Infectious diseases

In reply: We were interested in Gilles and colleagues’ response to our analysis of the uptake of interventions to prevent perinatal HIV transmission in Australia. As Gilles et al state, the reported rates of perinatal HIV transmission are low in Western Australia, where the choice of delivery modality is individualised. We agree that the additional benefit of elective caesarean section in women being treated with highly active antiretroviral therapy with an undetectable viral load is not known. We also agree that elective caesarean section is associated with potential risks, and women should have a choice regarding mode of delivery. This choice should be informed by other obstetric factors, maternal viral load, and the clinical setting in which delivery takes place. Geographic variation in such factors is likely, and will certainly contribute to differences across states in the uptake of preventive interventions. Ongoing national surveillance will help ensure that women with HIV infection and their children benefit as much as possible from evidence-based obstetric practices.

Michelle L Giles · Ann M McDonald · Elizabeth J Elliott · John B Ziegler · Margaret E Hellard · Sharon R Lewin · John M Kaldor

A 5-month-old boy with known congenital varicella syndrome presented to our hospital emergency department with generalised herpes zoster (shingles). The child was born in Australia. His Sri Lankan-born mother had developed chickenpox in the second trimester of pregnancy. Examination and investigation of the child at birth for complications of congenital varicella syndrome had revealed only skin changes on the left thigh (Box, A). A new vesicular rash had evolved over 3 days, initially involving right T8 (Box, B) and L4–5 (Box, C) dermatomes, then progressing to cover the entire body. There was no clinical evidence of visceral involvement. Cicatricial scarring had replaced the congenital skin changes (Box, D). Varicella zoster virus was isolated from vesicular fluid. Oral valaciclovir was prescribed for 7 days because the generalised nature of the rash demonstrated an insufficient immune response to varicella reactivation. The symptoms rapidly resolved, with no new scarring. A maternal chickenpox infection during pregnancy can be severe and life-threatening, and can also cause in-utero infection, which may be fatal or result in congenital abnormalities.1 Important features of congenital varicella syndrome include: dermatomal cicatricial scarring (highlighted by this patient); limb defects; intrauterine growth restriction; ophthalmological defects (chorioretinitis, optic atrophy, cataract); gastrointestinal or genitourinary abnormalities; neurological defects (developmental delay, seizures, deafness, limb paralysis, microcephaly).1 Shingles is caused by reactivation of varicella zoster virus. Childhood shingles is uncommon (incidence, 0.05%/year), rarely indicates primary immunodeficiency,2 and occurs more frequently following congenital infection (4.4%/year)2 or chickenpox infection during infancy (0.4%/year).2 Antiviral treatment of shingles in immunocompetent young children is not usually recommended, as complications (including post-herpetic neuralgia) are rare.3 Chickenpox has been mainly a childhood disease in Australia, but in many tropical countries it predominantly affects adults. Immigrants to Australia from these regions (including the mother of our patient) may remain susceptible to varicella infection.4 At least 5% of Australian women of childbearing age were born in tropical countries.5 Varicella vaccine is highly effective and is listed on the National Immunisation Program Schedule6 for childhood immunisation. Lowering the community prevalence of varicella infection by routine childhood immunisation can help protect non-immune adults and immunocompromised patients.1 Opportunistic, proactive identification and immunisation of non-immune adults, particularly for both prospective parents before pregnancy, could help prevent serious consequences. Cicatricial scarring and shingles in a 5-month-old infant with congenital varicella syndrome

Elizabeth K Nairn · Joshua Wolf · Jim P Buttery

To the Editor: The pattern of invasive pneumococcal disease (IPD) in Western Australia varies from that described in northern Queensland in a recent article by Hanna and colleagues.1 Their study showed a decline in IPD caused by serotypes included in the 7-valent pneumococcal conjugate vaccine (7vPCV) among Indigenous children and adults after the introduction of the vaccine in north Queensland. Over the same period, there was an increase among Indigenous adults in cases of IPD caused by serotypes not covered by the vaccine. However, the authors reported that there had been no increase in IPD caused by serotype 19A, a non-7vPCV serotype that has been increasingly predominant in other populations.2,3 In contrast to the disease pattern in north Queensland, serotype 19A has become the predominant disease-causing serotype in Western Australia, particularly among non-Indigenous people. Data from the WA Notifiable Infectious Diseases Database show that the incidence of IPD in WA fell from 10.7/100 000 in 2001 (n = 203) to 6.3/100 000 in 2007 (n = 132). In children aged < 5 years, there was a significant drop in overall IPD rate, attributable to the decline in disease caused by 7vPCV serotypes, among both Indigenous children (from 70/100 000 to zero) and non-Indigenous children (from 50/100 000 to 1.6/100 000) (Box). The rate of IPD caused by 7vPCV serotypes also declined among Indigenous and non-Indigenous adults, suggesting a herd immunity effect. From 2001 to 2007, the proportion of IPD cases caused by non-7vPCV serotypes increased among children aged < 5 years (from 19% to 91%) and children ≥ 5 years (from 33% to 72%). Serotype 19A was the only serotype that became more predominant, being responsible for 11 (8%), 14 (10%) and 26 (20%) cases of ICD in 2005, 2006 and 2007, respectively. In 2001, it accounted for 2.5% of cases in children < 5 years (1.6/100 000) and 0.8% of cases in children ≥ 5 years (0.1/100 000). By 2007, these figures had increased significantly to 34% of cases in children < 5 years (7.8/100 000) and 25% of cases in children ≥ 5 years (0.8/100 000). Interestingly, the increase in serotype 19A cases was seen only in non-Indigenous people (particularly children), with the number of cases remaining stable among Indigenous adults and children. Although numerous reports describe increasing prevalence of penicillin-resistant 19A strains,3,4 none of the WA isolates were penicillin-resistant. In summary, after the introduction of the 7vPCV, the rate of IPD caused by 7vPCV serotypes decreased significantly in WA. However, the rate of IPD caused by serotype 19A, a non-7vPCV serotype, increased in non-Indigenous people and in the population overall. These early trends have significant public health implications for vaccine policy. State and territory vaccination programs exist within the framework of the national immunisation program. However, jurisdictional expert advisory groups need local ongoing post-marketing surveillance, coupled with an understanding of historical trends and emerging serotypes, when formulating vaccine recommendations for their populations. Incidence of invasive pneumococcal disease (IPD) caused by serotypes included in the 7-valent pneumococcal conjugate vaccine (7vPCV), by age group and Indigenous status, Western Australia, 2001–2007 * The 7vPCV was funded for Indigenous children from July 2001 and for all Australian children from January 2005.

Carolien M Giele · Anthony D Keil · Deborah Lehmann · Paul G Van Buynder

To the Editor: Extended-spectrum-β-lactamases (ESBLs) are enzymes capable of hydrolysing penicillins, broad-spectrum cephalosporins and monobactams. Worldwide, ESBL-producing organisms are posing an increasing challenge for empirical antibiotic use and infection control. We recently carried out a review of microbiological isolates from clinical specimens taken from 2003 to 2007 at the Alfred Hospital, Melbourne. From 15 917 gram-negative bacilli, we identified 234 ESBL-producing organisms (1.5% of isolates) using double-disk synergy testing. Over the 5-year period, we noted three apparent changes in ESBL epidemiology relating to Escherichia coli isolates. First, E. coli became the most frequent organism in which ESBL production was observed, making up 55.6% of all ESBL-producing organisms in 2007 (up from 23.5% in 2003) (P = 0.03). Second, while the total number of E. coli isolates remained essentially constant over the study period, there was an increase in the proportion of E. coli isolates found to produce ESBLs: 1.8% of E. coli isolates in 2007 compared with 0.36% in 2003 (P < 0.001). The third and perhaps most striking change was in the epidemiology of ESBL-producing E. coli. In 2003, ESBL-producing E. coli infections were largely hospital-acquired, with 87.5% of isolates acquired after 48 hours in hospital or after a hospital admission in the previous 12 months. However, by 2007, ESBL-producing E. coli infections were found to be predominantly community-acquired, making up 62.2% of ESBL-producing E. coli isolates (P = 0.01). The increased proportion of community-acquired infections occurred despite a parallel increase in the frequency of hospital-acquired ESBL-producing E. coli infections (Box). Community-onset infections with ESBL-producing organisms have become increasingly recognised as important clinical entities.1 ESBL-producing E. coli bacteraemia is associated with higher mortality than bacteraemia caused by non-ESBL-producing organisms,2 a finding that has also been specifically demonstrated in the setting of community-acquired infections.3 Although local epidemiological data for infections with ESBL-producing organisms are not readily available, it appears that rates of community-associated infection vary greatly worldwide, with some regions of China reporting rates of ESBL-producing E. coli as high as 34% of all isolates.4 Although our study was limited by being a single-centre review, our findings are consistent with the emergence of multiresistant Enterobacteriaceae noted in Australian surveillance reports.5 It is not clear whether the change in our ESBL-producing isolates is reflective of local resistance patterns, or perhaps associated with travel to regions where ESBL-producing E. coli are known to be prevalent. Corroboration of these changes in other regions will be important for assessing the magnitude of this issue and responding appropriately, particularly in considering empirical antibiotic therapy for community-acquired gram-negative infections. Hospital-acquired (HA) versus community-acquired (CA) ESBL-producing E. coli isolates, Alfred Hospital, 2003–2007 E. coli = Escherichia coli. ESBL = extended-spectrum-β-lactamase.

Justin T Denholm · Michael Huysmans · Denis Spelman

The 21 August 1937 issue of the Medical Journal of Australia contained two articles on a hitherto unknown disease affecting abattoir workers and farmers — Q fever (with the “Q” standing for query). The first of these was by Edward Holbrook Derrick, Director of the Laboratory of Microbiology and Pathology, Queensland Health Department, Brisbane, and comprised his meticulous clinical descriptions and subsequent experiments to isolate the causative organism.1 During his research, Derrick sought the help of Frank Macfarlane Burnet, and the second article by Burnet and Mavis Freeman from the Walter and Eliza Hall Institute of Medical Research in Melbourne described their identification of the causative agent.2 Research breakthroughs frequently involve scientific collaboration, and attributing credit for the results of such collaborations can be difficult. In the light of some new information about Derrick’s experiments, I believe that he may not have received sufficient credit for his contribution to the discovery of the organism responsible for Q fever. When the MJA articles were published, Q fever appeared to be a disease localised to a small area of south-eastern Queensland. However, within a decade or so, it was shown to be of worldwide significance. Edward Derrick’s laboratory notes rediscovered Edward Derrick in his laboratory in 1937 taking rectal temperatures of guinea pigs. The guinea pigs were housed in second-hand battery jars, with two to a jar. In January 1994, I was asked by Professor L W Powell, Director of the Queensland Institute of Medical Research, to examine some cardboard boxes containing books and papers packed by Derrick before he died in 1976, to see whether there was anything important that should be kept. The boxes contained out-of-date textbooks, letters, photographs, notes of experiments and other memorabilia. One small package wrapped in newspaper contained an old exercise book cover, 13.2 × 21.2 cm, in which there were seven files of brown paper. Each file was stapled with a split-staple in the top left-hand corner, and on the top right-hand corner they were labelled Q1 to Q7 and they were in numerical order. Further examination of these notes revealed that they were laboratory notes comprising case histories and the results of guinea pig experiments. Correlation with Derrick’s MJA article of 1937 revealed that they were the laboratory notes relating to seven of the nine patients on which the article was based, and it was apparent that these notes had not been read by previous biographers. (A more detailed account of my findings, together with more than 300 digital images of the original documents, has been lodged in the Library of the Queensland Institute of Medical Research, and the Herston Medical Library, Brisbane.) Who was Edward Derrick?When Derrick was appointed to the position of Director of the Queensland Health Department Laboratory of Microbiology and Pathology in Brisbane in mid 1935, his previous experience included a year at the Walter and Eliza Hall Institute of Medical Research in Melbourne as a cancer research scholar in 1921 and a year as a pathology assistant at London Hospital in 1923. In the intervening period, he had survived a bout of tuberculosis and worked mostly as a country general practitioner in Australia. The laboratory he was in charge of was primitive even by standards of the time. It had a small staff of four, none of whom had tertiary qualifications. However, as Box 1 shows, Derrick’s appointment as Director of this laboratory was the beginning of a long and distinguished career as a research scientist and administrator. It was only a month after his appointment that Derrick was asked to investigate the cause of an obscure fever affecting meatworkers in a Brisbane abattoir processing dairy cattle (workers at a nearby abattoir processing steers for the international market had not been affected). He immediately set to work questioning the clinicians who had been treating the patients. Edward Derrick’s Q fever investigationsThe patients Derrick described in his MJA article presented between September 1935 and November 1936. Five were abattoir workers, another two were dairy farmers, and another worked in sewage construction. By examining the patients almost daily, and visiting some of them at their place of work, Derrick was able to make meticulous descriptions of their illnesses. He began by excluding other known causes of fever common in coastal Queensland. His working hypothesis was that it was likely to be a rickettsial infection, although it differed from the known rickettsias in that the patients did not have a skin rash or a positive Weil–Felix reaction. To isolate the causative organism, he began inoculating guinea pigs with patients’ acute-phase blood and urine samples with the aplomb of an experienced researcher. The inoculated guinea pigs became febrile and developed enlarged spleens, and he recorded their febrile response. His studies were done during the Depression, which explains Derrick’s use of second-hand battery jars (the casing of early batteries), and his method of recording his laboratory results on the cheapest paper available. Some extracts from the laboratory notes I discovered are described and illustrated in Box 2. He transmitted the infection serially in guinea pigs, investigated its properties in relation to heat, cold, and filterability, and studied the effect of dilution on its potency. He showed, by challenge and cross challenge, that the “strains” isolated from different patients were the same. This led to the development of a diagnostic test, albeit a cumbersome one, based on guinea pig immunity. Derrick also tried to identify the source of the infection and the manner of its transmission to patients. He visited Patient 3, a dairy farmer, at his farm where he looked for ticks or sick animals. He inoculated milk and cream (both raw and diluted) from the dairy into guinea pigs (they died from sepsis, but did not develop fever). He thought the infection might be transmitted by a biting vector, because he could only transmit it from one guinea pig to another by injection of infected liver and spleen. He attempted to infect other laboratory animals, mice and a few rabbits, without success, and rats with limited success. Overall, the results were compatible with Derrick’s hypothesis that a rickettsia-like organism, rather that a virus, was responsible for Q fever. Collaboration with Frank Macfarlane BurnetAt this stage, Derrick sent material from his patients and his guinea pig experiments to Frank Macfarlane Burnet at the Walter and Eliza Hall Institute of Medical Research in Melbourne. Burnet was one of the most prominent medical researchers in Australia at that time, and he already had an international reputation. Derrick was an unknown researcher working in an obscure peripheral laboratory, and he needed assistance from someone with an up-to-date, well staffed laboratory who had scientific support in the international arena. At a follow-up of Patient 5 on 17 September 1936, Derrick took a blood sample and sent half the serum to Burnet. Burnet’s laboratory notes (courtesy of Mr Gavan McCarthy, Director, Australian Science and Technology Heritage Centre, University of Melbourne) on 1 October 1936 read “abattoirs fever apparently successful early passage but now appears to have been lost”.3 On 5 October 1936, Derrick sent serum from Patient 7 to Burnet, and on 12 October he sent spleen and kidney from guinea pig D6 (Patient 7). Burnet’s laboratory notes on 30 November 1936 read “Abattoirs fever. Virus grown consistently. No spirochaetes or rickettsia seen”. After studying Derrick’s notes and drawings (see Box 2), I have wondered whether this comment could be interpreted as the report of a “consultant” to a “referring doctor” who has asked, “Could you please examine this material. I think that it contains a living organism. I have looked for many organisms, but I think it is likely to be a rickettsia”. (I could not find any correspondence that might shed light on this speculation either in Derrick’s or in Burnet’s papers that refer to this period of time.) On 1 January 1937 after further testing on D6 material, Burnet recorded, “Abattoirs fever: positive transmission to rats and mice. Enlargement of liver and spleen. In a rather variable proportion of mice numerous rickettsia seen. Sub inoculation to guinea pigs gives typical fever with immunity. Rickettsia seen.” In later communications, Burnet said that on this day he was confident that he had positively identified the organism causing Q fever. Interestingly, Burnet sent samples of D6 material to Rolla Dyer, head of the Rickettsia section at the National Institutes of Health in Washington, DC,4 and it was this strain that made it possible to show that it was identical to the organism that Herald Cox from Rocky Mountain Laboratory, Montana, USA, had isolated from ticks. Box 3 gives a summary of the current understanding of Q fever. A self-effacing scientistWe may never know whether Derrick should have received more recognition for his part in the identification of a rickettsia-like organism as the cause of Q fever. We do know that Derrick was responsible for having the organism named Rickettsia burneti5 (later changed to Coxiella burnetii as a result of Herald Cox’s contribution), and it is interesting to speculate as to why he did not ask for his own name to be included. Derrick was known for his retiring and self-deprecating nature, so it is quite possible that he shrank from taking the credit. He also knew (or guessed) that he had to act quickly to get a name in print because the group from Montana was about to publish its results on the “Nine Mile agent” in ticks. Rather than entering an argument with the more forceful Burnet, he may have decided to name it after him so that the answer would be a quick “yes” to his suggestion. It is interesting that Q or Query fever still bears the name given to it by Derrick when he was investigating its cause, and strangely it is a disease that continues to puzzle researchers. However, there has been a proposal for a name change. A seminar presentation in French, published in 1951, argued strongly that Q fever should be renamed Derrick–Burnet fever,6 and a Google search reveals that the use of this name is not uncommon. I would support this name change. 1 Edward Holbrook Derrick, CBE, MB BS, MD (1898–1976) 1921–23: Sir John Grice cancer research scholar, Walter and Eliza Hall Institute of Medical Research, Melbourne. Pathology assistant, London Hospital 1924: Contracted tuberculosis and, abandoning plans to become a medical missionary, returned to Australia to fight the disease (his brother had died of TB), hoping the climate would be curative 1925–34: Locum general practitioner, mostly in small country towns in the eastern states of Australia. With his health restored, he began private practice in Brisbane in 1934 1935–46: Director of the Laboratory of Microbiology and Pathology, Queensland Health Department, Brisbane. Conducted the first research on Q fever, collaborating with Frank Macfarlane Burnet to identify the causative organism. Studied other infectious diseases in Queensland, being the first to isolate Leptospira pomona. Suggested the establishment of a research institute to focus on Queensland diseases, and chaired an advisory committee that set up the Queensland Institute of Medical Research (QIMR) 1947–66: Deputy Director, QIMR, and in 1961 became Director. Continued investigations of leptospirosis and scrub typhus, and set up a virology unit. Conducted studies on asthma incidence 1966–73: Director of the Queensland Asthma Foundation’s Research Bureau Awards include: CBE; the Commonwealth Department of Health’s Cilento Medal (shared with Burnet); Britannica Australia Award for Medicine; Medal of the Australian and New Zealand Association for the Advancement of Science; Honorary Doctorate of Science (University of Queensland) Publications: Almost half of his 128 scientific publications were published in the Medical Journal of Australia, which also published a Festschrift issue in his honour in 1967 Source: Doherty RL. Derrick, Edward Holbrook. Australian dictionary of biography. Vol 13. Melbourne: Melbourne University Press: 620-621. 2 What Edward Derrick’s laboratory notes revealed 3 Q fever Q fever is a zoonosis, the causative organism Coxiella burnetii occurring worldwide (except in New Zealand) in mammals, birds and ticks. C. burnetii is an obligate intracellular organism, first classified as a rickettsia. Recent studies and genome sequencing suggest that it is a γ-Proteobacteria, order Legionellales, but with characteristics in common with bacteria in the genus Rickettsia. Q fever infection in humans may be asymptomatic; or it may cause an acute illness (usually a flu-like illness, pneumonia, or hepatitis), or a potentially fatal chronic illness (predominantly endocarditis). C. burnetii is disseminated mostly as aerosols or fomites from animals, particularly parturient animals. It is highly infectious, affecting abattoir workers and farmers, as well as researchers and laboratory technicians. Australia is the only country with a Q fever vaccine. C. burnetii also forms spores (0.2 × 0.5 μm) that resist heat and desiccation, and persist for long periods.

Robin A Cooke MD, FRCPA, FRCPath

A 62-year-old woman presented with left frontotemporal pain, scalp tenderness and raised levels of inflammatory markers. Temporal arteritis was considered likely, and symptoms resolved with prednisone therapy. This delayed diagnostic bone biopsy until a soft tissue abscess formed, and Pott's puffy tumour associated with Prevotella osteomyelitis of the frontal bone was diagnosed. This case highlights the value of early histopathological examination, and is a reminder of a condition seen frequently in the pre-antibiotic era. Clinical recordA 62-year-old woman was referred with a 6-month history of spontaneous left frontotemporal scalp pain. Initially, the pain was associated with a soft swelling over the scalp and resolved within 6 weeks. It recurred 4 months later, without associated swelling, localised to the left frontal region and became progressively more severe, disturbing the patient’s sleep. She remained systemically well and had no history of fever, sinusitis, dental infection or diabetes mellitus. Investigation by the patient’s general practitioner revealed raised erythrocyte sedimentation rate (130 mm/h; reference range [RR], < 20 mm/h), C-reactive protein (66 mg/L; RR, < 3 mg/L) and alkaline phosphatase (121 U/L; RR, 25–100 U/L). There was no paraprotein in the serum or urine. A plain radiograph revealed apparent osteolysis (Box, A) and a bone scan revealed intense uptake of technetium-99m-methylenediphosphonate in the skull (Box, B). A computed tomography (CT) scan confirmed diffuse lucency in the left frontal bone, without evidence of underlying sinusitis. These radiological and scintigraphic features suggested osteoporosis circumscripta cranii (the lytic phase of Paget’s disease of the skull), although the raised inflammatory markers were inconsistent with this diagnosis. A specialist opinion was sought. At review, the patient was afebrile and results of physical examination were normal except for marked tenderness over the left temporal region, raising the possibility of giant cell arteritis. Urgent temporal artery biopsy was arranged while the patient began oral prednisone therapy (80 mg per day). Her condition improved dramatically — the pain was alleviated and levels of inflammatory markers decreased — but no histological evidence of vasculitis in the temporal artery was found. A presumptive diagnosis of biopsy-negative giant cell arteritis was made, and oral corticosteroid therapy was continued with a tapering regimen. Prophylactic trimethoprim–sulfamethoxazole (320 mg/1600 mg twice per week) was administered to prevent Pneumocystis infection; concurrently, bisphosphonate therapy was begun (40 mg alendronate per day) for suspected osteoporosis circumscripta cranii. The occurrence of two separate pathological processes was considered improbable, and a skull biopsy for definitive diagnosis was discussed with the patient. However, she was reluctant to undergo further invasive testing because of the rapid symptomatic improvement. She was monitored clinically and biochemically at regular intervals while the prednisone dose was reduced over the following 6 months. Throughout this period, she remained pain-free and systemically well, with normal levels of inflammatory markers. Six months after initiation of corticosteroid therapy, while the patient was taking 10 mg of prednisone per day, she developed a tender fluctuant swelling over the left frontal region of the scalp. The swelling enlarged rapidly, and a CT scan revealed a 6 × 11 × 4.5 cm collection overlying the left frontal bone (Box, C). Neurosurgical consultation and exploration of the swelling were arranged. During exploratory surgery, copious malodorous pus was drained and a biopsy sample of the underlying skull, which appeared discoloured, was taken. A pure growth of Prevotella sp., an anaerobic gram-negative rod-shaped bacterium, was isolated on culture of the pus. The organism was identified as either Prevotella melaninogenica or Prevotella oralis. Histopathological examination of the biopsy sample revealed infiltration of the marrow spaces by neutrophils (Box, D), and the presence of plasma cells with admixed fibrosis (Box, E), consistent with concurrent acute and chronic osteomyelitis. The diagnosis was revised to Prevotella osteomyelitis of the frontal bone with associated soft tissue abscess (Pott’s puffy tumour). Prednisone and alendronate were withdrawn, and the patient was treated with intravenous antibiotics for 6 weeks. As the organism was penicillin-resistant, clindamycin (600 mg four times per day) was administered for 2 weeks, and this was followed by ertapenem (1 g per day) as outpatient therapy. The intravenous antibiotics were combined with oral metronidazole (400 mg three times per day) and were followed by treatment with oral clindamycin (300 mg four times per day) for another 6 weeks. The patient’s condition responded rapidly to medical management and she remained clinically well with normal levels of inflammatory markers at 12-month follow-up. A subsequent CT scan of the calvaria showed resolution of the lytic changes without bony sequestrum. DiscussionAnaerobic organisms predominate in head and neck infections, occurring in a mixed growth in more than 90% of dental, oral and neck space infections.1 Clinically relevant anaerobes include the gram-negative rods Bacteroides, Prevotella, Porphyromonas, Fusobacterium and Bilophila, and gram-positive rods (eg, Clostridium, Actinomyces and Propionibacterium) and cocci (eg, Peptostreptococcus).1 Despite frequently being found in mixed bacterial populations, Prevotella sp. was isolated as a pure growth in our patient. Although trimethoprim–sulfamethoxazole therapy (used as Pneumocystis prophylaxis in our patient) is generally thought to lack useful activity against anaerobes,1 it may have suppressed the infection. Osteomyelitis of the skull is uncommon; recognised clinical syndromes include frontal bone osteomyelitis secondary to frontal sinusitis, and skull base osteomyelitis associated with malignant otitis externa. Skull osteomyelitis may also result from direct inoculation during surgery or occur in association with retrograde septic thrombophlebitis.2 Haematogenous seeding of bacteria in the skull is rare. Although our patient had no clinically or radiographically recognised sinusitis or history of dental instrumentation or infection, it is likely that the organism originated in the oral cavity or frontal sinus. The duration of the history suggests that chronic osteomyelitis may have accounted for our patient’s initial symptoms, but, if present, Paget’s disease of the skull may have predisposed to bacterial seeding. Paget’s disease is a reported risk factor for osteomyelitis of the jaw.2 Pott’s puffy tumour is a complication of frontal osteomyelitis that was first described by Sir Percival Pott in 1760.3 It appears as a circumscribed swelling on the forehead, representing a subperiosteal abscess that forms when infection breaks through the frontal bone.2 Epidural abscess, subdural empyema, brain abscess and cortical vein thromboses have been described in association with Pott’s puffy tumour. It was predominantly seen in children and adolescents before the widespread availability of antibiotics.2,4 In our patient, the administration of corticosteroids masked the underlying anaerobic infection until dose tapering permitted an abscess to form. Our patient illustrates a diagnostic challenge. It seemed unlikely that two unrelated diagnoses would account for a single presentation, but the prompt clinical response to corticosteroids led to a delay in diagnostic bone biopsy. The final diagnosis of frontal bone osteomyelitis with subperiosteal abscess is a reminder of a condition seen commonly in the pre-antibiotic era. Radiography and computed tomography (CT) scans, and bone biopsy specimens, of a patient with Pott’s puffy tumour associated with Prevotella osteomyelitis of the frontal bone A: Plain radiograph of the skull before corticosteroid therapy, showing patchy osteolytic areas in the frontal cranium. B: Delayed skull spot views on a bone scan before corticosteroid therapy, showing accumulation of technetium-99m-methylenediphosphonate. C: CT scan of brain (using intravenous iopamidol contrast medium) after 6 months of corticosteroid therapy showing a large collection over the left frontal bone. D: Bone biopsy specimen taken after 6 months of corticosteroid therapy, showing infiltration of the bone marrow spaces by neutrophils and scattered osteoclastic giant cells adjacent to the bony trabeculae, indicating active inflammation (haematoxylin and eosin stain; original magnification, × 400). E: Bone biopsy specimen taken after 6 months of corticosteroid therapy, showing plasma cells with admixed fibrosis, indicating chronic inflammation (haematoxylin and eosin stain; original magnification, × 400).

Lyndal J Tacon MB BS · Jonathon F Parkinson MB BS · Bernard J Hudson FRACP, FRCPA · Janice M Brewer MB BS, FRCPA · Nicholas S Little MB BS, FRACS · Roderick J Clifton-Bligh FRACP, PhD

Objective: To evaluate the immune status and vaccination needs of first-year medical students in relation to bloodborne viruses and common vaccine-preventable diseases.Design, setting and participants: Survey of first-year medical students at the University of New South Wales, Sydney, NSW, attending a mandatory screening and vaccination clinic, 2002–2005.Main outcome measures: Self-reported history of vaccination or natural infection; serological evidence of immunity to measles, mumps, rubella and varicella (presence of specific IgG) and hepatitis B (presence of hepatitis B virus surface antibodies) or infection with hepatitis B and C viruses and HIV; and Mantoux test results.Results: 733 students attended the clinic (85% of those enrolled). Four students were positive for HBsAg and four had hepatitis C antibodies. None were HIV-positive. Twenty-nine per cent (216/733) were not immune to hepatitis B, 33% (238/724) to mumps, 26% (190/724) to measles, 13% (91/724) to rubella and 10% (75/724) to varicella. About 23% (91/237) needed further testing for tuberculosis. Immunity corresponded poorly with self-reported history of vaccination. More students reported vaccination against rubella (96%), measles (81%) and mumps (80%) than were immune, and fewer reported vaccination against hepatitis B (44%).Conclusions: Many students were not immune to vaccine-preventable diseases, and a small number had a previously undiagnosed bloodborne virus infection (hepatitis B or C). The level of immunity to vaccine-preventable infections was unacceptable and justified the provision of an easily accessible program for screening and vaccination.

Adrienne J Torda FRACP, GradDipBioethics, PhD

Clinical record A previously healthy 11-year-old boy presented to the Royal Children’s Hospital (RCH) with a 20 × 12 cm necrotising wound of the left popliteal fossa (Figure A). A further inflammatory lesion was evident on the anteromedial left thigh, extending into the groin. The boy was febrile and cachectic, weighing 30 kg. The patient had a history of a suspected insect bite in the area of the popliteal fossa 5 months earlier. The suspected bite wound had developed into an 8 cm necrotic lesion over several months. The patient had initially presented to a regional centre (a few days after the suspected bite), where he was treated with oral twice-daily Augmentin Duo Forte (amoxycillin–clavulanate) (GlaxoSmithKline Australia) 750 mg, excisional debridement and split-skin grafting, with 90% graft take. The wound was treated topically with dressings. The patient then emigrated with his family to Dubai. The wound subsequently broke down and was serially debrided, with further skin grafting and antibiotic coverage with amoxycillin and ciprofloxacin. Despite 4 weeks of treatment, the wound progressed and the family was referred by a doctor in Dubai to the RCH. Investigations at our hospital revealed a white cell count of 27.4 × 109/L (reference range [RR], 4.5–13.5 × 109/L), a C-reactive protein level of 29 mg/L (RR, < 8 mg/L) and an albumin level of 26 g/L (RR, 33–47 g/L). An ultrasound scan confirmed the presence of a necrotic lymph nodal mass in the left groin. Antibiotic therapy with 6-hourly intravenous Timentin (ticarcillin–clavulanate) (GlaxoSmithKline Australia) 1.5 g was commenced. Wound and tissue cultures revealed the presence of Staphylococcus aureus and Prevotella species. Although fungal cultures were requested, no fungal pathogen was isolated. The popliteal fossa wound and necrotic inguinal nodes were surgically debrided over the following 2 weeks. This revealed extensive necrosis of the biceps femoris and semimembranosus muscle, with undermining subcutaneous fat necrosis immediately adjacent to the wound. Ten centimetres of sciatic nerve and the popliteal vessels were exposed. Both wounds were treated by topical negative pressure (vacuum) dressing (VAC Therapy System, Kinetic Concepts Inc, San Antonio, Tex, USA). When the patient failed to improve after 5 days of intravenous antibiotic treatment, clinical suspicion of an atypical disease was heightened. Multidisciplinary discussions led to a specific request to the microbiology department to attempt to identify fungal disease. Further tissue cultures under specific conditions (see below) showed growth of the fungus Saksenaea vasiformis. Histopathological analysis of resected tissue revealed extensive subcutaneous fat necrosis with calcification and many non-septate hyphae with irregular diameters and branching — features consistent with zygomycosis (mucormycosis).1 These features were not seen on Gram stain. Antifungal therapy was initiated with amphotericin B 45 mg given via central venous line over 24 hours initially and then intravenous liposomal amphotericin B 150 mg daily. Major predisposing factors to zygomycosis were excluded: specifically, hyperglycaemia, ketoacidosis and immunosuppressive disorders.1 Notable findings included a raised IgE level. Although this can be associated with hyper-IgE syndrome, the patient had no other signs of this disease. After 5 weeks of treatment with amphotericin B, the patient became unwell, with a high fever and moderate renal impairment. His creatinine level had increased from 0.06 to 0.17 mmol/L (RR, 0.03–0.08 mmol/L); his urea level was 18.7 mmol/L (RR, 2.1–6.5 mmol/L), and the glomerular filtration rate was 29 mL/min (RR, 100–140 mL/min). A renal ultrasound scan revealed parenchymal fungal spores (Figure B). Amphotericin B treatment was ceased and twice daily oral posaconazole 400 mg commenced. Renal function normalised within about 7 days. Follow-up imaging 6 weeks later revealed resolution of renal fungal disease. After 6 weeks of antifungal treatment and no growth evident on serial tissue cultures, the wounds were surgically closed. The popliteal fossa wound was treated with a pedicled medial gastrocnemius muscle flap and skin graft to cover the exposed neurovascular structures. The groin wound was closed with a sartorius muscle turnover flap and skin graft. Both the wound and donor sites fully healed without complication (Figure C). A: Necrotising wound of the left popliteal fossa on presentation. B: Renal fungal spores (arrow). C: Healed wound after 6 weeks of antifungal treatment. Since it was first isolated in 1953,2 Saksenaea vasiformis has been reported to cause human infection in about 30 cases. In only two cases has disseminated disease been reported, both occurring in immunocompetent patients and having fatal outcomes.3,4 S. vasiformis belongs to the class Zygomycetes and order Mucorales. The usual manifestation of disease is reported to be skin and soft-tissue infections, most commonly occurring secondary to trauma,1 but can also follow haematogenous dissemination. Lessons from practice Multidisciplinary care is fundamental in dealing with complex or unusual conditions. Always consider atypical pathogens, particularly fungi, when a condition fails to respond to the perceived ideal treatment. If considering a fungal pathogen, consult microbiological opinion to aid identification of the species. Posaconazole can be used safely and successfully in children to treat disseminated fungal disease. Although the two previously reported cases of disseminated S. vasiformis infection were fatal, our report details the successful treatment of disseminated disease by a combination of surgery and systemic antifungal therapy. This case thus highlights several important issues in the treatment of zygomycosis. A multidisciplinary team approach is essential for a successful outcome. Exclusion of underlying immunodeficiency is paramount, as its presence often leads to a fatal outcome.1 Surgical treatment combined with appropriate antifungal therapy is the mainstay of treatment. In the case we describe, the patient required serial debridements and the use of vacuum dressings until microbiological evidence of eradication of fungi was achieved. Vacuum dressings were a good alternative to more labour-intensive and painful forms of dressing. The dressings were changed in theatre every 3–5 days. Negative pressure dressings have been shown to improve wound healing by increasing tissue oxygenation via a reduction of interstitial fluid5,6 and reducing bacterial counts in the wound.7 Diagnosis and identification of the fungus is important. Zygomycosis must be suspected in any wound that is worsening despite appropriate treatment. Tissue culture, rather than routine wound swabs, provides the most appropriate specimen. It is important to inform the microbiology laboratory of clinical suspicion of zygomycosis. The tissue should be cultured intact to preserve the viability of the irregularly septate zygomycete hyphae. This also ensures that cultures are incubated for the extended period necessary for fungal isolation. S. vasiformis is a fast-growing organism and can usually be isolated from culture within 72 hours.1,8 Once isolated, full identification for fungi may require extended time and specialist media in a reference laboratory. Antifungal therapy is essential to the treatment of this organism, and amphotericin B has traditionally been the agent of choice. However, its significant side effects, notably nephrotoxicity, often affect treatment, as seen in this case. Our patient’s renal impairment resolved after cessation of amphotericin treatment, confirming its nephrotoxicity. Treatment with posaconazole, a new generation triazole antifungal, was initiated after withdrawal of amphotericin treatment, without leading to any complication or relapse of the disease. There is little information on the treatment of zygomycosis with posaconazole. To our knowledge, ours is the first reported case of successful salvage treatment of disseminated zygomycosis with this drug. Posaconazole has been shown to be effective against zygomycosis when other therapy has been ineffective or complications have occurred due to the therapy.9 As posaconazole is not generally used in children under the age of 13 years, its safety profile in children is unknown. The drug is available as an oral suspension and is generally administered at a dose of 800 mg daily in divided doses. The patient described here received 400 mg twice daily without complication. The duration of therapy is dictated by the presence of disease. Minor common side effects include nausea and headache. Serious side effects are rare, but hepatic impairment may occur, so liver function should be monitored every 2–3 weeks during therapy. Posaconazole interacts with several immunosuppressive agents and has few contraindications. In conclusion, this report shows that disseminated zygomycosis, specifically S. vasiformis infection, may occur in immunocompetent individuals. It also shows how, with multidisciplinary care, mortality may be avoided.

Dean J Trotter MB BS · Gena Gonis BSc(Hons), FASM · Erin Cottrill BAppSc(Lab Med) · Christopher Coombs MB BS(Hons), FRACS(Plast)

An immunocompetent patient developed a necrotising soft tissue infection after being pecked by a magpie. The infection was caused by the fungus Saksenaea vasiformis, an uncommon human pathogen. Special culture techniques are required to induce sporulation to enable identification of the organism. Clinical recordAn 84-year-old woman presented to our hospital emergency department with cellulitis of the left lower leg. There was a small, dry eschar and some adjacent purplish discolouration (Box 1, A). Eleven days previously, she had been pecked above the left ankle by a magpie (Gymnorhina tibicen), which her daughter kept as a pet. The woman reported that within a week of the pecking incident she had experienced pain, swelling and redness on the lower leg near the injury site. Worsening symptoms had led her to present to hospital. She had a history of acute myocardial infarction many years previously and mild chronic obstructive pulmonary disease. Surgical history included a hysterectomy and varicose vein ligation. She was an ex-smoker. At the time of admission, capillary refill in the foot was sluggish and the patient was unable to bear weight on the affected leg. There was no fever, and the white cell count (8.9 × 109/L) was within the normal range. Treatment with intravenous dicloxacillin was commenced. The patient’s leg failed to improve during the first week of treatment (Box 1, B), despite the addition of metronidazole on Day 5 after admission and gentamicin on Day 6. The antibiotics were changed to ticarcillin–clavulanic acid on Day 9. The patient had low-grade fevers from Day 7 and her white cell count progressively rose to 31.1 × 109/L. A Doppler ultrasound scan of the thigh on Day 11 showed occlusion of the superficial femoral artery with reperfusion by collateral vessels, consistent with atherosclerotic peripheral vascular disease. Surgical exploration was performed on the same day, with wide resection of necrotic skin and subcutaneous tissue. Operative findings were of occluded vessels with absent blood flow in the areas of necrosis. Bacterial culture of the necrotic tissue showed profuse growth of Escherichia coli and Klebsiella pneumoniae, which led to a change in antibiotic treatment to ceftriaxone. Histopathological examination of the debrided tissue showed coagulative necrosis with scattered fungal hyphae, especially within blood vessels. The hyphae had occasional septa and branched at variable angles. The more viable areas contained acute inflammatory cells. A white downy fungus grew in culture from a tissue specimen after 5 days, but the fungus was difficult to identify as it failed to sporulate in culture. When subsequently grown on Czapek Dox agar, the isolate eventually produced vase-shaped sporangia typical of Saksenaea vasiformis (Box 2). Treatment with intravenous amphotericin B was commenced on receipt of the histopathology results. However, the patient’s foot became progressively more ischaemic, with development of frank gangrene by Day 16 after admission. Above-knee amputation was performed on Day 17. A computed tomography scan of the chest showed no evidence of pulmonary fungal infection. The antimicrobial agents were ceased 6 days after surgery, and the patient was eventually discharged to a nursing home on Day 44. DiscussionFungi of the class Zygomycetes are ubiquitous in nature, being found in soil and decaying organic matter. However, they are uncommon human pathogens. Zygomycosis in humans is usually seen either in immunosuppressed patients or in immunocompetent people after cutaneous inoculation from trauma or surgery. S. vasiformis was first described in 1953 by Saksena as a new zygomycete isolated from forest soil in India.1 Infection due to S. vasiformis was first observed in 1977 in a young man who had sustained severe cranial trauma in a motor vehicle accident. The infection involved the eye and brain.2 A total of 29 cases of human infection due to S. vasiformis have since been reported in the English language literature.3,4 Most cases occurred as cutaneous zygomycosis in immunocompetent patients after traumatic inoculation. S. vasiformis typically requires special culture techniques to induce sporulation and enable definitive identification. It shares these characteristics with Apophysomyces elegans, another zygomycete.5 Reports in the literature of skin or soft tissue infections following bird pecking injuries are sparse. These include a Pseudomonas aeruginosa infection of the finger after a swan bite6 and a Bacteroides scalp infection after an owl attack.7 More serious infections relating to trauma involving a bird have included septic arthritis of the knee after a chicken bite8 and a fatal brain abscess in a child caused by a rooster peck.9 Zygomycoses have been transmitted by insect or spider bites, with the pathogens reported as Rhizopus spp,10,11 Apophysomyces elegans12 and Mucor hiemalis.13 The infection in our patient was in some ways typical of infection with S. vasiformis, in that it occurred in an immunocompetent patient after trauma, albeit of an unusual nature. The presence of pre-existing peripheral vascular disease may have contributed to the aggressive course of the infection in this patient. Zygomycetes are rapidly growing fungi with a tendency to invade blood vessels, causing occlusion and infarction. An unusual infective agent must be considered in the setting of worsening soft tissue infection despite broad-spectrum antibiotic therapy, and early debridement accompanied by fungal culture may enable diagnosis. Trauma related to a bird-pecking injury should be added to the list of predisposing risk factors for zygomycosis, as exemplified by this case. 1 Appearance of patient’s left leg 2 Microscopic appearance of the fungus, showing typical vase-shaped sporangium

Paul A Wilson BSc, BMed(Hons)

To the Editor: Buruli ulcer, caused by the bacterium Mycobacterium ulcerans, leads to the destruction of skin and sometimes bone. It has been reported in many tropical countries in Africa and in some temperate regions of Australia, Japan and China.1 In 2004, the World Health Organization recommended treatment with the combination of oral rifampicin and intramuscular streptomycin (or amikacin) for 8 weeks.2,3 In-vitro studies and new data from mouse models suggest that combinations of rifampicin with clarithromycin, rifampicin with moxifloxacin, or clarithromycin with moxifloxacin may be as effective as rifampicin and streptomycin.4,5 In June 2007, a woman who was 6-months pregnant with her first child and had a 7-month history of Buruli ulcer on her right upper limb (Box 1, A) was admitted to the Buruli ulcer treatment centre in Allada, Benin. She was otherwise in good health, and the fetal heart beat was normal. Routine laboratory examinations, including HIV serology tests, found no abnormalities. Swabs from the ulcer were positive for acid-fast bacilli by Ziehl–Neelsen stain, and for IS 2404 (DNA sequence specific for Mycobacterium ulcerans) by polymerase chain reaction testing, but no growth of M. ulcerans was obtained on culture. Histopathological analysis of punch biopsy specimens showed typical features of Buruli ulcer. As streptomycin is contraindicated in pregnancy, we treated the patient with a combination of oral rifampicin (600 mg daily) and oral clarithromycin (500 mg twice daily) for 56 days, beginning 2 weeks after presentation. The treatment was well tolerated. We monitored the clinical response through serial photographs (Box 1) and measurements of the circumference of the affected and unaffected limbs at defined points (Box 2). The patient gave birth to a healthy boy weighing 2.25 kg in September 2007, 2 weeks after completing antibiotic treatment. She underwent skin grafting a month later. The lesion healed without functional limitation (Box 1, D), and the patient was discharged in December 2007. At that time, the surface area affected by the lesion was reduced by 55%. To our knowledge, this is the first report of successful treatment of Buruli ulcer using fully oral treament with rifampicin and clarithromycin alone. We hope our experience will contribute to future discussion and studies to find an oral treatment for this devastating disease. 1 Serial views of Buruli ulcer in a woman treated with rifampicin and clarithromycin A: At presentation. B: After 4 weeks' antibiotic treatment. C: On completion of antibiotic treatment (8 weeks). D: At hospital discharge after skin grafting, showing full movement of the elbow joint (23 weeks). 2 Clinical response to treatment Week after treatment start 0 4 8 23 Limb circumference (cm) At wrist Affected limb 21 17.5 16.5 15 Unaffected limb 14 14 14 14 % difference 50% 25% 18% 7% At mid-arm Affected limb 36 33 30 25 Unaffected limb 22 22 22 22 % difference 64% 50% 36% 14% At elbow Affected limb 34 21 21 21 Unaffected limb 23 23 23 23 % difference 48% − 9% − 9% − 9% Lesion dimensions Diameter (cm)* 30.3 23.8 22.5 20.3 Area Estimate (cm2) 722 446 397 325 % reduction — 38% 45% 55% * Median diameter.

Ange D Dossou · Ghislain E Sopoh · Christian R Johnson · Yves T Barogui · Dissou Affolabi · Sévérin Y Anagonou · Théophile Zohoun · Françoise Portaels · Kingsley Asiedu

To the Editor: Kaposi’s varicelliform eruption (KVE) is a disseminated cutaneous infection caused by herpes simplex virus (HSV) in patients with predisposing factors such as atopic dermatitis, widespread skin injury and sun exposure.1-5 I report a patient with KVE but no apparent predisposing factors. A 54-year-old man presented with a 3-day history of a rapidly progressing vesiculopustular rash on his trunk, legs, arms and hands (Box). He reported a burning skin sensation and had a temperature of 38.2°C. He had no labial or oral erosions, and no history of skin disease, HSV infection or any systemic disease. He was not taking any medication and reported no excessive sun exposure before symptom onset. Haematological, biochemical and immunological parameters, including levels of C-reactive protein, immunoglobulins, complement components, lymphocyte blastogenesis and natural killer cell cytolytic activity were normal. An HIV test was negative. Skin swabs from the lesion were positive for HSV-1 by polymerase chain reaction (PCR) testing; HSV-1 was also isolated on culture. Cultures were negative for bacterial, fungal and mycobacterial pathogens. A diagnosis of KVE was thus established. Based on past experience treating KVE with a combination of oral valaciclovir and vidarabine ointment, which accelerated resolution of symptoms,6 I treated the patient with oral valaciclovir (1 g three times per day) and vidarabine ointment (three times per day). The lesions were completely healed after 7 days of treatment. HSV-1 antibody titres on Days 1 and 7, respectively, were: IgM, 3.1 and 5.2 (reference range, < 0.8); and IgG, < 2.0 and 4.7 (reference range, < 2.0). HSV-2 IgM and IgG antibody titres on Days 1 and 7 were within reference ranges (< 0.8 and < 2.0, respectively). This case is unusual as it occurred in an otherwise healthy patient. KVE is usually associated with healing second-degree burns, peribuccal dermabrasion and laser skin resurfacing,2-4 and sun exposure in patients with recurrent HSV infection.5 The origin of the patient’s HSV-1 infection was not identified: there was no outbreak of HSV infection in his city of residence; his wife and two children were healthy and had no systemic or skin diseases; PCR testing of their saliva for HSV-1 and HSV-2 DNA 3 days after the patient’s presentation gave negative results; and the patient had no apparent contact with HSV-infected patients before onset of symptoms. KVE has been successfully treated with intravenous aciclovir (three times per day) or oral aciclovir (five times per day).2,5 However, intravenous aciclovir requires hospital admission, and compliance with the dosage regimen of oral aciclovir is troublesome. In contrast, oral valaciclovir (three times per day) and vidarabine ointment do not require hospital admission and are easier for patients.1,3,6 Oral valaciclovir is also very effective for preventing herpes infection.7 This case highlights that KVE should be considered in otherwise healthy patients with a sudden, rapidly progressing vesiculopustular rash. Vesiculopustular lesions in a patient with Kaposi’s varicelliform eruption

Hajime Kimata

Objective: To assess the impact of a long-term comprehensive control program for sexually transmitted infections (STIs) in remote Aboriginal communities in Central Australia, and to investigate a recent rise in gonorrhoea prevalence.Design: STI prevalence was determined from annual, cross-sectional, population-wide, age-based screening, 1996–2006. During 2006, gonococcal isolates were obtained by on-site culture and tested for antimicrobial susceptibility.Setting: Six remote clinics on the Anangu Pitjantjatjara Yankunytjatjara (APY) Lands, South Australia, which are served by Nganampa Health Council, an Aboriginal community-controlled health service.Participants: All resident Aboriginal people aged 14–40 years at the commencement date of each annual population-wide screen.Main outcome measures: Multivariable logistic regression models were used to compare prevalence of chlamydial infection, gonorrhoea and syphilis measured during each annual population-wide screen; antimicrobial susceptibility of gonococcal isolates obtained in 2006.Results: Between 1996 and 2003, there was a significant reduction in prevalence of gonorrhoea and chlamydial infection, by 67% and 58%, respectively. Subsequently, chlamydia prevalence rate plateaued, but there was a rapid rise in prevalence of gonorrhoea. Syphilis prevalence decreased linearly over the study period (odds ratio, 0.81; P < 0.001). During the first 6 months of 2006, 89 gonococcal isolates were obtained, 39 through on-site culture during the 6-week screening period, and all were sensitive to penicillin (in the less-sensitive category).Conclusions: The decrease in STI prevalence asssociated with the program was maintained until 2006 for chlamydial infection and syphilis, but not for gonorrhoea, which rose in prevalence after 2003. There was no change in antimicrobial resistance to explain this rise, and gonorrhoea transmission dynamics and travel of core transmitters to regions without STI control programs might be responsible.

Rae-Lin Huang MB BS(Hons), MPH, FRACGP · Paul J Torzillo MB BS, FRACP, FJFICM · Vivien A Hammond RN, RM, GradDipNursing · Stephanie T Coulter BLabMed · Adrienne C Kirby BSc(Hons), MSc

To the Editor: In the preceding article, we report on a substantial rise in prevalence rates of gonorrhoea in a population in remote Central Australia.1 This rise occurred in the context of a sustained major reduction in sexually transmitted infections (STIs) in the region, achieved by a comprehensive program of STI control, described in the article1 and previously.2 We found that the gonorrhoea outbreak was not due to penicillin resistance of the causative organism, and we hypothesise that it was due to the introduction and dominance of a more infectious clone.3,4 This rise in gonorrhoea in a region widely acknowledged to have the most successful STI control program in the country prompted several commentators to argue that both this program, and screening as a measure for STI control in remote Indigenous communities, had failed, and to advocate a range of other approaches.5 We recently completed the analysis of the 2008 annual population-wide STI screen, which achieved a 78% participation rate among eligible participants. These data strongly suggest that the gonorrhoea outbreak seen over the previous 4 years has been controlled (Box). Furthermore, the current prevalence rates are among the lowest seen in the past decade. These findings suggest that a comprehensive STI control program, such as that delivered by the Nganampa Health Council, can not only reduce STI rates, but also control outbreaks, provided the program is sustained. During most of the past decade, the prevalence of syphilis remained below 1%, of chlamydial infection below 6%, and of screening test-positive gonorrhoea below 8%, as measured during the annual population-wide screens. This program should be replicable in other regions, if appropriate resources and expertise are applied, thus providing an opportunity to improve an important area of Indigenous health using current public health knowledge. Age-adjusted prevalence rates of chlamydial infection, gonorrhoea and syphilis among 14–40-year-olds on the APY Lands, 1996–2008 APY = Anangu Pitjantjatjara Yankunytjatjara.

Rae-Lin Huang · Paul J Torzillo · Adrienne C Kirby

Mumps has re-emerged as an infection in the developed world. Its epidemiology has changed, with the majority of cases now primarily affecting adolescents and adults. While mumps is easily suspected if parotitis is present, parotitis is absent in 10%–30% of symptomatic cases. Mumps is a systemic infection with a variety of extra-parotid complications. In Australia, mumps diagnosis is confirmed by antibody testing and reverse transcriptase-polymerase chain reaction techniques. Suitable specimens for testing are serum, saliva, urine and cerebrospinal fluid. Treatment is generally supportive, although intravenous immunoglobulin therapy may have a future role in mumps management. Interferon alpha-2b treatment may be considered specifically for mumps epididymo-orchitis. Mumps vaccine is included in the measles–mumps–rubella (MMR) vaccine. In Australia, this vaccine is routinely administered at the ages of 1 and 4 years. Serious reactions to the mumps components of the MMR vaccine are rare.

Sanjaya N Senanayake BSc(Med), MAppEpid, FRACP

To the Editor: Streptococcus suis is an emerging zoonosis in humans and a common pathogen in Australian pigs.1 However, only two cases of human infection have previously been reported in Australia.2,3 We recently treated two Australian piggery workers, from the same town in New South Wales, for S. suis endocarditis. The first patient, a previously healthy 46-year-old woman, presented in October 2006 with a 3-month history of fatigue, anorexia, night sweats and weight loss of 20 kg. Her job involved hands-on work at a piggery. She was afebrile, with blood pressure of 145/50 mmHg, bilateral clubbing, splenomegaly, and a long diastolic murmur without evidence of heart failure. Transthoracic echocardiography confirmed severe aortic regurgitation associated with a vegetation. Blood cultures grew S. suis. The patient was treated with benzylpenicillin (1.8 g, 4-hourly for 6 weeks) and gentamicin (60 mg, 8-hourly for 2 weeks). Severity of aortic regurgitation necessitated aortic valve replacement. The second patient, a 58-year-old man, presented in January 2008 with headache, fever (38.7°C), neck stiffness and confusion. He had been unwell for 1 month with fevers, sweating, fatigue and weight loss of 6 kg. His job involved transporting pigs from local piggeries, including the one at which the first patient worked, to an abattoir, and involved direct contact with pigs. On admission, he was treated with ceftriaxone (2 g) and benzylpenicillin (2.4 g). Cerebrospinal fluid (CSF) examination showed leukocytosis (10 300 × 106/L; reference range, < 5 × 106/L) with 95% polymorphs. Scanty gram-positive cocci were visible, but there was no growth on culture of the CSF. Blood cultures grew S. suis. Transthoracic echocardiography revealed an aortic valve vegetation with trivial regurgitation. The patient was then treated with benzylpenicillin (1.8 g, 4-hourly for 4 weeks) and gentamicin (80 mg, 8-hourly for 2 weeks), and made a full recovery. Both cases were investigated by the NSW Department of Health, including assessment of workplace practices, staff education and rates of porcine infection at the piggeries and abattoir at which the patients had worked, but no significant factors for infection were identified. Since the first reported human infection with S. suis in Denmark in 1968,4 more than 400 cases have been reported, including an outbreak in China in 2005 that affected 215 people.5 The most common manifestations are meningitis (affecting 72.5% of patients) and bacteraemia (24.2%); endocarditis is relatively uncommon (1.1%).5 In a series of 16 cases of S. suis endocarditis, the mean period between onset of symptoms and diagnosis was 23 days, and seven patients required valve replacement.6 Similarly, our patients had subacute presentations: severe aortic regurgitation and secondary meningitis. In Australia, it is likely that there have been other S. suis infections in humans that have gone unrecognised because of mild presentations, difficulties with laboratory diagnosis, and empirical treatment of unrecognised infection. While it is unlikely that S. suis is a common zoonosis in Australia, these cases show that it is an occupational hazard in Australian piggeries, with potential public health, animal health and medicolegal implications.

Karina J Kennedy · Assad A Jadeer · Chong W Ong · Sanjaya N Senanayake · Peter J Collignon

Objectives: To describe all cases of staphylococcal pyomyositis in the Geelong region of Victoria over 110 months, to estimate the incidence of this disease, and to describe the clinical outcomes and identify any predisposing factors.Design, participants and setting: A prospective case series identified by clinical features (local pain and fever) and magnetic resonance imaging (MRI) findings (hyperintense signal on T2-weighted scan), among patients presenting to Geelong Hospital, Victoria between 1 April 1998 and 1 June 2007.Main outcome measures: Estimation of incidence, clinical course and identification of predisposing factors.Results: We estimate an annual incidence of 0.5 cases per 100 000 person-years, and propose a recent history of vigorous exercise (six of 11 patients) and underlying skin condition (five of 11 patients) as possible predisposing factors. MRI showed eight patients had osteomyelitis and one had septic arthritis. All patients had bacteraemia and one had mitral valve endocarditis. The duration of intravenous antibiotic therapy varied between 4 and 12 weeks, and all patients were completely cured.Conclusion: Pyomyositis should be considered in patients presenting with local pain, fever, muscle tenderness, and a recent history of vigorous exercise or underlying skin condition. MRI may guide non-surgical management.

Andrew A Block MB BS, BMedSci, FRACP · Catherine Marshall MB BS · Alison Ratcliffe MB BS, FRACP · Eugene Athan MB BS, FRACP

To the Editor: Cunningham and colleagues discussed the rationale for using a live attenuated vaccine against varicella zoster virus (VZV) in preventing herpes zoster (HZ) in an older population.1 They also noted the difficulties in using a live vaccine in immunocompromised adults. Although generally considered less immunogenic than its live counterpart, an inactivated VZV vaccine would be ideal for vaccinating immunocompromised hosts. There is little information in the medical literature on inactivated VZV vaccines. However, the studies that do exist tested inactive vaccine on adult populations and showed favourable performance when compared with a live vaccine.2,3 Despite these promising results, the inactivated vaccine seems to have gone out of favour. Furthermore, if an inactivated VZV vaccine was used in the childhood vaccination programs against varicella, then it would simultaneously solve two problems caused by the vaccine strain of the virus, namely the development of infectious varicella and the reactivation of the vaccine strain as HZ.4 Cunningham and colleagues discussed the benefits of vaccinating an older population with VZV vaccine,1 but did not raise the intriguing possibility that the vaccination program might reduce rates of listeriosis in older people.4 A recent study examined the T-cell response in mice to latent herpesvirus infection, and found that it led to activation of macrophages that, surprisingly, protected the host against subsequent infection with other pathogens such as Listeria monocytogenes.5 Given that protection from HZ through vaccination is achieved by stimulating T-cell numbers above a critical threshold for HZ,6 it could be hypothesised that VZV vaccinees may be protected against listeriosis, an infection to which older people are more susceptible. The basis of this hypothesis is that macrophage activity would be stimulated by the T-cell response to the VZV vaccine, thereby providing cross-protection against L. monocytogenes. Prospective follow-up of vaccinees in Australia over time could refute or confirm this hypothesis.

Sanjaya N Senanayake

Objective: To investigate the first reported cases of strongyloidiasis in the Solomon Islands, and to establish whether this disease poses a risk to personnel of the Regional Assistance Mission to Solomon Islands (RAMSI).Design, setting and participants: Retrospective review of the pathology database of the RAMSI Medical Facility in Honiara, Solomon Islands, for the period 1 July 2006 – 30 September 2007.Main outcome measures: Number and clinical features of confirmed cases of Strongyloides stercoralis infestation, as diagnosed by serological tests or faecal microscopy.Results: Fourteen confirmed cases of strongyloidiasis in previously healthy RAMSI participants were identified. Of 13 patients with notes available, symptoms documented at presentation included epigastric pain (10 patients), diarrhoea (7) and urticaria (4). Clinical disease in all patients responded to oral antihelminthic therapy (albendazole or ivermectin).Conclusions: Strongyloidiasis is endemic in the Solomon Islands and a risk for RAMSI personnel. Australian medical professionals should be aware of this potentially fatal and lifelong infestation, particularly the importance of an occupation history, appropriate diagnostic tests, effective treatment and adequate follow-up to document cure. We recommend implementation of a postdeployment screening program for strongyloidiasis.

David A Pattison MB BS · Richard Speare MB BS, PhD, FAFPHM

To the Editor: The recent call by Robotin and colleagues for a national strategy to respond to the increasing incidence of hepatitis B and hepatocellular carcinoma (HCC) in Australia1 is timely. I would like to add the following comments. First, a comprehensive Australian hepatitis B strategy should include prisoners and Indigenous Australians. Among Australian prisoners, hepatitis B carrier prevalence is 3%–5% — more than three times the national average — and prevalence of hepatitis C, which independently and synergistically increases the risk of severe liver disease, exceeds 30%.2 In addition, of 526 acute hepatitis B notifications in Australia in 2000–2002, 57 were in Indigenous Australians, a notification rate more than four times that in non-Indigenous Australians. Indigenous people are 12 times more likely to die of liver cancer than the general Australian population.3 Second, in New South Wales, the median age of diagnosis of HCC was found to vary significantly by country of birth;4 it was 5 years younger in the Asian-born group than the Australian-born group overall (64 v 69 years), and 9 years younger in those who were hepatitis B carriers (57 v 66 years) (P < 0.001 for both differences). Early onset of HCC among Asian-born Australians may be a result of hepatitis B infection in the perinatal and early childhood period. However, other factors that promote progression to HCC, such as diabetes, alcoholism, and inadequate health care access, are amenable to targeted public health interventions. Third, hepatitis B e antigen (HbeAg) positivity is strongly associated with high hepatitis B virus DNA counts (≥ 100 000 copies/mL), which are in turn highly predictive of cirrhosis and HCC risk. It is thus counterintuitive that — as implied by Robotin et al — hepatitis B carriers who are positive for HbeAg are less likely to progress to cirrhosis and HCC than those who have undergone seroconversion and are positive for hepatitis B e antibody. In fact, HBeAg positivity is associated with increased risk of HCC and liver-related mortality.5,6 Finally, the omission of hepatitis B vaccine — the world’s first anticancer vaccine — from Robotin et al’s list of elements of a public health response to hepatitis B and liver cancer is unfortunate. Hepatitis B vaccination is essential to any credible medium- and long-term strategy to prevent hepatitis B infection and, by extension, HCC, both in Australia and globally.

Niyi Awofeso

In reply: We agree with Awofeso that prisoners and Indigenous people have an increased risk of developing chronic hepatitis B. However, as no large-scale population-based studies of hepatitis B prevalence have been published in Australia, estimates of the risk vary widely.1 A national hepatitis B strategy may provide additional impetus for obtaining high-quality data. We also concur that modifiable behavioural factors may play a role in the age of hepatocellular carcinoma diagnosis, but differences in clinical course between Asian and white Australians,2 and the specific viral genotypes prevalent in Asia,3 are likely to be more important. Although white populations who undergo hepatitis B e antigen (HbeAg) seroconversion and develop hepatitis B e antibodies have a good prognosis, this is not so for Asian populations,2 or for other populations who are mostly infected in childhood, such as Indigenous Australians and Māori in New Zealand. The median age of HBeAg seroconversion in Asian patients with chronic hepatitis B is 34.5 years,4 while the median age at diagnosis of hepatocellular carcinoma of Asian patients quoted by Awofeso is 57 years, by which age most would have seroconverted. Australia has been successful in primary prevention of hepatitis B through vaccination (albeit less so in migrants, some Indigenous communities and catch-up vaccination), and hence the omission of vaccination from our “wish list” for a public health response. However, Australia has been less successful in secondary and tertiary prevention. We hope that a national strategy would be a catalyst for these interventions to be given the priority they deserve.

Monica C Robotin · Jacob George · Rajah Supramaniam · Freddy Sitas · Andrew G Penman

Objective: To analyse the uptake of interventions known to reduce the risk of perinatal HIV transmission among Australian women with HIV infection (who knew their HIV status before delivery), and identify predictors of uptake.Design: Retrospective analysis of perinatal HIV surveillance data in Australia.Patients: Women reported as having HIV infection and having given birth to a child (1982–2005) were identified through three mechanisms: an informal network of clinicians (1982–1993); an active surveillance program through paediatricians (since 1993); and state health department reports of children born to women newly diagnosed with HIV (since 1995).Main outcome measures: Uptake of interventions — avoidance of breastfeeding (after 1985), use of zidovudine during pregnancy (after 1994), and elective caesarean section (after 1999). Factors associated with uptake of these interventions were identified by univariate and multivariate analyses.Results: 367 live births were reported in 291 women with HIV infection. Among the subgroup diagnosed with HIV infection before delivery, 4/255 (1.6%) elected to breastfeed (post 1985), 44/185 (24%) did not receive zidovudine (after 1994), and 41/118 (35%) did not have an elective caesarean section (after 1999). In multivariate analysis, there were significant differences in uptake of zidovudine and elective caesarean section according to year of birth and state in which the birth took place.Conclusion: In Australia between 1982 and 2005, uptake of interventions to reduce mother-to-child transmission of HIV was high. There were significant differences associated with use of zidovudine and mode of delivery according to location of delivery and year of birth.

Michelle L Giles MB BS, FRACP · Ann M McDonald BSc, MPH · Elizabeth J Elliott MD, FRCP, FRCPCH · John B Ziegler MD, FRACP · Margaret E Hellard FRACP, FAPHM, PhD · Sharon R Lewin MB BS, FRACP, PhD · John M Kaldor PhD

Two children with advanced lung disease underwent successful cadaveric bilateral lobar lung transplantation, using lungs “cut down” from deceased adult donors — the first reported use of the technique in Australia. This approach, while it cannot address the lack of donor organs, may enable us to redress any size bias limiting paediatric lung transplantation. Clinical recordsPatient 1A previously healthy 9-year-old girl presented in early 2007 with an upper respiratory tract infection that progressed over 10 days to respiratory failure, requiring intubation and ventilation with high inspiratory pressures. Subsequent tracheal aspirates were positive for Mycoplasma (by polymerase chain reaction), with consistent serological results (antibody titres, 1 : 640). Computed tomography of the chest demonstrated widespread bronchiectasis (Box 1, A). Although she was extubated 6 weeks after initial presentation, she remained in hypercapnic respiratory failure (Pco2, 80 mmHg), requiring continuous oxygen supplementation (5 L/min) and bilevel non-invasive positive-pressure ventilation (BiPAP). She was listed for lung transplantation in May 2007, but, given the severity of her lung disease and in the absence of appropriately matched donor organs, the transplant team gave early consideration to cadaveric bilateral lobar transplantation using an adult “oversized” donor. This was performed in August 2007. Patient 2A 13-year-old girl with cystic fibrosis was referred for consideration of lung transplantation. She had been diagnosed with cystic fibrosis at birth (Δ508 homozygous, without liver, sinus or diabetic sequelae), and over the preceding 2 years developed progressive bronchiectasis (Box 1, B), necessitating supplemental oxygen and initiation of nocturnal BiPAP. She was initially listed for either lung transplantation or heart–lung transplantation; however, after 9 months of progressive respiratory failure (Pco2 increased to 46 mmHg; forced expiratory flow in 1 second [FEV1], 16%; forced vital capacity [FVC], 28% predicted), the transplant team considered cadaveric bilateral lobar transplantation, which was performed in September 2007. Surgical procedure and clinical courseBoth children underwent cadaveric bilateral lobar transplantation as described by Starnes and colleagues1 for living-related lung transplantation. Briefly, the donor right lower lobe was resected, and the right upper and middle lobes were implanted, the anastomosis being performed at the right main bronchus. On the left, the inferior pulmonary vein, interlobar artery distal to its lingular branch, and bronchus were transected, and the lower lobe removed. Size mismatch was compensated for by seating the donor bronchus inside the recipient bronchus, while pulmonary vessel mismatch was taken up in the suture lines. Neither patient required cardiopulmonary bypass, and resected lobes were not used further. Following surgery, both children were established on an internationally standardised immunosuppression regime, comprising prednisolone, tacrolimus and mycophenolate mofetil.2 Both patients made a good postoperative recovery, with short intensive care unit stays. Patient 1 required a longer inpatient stay for treatment of pneumonia. Neither patient developed allograft rejection, and lung function gradually improved (Box 2). Both patients were discharged to their respective tertiary hospitals for continuing follow-up. Both patients were well and without complication at follow-up 10 and 9 months postoperatively, respectively. DiscussionTo our knowledge, these are the first reported cases of cadaveric bilateral lobar transplantation in Australia. They demonstrate its efficacy as a means of reducing waiting-list mortality for paediatric lung transplantation recipients. Lung transplantation is now an established treatment for patients with severe end-stage lung or pulmonary vascular disease. Despite attempts to increase organ donation worldwide, the number of patients requiring lung transplantation far exceeds the availability of donor lungs. In Australia, this is of particular concern for children awaiting appropriate size-matched donor organs.3 Review of the Australian and New Zealand Organ Donation Registry between 2002 and 2006 revealed that very few lungs are retrieved from paediatric donors younger than 14 years (26/497 lung donors).4 The number of children with severe lung disease warranting consideration of lung transplantation, both globally and in Australia, is, fortunately, very small. The most recent data from the International Society for Heart and Lung Transplantation show that only 65 paediatric lung transplantations were performed worldwide in 2005.2 However, of concern is that waiting-list mortality is greater for children than for adults — a worrying trend as fewer paediatric lung transplantations have been performed per annum, while adult lung transplantation numbers have increased.5 In Australia during 2006, 181 donor lungs were offered for lung transplantation, with only seven paediatric donors contributing, all of whom were aged 6–14 years (Ross Pettersson, Australian and New Zealand Cardiothoracic Organ Transplant Registry and Heart Transplant Data Manager, St Vincent’s Hospital, Sydney, NSW, personal communication). Despite an active policy of utilising “extended” donor organs (eg, from older donors or donors with previous cancer, smoking or aspiration history) wherever possible, only 30%–50% of available lungs are actually suitable for transplantation,6 further diminishing the number of available donor lungs, which is low by international standards.7 In the absence of appropriately size-matched organs, children from our institution have died while on the waiting list (2/9 listed in 2000–2007); after reviewing the 2007 donor referrals, it became apparent that the children described here would most likely have died while waiting. Minimising paediatric waiting-list mortality requires consideration of non-traditional donor sources, such as live donors, who have been used in small numbers in the United States and Japan.8 The technique involves a bilateral lobar transplantation, typically taking one lobe from each of two larger, usually related, adult donors. Outcomes for living-donor bilateral lobar transplantation are similar to cadaveric lung transplantation, but there are significant ethical and technical issues with such an approach, and a potential 300% mortality rate. The number of these procedures being performed is declining.5 To our knowledge, no centre presently offers this service in Australia. In adults, cadaveric lungs have been cut down to facilitate lung transplantation where size mismatch between donor and recipient could prevent transplant.9 Typically, this involves non-anatomical “lung shaving” or anatomical lobar resection. Rarely is this a bilateral extensive procedure, given the potential complications, including persistent air leaks, airway stenoses and stump dehiscence. Lobar transplantation is not specific to lung transplantation and has become common practice in liver transplantation; lessons may be learned from these experiences.10 Paediatric lobar transplantation has not been widely performed outside of the living-related scenario, but despite the additional surgical complexity, outcomes have proven comparable to cadaveric lung transplantation.8,9 Starnes and colleagues’ work suggests our two patients can be expected to ultimately achieve near-normal lung function,11 and their total lung capacity will increase as they grow.12 Cutting down cadaveric adult donor lungs for use in paediatric recipients raises ethical and practical issues about removing donor lungs from an already insufficient adult pool. Should lungs that might “perfectly” match an adult be cut down for a paediatric patient? Is a child more deserving than an adult? Our approach to reducing waiting-list mortality is to perform transplantation on recipients with the most severe lung disease at the first opportunity, and both these children satisfied that criterion. In conclusion, our cases illustrate the difficulty experienced by many centres in acquiring an adequate number of donor lungs to service the needs of the paediatric lung transplantation waiting list. Using cut-down adult donor lungs had a good outcome in both our patients. Such an approach is likely to expand the donor pool available for children needing lung transplantation, thereby reducing the high waiting-list mortality experienced by this age group. 1 Computed tomography scans of the two patients’ lungs before transplantation A: Patient 1 had cysts and lung destruction after Mycoplasma infection (arrows). B: Patient 2 had severe cystic fibrosis-related bronchiectasis (arrows). 2 Clinical course after cadaveric bilateral lobar transplantation in two children Patient ICU days Hospital days Respiratory infection in first 3 months Biopsy (ISHLT grade) 30 days 90 days 180 days FEV1 (% pred) FVC (% pred) FEV1 (% pred) FVC (% pred) FEV1 (% pred) FVC (% pred) 1 2 27 Pseudomonas, Staphylococcus A0 0.89 (40%) 0.90 (37%) 1.02 (46%) 1.33 (54%) 1.26 (55%) 1.81 (78%) 2 2 11 Staphylococcus A0 1.12 (72%) 1.27 (71%) 1.17 (75%) 1.45 (81%) 1.11 (63%) 1.66 (94%) ICU = intensive care unit. ISHLT = International Society for Heart and Lung Transplantation. FEV1 = forced expiratory flow in 1 second. pred = predicted. FVC = forced vital capacity.

Dominic T Keating MD, MRCPI · Glen P Westall FRACP, PhD · Silvana F Marasco MS, FRACS · Jacquie H Burton DipAppSci(Nursing), BN, GradDipPaed · Mark R Buckland MB BS, FANZCA · Colin F Robertson MSc(Epi), MD, FRACP · Trevor J Williams MB BS, FRACP, MD · Gregory I Snell MB BS, FRACP, MD

To the Editor: A 37-year-old man was referred to our emergency department with an acute 7 cm abscess of the buttock. The abscess was incised, and the patient was prescribed oral β-lactam antibiotics and discharged. After 48 hours, culture of samples from the abscess showed methicillin-resistant Staphylococcus aureus with a community-acquired antibiotic resistance pattern (CA-MRSA). The isolate was resistant to β-lactam antibiotics, but sensitive to trimethoprim, gentamicin, and tetracycline. Unusually for an Australian CA-MRSA strain,1 the isolate was also resistant to erythromycin and ciprofloxacin. On reviewing the patient’s history, it was noted that he was a previously well United States resident who had visited Australia and New Zealand as part of the support team for an international rock band. Further testing was undertaken, and the isolate tested positive for genes coding for the Panton–Valentine leukocidin toxin, associated with staphylococcal virulence (eg, recurrent furunculosis, abscess formation, and necrotising pneumonia).2 Pulsed-field gel electrophoresis (performed by the Gram-Positive Bacteria Typing and Research Unit, Department of Microbiology and Infectious Diseases, Royal Perth Hospital, WA) confirmed the isolate as the ST8-MRSA-IV strain, also known as USA300. Most CA-MRSA strains remain susceptible to a majority of non-β-lactam antibiotics, including clindamycin, trimethoprim–sulfamethoxazole, tetracyclines and fluoroquinolones. This helps distinguish CA-MRSA isolates from the typically multiresistant hospital strains, and facilitates oral outpatient therapy. USA300 is the dominant strain causing CA-MRSA infections in the US.3 Among 422 patients with soft-tissue infections presenting to 11 US emergency departments in 2004, 59% of cases were caused by CA-MRSA, of which 99% were USA300. Recent reports indicate that multiresistance is emerging within this strain, with acquisition of resistance to erythromycin, clindamycin, mupirocin and fluoroquinolones. An increasing association of USA300 infections with buttock and perineal infections is also reported, as well as potential sexual transmission, particularly among men who have sex with men. Our case highlights the ease of international spread of microorganisms. Arguably, a “one-night stand” tour could be an ideal vehicle for microbial dissemination. CA-MRSA was not considered in the patient’s initial assessment, and the patient was discharged with oral β-lactam antibiotics and no planned follow-up. Moreover, the isolate may not have been identified as the “epidemic” USA300 strain without more involved tests. A recent study documented a rising incidence of USA300 isolates in Western Australia between 2003 and 2007. Of 61 patient isolates, 35 were diagnosed in 2007 (Pearson J, Coombs G, Christiansen K, et al. USA300 MRSA identified in the Australian community [abstract PP3.2]. Abstract presented at the Australian Society for Antimicrobials 9th Annual Scientific Meeting; 2008; Feb 21–23; Sydney). Our case suggests we should be more alert to CA-MRSA infection presenting with furunculosis and soft tissue infections, not only in Indigenous communities and young people, but also in international travellers and patients whose infections fail to respond to usual therapy. It also reinforces the value of incision and drainage. As β-lactam susceptibility is no longer assured, such specimens should routinely undergo culture and susceptibility testing.

Thomas Gottlieb · Wei-Yuen Su · John Merlino · Elaine Y-L Cheong

Objective: To investigate a reported increase in tinea capitis in an English-language school to determine if it was an outbreak and whether control measures were warranted.Design: Cross-sectional study.Setting and population: Primary school children enrolled at an English-language school in an outer suburb of Melbourne were screened for tinea capitis in November 2005 by clinical examination, collection of scalp, skin or nail specimens where clinically indicated, and scalp brushing.Main outcome measures: Clinical diagnosis of tinea capitis confirmed by microscopy and culture.Results: Parental consent was obtained for 180 children (98%), of whom 153 (85%) were screened. Dermatophytes were isolated from 21% (32/153) of the children screened, comprising 23 infected children (cases) and 9 carriers. Three dermatophyte species were identified: Trichophyton soudanense, Trichophyton violaceum and Microsporum audouinii. Cases and carriers were significantly different to non-cases by ethnicity (P = 0.010): a higher proportion came from Africa, notably Sudan, and Arabic countries.Conclusions: Although our result may reflect what is expected in these migrant groups, tinea capitis caused by these three dermatophyte species is rare in Australian school children. Tinea capitis may continue to be a problem in these groups on account of continuing migration.

Michelle E McPherson BSc/BA, MPH, MAppEpid · Alan J Woodgyer BSc(Hons) · Kleete Simpson BSci(Med), MB BS(Hons), MPH · Alvin H Chong MB BS

Objective: To examine trends in invasive pneumococcal disease (IPD) in Indigenous people in north Queensland following the introduction of the 7-valent pneumococcal conjugate vaccine (7vPCV).Design: Trends in IPD were compared over three 3-year periods: before the introduction of 7vPCV for Indigenous children (1999–2001), and two consecutive periods after its introduction (2002–2004 and 2005–2007).Main outcome measures: Incidences of IPD in Indigenous children and adults in 1999–2001 and 2005–2007; trends in IPD caused by 7vPCV and non-7vPCV serotypes; and trends in indirect protective effects and emergence of non-7vPCV serotype IPD.Results: From 1999–2001 to 2005–2007, there was a 60% decline in IPD, with the virtual elimination of 7vPCV serotype IPD in young (< 5 years) Indigenous children. There is no evidence yet of an increase in non-7vPCV serotype IPD in these children. Although the annual incidence of IPD in Indigenous adults remained virtually unchanged, there was a 75% decline in 7vPCV serotype IPD in these adults (χ2trend = 11.65, P < 0.001). However, the incidence of IPD caused by non-7vPCV serotypes more than tripled in adults (χ2trend = 7.58, P = 0.006). Serotype 1 IPD has been prominent over the 9 years, but there is no evidence of a recent increase in serotype 19A IPD.Conclusions: Vaccinating Indigenous children with 7vPCV has protected Indigenous adults in north Queensland through an indirect “herd immunity” effect. However, this benefit has been offset by a recent increase in non-7vPCV IPD in Indigenous adults. Newer pneumococcal conjugate vaccines could prevent, both directly and indirectly, a considerable amount of the persisting IPD in Indigenous people in the region.

Jeffrey N Hanna MPH, FAFPHM · Jan L Humphreys · Denise M Murphy DipMedTech