recurrent nature of OM. Researchers from WA, Queensland and the Northern Territory highlighted the importance of investigating the interactions between bacteria and viruses in the pathogenesis of OM. Delegates acknowledged that further research is needed to determine the clinical significance of Haemophilus haemolyticus, Alloiococcus otitidis and polyoma viruses in OM. Associate Professor Peter Richmond (School of Paediatrics and Child Health, UWA) noted that children vaccinated with pneumococcal conjugate vaccine were protected from life-threatening disease, but cautioned that children who have normal antibody responses may still experience OM. He reasoned that more appropriate assays are required to adequately assess antibody function. Professor Jennelle Kyd (Deputy Vice-Chancellor [Academic and Research], Central Queensland University [CQU], Rockhampton, Qld) emphasised that evaluation of vaccine effectiveness should include measurements of mucosal immunity. Researchers from CQU and the University of Newcastle in New South Wales are using cell culture models to further our understanding of the interactions between external risk factors (eg, cigarette smoke), otopathogens and host immunity. Researchers from CQU have also developed animal models to enhance our understanding of OM pathogenesis, support OM vaccine development and optimise antigen delivery. A study of 1000 non-Indigenous families in WA led by Dr Sarra Jamieson (Division of Genetics and Health, TICHR) demonstrated that immunological genotypes were associated with OM susceptibility. Together, this led to the conclusion that further immunological studies in other populations and settings are warranted. Environmental studies, intervention programs and clinical trialsAssociate Professor Deborah Lehmann (Division of Population Sciences, TICHR) stressed that crowding at home is the strongest predictor of nasopharyngeal carriage of otopathogens in Indigenous children, whereas daycare attendance is the strongest predictor in non-Indigenous children. Delegates agreed with previous assertions that “reducing overcrowding is the key to fighting the disease”.5 Lehmann reported that exposure to environmental tobacco smoke increases the risk of OM 1.6-fold, and that reducing exposure to tobacco smoke could reduce the risk of OM by up to 27%. The link between hygiene and OM generated much discussion. Delegates agreed that further evidence is required to optimise hygiene education and practices in order to improve ear and general health. Such evidence may be forthcoming from an ongoing intervention study (promoting regular ear screening, frequent hand washing and reduced smoke exposure) of Indigenous children in WA. Debra Fernando (Sax Institute, Sydney, NSW) described the Study of Environment on Aboriginal Resilience and Child Health, which is examining ear disease, mental health, housing and environmental factors in urban Indigenous children from NSW. Preliminary findings indicate that over a third of the cohort had some middle ear abnormality detected by otoscopy. Associate Professor Chris Perry (School of Health and Rehabilitation Sciences, University of Queensland, Brisbane, Qld) updated delegates on the Deadly Ears program that involves a team of ear, nose and throat surgeons, audiologists, speech pathologists, nurses and Indigenous health workers. They provide screening, surgery, rehabilitation and educational services to remote Indigenous communities in Queensland. Associate Professor Amanda Leach (Child Health Division, Menzies School of Health Research [Menzies], Darwin, NT) described the PREV-IX_COMBO randomised controlled trial (ACTRN12610000544077; NCT01174849) that will compare the effect of two new pneumococcal conjugate vaccines (Prevenar13 [Wyeth] and Synflorix [GlaxoSmithKline]) and a combination schedule of these vaccines on immunogenicity, nasopharyngeal carriage and OM prevalence in Indigenous infants. Associate Professor Ross Andrews (Child Health Division, Menzies) noted that recruitment for the PneuMum study (NCT00714064) — assessing the effect of maternal pneumococcal vaccination on early-onset OM in Indigenous infants — is nearing completion. As highlighted by Associate Professor Peter Morris (Child Health Division, Menzies), trials such as PREV-IX_COMBO and PneuMum provide data for evidence-based guidelines that can be used to change policy and practice and, ultimately, to improve health outcomes. Research priorities and recommendationsThe OMOZ workshop enabled delegates to identify specific research priorities and recommendations, particularly those involving interagency participation, that could help reduce the burden of OM in Australia (Box). Research prioritiesFurther research into interventions to reduce ear disease in Indigenous communities is urgently required. The manner in which studies are conducted is critical if research is to be sustainable and meaningful to Indigenous communities. Involvement of Indigenous people in research will allow important questions to be addressed and promote research skills within Indigenous communities. Research into ear health in urban Indigenous children is urgently required. Further studies are required to determine whether the incidence of OM can be reduced by modifying risk factors such as hygiene practices, breastfeeding duration, cigarette smoke exposure and household crowding. Diagnostic accuracy is required to ensure appropriate treatment. Laboratory and clinical protocols should be standardised for accurate interpretation and comparison of research findings. Bacterial and viral density and diversity studies are required to help explain the vast difference in risk of OM between Indigenous and non-Indigenous children. RecommendationsResearch that strengthens the evidence for action (and the anticipated health benefits) must be clearly communicated to health care providers, policy leaders and the broader community. OM with tympanic membrane perforation for greater than 2 weeks’ duration must be considered a chronic disease. To reduce the unacceptably high levels of OM in Indigenous children, broader initiatives are required. Interagency collaboration should focus on promoting an agreed set of short-, medium- and long-term strategies. An ear health and hearing taskforce led by Indigenous Australians (supported by researchers, policymakers, clinicians and public health workers) is needed. This taskforce should inform government agencies about options for improving ear health and hearing in Indigenous Australians until the problem of OM is solved. Long-term funding is crucial to enable the conduct of long-term research and intervention studies that are required to address the large and complex problem of OM in both Indigenous and non-Indigenous children. As OM in Indigenous children is often asymptomatic, health care professionals should be encouraged to examine Indigenous children’s ears regularly. Immunisation data from the Australian Childhood Immunisation Register should be made available to facilitate evaluation of vaccine impact through data linkage. An OM research advisory board should be established to communicate research findings that have the greatest potential to influence policy and practice. Researchers should use the EarInfoNet website (http://www.healthinfonet.ecu.edu.au/other-health-conditions/ear) to share research findings with the community, promote standardisation of research methods, raise awareness of research expertise within Australia, and foster collaboration among researchers. We are listening — are you?The inaugural OMOZ workshop was timely and highly successful. It highlighted that OM is a major but unrecognised public health issue in Australia. Researchers are aware of the complexity of the condition, the gaps in knowledge about the pathogens and their interaction with the host, the difficulty of accurate diagnosis, and the challenges of prevention and appropriate treatments. However, they are optimistic that with enhanced awareness and stronger collaborative efforts with health care providers, policy leaders and the community, the burden of OM in Australia can be reduced. We all need to listen ... and take action. Keys to reducing the burden of otitis media (OM) in Australia Prevention — known risk factors for OM must be addressed. The costs and benefits of reducing the risk of severe disease should be quantified. Intervention — defined and evaluable interventions to prevent and treat OM are required. We must establish how, where and when to intervene. Treatment — children at high risk of severe OM should be identified early and treatment options should be enhanced. Investigation — ongoing laboratory research is essential to understand host–pathogen interactions and to develop and evaluate OM treatments and vaccines. Participation — involvement of Indigenous people in prioritisation, implementation and transfer of research is critical to sustainable improvements in ear health. Communication — research findings should be conveyed to the broader community, particularly health care service providers and policy leaders.

Lea-Ann S Kirkham PhD · Selma P Wiertsema PhD · Heidi C Smith-Vaughan PhD · Ruth B Thornton BSc(Hons) · Robyn L Marsh BSc(Hons) · Deborah Lehmann MB BS, MSc · Amanda J Leach BAgSc(Hons), MAgSc, PhD · Peter S Morris MB BS, FRACP, PhD · Peter C Richmond MB BS, FRACP

The Australian Government’s recent decision not to renew federal funding for the Master of Applied Epidemiology (MAE) program at the Australian National University (ANU) puts the nation’s public health response capacity at serious risk. This program has provided the investigative backbone to the Communicable Diseases Network Australia for nearly 20 years. A charitable view is that its disestablishment came about as an administrative accident — collateral damage when Cabinet decided to terminate the much larger Public Health Education and Research Program (PHERP) after a 20-year funding cycle had reached its promised end. Funding for the MAE was rolled into the PHERP quite recently as an administrative convenience, after being supported through a distinct funding stream for most of its life, but the two are in fact very different types of public health activity. Although other PHERP-funded courses are traditional campus-based degree programs, the MAE puts its intake of outstanding health professionals through intensive field apprenticeships as disease detectives. Over 2 years, trainees undertake brief campus-based training blocks, but, for most of their time, they are placed at health agencies around the nation where they are immersed in disease surveillance and outbreak investigations. They serve as a flying squad to respond at short notice to unusual infectious disease events that present potential threats to the population’s health.1 The program has been a bargain for the government, with a budget under $2 million per year (the cost of about six tertiary hospital beds), which meets trainees’ stipends and supports a small team of academic supervisors. Over two decades, 160 MAE trainees have played central roles in stemming the spread of about 200 epidemics, including severe acute respiratory syndrome (SARS), pandemic (H1N1) 2009 influenza, Hendra virus, food-borne infections, and many others. Their work has generated over 500 academic publications, often of national and global public health significance.2-4 The program was originally modelled on the world-renowned Epidemic Intelligence Service at the Centers for Disease Control and Prevention (CDC) in the United States. The Australian MAE has helped spawn equivalent programs in China, India, Indonesia and Malaysia. In addition to serving as a standing national response team during their 2-year apprenticeship, graduates of the MAE program have gone on to become national, and in some cases international, leaders in public health. The employment distribution of 104 non-Indigenous graduates who completed a survey recently is shown in the Box. The MAE has a particular emphasis on supporting Aboriginal and Torres Strait Islander trainees, recognising that the burden of infectious diseases in Australia falls disproportionately on the Indigenous population. Placements have been made in settings that have allowed Aboriginal trainees to work closely with Aboriginal communities. Twenty-seven Aboriginal MAE graduates have gone on to make a unique contribution to several areas of Aboriginal health and have become role models for Aboriginal health research in Australia.5 Thirteen of these have used their training in this program as a portal of entry to PhD candidacy. A review of the program commissioned jointly by the Australian Government and ANU in February 2010 was unequivocal in recommending that it should continue as a key element of Australia’s disease control activity.6 The MAE program was born as a response to the urgent need, recognised during the early years of the HIV epidemic, for Australia to upgrade its national disease intelligence capacity. It was initiated with assistance from the US CDC, and its first Australian Director was the late Professor Aileen Plant, who would be appalled at its disappearance with no apparent replacement in sight. This will leave Australia vulnerable at a time when increasing population movements, changing climate and other pressures increase the likelihood that we will face new pandemics and the re-emergence of old ones.7 Although Australia is now one of few industrialised nations that has no national centre for disease control, the MAE program at least represented one of the essential elements that such a national organisation would provide.1 Infections respect neither state nor national boundaries, and under Australia’s political structure their control can only be achieved through a consistent, coordinated effort by the federal and jurisdictional governments. The ongoing human resource represented by the MAE trainees is a highly cost-effective insurance policy that we cannot risk losing in the challenging times ahead. Non-Indigenous Master of Applied Epidemiology graduates by current employer and type of work, 1991–2010 Employment classification Institution Epidemiologist Other public health Policy advisor Academic Other research Clinician Laboratory Total Federal government 6 — — — — — — 6 State government 22 9 2 — 1 — 1 35 Research institute 11 — — 3 2 — — 16* International health organisation 7 2 2 — 1 — 1 13† Non-government organisation 2 — 2 — — — — 4 Private enterprise — 1 1 — — 2 — 4 Hospital 1 — — — — 5 — 6 University 4 — — 16 — — — 20 Total 53 12 7 19 4 7 2 104‡ — = zero or not applicable. * Eight of the current jobs are at research institutes that provide services to government in communicable disease surveillance. † Ten of the current jobs are with the World Health Organization. ‡ Twenty-nine students did not complete the survey.

Robert M Douglas MD, FRACP, FAFPHM · Fiona J Stanley MD, MSc, FAFPHM · A Rob Moodie MB BS, MPH, FAFPHM · Anthony I Adams MB BS, MPH, FAFPHM · John M Kaldor PhD

We report the first Australian case of treatment of infant botulism with a human botulinum antitoxin developed in the United States by the California Department of Public Health. Our patient’s clinical improvement was rapid, and although the product is expensive, cost-analysis supports the economical viability of its use. In future cases of suspected infant botulism, we recommend that Australian clinicians promptly obtain and administer this antitoxin to their patient. Clinical recordA 5-month-old girl who was fully breastfed presented to the emergency department at a tertiary children’s hospital with poor feeding and lethargy. She was afebrile and mildly dehydrated, with a poor suck and a weak cry. Laboratory testing revealed a normal full blood examination and mild derangement of electrolytes consistent with dehydration. Blood cultures were sterile, and cerebrospinal fluid examination was normal. Formal neurological examination revealed bilateral ptosis, low muscle tone, globally reduced muscle strength and no gag reflex. Deep tendon reflexes were absent, and pupillary reflexes were preserved. Nerve conduction velocities and electromyography were normal. Further history revealed no recent ingestion of honey and no passage of bowel motions for 10 days. She had not received oral polio vaccine and had no history of overseas travel. The patient was transferred to the hospital’s paediatric intensive care unit (PICU), where we established a working diagnosis of infant botulism, pending confirmatory investigations. The patient was electively intubated and ventilated on Day 3 of her hospital admission. Faecal fluid was obtained per rectum for a mouse toxin bioassay. We telephoned the California Department of Public Health’s Infant Botulism Treatment and Prevention Program (IBTPP) in the United States to purchase BabyBIG (botulism immune globulin [intravenous human]) (Massachusetts Public Health Biologic Laboratories and Cangene Corporation, Boston, Mass, USA), which we received 48 hours later. A single infusion of BabyBIG was administered on Day 7 of the child’s admission to hospital, with no adverse consequences. The product cost US$43 500. The diagnosis of infant botulism was confirmed by the mouse bioassay, with growth of toxin B-producing Clostridium botulinum from faeces. The child was extubated on Day 10 of her PICU admission, discharged from the PICU on Day 16, and discharged home on full enteral feeds on Day 24. Follow-up physiotherapy showed gross motor delay with postural weakness, which had resolved by 2 months after discharge. DiscussionThis is the first case of infant botulism in Australia in which BabyBIG has been used (personal communication, Dr Stephen Arnon, Chief, IBTPP, California Department of Public Health, 21 March 2009). While an uncommon disease, Australia has had about one case per year since 1999.1 Infant botulism arises from ingestion of C. botulinum spores and growth of the organism in the gastrointestinal tract, producing botulinum toxin, which binds irreversibly to receptors at the neuromuscular junction, producing flaccid paralysis. Ingestion of honey is a classic risk factor, although frequently no specific source of the infection is found. Intensive supportive care is required until muscular function recovers — a process which takes weeks to months, usually with extended hospitalisation and artificial ventilation. BabyBIG was developed by the California Department of Public Health and registered with the US Food and Drug Administration (FDA).2 The product is derived from serum donations from individuals immunised with pentavalent botulinum toxoid, a vaccine developed by the US military. Purification and preparation of the product is in line with FDA licensing requirements for processing human plasma, including screening of donors and testing plasma for transmissible diseases. The product comes as a lyophilised powder of immunoglobulin G, stabilised with 5% sucrose and 1% human albumin, and contains neutralising antibodies against botulinum toxins A and B. The product has a half-life of about 28 days, and a single infusion is calculated to neutralise all absorbed botulinum toxin for at least 6 months. BabyBIG was initially assessed in a randomised, double-blind, placebo-controlled trial conducted between 1993 and 1997.3 The trial involved 129 Californian infants with botulism, treated on Days 0–3 of hospital admission, and showed significant decreases in duration of ventilation (by 2.6 weeks [P = 0.01]), length of PICU stay (by 3.2 weeks [P < 0.001]), length of hospital stay (from 5.7 weeks down to 2.6 weeks, [P < 0.001]), and mean hospital costs per patient (of US$88 600 [P < 0.0001]). Subsequent open-label, US-wide use of the product on 382 infants showed similar results in the 366 infants who received BabyBIG within 7 days of admission.3 The product was initially only available to infants in North America, but since 2003 has been exported internationally on a case-by-case basis. A subsequent review has shown that only 5% (32) of 681 cases treated with BabyBIG since 2003 have been misdiagnoses, with no adverse events occurring as a consequence of the infusion in any infants.4 Although the cost of the treatment is substantial, evidence has shown the intervention to be economically sound. In our case, a conservative estimate of costs saved just from reduced requirement for intensive care ranged from A$28 000 to A$117 600, based on an estimate of A$4000 per intensive care day. The social and emotional benefits of early discharge and recovery to the child and her family are obvious. In cases of suspected infant botulism, we recommend that Australian intensive care physicians and paediatricians promptly obtain and administer BabyBIG to their patient. All experience to date encourages pre-emptive treatment without waiting for confirmation by diagnostic testing. Despite long distances in sourcing the product, with good communication, this process can provide a timely, safe, effective and cost-saving treatment for infant botulism.

Meryta L A May MB BS, FRACP, FRCPA · Michael A Corkeron MB BS, FANZCA, FCICM · Mark Stretton MB BS, FRACP

To the Editor: As public health professionals, we strongly support Givney’s call for the creation of an Australian national authority for disease prevention and control.1 This proposal is by no means a new one,2 but its relevance has, if anything, increased with time. Such an authority would structure and coordinate responses to emerging disease threats, as well as ensure that Australia has the national public health infrastructure required to coordinate the increasingly complex strategies needed for disease surveillance more generally. Human papillomavirus (HPV) surveillance is a recent case in point. Between 2007 and 2009, Australia delivered what remains the world’s most widely targeted HPV vaccination program, offering free vaccination with quadrivalent HPV vaccine to all girls and women aged 12 to 26 years. Australia’s excellent cancer registries will be able to accurately monitor the anticipated decline in cervical cancer incidence, but it will not occur for decades. In the meantime, we need to track more immediate vaccine impacts, such as the incidence of genital warts, incident Pap smear abnormalities and type-specific HPV infection. Specialist groups are initiating their own studies in these areas, with funding from a combination of government and industry sources, but there is no coordinated system for bringing together the key components of surveillance, and for ensuring that they are properly funded and analysed. The surveillance requirements for an HPV vaccination program are complex because of the multiple outcomes of vaccination, varying time scales over which these outcomes are expected, and the range of stakeholders involved in the fields of immunisation, cancer control and sexual health. No clear ownership or responsibility for comprehensive surveillance is apparent in Australia. In the United States, the Centers for Disease Control and Prevention have taken responsibility for coordinating HPV surveillance,3 and in the United Kingdom efforts are led by the Health Protection Agency, with planning and funding for comprehensive surveillance having been established at the outset of the immunisation program. The creation of an independent, well resourced body that is expert in disease control and prevention will ensure that Australia is best placed to respond to emerging disease threats as well as able to obtain maximum value from the implementation of prevention strategies.

Julia M L Brotherton · John Kaldor · Marion Saville

To the Editor: Givney’s recent letter restated the case for a national centre for disease control.1 His arguments for national planning, and particularly for a non-politicised approach to coordination and modification of responses to public health threats based on evidence, will be welcomed by many. A clear example of the validity of his case is provided by the recent pandemic (H1N1) 2009 influenza. In hindsight, despite certain risk groups being severely affected,2 the 2009 influenza season was generally mild.3,4 However, the public health response, based on the agreed pre-pandemic plans, was personnel-intensive and long-lasting.5 Crucially, there was a need for a well trained, flexible epidemiological workforce to rapidly analyse data to inform any response. Here, we highlight the contributions of Master of Applied Epidemiology (MAE) staff and students to this component of the response. The MAE program has operated as Australia’s only field-based epidemiology training program since 1991. MAE staff and students were enlisted to the response within days of the pandemic alert, as they constitute the only readily available epidemiological capacity in Australia. A survey conducted in February 2010 indicated that between April and December 2009, 18 students and five MAE staff members contributed 1159 person-days (3.2 person-years) to the response at local, state and national levels and internationally in New Zealand and with the World Health Organization. Contributions included establishing and evaluating surveillance systems, data analysis and reporting, training and supervision, rapid assessment and longer-term research projects. Areas covered included: border screening; investigation of clusters of cases related to air arrivals; school, prison and household transmission studies; analysis of state and national data; and establishment of a hospital-based sentinel surveillance system. Research findings have been disseminated widely via government reports, seminars, conference presentations and peer-reviewed publications. During the pandemic, the MAE program provided epidemiological “surge capacity”. This vital technical input to higher-level analysis allowed policy responses to changing evidence, a contribution that needs to be maintained and strengthened if Australia is to respond appropriately to future emerging disease threats. A logical home for a field epidemiology training program such as the MAE would be a national centre for disease control, with strong linkages to one or more academic institutions. We therefore echo Givney’s call for the establishment of an Australian centre, providing independent, evidence-based advice to governments, and incorporating a strong commitment to workforce capacity building and sustainability.

Paul M Kelly · Kamalini Lokuge · Hassan Vally · Alexander S Cameron

Liver abscess due to Klebsiella pneumoniae infection has been widely reported in Asia, but rarely reported in Australia until now. We describe four previously well Asian-born patients who presented across Australia with community-acquired K. pneumoniae liver abscesses. With prompt recognition, appropriate antibiotics and early drainage, outcome is significantly improved, although vigilance for metastatic complications is essential. Clinical recordsDuring 2008 and 2009, four patients (two men, two women) presented around Australia with community-acquired Klebsiella pneumoniae liver abscesses (KPLAs). All four patients were previously well and did not have diabetes. Patients 1, 2 and 3 were Australian residents who were born in Asia and had recently visited there; Patient 4 was visiting from China. All patients presented to hospital after several days of gastrointestinal and other symptoms. Liver abscess was shown on computed tomography scans, and K. pneumoniae infection was diagnosed following culture of abscess fluid or blood. Patients were treated with appropriate antibiotics and pigtail catheters for drainage; Patients 3 and 4 required surgical treatment. Patients 1, 2 and 3 were well at follow-up; Patient 4 returned to China and was lost to follow-up. Patient 3 suffered a recurrence about 10 months after her first presentation, but this was too remote to be clearly attributable to her short course of antibiotics (only 10 days). Box 1 summarises the clinical and microbiological details of the four patients. DiscussionA community-acquired Klebsiella pneumoniae primary invasive liver abscess syndrome has been recognised in Asia for more than 20 years, with almost 1000 reported presentations published by 2008; it has been reported less frequently in other regions.1 K. pneumoniae infection accounted for over 80% of primary liver abscesses reported from Taiwan in the 1990s.2 Increasingly, cases have been seen outside Asia, primarily among patients of Asian ethnicity, including in the United States.1,3 It has only rarely been reported in Australia until now.4,5 Of interest are an absence of prior hepatobiliary disease, an association with diabetes, and a risk of metastatic spread.6 Community-acquired KPLA has been associated with severe metastatic complications, including endophthalmitis. The reasons for the changing epidemiology away from Escherichia coli as the leading cause of pyogenic liver abscess are unclear, although selective pressure for Klebsiella through widespread amoxicillin use, to which it is almost universally resistant, has been postulated.7 A genetic predisposition is possible, given the disease is seen almost exclusively in patients of Asian ethnicity, even outside Asia, and very rarely in those of Caucasian origin.8,9 K. pneumoniae is frequently found as part of normal faecal flora, and spread to the liver is thought to occur from the intestines via the portal system.1 Ordinarily, any bacteria reaching the liver would then be phagocytosed and killed, and failure of this defence is presumed to lead to the formation of liver abscesses.1 Diabetes was present in about 50%–70% of patients reported from Taiwan,6 presumably conferring susceptibility by impairing neutrophil-mediated defence,10 and this also appears to be a risk factor for metastatic complications.6 It is interesting to note that none of the patients in our small sample had diabetes. Bacterial virulence is also of major importance, as the condition often affects previously healthy individuals. The presence of capsular polysaccharides of K. pneumoniae serotype K1 or K2 has been strongly associated with virulence through resistance to phagocytosis;10,11 our patients were all infected with one of these two serotypes. Commonly, K. pneumoniae strains causing liver abscess are hypermucoviscous, as defined by an unusual, highly mucoid colony appearance on culture, a feature strongly associated with the K1 or K2 serotype.11 This stickiness is the basis of the “string test”, which can be performed easily in the laboratory. The string test is a quick, useful investigation in this setting (Box 3).7 A colony that stretches more than 5 mm using a standard inoculation loop tests positive for hypermucovisosity.3 The geographical distribution of KPLA may be explained by the finding that K. pneumoniae isolates from Taiwan were far more likely to have a hypermucoviscous phenotype and to belong to K1 or K2 serotypes than those in other countries except South Africa, where invasive disease is also seen.12 Indeed, of the many K. pneumoniae capsular serotypes isolated from patients in an Australian tertiary hospital inpatient setting, K1 and K2 accounted for only 10 of 293 (3.5%) presentations.13 All our patients had recently been in Asia, which raises the possibility of exposure to these virulent strains of the organism. However, case reports from the US have involved emigrants from Vietnam and Korea who had not travelled home for some years.1 A third-generation cephalosporin such as ceftriaxone is usually an effective treatment, with good penetration of vitreous fluid and cerebrospinal fluid, allowing it to reach metastatic lesions in these locations.12 In the case of endophthalmitis, systemic antibiotics should be combined with intravitreal injections. Treatment is required until clinical state, biochemistry and radiology indicate resolution, often requiring antibiotics for 4 to 6 weeks. Another mainstay of therapy is computed tomography- or ultrasound-guided percutaneous abscess drainage. Surgical drainage may be necessary when percutaneous techniques have failed, as was seen in our Patients 3 and 4. Metastatic spread not uncommonly complicates KPLA; reports from Taiwan estimate the frequency of this at between 3.5% and 20%.12,14 Endophthalmitis, lung abscesses and meningitis are the more common complications. Ophthalmological and other organ review is therefore indicated when KPLA is diagnosed. Visual recovery in patients with endophthalmitis is often poor; a high index of suspicion and early intervention before visual changes are noted may improve outcome. Response to antibiotics and drainage is generally good. In contrast with patients with underlying biliary tract disease, long-term recurrence rates in patients with spontaneously occurring liver abscess appear to be low.15 Given the emerging global trend of K. pneumoniae liver abscesses, Australian clinicians should be mindful of this condition, particularly, but not exclusively, in patients of Asian origin with abdominal infection or whose cultures reveal this organism. In this setting, a hypermucoviscous isolate of K. pneumoniae may belong to serotype K1 or K2, and be associated with metastatic infection, particularly endophthalmitis, lung abscess and meningitis. 1 Clinical and microbiological details of four patients with community-acquired Klebsiella pneumoniae liver abscesses Patient 1 Patient 2 Patient 3 Patient 4 Year, state of presentation 2008, Victoria 2008, Victoria March 2008, Western Australia; Jan 2009, South Australia 2009, Northern Territory Demographics M; 33 y; Filipino-born; Victorian resident for 2 y F; 52 y; Malaysian-born; long-term Victorian resident F; 67 y; Malaysian-born; long-term SA resident M; 52 y; Chinese cargo ship sailor, passing through the NT Recent travel/contacts Lived with Filipino friends. Trip to Middle East via India 1 month prior Trip to Malaysia 6 weeks prior Trip to Malaysia between presentations Visiting from China Features on presentation 2 days of vomiting, myalgias, fevers and rigors; hypotension, mild epigastric tenderness, RUQ tenderness Several days of aches, rigors, diarrhoea; hypotensive, febrile 2008: 3 days of epigastric pain, low-grade fevers; 2009: 5 days of malaise, vomiting, RUQ pain 5 days of fever, jaundice, RUQ pain Notable investigations First abdominal U/S normal; CT of abdomen: 5 cm septate liver lesion (Box 2) Abdominal U/S: 9 cm multiloculated liver abscess; confirmed on CT of abdomen 2008: CT of abdomen: 3 cm liver lesion, near-resolved after 2 months; 2009: CT of abdomen: 6 cm liver abscess, progressed to 7.5 cm with central necrosis 1 week later CT abdomen: 8 cm multiloculated lesion Microbiology K. pneumoniae cultured on three sets of BC and abscess fluid; string test positive (Box 3) Resistant to ampicillin; sensitive to amoxicillin/clavulanic acid, ciprofloxacin, gentamicin K. pneumoniae BC and abscess fluid Resistant to ampicillin; sensitive to amoxicillin/clavulanic acid, ciprofloxacin, gentamicin 2008 and 2009: K. pneumoniae BC Resistant to ampicillin; sensitive to amoxicillin/clavulanic acid, cephazolin, ceftriaxone, gentamicin K. pneumoniae abscess fluid Resistant to ampicillin; sensitive to amoxicillin/clavulanic acid, cephazolin, ceftriaxone, gentamicin Serotype K1 K1 2008: isolate not serotyped; 2009: K2 K2 Drain/surgery Pigtail catheter Pigtail catheter 2008: no drainage; 2009: pigtail catheter then laparotomy for ongoing sepsis, with drainage of abscess and cholecystectomy Pigtail catheter, then laparotomy and chest drain Antibiotics Rationalised to ceftriaxone for 2 weeks; discharged on oral amoxicillin/clavulanic acid for 2 months Rationalised to ceftriaxone for 1 month; discharged on oral cotrimoxazole for 11 weeks (rash with ciprofloxacin) 2008: 1 week ceftriaxone then 5 days of amoxicillin/clavulanic acid; 2009: 3 weeks ceftriaxone then 1 week amoxicillin/clavulanic acid Initially timentin for 2 weeks; discharged on oral ciprofloxacin for at least 1 month Complications Brief acute renal impairment (creatinine to 180 μmol/L); 24 hours of septic shock requiring ICU 24 hours of septic shock requiring ICU 2009: 48 hours of septic shock requiring ICU Rupture through liver capsule and subphrenic collection and empyema, requiring laparotomy and chest drain BC = blood culture. CT = computed tomography. ICU = intensive care unit. RUQ = right upper quadrant. U/S = ultrasound. 2 Abdominal computed tomography scan showing a 5 cm abscess (arrow) in the right lobe of the liver in Patient 1 3 String test of a Klebsiella pneumoniae isolate demonstrating hypermucoviscosity Photo: Adam Jenney

James R Anstey MB BS · Timothy N Fazio · David L Gordon FRACP, FRCPA, PhD · Geoff Hogg BM BS, FRACP, FRCPA · Adam W Jenney MB BS, FRACP, PhD · Matthias Maiwald MD, FRCPA, D(ABMM) · Jonathan J Wilksch BSc(Hons)

Aim: Design, setting and participants: Retrospective observational study of patients who were tested for influenza A after being admitted to hospital through emergency departments of the Sydney South West Area Health Service from 15 June to 30 August 2009.Main outcome measures: The association of factors such as age, diagnosis at admission, hospital and week of admission with rates of testing and detection of influenza A.Results: 17 681 patients were admitted through nine emergency departments; 1344 (7.6%) were tested for influenza A, of whom 356 (26.5%) tested positive for pandemic influenza. Testing rates were highest in 0–4-year-old children, in the peak period of the outbreak, and in patients presenting with a febrile or respiratory illness. Positive influenza test results were common across a range of diagnoses, but occurred most frequently in children aged 10–14 years (64.3%) and in patients with a diagnosis at admission of influenza-like illness (59.1%). Using multivariate logistic regression, patients with a diagnosis at admission of fever or a respiratory illness at admission were most likely to be tested (odds ratios [ORs], 15 [95% CI, 11–21] and 17 [95% CI, 15–19], respectively). These diagnoses were stronger predictors of influenza testing than the peak testing week (Week 4; OR, 7.0 [95% CI, 3.8–13]) or any age group. However, diagnosis at admission and age were significant but weak predictors of a positive test result, and the strongest predictor of a positive test result was the peak epidemic week (Week 3; OR, 120 [95% CI, 27–490]).Conclusion: The strongest predictor of a clinician’s decision to test for influenza was the diagnosis at admission, but the strongest predictor of a positive test was the week of admission. A rational approach to influenza testing for patients who are admitted to hospital for acute care could include active tracking of influenza testing and detection rates, testing patients with a strong indication for antiviral treatment, and admitting only those who test negative to “clean” wards during the peak of an outbreak.

Andrew Jardine PhD, MAE · Stephen J Conaty MB BS, MPH, FAFPHM · Michelle A Cretikos MPH, PhD, FAFPHM · Wei-Yuen Su MB BS · Iain B Gosbell MD, FRACP, FRCPA · Sebastiaan J van Hal MB ChB, FRACP, FRCPA

To the Editor: Nelson and colleagues1 referred to the limited community data from the Melbourne Medical Deputising Service (MMDS) that was analysed by Carville et al.2 MMDS consultations also represent general practice consultations, although the majority of MMDS consultations occur after hours. We can now provide an update on MMDS consultations from January 1998 to June 2010, stratified by age. De-identified data were extracted from the MMDS database for diagnoses that included the terms “chicken pox” or “varicella” and “shingles” or “zoster”, and patient age. Using the total consultations as the denominator, we calculated the crude and age-specific rates of varicella (chickenpox) and herpes zoster (HZ [shingles]) per 1000 consultations by week, and present the results here by year. These updated data support the conclusions reached by both groups of researchers that there has been a decrease in varicella cases and a rise in HZ cases in Australian general practice consultations since the introduction of a varicella vaccine in 2000. We had previously shown a decrease in hospitalisations and MMDS consultations for varicella and an uncertain effect on HZ up to 2007 after the introduction of varicella vaccine.2 The overall rate of varicella-related MMDS consultations continued to decline from 2007 to 2010, with an annual average rate of 3.3/1000 consultations in 2000 decreasing to 1.5/1000 consultations in 2007 (P < 0.001, 2000–2007) and to 1.0/1000 consultations for the first half of 2010 (P = 0.043, 2007–2010). Decreasing rates of varicella-related consultation were seen in all age groups, although an apparent increase in the consultation rate for children aged less than 5 years in 2010 might be explained by a summer peak in varicella infection and incomplete annual data (Box 1).3 The trend in HZ-related MMDS consultations showed an increase in the annual average rate from 1.7/1000 consultations in 2000 to 2.7/1000 consultations in 2007 (P < 0.001, 2000–2007) and to 3.4/1000 consultations for the first half of 2010 (P = 0.020, 2007–2010). There was a substantial increase in the HZ-related consultation rates for people aged 70–79 years and 80+ years (Box 2). Our updated data support the recommendation for adding vaccination against HZ to the vaccine schedule for older Australians,1 although the optimal age at which this should occur remains to be determined. 1 Varicella (chickenpox)-related consultation rates, by age group, 1998 to June 2010* * Data from the Melbourne Medical Deputising Service database. 2 Herpes zoster (HZ [shingles])-related consultation rates, by age group, 1998 to June 2010* * Data from the Melbourne Medical Deputising Service database.

Kristina A Grant · Kylie S Carville · Heath A Kelly

To the Editor: We read with interest the article by Seed and colleagues1 about the collection and distribution of blood from two donors diagnosed with Plasmodium vivax malaria following travel to Papua New Guinea (PNG). Although the potentially infectious blood components were recalled before transfusion, this case underscores the complexity of managing the risk of transfusion-transmitted malaria (TTM). Three points in particular are worth noting. First, the donors were asymptomatically harbouring infection at donation following routine foreign travel. (Between 1963 and 1999 in the United States, only one donor was implicated in TTM following routine travel, compared with more than 30 donors with lengthy residence in Sub-Saharan Africa.2) Second, both donors acquired malaria despite observing Australian guidelines for chemoprophylaxis. Finally, both were non-reactive on the enzyme immunoassay (EIA) used to screen their donations (Malaria EIA, NewLabs, Newmarket, United Kingdom) after intervals of 4 and 13 months between return from PNG and their donations. Interestingly, chemoprophylaxis for these donors was both the cause and a potential solution for the “near-miss” event. The primary prophylactic regimens used were sufficient to modify the primary infection such that antibody response to the blood-stage antigens, on which the EIA is based, occurred only after relapse months later. Had the donors taken primaquine following their travel, the parasitaemia triggered by the hepatic hypnozoite forms that characterize P. vivax infections might well have been prevented. Although primaquine is not universally recommended for terminal prophylaxis, it is consensually recommended for terminal prophylaxis for travellers who have had “intense” or “significant” exposure to P. vivax or Plasmodium ovale, such as PNG would offer.3 Seed and colleagues suggest the need for an exception to blood service management practices for donors who have recently visited a geographic area with distinct epidemiological risk for malaria. Noting the disproportionate risk associated with travel to PNG, they suggest excluding donors with a history of recent visits to PNG from routine testing for malaria (and excluding their donations from fresh component production for an appropriate period). In the United States, regulators are similarly considering carving out an exception for travellers to Mexico,4 a low-risk country where the areas associated with most (approximately 75%) malaria deferrals report near-zero malaria risk (our unpublished data). US data suggest that more than 45 000 donors will be recovered annually if the Mexican state of Quintana Roo is exempted from the deferral requirements, and regulators are weighing this benefit against the exquisitely low added risk. The outcome of this deliberation is pending, but the fact that risk gradients within a given risk category are prompting consideration of differentiated management in two countries is notable.

Bryan R Spencer · Louis M Katz

To the Editor: Children have been seen as a key priority group for pandemic (H1N1) 2009 influenza (“swine flu”) vaccination. In Australia and New Zealand, children aged 0–4 years had the highest population rate of intensive care unit admissions for swine flu.1 From 3 December 2009, the Australian Government provided free H1N1-specific influenza vaccine for all Australians aged 6 months and older. However, it was not known how parents and other caregivers would respond to the offer of vaccination. We sought to determine caregivers’ intentions regarding whether their child would receive the pandemic vaccine. The study was approved by the human research ethics committee of the Children’s Hospital at Westmead and was conducted in November and December 2009, immediately before, and alongside, the commencement of the pandemic vaccination program for children. A paper-based questionnaire (with an alternative web-based option) was sent to caregivers of children aged 6 months to 5 years who were attending 16 long-day-care centres across metropolitan Sydney. It included questions about attitudes, behaviour, intentions and beliefs regarding swine flu, seasonal influenza and vaccines. We analysed responses using SPSS, version 17 (SPSS Inc, Chicago, Ill, USA) and conducted univariate analysis (as factors had high collinearity) to search for factors associated with caregivers’ intention for their child to receive the pandemic vaccine. The response rate was 44% (431/972). Most respondents had families of two children (47%) or one child (41%); 90% were mothers; and 48% had a postgraduate education. Caregivers were asked to report in relation to their eldest child attending the day-care centre (mean age, 38 months). Three children (out of 427 responses; 0.7%) had already received the pandemic vaccine; 23% of caregivers (92/400) said they would have their child vaccinated; 54% (217/400) were unsure; and 22% (87/400) would not. Intentions regarding seasonal influenza vaccination were similar. Factors associated with caregivers’ intention to have their child vaccinated with pandemic vaccine are shown in the Box. Those with the strongest associations included caregivers’ intention to have their child vaccinated against seasonal influenza in 2010 and belief that seasonal influenza vaccine is completely safe or only a slight risk. Factors not significantly associated with respondents’ intention to have their child vaccinated with the pandemic vaccine were the respondent’s age group, sex, education level, language spoken at home, and number of children in the household. The study indicated that at the commencement of the Australian pandemic influenza vaccination program for children, there was significant uncertainty among this sample of relatively highly educated respondents. The proportion of respondents intending to have their children vaccinated was far lower than recent Australian estimates (6% of children aged 4 years and under).2 Our findings suggest that, despite the acknowledged severity of pandemic influenza, respondents’ concerns about vaccine safety were influencing their intentions. Indeed, the program commenced in a context of public debate about the response to the influenza pandemic and the vaccination program, including concerns about the safety of using multi-dose vials for vaccine delivery.3,4 Among respondents intending for their child to have the pandemic vaccine, the association with the child having had a previous influenza vaccination suggests that, having once taken up vaccination, respondents were more likely to intend to do so again. More recent events in Australia leading to suspension of use of all three 2010 seasonal influenza vaccines for children under 5 years of age are likely to further increase safety concerns.5 While two vaccines have since been reinstated, these events present a significant challenge for future influenza vaccination programs. Providers are likely to have an important role in communicating recommendations and addressing caregivers’ concerns. Factors associated with caregivers’ intentions for their child to receive the pandemic (H1N1) 2009 influenza vaccine Survey responses Intention “yes” (n = 92) Number OR (95% CI) Would you have your child vaccinated against seasonal flu in 2010? (n = 396) No 8 1.00 Unsure 33 2.29* (1.11–5.15) Yes 51 17.49* (7.55–40.50) How safe do you think the seasonal flu vaccine is for children aged 1 to 5 years? (n = 396) Moderate/high risk 7 1.00 Don’t know 19 2.04 (0.82–5.07) Completely safe/slight risk 66 6.64* (3.00–15.22) How safe do you think the seasonal flu vaccine is for babies aged 6 to 11 months? (n = 395) Moderate/high risk 21 1.00 Don’t know 36 1.35 (0.75–2.44) Completely safe/slight risk 35 4.32* (2.27–8.22) Did your child receive seasonal flu vaccination in 2009? (n = 394) No 77 1.00 Yes 15 3.48* (1.65–7.36) How concerned do you feel about your child catching the flu? (n = 396) Not at all/ a little/ moderately 31 1.00 Very/extremely 61 2.46* (1.46–4.17) Does your child have any medical conditions requiring ongoing visits to a health care professional? (n = 396) No 76 1.00 Yes 16 2.00† (1.03–3.87) The flu vaccine can give you the flu. (n = 396) Agree 24 1.00 Don’t know 23 1.18 (0.62–2.23) Disagree 45 1.82† (1.04–3.20) OR = odds ratio. * P ≤ 0.01. † P ≤ 0.05.

Julie Leask · Maria Yui Kwan Chow · Catherine King · Robert Booy

Objective: To compare trends in invasive pneumococcal disease (IPD) in non-Indigenous people in north Queensland before and after the introduction of funded pneumococcal vaccines, and to examine the proportion of cases that occurred after vaccine roll-out that could be vaccine-preventable.Design, setting and participants: In 2005, a 7-valent pneumococcal conjugate vaccine (7vPCV) for non-Indigenous children and a 23-valent pneumococcal polysaccharide vaccine (23vPPV) for non-Indigenous adults aged ≥ 65 years were made freely available. Trends in IPD in the non-Indigenous estimated resident population in north Queensland (about 581 850 in 2006) were compared between the 4 years before (2001–2004) and after (2006–2009) the vaccines were rolled out.Main outcome measures: Incidences and serotypes of IPD in non-Indigenous people.Results: After the introduction of the vaccines, there were significant declines for all ages in the average annual incidence of IPD (− 34%; P < 0.05) and 7vPCV serotype IPD (− 77%; P < 0.05). In children aged < 5 years, there was a 91% decline in the incidence of 7vPCV serotype IPD (P < 0.05); in adults aged 15–64 years and ≥ 65 years there were 62% and 77% declines, respectively, in 7vPCV and 23vPPV common-serotype IPD (P < 0.05). There was a 188% increase in 23vPPV-only serotype IPD in adults aged 15–64 years (P < 0.05), whereas there was no significant change in adults aged ≥ 65 years. Serotype 19A was the most frequently identified serotype in 2006–2009, causing 19% of all IPD in those 4 years.Conclusions: There is circumstantial evidence that 7vPCV has had a powerful indirect effect in preventing IPD in adults in north Queensland; 23vPPV may have had a direct effect in adults aged ≥ 65 years. It is likely that with combined direct and indirect effects, newer conjugate vaccines could prevent more IPD than could be prevented with the two current vaccines.

Jeffrey N Hanna MPH, FAFPHM · Jan L Humphreys RN · Denise M Murphy DipMedTech · Helen V Smith GradDipPH, BApplSci, MASM

Objective: Design, setting and participants: Vaccination data for Western Australians aged 10 years and older were obtained from two sources: the WA Pandemic Influenza Vaccination Database (PIVD; which collected reports of pandemic influenza vaccinations from vaccination providers statewide) for the period 30 September 2009 to 31 January 2010, and the WA Health and Wellbeing Surveillance System (HWSS; a continuous population-based telephone survey) for the period 1 December 2009 to 31 January 2010. Data from the PIVD was used to impute vaccination coverage estimates for at-risk subpopulations not assessed in the HWSS interviews.Main outcome measures: Vaccination coverage of Western Australians aged 10 years and older and of subgroups targeted by the national pandemic (H1N1) 2009 influenza vaccination campaign.Results: A total of 171 789 pandemic influenza vaccinations were reported to the PIVD by 31 January 2010 and 88% of these were administered by 1 December 2009. Based on HWSS data, vaccination coverage of persons aged 10 years and older was 14.5% (95% CI, 12.6%–16.6%) and of persons aged 18 years and older was 15.3% (95% CI, 13.3%–17.6%). Based on PIVD data, coverage in adults ranged from 10.3% in pregnant women to 52.8% in health care workers.Conclusions: Our estimate of pandemic influenza vaccination coverage in the adult population of WA is comparable to the national estimate of 19%, but it did not reach levels considered sufficient to interrupt community transmission. Future influenza vaccination programs should target groups at increased risk of severe influenza, such as pregnant women.

Donna B Mak MB BS, MPH, FAFPHM · Alison M Daly BA(Hons), BA(Ed) · Paul K Armstrong MBBS, MAE, FRACP · Paul V Effler MD, MPH, FAFPHM

Objective: Design, setting and participants: Cross-sectional study of consecutive patients attending the Joondalup Health Campus public antenatal clinics in WA in January 2010.Intervention: Audit of uptake of the H1N1-specific vaccine.Main outcome measures: Rate of H1N1-specific vaccination, and reasons for not being the vaccinated.Results: 479 of 541 women who attended the clinics (88.5%) were included in the audit. Three women had been infected with pandemic influenza in the preceding influenza season, leaving 476 women who were eligible for vaccination in pregnancy. Of these 476 women, only 33 (6.9%) had been vaccinated. Of the remaining 443 women who were eligible to receive the vaccine but had not been vaccinated, 63.9% had not been offered vaccination despite multiple visits to their general practitioners during pregnancy, 19.6% had been advised by their GPs against vaccination in pregnancy, and 61.6% stated that they would decline vaccination if offered because of safety concerns.Conclusions: Uptake of H1N1-specific influenza vaccine in pregnant women was poor. Reasons for this relate both to vaccination not being offered to or actively sought by the women, as well as concerns — of both the women and their GPs — about vaccine safety in pregnancy. Uptake in this setting may improve if vaccination is offered through public antenatal clinics with concurrent safety education for obstetricians and vaccination providers.

Scott W White MB BS · Rodney W Petersen MB BS, MBA, FRANZCOG · Julie A Quinlivan MB BS, PhD, FRANZCOG

Clinical records Patient 1 A 59-year-old man infected with HIV presented to hospital with sudden onset of tinnitus, vertigo and hearing loss in his right ear. An audiogram showed moderate bilateral sensorineural hearing loss, which was worse on the right. A magnetic resonance imaging scan of his brain showed no abnormalities. He was diagnosed with Meniere’s disease and managed symptomatically. Symptoms worsened over the following months, and he was reviewed in the neurology and ear, nose and throat (ENT) clinics of another tertiary hospital. Both clinics agreed with the diagnosis of Meniere’s disease. Serological tests for syphilis were performed 12 months after symptom onset. The rapid plasma reagin (RPR) and Treponema pallidum particle agglutination (TPPA) test results were reactive, with the RPR test showing a titre of 1:128. Cerebrospinal fluid (CSF) examination showed a mild lymphocytic pleocytosis and a reactive TPPA test result but a negative RPR test result (Box 1). A diagnosis of otosyphilis was made and the patient was treated with intravenous benzylpenicillin 2.4 million units 4 hourly and oral probenecid 2 g daily for 2 weeks, followed by three doses of weekly benzathine penicillin 2.4 million units intramuscularly. His symptoms stabilised but did not improve. Patient 2 A 30-year-old man infected with HIV presented to an HIV clinic having had tinnitus, hearing loss and imbalance for 3 months. He was referred to ENT clinics in two tertiary hospitals, both of which diagnosed Meniere’s disease. Audiological tests showed mild right sensorineural hearing loss. Serum RPR and TPPA test results were reactive, with an RPR titre of 1:516. CSF examination showed a mildly elevated protein level, but no other abnormalities (Box 1). A diagnosis of otosyphilis was made, and the patient was treated for 2 weeks with benzylpenicillin 2.4 million units 4 hourly. His symptoms resolved completely, and an audiogram performed 6 months after treatment showed that his hearing had returned to normal. The recent increase in early syphilis infections in Australia has been accompanied by the re-emergence of disease manifestations unfamiliar to modern clinicians. Otosyphilis is a rare cause of sensorineural hearing loss and dizziness, and is important for clinicians to consider because the hearing loss is potentially reversible with early diagnosis and treatment. We report two cases of otosyphilis occurring in patients infected with HIV. In both cases, the diagnosis of otosyphilis was initially missed, despite review by several specialist medical units. Cochleovestibular dysfunction is a well described complication of congenital and acquired syphilis. In acquired syphilis, it can occur at any stage of infection. In the pre-penicillin era, hearing loss was reported in 17% of patients with early latent infection and in 80% with symptomatic neurosyphilis.1 Cochleovestibular symptoms of neurosyphilis can occur via two main mechanisms. First, the eighth cranial nerve may be affected, for example in acute syphilitic meningitis. In these situations, hearing loss is usually accompanied by other neurological deficits, and findings on cerebrospinal fluid (CSF) examination will usually be abnormal. Second, and more commonly, hearing loss and vestibular symptoms present without features of coexisting neurosyphilis. These symptoms may occur at any stage of syphilis and are thought to result from direct damage to the vestibulocochlear apparatus. During dissemination, spirochaetes invade the inner ear perilymph, leading to inflammation of the labyrinthine structures and otic capsule. CSF parameters are usually found to be normal but, histologically, fibrosis and ischaemic necrosis of labyrinthine structures are seen2 and endolymphatic hydrops is common. These pathological findings are identical to those of Meniere’s disease, explaining the similar clinical features. Symptoms may be sudden or insidious in onset, and include bilateral (but often asymmetrical) sensorineural hearing loss, tinnitus and vestibular symptoms ranging from dizziness to severe vertigo. These symptoms closely resemble those of Meniere’s disease. Audiological testing shows sensorineural hearing loss, classically affecting low or high frequencies while sparing middle frequencies, and speech discrimination is poor. Without treatment, otosyphilis will progress to profound deafness over months to years. Symptoms can fluctuate markedly over time, but the overall course is one of deterioration.3 There is no established case definition for otosyphilis, but the diagnosis should be made on the basis of a typical clinical presentation and positive serological test results for syphilis. This approach is purposely “over inclusive”, as otosyphilis is a potentially reversible cause of hearing loss. The optimal treatment for otosyphilis is not established. The published literature is limited, consisting of case reports and small case series, but indicates that intravenous therapy is required. Intramuscular penicillin penetrates the perilymph poorly, and there are numerous reports of treatment failure when patients with otosyphilis are treated with penicillin regimens for latent syphilis. In one report, spirochaetes were recovered directly from a patient’s perilymph after treatment.4 Intravenous penicillin G at a dose of 18–24 million units per day, administered as 3–4 million units every 4 hours for 14 days, is the regimen recommended by the United States Centers for Disease Control and Prevention for treatment of otosyphilis. Probenecid is sometimes added, as are subsequent courses of intramuscular or intravenous penicillin.5 There is no high-level evidence to support any of these approaches. Steroids are commonly coadministered, although there are few supporting clinical data. The rationale is that inflammation of the endolymphatic duct appears crucial to the pathogenesis of otosyphilis. A typical steroid treatment regimen is prednisolone at a dose of 0.5–1.0 mg/kg tapered over 1–2 months. Regardless of the penicillin regimen used or whether steroids are employed, treatment outcomes are uniformly poor. Studies consistently show that auditory symptoms abate for only 30% of patients, while 7%–15% have improved results in audiological or speech discrimination tests. Tinnitus and dizziness have better outcomes, with 70%–80% of patients reporting improvement. Factors associated with better outcomes include duration of symptoms less than 5 years, age less than 60 years and fluctuating hearing loss.6 Both of these patients had HIV infection. Rates of syphilis are known to be substantially higher in the HIV-positive population.7 Otosyphilis has previously been described in patients infected with HIV, but relevant published literature is sparse. Patients co-infected with HIV and syphilis appear no different to HIV-negative patients in their clinical features, severity of disease or likelihood of developing this manifestation of syphilis. In both of the cases we report, the diagnosis of otosyphilis was missed despite review by several specialist medical units. In the past few years, rates of early syphilis have risen markedly in Australia, predominantly among homosexual men.8 Relevant practitioners should be aware of this diagnosis in patients presenting with the symptoms described here, especially those at risk of syphilis, such as sexually active homosexual men, including those with HIV infection. Current guidelines recommend syphilis screening in sexually active homosexual men at least annually (up to every 3 months in those at higher risk) and at regular intervals in individuals infected with HIV.9 1 Cerebrospinal fluid and serological test results for two patients with HIV and otosyphilis Patient 1 Patient 2 Cerebrospinal fluid Appearance Clear, colourless Clear, colourless White cell count (× 106/L) 1 polymorph 8 lymphocytes 0 polymorphs 1 lymphocyte Red cell count (× 106/L) 0 0 Protein (g/L) (reference range, 0.15–0.45 g/L) 0.52 0.7 Glucose (mmol/L) (reference range, 2.5–5 mmol/L) 2.7 2.7 Microbiological culture and sensitivity Nil Nil Treponema pallidum DNA polymerase chain reaction test Not detected Not detected Serum Rapid plasma reagin (titre) Reactive (1:128) Reactive (1:516) T. pallidum particle agglutination Reactive Reactive Lessons from practice Consider the possibility of otosyphilis in any patient (especially those with HIV infection or at risk of syphilis and/or HIV infection) presenting with auditory symptoms, particularly sensorineural hearing loss with tinnitus and vestibular dysfunction. Positive serological test results for syphilis will establish the diagnosis. All sexually active men who have sex with men should be screened for syphilis at regular intervals. Otosyphilis must be treated with intravenous penicillin regardless of findings of cerebrospinal fluid testing.

Janet M Pasricha MB BS(Hons) · Tim R Read MB BS, FAChSHM · Alan C Street MB BS, FRACP

To the Editor: We report a case of measles in a 24-year-old man who returned from the Fédération Internationale de Football Association (FIFA) World Cup in South Africa in July 2010. Despite Australian health alerts about measles in South Africa,1 the patient had received no pretravel medical advice or vaccinations. Six days after returning home to the Northern Territory, the patient developed fever, headache and myalgia. The following day he developed vomiting, diarrhoea, and productive cough, with a widespread rash appearing the subsequent day. He visited two general practitioners, was prescribed doxycycline and then admitted to hospital on Day 6 of his illness. On examination, his temperature was 38.9ºC; pulse, 112 beats per minute; blood pressure, 133/72 mmHg; and oxygen saturation, 96% on room air. He had conjunctivitis, a widespread blanching maculopapular rash involving his face, trunk, limbs, hands and feet (Box) and cervical lymphadenopathy. He had bilateral basal lung crackles and tender hepatomegaly. Investigations showed thrombocytopenia (platelet count, 148 × 109/L; reference range, 150–450 × 109/L); hyponatraemia (sodium concentration, 131 mmol/L; reference range, 132–142 mmol/L); and abnormal liver function test results (alanine transaminase concentration, 417 U/L [reference range, < 40 U/L]; alkaline phosphatase concentration, 236 U/L [reference range, 39–117 U/L]). His chest x-ray was normal. The following day, measles virus RNA was detected from a throat swab, and the patient was put into respiratory isolation and therapy with doxycycline ceased. He made a full recovery. The patient reported receiving childhood vaccinations, and while he thought he may have received one measles, mumps and rubella vaccination, he had not had two. Follow-up was required for 84 identified contacts, with no measles cases subsequently notified in the NT. The FIFA World Cup is the world’s largest single-sport event, with an attendance this year of over 3 million people. Mass gatherings may be associated with outbreaks of communicable diseases such as meningococcal disease, measles and pandemic (H1N1) 2009 influenza, in addition to an increased risk of sexually transmitted diseases.2 These risks should be considered when seeing patients who have travelled to such events, in addition to country-specific health risks. Recent data from the GeoSentinal surveillance network showed that a systemic febrile illness was the most common presenting syndrome among travellers returning from South Africa. Most of these cases of illness (54.5%) were due to spotted fever group rickettsiosis.3 The risk of acquiring rickettsiosis increases among travellers visiting game parks, with an incidence of African tick bite fever (Rickettsia africae) among short-term safari tourists of 4.0%–5.3%.4 Measles has rarely been reported in travellers returning from South Africa,2 but the country is in the midst of a measles epidemic, with 17 354 confirmed cases between January 2009 and 12 August 2010.5 Measles presents with fever, cough, rhinorrhoea and conjunctivitis, followed by a widespread rash. The incubation period is usually 7–10 days, but may be up to 18 days. The virus is highly infectious, from 5 days before to 4 days after the onset of rash. Young adults from non-endemic countries such as Australia are at particular risk, as they may only have had one childhood vaccination for measles, with consequent inadequate protection. Although measles has been eliminated in Australia,6 sporadic outbreaks continue to occur,7 and travellers returning from overseas create an ongoing potential for the re-establishment of endemic measles. Given the public health implications of a delayed diagnosis, doctors must be alert to possible cases of measles in travellers returning from endemic countries. The patient’s widespread maculopapular blanching rash

Bridget E Barber · Krispin M Hajkowicz · Vicki L Krause · Kevin G Freeman · Bart J Currie

The epidemiology of influenza pandemics demands that Aboriginal and Torres Strait Islander people occupy centrestage in future planning The first wave of pandemic (H1N1) 2009 influenza (pH1N1) broke more heavily on Australia’s Aboriginal and Torres Strait Islander populations than on non-Indigenous Australians. The burden of disease in Aboriginal and Torres Strait Islander people was highlighted by the first Australian death associated with pH1N1 infection: a young Aboriginal man from a remote area of Western Australia who died on 19 June 2009 in an Adelaide hospital.1 The differences between the populations are stark, with Aboriginal and Torres Strait Islander people indisputably over-represented in severe pH1N1 disease. In the Top End of the Northern Territory, pH1N1 rates of notification, hospital admission and intensive care unit (ICU) admission were higher for Aboriginal and Torres Strait Islander people than for the non-Indigenous population (3.5 times, 12 times and 5 times, respectively).2 Similar profound differences have been recorded for Aboriginal communities in New South Wales: Aboriginal people hospitalised with pH1N1 were younger than their non-Aboriginal counterparts (median age of 24.5 years compared with 31.7 years), and the age-standardised rate ratios for Aboriginal to non-Aboriginal admissions to hospital, admissions to ICU and death during the 2009 pandemic wave were 3.2, 4.0 and 4.5, respectively.3 Overall, from May to October 2009 in Australia, Aboriginal and Torres Strait Islander Australians, who comprise 2.5% of the population, accounted for 16.0% of hospitalisations with pH1N1 and 9.7% of pH1N1 admissions to an ICU.4 A fivefold increase in risk of death due to pH1N1 was also reported.5 This experience demands a greater focus on the needs of Aboriginal and Torres Strait Islander communities and their prioritisation in future pandemic planning. We should not have been surprised, as history tragically demonstrates disproportionate morbidity and mortality for Aboriginal and Torres Strait Islander people in previous pandemics.6 It is thus exceedingly disappointing to discover no mention of Aboriginal and Torres Strait Islander Australians in the revised National Action Plan for Human Influenza Pandemic (NAP).7 The 2010 NAP fails to identify Aboriginal and Torres Strait Islander people as a high-risk group during the H1N1 2009 pandemic, although it acknowledges other risk groups that have been recognised internationally and in Australia: severe cases occurred in people with underlying chronic conditions such as respiratory diseases, cardiovascular disease, diabetes, autoimmune disorders and obesity. Pregnant women were also at an increased risk of serious disease.7 It is inexplicable that while Aboriginal and Torres Strait Islander people were identified as a priority group for the rollout of the pH1N1 influenza vaccination — a commendable and necessary preventive strategy — they are overlooked in the NAP.8 Although the Australian Health Management Plan for Pandemic Influenza9 states an equity commitment, and a subsequent appendix10 produced during the “Protect” phase of the 2009 pandemic endorsed the need for partnership between all health care providers in case and contact management among the Aboriginal and Torres Strait Islander population, respectful partnership between governments and Aboriginal and Torres Strait Islander communities to identify culturally appropriate and effective prevention and mitigation strategies enjoys no mention. Given that the NAP is the peak plan for guiding preparations for future pandemics, there is a fundamental need for governments to acknowledge and respond effectively to the specific requirements of Aboriginal and Torres Strait Islander people. Prevention and preparedness must include government support of planning in respectful partnership with Aboriginal and Torres Strait Islander communities, health organisations and representative bodies. Mandating this support and partnership at all levels of government will allow a greater understanding of infection risk and identification of cultural, social, economic and health service factors that may contribute to poor health outcomes, and ensure culturally safe and effective prevention and mitigation strategies. A national project, funded by the National Health and Medical Research Council, working with Aboriginal and Torres Strait Islander communities and health services in NSW, Queensland and Western Australia is learning about feasible and culturally appropriate containment strategies.11 A strong theme emerging from this work is the message to government: “Ask us, listen to us, share with us”. The ability of Aboriginal and Torres Strait Islander communities to develop novel practical mitigation measures has been a particular feature of this respectful engagement that has already informed government strategies in NSW.3 The epidemiology of the current and previous influenza pandemics demands that Aboriginal and Torres Strait Islander people occupy centrestage in future planning. Solutions to limit the burden on Aboriginal and Torres Strait Islander populations exist, but respectful partnership is necessary to unearth them. The partnership must not be a token one, but one developed through engagement with communities, and with the flexibility to be localised to meet the specific needs of diverse urban, rural and remote Aboriginal and Torres Strait Islander communities in all states and territories. Health information delivered with a local flavour is a key message from the project. “Ask us, listen to us, share with us” is a strong message that governments must heed if the impact of pandemic influenza on Aboriginal and Torres Strait Islander communities is to be limited.

on behalf of the Aboriginal and Torres Strait Islander Community Influenza Study Group

Circumcision now to prevent heterosexual HIV transmission in 2030 makes sense Australia is rightly proud of its response to HIV. Thanks to superb formulation of public policy in the early days of the epidemic, it is not only a low-prevalence country but an international leader in many aspects of its clinical and public health responses. To maintain this fine record, Australia should change policy so that infant male circumcision rates are boosted in the face of rising heterosexual transmission of HIV. Regular surveillance indicates that HIV in Australia is slowly following the trend in Western Europe and North America toward an increased proportion of transmission occurring through heterosexual contact.1 Although the epidemic in Australia is likely to remain concentrated for some time among men who have sex with men, the proportion of new diagnoses attributable to heterosexual contact has risen from the negligible levels of the epidemic’s early days.1 The World Health Organization, the Joint United Nations Programme on HIV/AIDS and the Global Fund to Fight AIDS, Tuberculosis and Malaria have endorsed male circumcision to control HIV attributed to heterosexual contact in hyperendemic areas, stating: “The efficacy of male circumcision in reducing female to male transmission of HIV has been proven beyond reasonable doubt. This is an important landmark in the history of HIV prevention.”2 This raises the question of whether low-prevalence countries such as Australia — with an increasing proportion of HIV cases attributed to heterosexual contact — should consider increasing the rate of infant male circumcision to reduce future HIV infections. The protection conferred to heterosexual males by circumcision is similar in hyperendemic and low-prevalence settings.3-5 In 2008, the Centers for Disease Control and Prevention (CDC) concluded that male circumcision “may also have a role in the prevention of HIV transmission in the United States”.3 The CDC is now formulating a new policy.4 Being a low-prevalence country does not preclude a population-wide approach to HIV prevention. For example, we test pregnant women to prevent cases of vertical HIV transmission. Infant male circumcision would be a comparable, albeit more interventionist, population-wide strategy. A wealth of research has shown that the foreskin is the entry point that allows HIV to infect men during intercourse with an infected female partner.5,6 Soon after the HIV pandemic was first recognised, much lower HIV prevalence was found in areas of sub-Saharan Africa where more than 80% of males had been circumcised than in areas where the circumcision rate was less than 20%.5,6 These findings were then replicated in Asia.7 In Australia, infant male circumcision was once routine, but plummeted in the 1970s. Circumcision of males is now referred to by many as a “surgical vaccine” against a wide variety of infections and adverse medical conditions over the lifetime.5,6,8,9 The public health benefits include protection not just from sexually transmitted HIV, but also from some common sexually transmitted infections and other conditions.4-6 Although it can be performed at any age, the ideal time is infancy, when adverse effects are uncommon.4-6 Considerable evidence, including data from randomised controlled trials, shows that male circumcision has no adverse effects on sexual function, sensitivity or satisfaction.4-6,8 At present, the major obstacle to increasing the rates of infant male circumcision in Australia is an influential Royal Australasian College of Physicians policy, which has been criticised on scientific grounds.10 A draft of a new policy has also been criticised in a detailed petition by 38 academic and clinical experts (including Fellows of the College). Another barrier is the Medicare rebate, which has been reduced steadily in real terms over many years. No state or territory Department of Health except Queensland Health allows elective infant male circumcision to be performed in public hospitals. Despite official discouragement, Medicare statistics show a rise in the rate of infant male circumcision in Australia from 13% in 1998 to 19% in 2009. Boosting the rate in Australia, as a long-term strategy to reduce HIV transmission (in combination with other interventions), is sound public health policy. Male circumcision is one of the most powerful interventions that is currently available in the fight against HIV.8,9 The prospect of the availability of a vaccine over the next 20 years is unlikely. Thus, circumcision now to prevent heterosexual HIV transmission in 2030 makes sense. In addition to preventing HIV transmission, other benefits, high cost-effectiveness11 and risk–benefit balance5,10,11 justify acceptance of male circumcision as a sensible public health measure.3,5,6 It should be viewed as part of a safer sex package. Condom use remains essential, with promotion of condom use plus circumcision of males being analogous to seatbelts plus airbags for reducing the road toll. Australia would also be acting compassionately if it promoted infant male circumcision in the Asia–Pacific region, especially in Papua New Guinea where a generalised HIV epidemic has become well established. A commitment to increasing infant male circumcision should complement earlier commitments to other strategies for prevention of sexually transmitted infections, including condom use. Twenty-nine years after the existence of this epidemic was first announced, it is clear that a new chapter has opened with the recognition that male circumcision substantially reduces female-to-male HIV transmission. Australia would be wise to take advantage of this knowledge.

David A Cooper MD, DSc · Alex D Wodak AM, FRACP, FAChAM, FAFPHM · Brian J Morris PhD, DSc, FAHA

Consensus recommendations for managing chronic suppurative lung disease (CSLD) and bronchiectasis, based on systematic reviews, were developed for Australian and New Zealand children and adults during a multidisciplinary workshop. The diagnosis of bronchiectasis requires a high-resolution computed tomography scan of the chest. People with symptoms of bronchiectasis, but non-diagnostic scans, have CSLD, which may progress to radiological bronchiectasis. CSLD/bronchiectasis is suspected when chronic wet cough persists beyond 8 weeks. Initial assessment requires specialist expertise. Specialist referral is also required for children who have either two or more episodes of chronic (> 4 weeks) wet cough per year that respond to antibiotics, or chest radiographic abnormalities persisting for at least 6 weeks after appropriate therapy. Intensive treatment seeks to improve symptom control, reduce frequency of acute pulmonary exacerbations, preserve lung function, and maintain a good quality of life. Antibiotic selection for acute infective episodes is based on results of lower airway culture, local antibiotic susceptibility patterns, clinical severity and patient tolerance. Patients whose condition does not respond promptly or adequately to oral antibiotics are hospitalised for more intensive treatments, including intravenous antibiotics. Ongoing treatment requires regular and coordinated primary health care and specialist review, including monitoring for complications and comorbidities. Chest physiotherapy and regular exercise should be encouraged, nutrition optimised, environmental pollutants (including tobacco smoke) avoided, and vaccines administered according to national immunisation schedules. Individualised long-term use of oral or nebulised antibiotics, corticosteroids, bronchodilators and mucoactive agents may provide a benefit, but are not recommended routinely.

Anne B Chang MPHTM, PhD, FRACP · Scott C Bell MB BS, MD, FRACP · Cass A Byrnes MB ChB, MD, FRACP · Keith Grimwood MB ChB, MD, FRACP · Peter W Holmes MB BS, FCCP, FRACP · Paul T King MB BS, FRACP, PhD · John Kolbe MB BS, FRACP · Louis I Landau MB BS, MD, FRACP · Graeme P Maguire MB BS, FRACP, PhD · Malcolm I McDonald MB BS, FRCPA, PhD · David W Reid MB ChB, MRCP, FRACP · Francis C Thien MB BS, MD, FRACP · Paul J Torzillo MB BS, FRACP, FJFICM

From 1967, the Australian Human Pituitary Hormone Program offered treatment for short stature and infertility using human cadaver-acquired pituitary hormones (human growth hormone [hGH] and human pituitary gonadotrophin [hPG]). The program was suspended in 1985 when a growth-hormone recipient in the United States developed Creutzfeldt–Jakob disease (CJD), an incurable and rapidly progressive neurodegenerative disorder. Since this time, recipients have lived with the significant anxiety that they have an elevated risk of developing CJD. Furthermore, additional CJD infection control measures are required when recipients undergo some types of surgery. As it is 20 years since the last Australian pituitary hormone recipient developed CJD, we evaluated the risk for Australian recipients of developing iatrogenic CJD, and compared Australian data with data from New Zealand and selected other countries who had pituitary hormone programs. Our evaluation indicates that pituitary hormone recipients in Australia have the lowest risk of developing iatrogenic CJD, and that Australia is the only country not to have experienced ongoing CJD-related deaths. Thus, we believe that: in the Australian hGH recipient cohort, the risk of developing CJD is sufficiently low for this cohort to no longer require additional infection control measures in the health care setting; and in the Australian hPG recipient cohort, if another 5 years elapses with no further occurrence of CJD in this group, the hPG recipient cohort could also be considered as not requiring additional infection control measures in the health care setting. These recommendations should not be misunderstood as implying that there is no ongoing risk, but that the risk is acceptably low and generally in keeping with guidelines that stratify the risk.

Alison Boyd DipAppSci(Nursing), GradDipGenCoun · Genevieve M J A Klug BSc(Hons), PostGradDipEpiBioStat · Lawrence B Schonberger MD, MPH · Amelia McGlade BSc · Jean-Philippe Brandel MD · Colin L Masters MD · Steven J Collins MD

Identifying the emerging threats for which we must be vigilant In 1922, infectious diseases accounted for 15% of all deaths in Australia, but this rate declined dramatically to 1% by 2007 due to a combination of antibiotics, vaccination and public health measures. Yet infectious diseases continue to feature prominently in Australia. The Australian Institute of Health and Welfare has just released its biennial publication on the health of the nation, Australia’s health 2010 — a statistical and informed commentary that examines a variety of health issues dominating the national landscape.1 Here, I summarise the report’s chapter on infectious diseases to paint a picture of where we are today and the challenges we may well face in our future. Among vaccine-preventable diseases, invasive meningococcal disease remains one of the most feared. However, notification data continue to show a pleasing trend of decreasing cases annually.1 Much of this decline can presumably be attributed to the introduction of the meningococcal C conjugate vaccination program in 2003.2 Not surprisingly, cases of the B strain, for which there is no vaccine, dominate the notifications, although numbers have been stable and certainly haven’t increased. Similarly, rates of invasive pneumococcal disease remain steady and well below those seen before the introduction of universal infant vaccination in 2005.1 Concerns continue that there will be a surge of invasive pneumococcal disease due to non-vaccine serotypes — so-called serotype replacement — following introduction of the conjugate vaccination program that will offset any reductions from the program; however, this has not yet happened. Pertussis notifications reached unprecedented levels in 2008 and 2009, with a particularly large increase in the proportion of cases in 0–4-year-olds — the group most vulnerable to severe disease from pertussis.1 Yet it is likely that this increase in notifications can at least partly be explained by increased testing and easier access to better tests, such as polymerase chain reaction (PCR). The world experienced its first influenza pandemic in 41 years with the outbreak of pandemic (H1N1) 2009 influenza (popularly known as “swine flu”). There were over 45 000 laboratory-confirmed notifications of influenza in Australia in 2009, eclipsing those of previous years — by comparison, in 2007, the other severe influenza year in recent times, there were 10 445 notifications. However, there was undoubtedly more testing conducted in 2009. The figure shown in the Box elegantly demonstrates how the swine flu virus behaved like a typical pandemic strain, predominantly affecting adolescents and young adults, while the 2008 “standard” seasonal strain mainly targeted people at the extremes of age.1 Although pandemic influenza has had the highest profile in recent times, chlamydia, with over 62 000 notifications, was the most highly notified infection in Australia in 2009 and remains an important issue among the sexually active. However, as with pertussis and influenza, increased testing has almost certainly contributed to the large number of infections seen recently.1 From 2000 to 2009, there was a decline in rates of newly diagnosed hepatitis B and C infections. Particularly among adolescents and young adults, this decline may be due to factors such as a reduction in injecting drug use and a vaccination program for adolescents against hepatitis B infection. Despite this, however, chronic hepatitis B and C infections are looming as long-term challenges for Australia.1 One model predicts that the 2008 figure of 187 000 people living in Australia with chronic hepatitis B infection could markedly increase to 276 000 cases in 2017 if current practices and resources remain unchanged. This would be associated with a large increase in hepatitis B-related deaths, including those from hepatocellular cancer.3 It is estimated that 212 000 people were living with chronic hepatitis C infection in Australia in 2008, and these people are at risk of similar chronic sequelae as those with chronic hepatitis B infection.4 Challenges include increasing awareness of the diseases and improving access to treatment for affected people, many of whom are from marginalised groups (eg, non-English speaking migrants, Indigenous Australians and injecting drug users). The federal government has responded to these challenges by releasing its first national hepatitis B strategy and third national hepatitis C strategy.4,5 A dengue outbreak featured prominently in northern Queensland between November 2008 and June 2009. Around 1000 cases occurred during this 8-month period, matching the total for the preceding 9 years. The outbreak was characterised by all four strains of dengue circulating, including a virulent DENV-3 strain that had a shorter incubation period within both mosquitoes and humans.1 Hendra virus infection remains unique to Queensland, where outbreaks continue to occur, causing much angst among the public and communicable disease services alike. In 2008 and 2009, Hendra virus, which is transmitted to humans from infected horses, caused the deaths of two veterinary workers.1 There are two emerging infections of concern in Australia. First, hypervirulent Clostridium difficile (also known as PCR ribotype 027 or NAP1) infection has become well established in the health care systems of many northern hemisphere nations in recent years, with high case-fatality and bowel-resection rates. Although a milder form of the infection has been well established here for years, Australia had remained free of this particular hypervirulent strain until our first imported case was detected in Western Australia in 2009.6 This was followed in May 2010 by an outbreak among patients in a Melbourne hospital,7 raising concerns that it may become established in Victoria before spreading elsewhere. Second, the appearance of multiresistant gram-negative organisms such as Escherichia coli in returning travellers, especially those arriving from Asia, is of concern. Although colonisation with these organisms in the bowel is asymptomatic, the problem arises when they cause symptomatic illness, typically in the urinary tract. Few antibiotics are available to treat such infections, and they are often expensive (eg, carbapenems) or dangerous (eg, potential nephrotoxicity and ototoxicity from amikacin). One study found that, while 8% of travellers were colonised with multiresistant E. coli before leaving Australia, almost 50% were colonised on their return.1,8 (It appears that Customs officials may have to worry about more than concealed drugs in travellers’ bowels on their return to Australia!) The health inequities experienced by Australia’s Indigenous peoples are well recognised and apply to many infectious diseases. One example is acute rheumatic fever and rheumatic heart disease. Indigenous people in the Northern Territory have one of the highest rates in the world of these conditions and are around 20 times more likely to die from rheumatic heart disease than non-Indigenous Australians.9 Despite the advances in combating acute and chronic infectious diseases over the past century, both continue to present challenges to our health system, especially for certain Indigenous populations. Multiresistant gram-negative bacterial infections acquired from overseas and hypervirulent C. difficile infection are emerging threats in Australia for which we must be vigilant. This is in addition to infections caused by the already established multi-resistant nosocomial pathogens such as vancomycin-resistant enterococci. The need to isolate affected patients and use expensive antibiotics to treat them only further burdens the hospital system. A mandatory reporting system for certain hospital-acquired infections could be one way to address this. Although childhood immunisation programs have generally been successful, we need to be watchful for resurgent infections, such as pertussis, where immunity from childhood vaccination has waned. Finally, as last year’s swine flu outbreak demonstrated, a pandemic has the potential to consume considerable resources and generate widespread concern. While the 2009 influenza outbreak has passed, the potential for further pandemics and the need to prepare for them persist. Avian influenza, which continues to cause human infections overseas, immediately comes to mind in this regard. Age distribution of influenza notifications in a pandemic year (2009) versus a standard seasonal year (2008)* * Reproduced from Australia’s health 2010 with permission of the Australian Institute of Health and Welfare.1

Sanjaya N Senanayake FRACP, MAppEpid, MB BS

To the Editor: National best practice guidelines recognise that accurate data on the health of Indigenous Australians are crucial to improving health service delivery.1 The draft revision of the RACGP Standards for general practices acknowledges the need for improvement and requires that a practice demonstrates how it routinely records, in active patient health records, self-identified Aboriginal and Torres Strait Islander status.2 This is a commendable improvement but should be further strengthened, requiring that Indigenous status be recorded for at least 90% of active patients, the level required for a history of allergies. Improved record keeping in general practice has resulted in the potential to improve Indigenous identification among patients notified with a communicable disease. This enables the documentation of health disadvantage, and allows evaluation of measures aimed at closing the gap in health outcomes between Indigenous and non-Indigenous people. Demographic data in the NSW notifiable diseases database (NDD) were audited for all 258 Hunter New England (HNE) Salmonella infection notifications in 2007 by interviewing patients and their referring general practitioners. Interviews were completed for 83% of patients. Indigenous status was poorly recorded. The NDD listed three patients with salmonellosis as Aboriginal, but showed an unknown status for 87%. Among patients who had attended a GP during their illness (66%), practice records listed two as Aboriginal, but Indigenous status was unknown for 70%. Most GPs (95%) reported using electronic medical records, and 89% completed pathology requests with practice software. Many GPs (60%) requested information on how to appropriately ask about a patient’s Indigenous status. Interviews with patients who had been notified as having had salmonellosis identified 13 as Aboriginal, and no resistance to identification was encountered. The crude salmonellosis notification rates per 100 000 population were 42.2 (95% CI, 19.3–65.1) for Aboriginal HNE residents and 25.5 (95% CI, 21.7–28.6) for non-Aboriginal HNE residents which, while not statistically significant for this small sample, suggests a differential salmonellosis burden, consistent with studies elsewhere.3 The true burden of disease was likely to have been substantially higher, as many infections are not notified.4 The differential burden may also be an underestimate if Aboriginal HNE residents were less likely to be notified than non-Aboriginal residents due to, for example, reduced access to health services. The widespread availability of electronic practice software for generating pathology requests provides a new opportunity to substantially improve Indigenous identification in communicable disease notifications.3 Indigenous status should be routinely recorded by GPs and automatically included on their pathology request forms and subsequent laboratory notifications. There is now a need for a coordinated national approach to ensure consistent inclusion of Indigenous status on all laboratory notification data.

Anthony D Merritt · April R Roberts-Witteveen · David N Durrheim

To the Editor: Seizures can be precipitated by treatment with praziquantel in patients with underlying neurocysticercosis, but this is rare and has not previously been described in Australia. We describe the case of a patient who developed seizures after antischistosomal therapy. An asymptomatic 23-year-old Burmese man underwent migrant health screening by his local doctor a month after arriving in Australia. His schistosomal serological results were positive (titre, 1:32) and he received three doses of 600 mg praziquantel. Three days later, he experienced several generalised tonic–clonic seizures in short succession, each lasting a few minutes. A magnetic resonance imaging (MRI) scan revealed three ring-enhancing lesions less than 1 cm in diameter, suggestive of neurocysticercosis. He was treated with phenytoin and also received dexamethasone for 1 month. A repeat MRI scan 6 months later showed significant reduction in the size of the lesions, to less than 3 mm. Phenytoin therapy was ceased after 3 months, with no seizures at last review (6 months). In view of the temporal association between the treatment and the seizures in this previously asymptomatic patient, we believe the seizures were precipitated by the praziquantel therapy. Cysticercosis, which is endemic across the developing world, is caused by the helminth Taenia solium. Clinical disease, including neurocysticercosis, is often asymptomatic. Symptomatic neurocysticercosis often presents as seizures, especially as the cysts degenerate, and is the commonest cause of acquired, late-onset epilepsy in the developing world.1 The benefit of treatment remains controversial, especially when there are only a few cysts.1-3 Praziquantel and albendazole therapy accelerate cyst degeneration, and subsequent inflammation may precipitate seizures, which are sometimes pre-emptively managed with corticosteroids.1 There is conflicting evidence on the benefit of treatment for long-term seizure frequency.2,3 Although screening for some parasitic infections in refugees in Australia is recommended,4 this does not include cysticercosis. Serological tests for T. solium cannot differentiate between active and past infections, have limited sensitivity, are not widely available in Australia, and cannot differentiate between neurocysticercosis and cysticercal disease elsewhere.5 The only reliable method for diagnosis is neuroimaging, which is impractical for mass screening. Nevertheless, we advocate a high degree of suspicion for neurocysticercosis in migrants from Taenia-endemic areas. Geographical origin alone is insensitive for identifying an at-risk population. A history of seizures, or the presence of subcutaneous nodules, should prompt investigation with serological testing and subsequent neuroimaging before consideration of treatment. In such symptomatic patients, this will allow the need for anthelmintic therapy to be assessed, along with consideration of adjunctive corticosteroid therapy.

Saliya S Hewagama · Jonathan D Darby · Harsha Sheorey · John R Daffy

To the Editor: In February 2009, a 68-year-old man presented to the Royal Victorian Eye and Ear Hospital within hours of developing an itchy, red left eye. The patient, who was otherwise healthy, lived in suburban Melbourne, usually with his pet dogs, but the last of his dogs had recently died. The patient was unsure if all his dogs had been dewormed regularly because he spends about 6 months a year in Europe. General inspection of the eye suggested subconjunctival haemorrhage. However, slit-lamp examination showed a mobile, tightly coiled structure within the subconjunctival blood. It grew increasingly agitated with higher slit-lamp light intensity (Box, A). Assessment of the patient’s visual acuity and the anterior and posterior chambers of the eyes was unremarkable. Blood tests revealed a positive filarial serology and eosinophilia. The patient was transferred to the operating theatre and, under topical anaesthesia, a 5 mm conjunctival incision was made and the mobile structure removed (Box, B and C). The patient was discharged with a prescription for prednisolone acetate 1% and chloramphenicol 0.5% eye drops (one drop four times a day). He made a full recovery. The extracted specimen was reviewed by one of us (D M S). The 150 mm worm was identified as a young adult female filarioid nematode, Dirofilaria immitis (commonly named dog heartworm) after comparisons with laboratory specimens of D. immitis and Pelecitus roemeri. Infection with either P. roemeri (kangaroo and wallaby knee worm) or Loa loa (loiasis) was excluded. Our specimen did not have lateral alae and the distance from anus to tail was shorter than would be expected for the kangaroo worm. In addition, the patient had never been to Africa where loiasis is endemic to several countries. Subconjunctival dog heartworm is rare, but its incidence is increasing in parts of the world.1,2 Dogs are the natural hosts and transmission to humans occurs through mosquito bites of the skin (into which the third-stage infective larva may escape). For an unknown reason, the worm sometimes takes an abnormal migratory route and ends up in the eye of the host. Ophthalmic cases have been reported in dogs.3,4 Careful measures to exterminate mosquitoes and deworm dogs and cats are important in limiting its transmission. Surgical extraction is the definitive treatment and further treatment with systemic anthelmintics is unnecessary.5 Humans are non-natural hosts for this parasite and, therefore, its life cycle cannot be completed within the human body. When a larva does evade the human immune system, as in the case of our patient, the chances of another larva being present elsewhere in an immunocompetent person seems remote. Furthermore, unless the larva becomes clinically apparent, it would be impossible to find. Subconjunctival Dirofilaria immitis infection in a 68-year-old man A: A whitish mobile structure coiled in the haemorrhagic subconjuctival space B: The female Dirofilaria species measuring about 150 mm C: Day 1 after removal of worm and necrotic temporal conjunctiva, exposing bare sclera

Elaine W Chong · Harsha Sheorey · Cheng Hean Lo · David M Spratt · Enrique Graue-Hernández