Infectious diseases

Patrick G P Charles,* M Lindsay Grayson,† Peter W Angus,‡ Joseph J Sasadeusz§ * Registrar, Department of Infectious Diseases, † Director, Infectious Diseases and Clinical Epidemiology, ‡ Director, Gastroenterology and Hepatology, Austin and Repatriation Medical Centre, Studley Road, Heidelberg, VIC 3084; § Director, and Infectious Diseases Physician, Victorian Infectious Diseases Service, Royal Melbourne Hospital, Melbourne, VIC. patrick.charlesATmh.org.au In reply: Magnavita correctly points out the need for a national policy on the management of healthcare workers who are either infected with or occupationally exposed to hepatitis C virus (HCV). Compulsory testing of healthcare workers is neither practical, logical nor fair in the current Australian healthcare environment. Firstly, most healthcare institutions do not currently have adequate staff health systems in place to ensure that staff are appropriately vaccinated against readily preventable diseases, such as hepatitis B, measles and varicella, let alone to test all staff for a disease such as hepatitis C, for which there is no vaccine. Secondly, awareness about important issues, such as healthcare worker transmission-risk assessment is embryonic (at best) in most institutions. The risk of HCV transmission from infected healthcare workers to their patients is generally considered to be extremely low, but probably depends on a number of factors, including the nature of the patient’s procedure and the healthcare worker’s injury and level of viraemia at the time. Simplistic legal opinions about such matters rarely help. Finally, we agree that the rights of healthcare workers are often neglected in this era of litigation-driven medicine. If these rights are not considered, and infected or exposed healthcare workers are simply excluded from all types of work without any appropriate risk assessment or compensation, then compliance with any form of postinjury testing is unlikely. However, rather than ignoring this important workplace issue, as we believe many Australian institutions currently do, a logical assessment of potential transmission risk is possible that is both fair to the patient and the infected worker. Stratification of healthcare workers according to their level of HCV viraemia and whether they are involved in exposure-prone procedures is a logical start — this we have attempted in our proposed guidelines.1 Some healthcare workers may avoid being tested so that they can have the protection of not knowing their serological status.2 However, recent studies suggesting the efficacy of early treatment of acute HCV infection3 mean that it will actually be in healthcare workers’ interest to know if they have recently acquired HCV infection — as long as they are treated in a manner that protects their health and workplace rights, while also protecting the rights of their patients.

Patrick G P Charles · M Lindsay Grayson · Peter W Angus · Joseph J Sasadeusz

A 53-year-old Asian man with type 2 diabetes mellitus presented to the Emergency Department with acute onset of generalised muscle cramps. He reported a 2-month history of polydipsia, polyuria and passing “milky” urine with blood clots. He had travelled widely throughout subtropical Asia. On examination, he was normotensive, with no lymphadenopathy, abdominal masses or oedema. Urinalysis showed marked proteinuria, glycosuria and haematuria. The urine protein excretion rate was later confirmed to be 15.57 g/24 h (reference interval [RI], 0.02–0.15 g/24 h). Urine triglyceride measurement and lipoprotein electrophoresis confirmed the appearance of chylomicrons in the urine after an oral fat tolerance test (Box 1). Biochemical analysis of serum showed the following levels: sodium 121 mmol/L (RI, 134–146 mmol/L), potassium 4.6 mmol/L (RI, 3.4–5.3 mmol/L), creatinine 46 μmol/L (RI, 60–105 μmol/L), glucose 19.7 mmol/L (RI, < 5.5 mmol/L), ferritin 16 mg/L (RI, 30–620 mg/L), 25-hydroxyvitamin D 11 nmol/L (RI, > 50 nmol/L), total cholesterol 5.2 mmol/L (RI, <5.5 mmol/L), and triglyceride 1.8 mmol/L (RI, < 1.8 mmol/L). The patient had marked hypoproteinaemia and hypoalbuminaemia, with a total protein level of 39 g/L (RI, 63–80 g/L) and albumin level of 21 g/L (RI, 35–50 g/L), respectively. The serum IgE level was also raised (2300 kU/L; RI, < 210 kU/L). The patient was mildly anaemic (haemoglobin level, 120 g/L [RI, 130–170 g/L]), with a normal erythrocyte sedimentation rate and C-reactive protein level. There was lymphopenia but no eosinophilia. No microfilariae or acid-fast bacilli were detected in thick blood films taken at midnight or in a urine sample. Serological and intradermal tests for filariae were also negative. A chest x-ray and computed tomography scan of the abdomen and pelvis were normal. A biopsy of the right kidney showed evidence of mild mesangial change, consistent with diabetes mellitus. Lymphoscintigraphy showed delayed lymphatic transport, particularly on the left side, but no physical obstruction to lymphatic drainage. Contrast lymphangiography demonstrated a grossly abnormal lymphatic system in the pelvis and groin with a unilateral left-sided lymphorenal communication (Box 2). A presumptive diagnosis of filariasis was made and the communication between the left kidney and the lymphatics was surgically disconnected. The chyluria recurred after surgery, but within 4 weeks of a therapeutic course of the antifilarial diethylcarbamazine there was complete resolution. Furthermore, the biochemical abnormalities reversed, consistent with urinary loss as the mechanism. At 3-year follow-up, the patient remained symptom-free and without chyluria. DiscussionChyluria is rare in Australia but common in many parts of the world, particularly where Wuchereria bancrofti, the main agent of filariasis, is endemic. It occurs, on average, 5–10 years after the worm has died, and so there may be no evidence of active filariasis. However, a therapeutic trial of diethylcarbamazine should be considered before undertaking surgery. As spontaneous remissions of chyluria have been reported, we can not be certain whether the antifilarial therapy was responsible for resolution of the chyluria in this case. 1: Oral fat tolerance test Urine of patient before a 75 g oral fat tolerance test (0 h) and at serial time points (0.5, 1, 2, 3, 4, and 5 h) after the test. 2: Contrast lymphangiography Contrast lymphangiogram, showing a grossly abnormal lymphatic system with a unilateral left-sided lymphorenal communication (arrow).

John R Burnett MB ChB, FRCPA, PhD · Gary G Sturdy MB BS · Suzzanne J Smith BSc(Hons) · Yuli Ten MB BS · Michael J McComish MB BS, FRACP

Objective: To describe an outbreak of Plasmodium vivax malaria in Far North Queensland in 2002.Design: Epidemiological and entomological investigations; molecular analyses of the infecting parasites.Main outcome measures: Case characteristics, adult and larval mosquito counts at the outbreak location, haplotyping of parasites in blood samples from different cases determined through sequencing of AMA1 and MSP1 genes.Results: A man with imported P. vivax malaria stayed at a camping ground 95 km north of Cairns in late September 2002. This led to an outbreak of P. vivax malaria in 10 adults who stayed at the camping ground in October. Large numbers of Anopheles farauti sensu lato larvae were present in stagnant pools in a creek at the camping ground, and many adult mosquitoes were collected nearby. Not only had most of the infected patients been exposed to mosquitoes at night, they were also less likely than other campers to have used insect repellents appropriately (odds ratio, 0.01; P < 0.001). Two different haplotypes of P. vivax, only one of which was detected in the imported case, were involved in the outbreak.Conclusions: Although local transmission of malaria is rare in Far North Queensland, the risk is probably higher in the dry season (September to December). Campers need to be aware of the increased risk of mosquito-borne diseases. Sexual recombination of multiple gametocytes in mosquitoes infected by the imported case may have resulted in the two haplotypes of P. vivax involved in the outbreak.

Jeffrey N Hanna MPH, FAFPHM · Scott A Ritchie PhD · Dianne L Brookes MPHTH · Brian L Montgomery MSc · Damon P Eisen MD, FRACP · Robert D Cooper PhD

After holidaying in Vanuatu, a 24-year-old man presented with pleuritic chest pain and chest wall tenderness thought to be musculoskeletal in origin. He developed fatal acute renal failure, jaundice, respiratory failure, myocarditis and rhabdomyolysis. Subsequent serological results showed a rise in serum titre of antibodies to Leptospira grippotyphosa, from 1 : 50 to 1 : 800, consistent with acute infection. Leptospirosis is a spirochaetal zoonosis uncommon in Australia. There were 245 reported cases in Australia in 2000 and 230 in 2001, most in Queensland.1 However, many cases would be mild and self-limiting, remaining undiagnosed and unreported.2 We describe a young man who developed multi-organ failure after presenting with pleuritic chest pain and chest wall tenderness. To our knowledge, this presentation of leptospirosis has not been reported previously. Clinical recordA 24-year-old man presented to an emergency department with a 1-day history of left-sided pleuritic chest pain. He worked as a metal machinist and was previously well. Two weeks before his presentation, he had returned from a 10-day trip to Vanuatu, where he had injured the sole of his foot on coral. After injuring his foot, he had swum in freshwater rivers. The physical examination revealed slight left-sided chest wall tenderness alone. The wound in his foot showed no sign of local inflammation. His full blood count, renal and liver function tests, coagulation profile, arterial blood gases and chest x-ray were all normal. He was admitted to hospital for observation and pain management. The initial diagnosis was musculoskeletal chest pain of unknown origin. Over the next 2 days, his condition deteriorated. He developed a non-specific erythematous rash, vomiting, diarrhoea and a mild headache. He was afebrile, had tachycardia (heart rate, 120/min), was hypotensive (blood pressure, 80/64 mmHg), hypoxic (Po2, 71.9 mmHg; Fio2, 0.6), jaundiced (bilirubin, 102 μmol/L [reference range (RR), 0–18 μmol/L]), and had abnormal renal function (creatinine, 356 μmol/L [RR, 70–110 μmol/L]). The white cell count was 13.4 × 109/L (RR, 4–11 × 109/L). A chest x-ray showed left lower lobe consolidation. A diagnosis of severe pneumococcal pneumonia was made. The differential diagnoses included atypical pneumonia and leptospirosis. He received intravenous fluids and penicillin (1.2 g twice daily), ciprofloxacin (200 mg daily) and metronidazole (500 mg twice daily), but became oliguric and required inotropic support. He was then transferred to a tertiary hospital for renal support. On admission to that hospital, he was alert with no evidence of meningism or conjunctivitis. He was febrile (39.2°C) and tachypnoeic with left-sided bronchial breathing on auscultation. His electrocardiogram (ECG) showed sinus tachycardia with inferolateral T wave inversion. After an initial period of continuous positive airway pressure ventilation by mask, he was intubated and ventilated for respiratory exhaustion. Continuous veno-venous haemodiafiltration was commenced for oliguric renal failure (urea, 22.9 mmol/L [RR, 3–8 mmol/L]; creatinine, 498 μmol/L) in association with increasing acidosis (pH 7.37; base excess, − 6.1 mmol/L). Antibiotics were changed to benzylpenicillin (1.2 g four times a day), erythromycin (1 g four times a day), ceftazidime (1 g three times a day, to cover possible melioidosis) and metronidazole (500 mg twice daily). All cultures remained negative, and no serology results were available. The chest x-ray showed cardiomegaly, extensive consolidation in the left upper and lower lobes, and some right-sided patchy opacification ( Box). Over the next 2 days, he required increasing inotropic support with infusions of adrenaline (2.22 μg/kg per minute), noradrenaline (2.22 μg/kg per minute) and vasopressin (3 U/h) to maintain adequate blood pressure. A transthoracic echocardiogram showed a mildly dilated left ventricle with a left ventricular ejection fraction of 35%–45% (RR, > 50%), and a mildly dilated right ventricle with moderate depressed contractility. He was in atrial fibrillation with intermittent runs of ventricular tachycardia and one episode of ventricular fibrillation that required cardioversion. Because of the possibility of an immunological diagnosis (eg, vasculitis or Wegener’s syndrome), he was treated with pulses of 1 g intravenous methylprednisolone and then started on maintenance dexamethasone (4 mg four times a day). A short synacthen test excluded adrenal insufficiency. He developed rhabdomyolysis and hyperkalaemia (7.1 mmol/L [RR, 3.5–5 mmol/L]), with flaccid upper limbs and rigid lower limbs. His creatinine phosphokinase (11 557 U/L [RR, 0–250 U/L]) and white cell count (59.4 × 109/L) continued to rise. On Day 8, he suffered an asystolic arrest from which he could not be resuscitated. Subsequent serological results showed a 16-fold rise in the titre of antibodies to Leptospira grippotyphosa by microscopic agglutination, from 1 : 50 on admission to 1 : 800 on the day of his death. All microbiological cultures remained negative, including four sets of blood cultures. Thick and thin blood films examined at the time for malaria parasites were negative. Serological testing for dengue fever and rickettsia was negative, as was that for seven other serovars of leptospiras, influenza viruses A and B, Mycoplasma, adenovirus, Chlamydia psittaci, Toxoplasma, Legionella, cytomegalovirus, Epstein–Barr virus and HIV. At autopsy, the right and left lungs were extensively mottled and haemorrhagic in appearance, with bilateral lobar- and bronchopneumonia. There was no evidence of pulmonary embolism. Sections of myocardium showed a diffuse, full-thickness interstitial neutrophilic infiltrate, indicating acute myocarditis. Both kidneys showed widespread acute tubular necrosis and multiple well-demarcated areas of infarction. No attempt was made to isolate leptospiras at autopsy. DiscussionLeptospirosis has not previously been described to present with pleuritic chest pain and chest wall tenderness. We report this patient so that leptospirosis can be considered as a cause of such a presentation and to emphasise that the disease can occur in travellers who visit endemic areas. We assume that the cause of our patient’s chest pain was probably early myalgia from his chest wall musculature, and the start of pulmonary manifestations of leptospirosis. About 90% of recognised cases of leptospirosis are mild and self-limiting, involving a spirochaetaemic phase followed by an immune phase. The former occurs after an incubation period of 1 day to 4 weeks, and causes fever, headache, myalgia, abdominal pain, nausea, vomiting and conjunctival suffusion. In the past, jaundice has been the indicator of severe disease (Weil’s syndrome), characterised by hepatic and renal impairment, haemorrhage and vascular collapse. However, recent studies show that jaundice is no longer an accurate marker of disease severity.2 Leptospira species are endemic in feral and domestic mammals, reptiles and amphibians. Rats and other rodents are the most important sources for human infection. This usually occurs through contact with urine-contaminated soil or water, contact with infected animal tissue, or through rat bites.3 Traditionally, farmers, sewer workers, miners, fishermen and meat workers have been at greatest risk of infection. However, outdoor leisure activities such as triathlons, swimming and rafting in fresh water provide opportunity for infection, particularly in endemic areas.4 A review of notifications in Australia between January 1998 and June 1999 shows that more than 60% of patients complained of one or more of headache, fever, chills, sweats and myalgia, 56% had nausea and vomiting, 15% had renal involvement, 15% had respiratory symptoms, and 4% had pulmonary haemorrhages.3 No deaths were reported in this period. The highest occupational group was banana farmers (19%), followed by meat workers (17%) and dairy farmers (11%). Whitewater rafting guides and tourists each accounted for 1%.3 Pathogenic leptospiras rapidly invade the bloodstream after penetrating skin or mucous membranes, and multiply in small blood vessel endothelium, resulting in damage and vasculitis in major organs. The mortality rate ranges from 4% to 10%, and adverse indicators are dyspnoea, oliguria, raised white cell count, abnormalities on ECG, and alveolar infiltrates on chest x-ray.5 Acute renal tubular necrosis, rhabdomyolysis, pulmonary haemorrhage, myocarditis with cardiac arrhythmias, meningitis, and uveitis are common manifestations of severe disease. Death is from multi-organ failure.6 There is no sensitive, specific, low cost, rapid and widely available diagnostic test for leptospirosis.2 Because of the non-specific nature of symptoms and lack of a rapid test, leptospirosis is difficult to diagnose. Although early antibiotic therapy may shorten the duration of renal failure and hospital stay,7 no decrease in the mortality rate has been demonstrated.5 Indeed, a recent Cochrane review of antibiotics for leptospirosis suggests that the evidence for their use is not convincing.8 Chemoprophylaxis is effective for people with potential risk of exposure. Oral doxycycline is highly efficacious, but is not recommended for long-term use. Chest x-ray of a patient with leptospirosis The x-ray shows cardiomegaly and extensive consolidation in the left upper and lower lobes, and some right-sided patchy opacification.

Fenton M O’Leary MB BS, MRCS · Jaspal S Hunjan MB BS, MBA, DDU · Ross Bradbury MB BS, FRACP, FRCPA · Govindasamy Thanakrishnan MRCP, FRACP, FJFICM

A previously well 30-year-old man presented with severe progressive back pain, joint pain and fever. Magnetic resonance imaging confirmed an epidural abscess. A sexual history revealed both risk factors for and previous symptoms of a sexually acquired infection. Neisseria gonorrhoeae was isolated from a rectal swab and from a wrist aspirate, consistent with disseminated gonococcal infection. The epidural abscess resolved clinically and radiologically after treatment for N. gonorrhoeae with ceftriaxone. Localised back pain and fever are important symptoms, which may indicate an epidural abscess or vertebral osteomyelitis. In assessing such a patient, a sexual history is often omitted, but it can provide useful information, as illustrated here. Clinical recordPresentation (Day 0): A 30-year-old man presented to hospital with an 8-day history of progressive severe thoracic back pain and a 5-day history of left knee pain. The back pain had occurred suddenly after lifting weights, and radiated to the right chest wall. Chiropractic manipulation and paracetamol had been unsuccessful in relieving the pain. His family history in relation to rheumatological or inflammatory disorders was unremarkable, and he had never used intravenous drugs. He had no symptoms of fever, conjunctivitis, urethritis, rash, early morning joint stiffness or neurological dysfunction. On initial examination he looked well but had a slightly raised temperature (37.8°C). There was tenderness over the fifth to the seventh thoracic vertebrae, and his left tibiofibular joint was erythematous and warm. Examination of the skin and of musculoskeletal, neurological and genitourinary systems showed no abnormalities. Initial investigations revealed a neutrophil leukocytosis of 9.5 × 109/L (reference range [RR], 1.7–7.0 × 109/L) and raised inflammatory markers: C-reactive protein, 73 mg/L (RR, < 3 mg/L); and erythrocyte sedimentation rate, 47 mm/h (RR, 0–10 mm/h). Test results for haemoglobin concentration, platelet count, serum electrolytes, renal and liver function, rheumatoid factor and antinuclear antibody were within normal limits. Blood cultures were negative. The patient was admitted to hospital after a magnetic resonance imaging scan of the thoracic spine revealed an epidural mass at T6/T7 level (Figure A, B). Day 1: A computed-tomography-guided biopsy of the epidural collection was undertaken. This revealed an acute inflammatory exudate with neutrophils. Cytological examination did not detect malignant cells, and no organisms were seen on Gram stain. The patient’s left wrist became painful, red and swollen, and an infectious diseases consultation was arranged. A sexual history revealed that the patient had experienced mild anal pruritis associated with a white anal discharge 3 months before presentation. This occurred after he had had sexual intercourse with multiple male partners, and it resolved without treatment. Microscopic examination of the fluid aspirated from the wrist joint revealed numerous pus cells and gram-negative diplococci on Gram stain (Figure C). Urethral, rectal and throat swabs were taken. A provisional diagnosis was made of disseminated gonococcal infection with an epidural abscess. Therapy was initiated with ceftriaxone 2 g intravenously twice a day. A single dose of 1 g azithromycin orally was also given to treat possible associated Chlamydia trachomatis infection. Serological tests for sexually transmitted diseases, including syphilis, HIV and hepatitis B virus infection, were negative. The patient’s regular sexual partner was treated with ceftriaxone 250 mg intramuscularly and azithromycin 1 g orally. Further contact tracing was not possible as the identity of other sexual partners was unknown. Day 3: Culture of the wrist aspirate and rectal swabs isolated Neisseria gonorrhoeae that was fully sensitive to ciprofloxacin and ceftriaxone, but resistant to tetracycline and penicillin. The urethral swab, throat swab and the epidural aspirate were sterile. Most of the patient’s symptoms resolved 48 hours after starting ceftriaxone. Course: The patient was discharged from hospital after 7 days and instructed to take oral ciprofloxacin 500 mg twice a day for 4 weeks. At review 1 month later: The patient’s symptoms had completely resolved and a repeat magnetic resonance imaging scan revealed total resolution of the epidural collection. The patient elected to go to his local doctor for follow-up serological testing. DiscussionEpidural abscesses are rare and in most cases are caused by Staphylococcus aureus.1 To our knowledge, this is the first reported case of disseminated gonococcal infection presenting as an epidural abscess. With an increasing incidence of N. gonorrhoeae infection in our community, clinicians need to be aware of the manifestations of disseminated gonococcal infection, and to consider it in the differential diagnosis of inflammatory syndromes in sexually active patients. Disseminated gonococcal infection is an uncommon manifestation of N. gonorrhoeae infection. It most commonly follows asymptomatic mucosal infections and is more common in women (female : male ratio, 3 : 1).2 The reported incidence of disseminated infection ranges from 0.5% to 3% of mucosal infections,3 and its incidence in Australia is increasing (predominantly in men who have sex with men).4 Patients typically present with either a triad of tenosynovitis, dermatitis and polyarthralgia without purulent arthritis, or purulent arthritis without skin lesions.2 These two syndromes are not exclusive and some overlap can occur. The most commonly involved joints are the knee, the elbow, and the joints distal to these. Other reported complications are rare and include osteomyelitis,5 meningitis,6 and overwhelming sepsis.7 The bones typically involved in gonococcal osteomyelitis are those adjacent to the sites of gonococcal arthritis, as the organism spreads through the synovium into the adjacent bone. In our patient, N. gonorrhoeae was isolated from the wrist and rectum, confirming disseminated gonococcal infection, which was temporally associated with an epidural abscess. Although N. gonorrhoeae was not isolated from the site of the abscess, complete symptomatic and radiological resolution followed antimicrobial therapy directed against N. gonorrhoeae. For the investigation of symptoms of localised back pain and fever, magnetic resonance imaging is the investigation of choice.8 Appropriate microbiological sampling is essential to determine the aetiological agent and guide antimicrobial therapy. Our case illustrates the importance of obtaining a sexual history, both for the differential diagnosis and for selecting investigations to perform. The recommended empirical treatment for N. gonorrhoeae infection in Australia is ceftriaxone, as more than 5% of isolates are resistant to penicillin, ciprofloxacin and tetracycline.9 Screening for other sexually transmitted infections, and contact tracing and treatment of sexual partners are important to control epidemics. A: T1-weighted sagittal magnetic resonance imaging scan through the cervical and thoracic spine shows an epidural abscess lying posteriorly to the T6 vertebral body (arrow). B: T1-weighted axial magnetic resonance imaging scan at T6 level shows a poorly defined extradural space-occupying lesion, extending through the right neural exit foramen (arrow) with a small paravertebral component. There was an associated effusion within the facet joint (not shown) and no evidence of bony erosion, destruction or oedema. C: Gram stain of wrist aspirate, revealing numerous polymorphs and gram-negative intra- and extracellular diplococci.

Sebastiaan J van Hal MB ChB(Hons) · Jeffrey J Post MB BS(Hons), FRACP

Donna B Mak,* Graeme H Johnson,† Lewis J Marshall,‡ Jacqueline K Mein§ * Public Health Physician, Department of Health Western Australia, 189 Royal Street, East Perth, WA 6000; † Medical Officer, Derby Aboriginal Health Service, Derby, WA; ‡ Head, Sexual Health Service, Fremantle Hospital, Fremantle, WA; § Public Health Medical Officer, Kimberley Population Health Unit, Broome, WA. makhoATbigpond.com To the Editor: We were pleased to read Chen and Donovan’s editorial which highlighted sex-based inequalities in control of genital chlamydial infection and argued for more screening of men for this infection.1 In the Kimberley region of Western Australia, where rates of genital chlamydial infection are among the highest in Australia, control strategies encompass both sexes.2 Although chlamydial infection was not notifiable in WA until 1993, it has been part of the sexually transmitted infections (STI) control program of the Kimberley Public Health Unit (now the Kimberley Population Health Unit) since the 1980s. Since 1989, regional STI management guidelines have recommended that testing for chlamydial infection (and gonorrhoea, syphilis, hepatitis B and HIV infection) be offered to all patients presenting with STI symptoms or as a sexual contact of an STI patient, and as part of antenatal, prison and well-person’s screenings.3,4 In 1996, empirical treatment for chlamydial infection with single-dose azithromycin (funded by the Kimberley Public Health Unit) was added to the standard treatment regimen, and antibody testing and culture were replaced by nucleic acid testing, which is more transport-robust and sensitive. This led to the introduction in 1997 of active health-service-initiated contact tracing for chlamydial infection (ie, sexual contacts reported by patients with chlamydial infection are actively sought by health staff and offered an STI consultation and empirical treatment). Between 11 June 2001 and 29 June 2002, WA Health Department staff (who contribute over 70% of the region’s STI notifications) notified 94 cases of chlamydial infection in female patients and 56 in male patients.5 Coinfection was common, with 61 patients (41%) also having gonorrhoea and four (3%) also having syphilis. Of the female patients, 30% were tested for chlamydia because they had self-presented with STI symptoms, 32% as part of antenatal or well-person’s screening, 36% because they had been reported as a sexual contact of a patient with STI, and 2% for unknown reasons. The corresponding proportions in male patients were 45%, 7%, 45% and 4%, respectively (Pearson χ2 = 12.6, df = 3; P = 0.006). Prevalence of chlamydial infection in the Kimberley antenatal population (69% of whom are screened for chlamydia) is 3% (95% CI, 2%–6%).6 Prevalence in 93 Kimberley men screened consecutively on admission to prison during 18 weeks in 1998–1999 was also 3% (95% CI, 1%–9%). During this same period, prevalence among 59 Kimberley men and 68 women presenting consecutively as STI contacts was 19% (95% CI, 11%–31%) and 22% (95% CI, 14%–33%), respectively (Mak DB, unpublished data). These data demonstrate that contact tracing contributes significantly to chlamydial case-finding, and support the addition of azithromycin to the Kimberley’s empirical STI treatment regimen. Empirical treatment and contact tracing for gonorrhoea over more than 15 years have been associated with decreases in the rate of gonorrhoea and the male : female ratio of cases in the Kimberley (Box). Seven to 8 years after introducing empirical treatment and contact tracing for chlamydial infection, rates have increased in both sexes, as has the proportion of male notifications (Box). Further progress in control of chlamydial infection requires continued provision of STI screening, treatment and contact-tracing services that are acceptable and accessible to both men and women. Notifications of chlamydial infection and gonorrhoea in the Kimberley region, 1993–2002

Donna B Mak · Graeme H Johnson · Lewis J Marshall · Jacqueline K Mein

Neil R Parker Public Health Physician, Darling Downs Public Health Unit, Public Health Services, Queensland Health, PO Box 1775, Toowoomba, QLD 4350. neil_parkerAThealth.qld.gov.au To the Editor: In May 2000 and December 2001, I vaccinated two women for Q fever (Q-Vax, CSL). Both had negative blood tests (IgG < 1:10 by immunofluoresence) and skin tests. Both had local reactions similar to those described by Mills et al.1 In both women, the skin test became positive after vaccination. The first woman had visited a farm on weekends, but had had no direct exposure to cattle, sheep or goats. Swelling at the vaccination site occurred within 72 hours, forming a lump 70 mm x 30 mm in size and causing significant discomfort. The skin test became positive at the same time. A surgeon excised the lesion 5 months after vaccination, and scarring resulted. The histological appearance was similar to that described by Mills et al,1 including a granulomatous panniculitis. The tissue was weakly positive for Coxiella burnetii by a polymerase chain reaction test (Professor B P Marmion, Institute of Medical and Veterinary Science, Adelaide). The skin test was still positive 7 months after vaccination. The second vaccine recipient lived on a cattle property and was involved with calving. She reported that her skin test became positive 5 weeks after vaccination (an observation confirmed by me a week later). The test was still positive at my final review 4 months after vaccination. Although the swelling at the vaccination site reached 50 mm × 20 mm, it caused little local pain or inconvenience. The lesion resolved spontaneously without scarring. The first of these cases had a much shorter onset period than that described by Mills et al.1 Their article did not document the fate of the skin tests, but based on the two cases I report here, and other cases notified to me by general practitioners, I suspect that prolonged positivity may be the rule rather than the exception.

Neil R Parker

Sandy J Berenger,* John K Ferguson† * Area Infection Control Consultant (and Clinical Nurse Consultant, Hunter Area Pathology Service, University of Newcastle), † Director, Department of Microbiology and Infectious Diseases, John Hunter Hospital, Locked Bag 1, Newcastle, NSW 2310. sberengerAThunter.health.nsw.gov.au To the Editor: Collignon and colleagues decry the reuse of “single-use” medical devices.1 Unfortunately, the focus on reuse of items labelled as single-use detracts attention from some of the more serious issues with cleaning of reusable instruments. All hospitals have cleaning failures that occur because some instruments are virtually impossible to clean. Examples include hollow instruments such as bone reamers, biopsy needles and tissue forceps. The actual sterilisation process (as described under Australian Standard [AS] 41872) is not at issue here. Rather, it is the poor design of instruments, and the lack of any standardised assessment process to determine whether an item is capable of being cleaned against that standard. One study found that most “sterilised” artery forceps had residual tissue, visible by light microscopy, representing an unknown, but real, infection risk.3 Most Australian hospitals do not examine surgical instruments under the microscope for grooves or cracks, and instrument sets remain in circulation for many years. In contrast, the most common “single use” critical items that are reused in many Australian hospitals are electrophysiological stimulation (EPS) and aberrant cardiac pathway ablation catheters; there have been no reports of significant mechanical or patient safety issues from reuse of a wide range of cardiac catheters, including EPS and ablation catheters.4 The sterilisation process itself has been validated for these items.5 At John Hunter Hospital, the process of reuse is controlled by a quality system that is far more stringent than the existing AS 4187 Standard. Devices are used for a set number of times before discard, and each catheter use is tracked to the specific patient and procedure. After cleaning, each catheter is examined under x 10 magnification to detect defects. The catheters are tested electrically at the point of use and patient consent is obtained before the procedure. The John Hunter Hospital program has operated for 6 years with an estimated cumulative cost saving of $6 million (compared with no reuse). Patient outcomes are monitored, and no adverse events have been detected. Clinicians express a high degree of satisfaction with the program. The same standard of equipment design, assessment and cleaning should be applied to all instruments that contact sterile tissue. Whether or not a company chooses to label its product “single-use” should not determine whether the item should or should not be reused. More often than not, such labelling serves to benefit financial return rather than patient safety. Hughes entreats us to cease reuse practices until there is incontrovertible proof of the safety of reuse.6 This statement should also apply to routine surgical items. In this era of zero risk tolerance, perhaps the consent process should make patients aware that reusable instruments processed under AS 4187 cannot be guaranteed to be free from human tissue contamination.

Sandy J Berenger · John K Ferguson

Clifford F Hughes Head, Department of Cardiothoracic Surgery, Royal Prince Alfred Medical Centre, Suite 304, 100 Carillon Avenue, Newtown, NSW 2042 (and former Chairman, Therapeutic Device Evaluation Committee). clifford.hughesATemail.cs.nsw.gov.au In reply: Berenger and Ferguson correctly raise the issue of sterilisation procedures for devices used in surgery. They have also described specific measures taken at their hospital for a specific device and, more importantly, have developed a system to ensure the highest quality of sterilisation process in a medical device. Of course, the use of any surgical device should be subject to the strictest sterilisation procedures. Most reuseable surgical instruments do have documented sterilisation protocols which include verification of the process used. All surgical instruments, whether designed for reuse or not, whether used for the first time or the tenth time, should be subject to the scrutiny, surveillance and meticulous records demonstrated by the John Hunter Hospital system. This hospital is to be congratulated on its attention to detail. Were similar stringent protocols in place across all disciplines and in all hospitals, the debate would cease to rage. More importantly, many devices could be safely and efficiently reused. Others may be considered too difficult to resterilise. Nevertheless, asepsis would, once again, be positioned where it belongs, as one of the key principles of surgery.

Clifford F Hughes

In 1978, when I was a Fellow in Ophthalmology at the Johns Hopkins Hospital in Baltimore, I went to a seminar given by one of the senior faculty (Maurice Langham) about work he was doing on an unusual disease called onchocerciasis. Although I must have learnt about onchocerciasis at medical school and during my ophthalmology training, it was such an esoteric tropical disease in small print that it had made no perceptible impact on me. Actually, onchocerciasis is a fascinating disease. It is also called river blindness, as those who are affected live along rivers and streams. It affects about 20 million people; 99% of these live in Africa, with a few in Latin America (see Box 1).1 In endemic areas, half will become blind before they die and, at any one time, some half a million people with onchocerciasis are blind. Onchocerciasis has had a devastating impact in Africa. All but the poorest of the poor have abandoned the endemic areas. In the worst affected villages, everyone is infected by the age of 14 or 15 years.1 People go blind in their 20s and 30s, just when these subsistence-farming families are raising children. Once blind, parents often need to be led to their fields by their young children. This has a devastating effect on all aspects of the villagers’ lives. There have been various attempts to treat and control onchocerciasis. During the Second World War, tens of thousands of Australian and American soldiers fighting in the Pacific islands were afflicted with lymphatic filariasis. Wartime drug development led to the discovery of diethylcarbamazine (DEC) that would halt the progression of, and sometimes cure, filariasis. After the war, DEC was tried on some people with onchocerciasis and was found to have a temporary holding effect.1,2 DEC was better than nothing, but its use was limited, as many infected people had a severe reaction to the treatment caused by the sudden death of billions of microfilariae, the so-called Mazzotti reaction.3 Sleeping sickness or trypanosomiasis is almost invariably fatal. During the First World War a drug called suramin was developed in Germany that could save some people with sleeping sickness, although it was very toxic. It was tested and found to be effective against onchocerciasis, but 2%–3% of those treated died and so it was not widely used.4 The World Health Organization had started a major program to control onchocerciasis by spraying breeding sites to control the black fly vectors. This program started in 1974 in 11 countries in West Africa. Breeding sites in rivers and streams were “bombed” each week with the aerial application of larvicide. This was an effective, if slow and expensive, method of controlling the disease in open savanna but, because of problems with aerial access, it could not be used in rainforest areas. This was the state of play as I listened to Langham in Baltimore describe the human studies to treat onchocerciasis he had recently done in Africa. After the lecture, I suggested some clinical trials he could do. It seemed so simple to me then: get a small team of two or three people and a bit of equipment to examine people and do a prospective randomised trial. I had had great lab training at the Royal Melbourne Hospital under Peter Morris (later Professor Sir Peter Morris), and I had had an extraordinary experience of working in the field with Professor Fred Hollows when I travelled throughout outback Australia on the National Trachoma and Eye Health Programme. I little suspected how much I still had to learn, but Langham proposed that I should do the study and offered to help me put it together. Within a few months I was starting a study in Liberia and another in Guatemala. I teamed up with a young infectious diseases doctor, Bruce Greene, who was at Hopkins and later went to Case Western University in Cleveland. This was the start of a very successful collaboration. As there were only a few ophthalmologists working on onchocerciasis, I was soon appointed to a WHO Scientific Working Group on Filariasis that included onchocerciasis. In the 1970s, WHO had started a drug-screening program under their Special Programs for Training and Research in Tropical Diseases. Pharmaceutical companies could send interesting compounds to be tested in WHO-supported laboratories in selected universities to see if their new drug had an effect against some of the targeted tropical diseases. In 1983, I was asked to chair a new WHO Scientific Working Group on Onchocerciasis Chemotherapy. Since the Second World War, major drug companies have scoured the world looking for new antibiotics, many of which came from fungi. In 1978, a Japanese scientist collected a fungus species that was to revolutionise the treatment of onchocerciasis from beside a golf course in Kawano, Japan — I have been told it was from beside the fifth fairway. This fungus made a compound that was called in the lab MK 933. Later, it was called ivermectin. It was not good as an antibiotic, but it was a very potent killer of parasites. It went to a WHO test laboratory where it created some interest, but then it disappeared. It was the pharmaceutical firm Merck and Co. that developed ivermectin and started to market it for veterinary use. It is now a worldwide product used to treat heartworm in dogs, and a whole range of parasites in sheep, cattle, horses, pigs and other animals.5 Dr Mohammed Aziz worked for Merck. He was originally from Bangladesh, and had worked in Africa with WHO where he learned about onchocerciasis. He insisted that MK 933 be tried in onchocerciasis. Once the veterinary product was successfully launched, he got his way, and he did a small pilot study in Senegal.6 The results were published in the Lancet and picked up by the New York Times, Le Monde and other newspapers. This was the first time that I, and others in the field, had heard of this drug. The study was somewhat unusual. The results seemed to be too good to be true. How could any drug kill the microfilaria without producing the intense Mazzotti reaction we saw with every other drug that killed microfilaria? This did not fit with any conceivable clinical, laboratory or theoretical explanation at the time. Besides, the study patients were only lightly infected, the investigators had not worked on “oncho” before, the study was funded by a drug company, and it was published simultaneously in the newspapers and the scientific literature. Maybe it was just wishful thinking, or artefact. Soon a series of parallel, randomised clinical trials were planned to more fully evaluate this very exciting new drug. These studies started after some further patients were treated in an open dose-ranging study. Bruce Greene and I undertook a study in Liberia. We treated men who had become heavily infected with onchocerciasis while working as rubber tappers on a plantation. In this controlled trial, 10 men received ivermectin, 10 received DEC, and 10 took placebos. We were very anxious for the first few days, as we expected to see similar reactions to those seen in patients treated with DEC. Some animal studies suggested even worse reactions were possible with ivermectin. Maybe some people would even die. We were elated six months later when our results showed that ivermectin was at least as effective as DEC, but safer.7 The two other parallel studies came up with similar results.8,9 Subsequently, one partial answer emerged for the lack of a Mazzotti reaction. It seems that, rather than killing the microfilariae in the tissues, the microfilariae are paralysed and then pass through the lymphatic system and die in the lymph nodes. We went back to Liberia and this time treated 300 people, men and women, to test different doses. We followed this group for 2 years. A tiny tablet of ivermectin cleared the microfilariae almost completely and people’s skin and eye signs improved dramatically.10,11 The adult worms were not affected, so ivermectin needed to be given once every year. By August 1987, Merck had enough data to register ivermectin for use in onchocerciasis. The chairman of Merck, Dr Roy Vagalos, announced that his company would provide the drug at no cost to treat anyone with onchocerciasis, anywhere in the world, for as long as it was needed.12 This was an unprecedented and extraordinarily generous and courageous decision. Although Merck was selling huge amounts of ivermectin to treat animals, there were some 20 million people with onchocerciasis, and maybe 40 million who would need treatment. Treatment had to be continued for at least 10 years. This was a huge commitment when each pill was worth US$3. However, Vagalos knew that if Merck did not do something, this breakthrough treatment could never be afforded by those who lived beyond the end of the road, the poorest of the poor. Ivermectin was now freely available. But how could it be distributed to the millions who needed it? There were other questions to be answered: for example, would ivermectin have rare but serious side effects? And what would happen if pregnant women inadvertently took a tablet? We then started another study of 30 000 people in Liberia to assess the community acceptance and safety, and to work out distribution strategies. We monitored every person, every month, investigating and documenting all births and deaths. We kept track of people as they moved, we caught and examined the biting black flies, and we thoroughly examined all the children. This huge study was very successful and confirmed the safety of ivermectin: it could be distributed to nearly everybody in the community.13,14 We showed that by treating the whole community we could reduce transmission and the incidence of new infection in children.15 Initially, the dose of ivermectin was adjusted for each individual’s weight, so everyone had to be weighed, but later work showed that height could be used instead.16 If children could walk under the stick, they got one pill; if they were too tall, they got two. By 1989, when our last Liberian study was finishing, several government and non-government organisations coordinated by WHO had started delivering ivermectin in pilot projects. Although Merck would deliver boxes of ivermectin to the national port, it still cost between 5 cents and $5 a tablet to get the ivermectin up-country and into people’s mouths. A lot of work was done to develop cost-efficient ways of community-based distribution. To supervise the distribution of the donated ivermectin, Merck created the Mectizan Expert Committee.1,17 This joint committee was based at the Jimmy Carter Presidential Centre in Atlanta and included representatives from WHO and Merck, and other experts. I had the privilege to serve on this committee in the early 1990s. In 1990, a Houston software developer, John Moores, read an article about ivermectin in the Houston Chronicle. He was so taken by this story that he started a foundation to support this work. I was also fortunate to be on the Board of the River Blindness Foundation and eventually John Moores gave US$25 million to the Foundation. It became clear that a lot more money would be needed to distribute ivermectin in the 28 African endemic countries. The River Blindness Foundation, the Carter Centre and other non-government organisations convinced the World Bank to start a special program to distribute ivermectin in Africa, worth about $300 million.18 Another smaller program was set up for the six endemic countries in Latin America. In 2002, nearly 50 million doses of ivermectin were given away free: over four million doses a month, treating about 100 people every minute. Despite local disturbances and civil war, ivermectin distribution programs are active in 25 of the 27 endemic countries and currently reach 45% of the “Ultimate Treatment Goal”, the total number of people required to be treated (see www.mectizan.org). The number treated each year continues to increase at an almost exponential rate, and progress is closely monitored by the Mectizan Expert Committee, WHO and non-government organisations. The commitment and strategies are in place to reach everyone who needs treatment and to eliminate onchocerciasis by the year 2020. Success has many parents, and failure only one. Obviously, many people were involved in the ivermectin story, but it has been a great thrill to be one of them and to have been a part of what must be one of the most significant breakthroughs in tropical medicine in the past 25 years. 1: Onchocerciasis endemic areas Two onchocerciasis control programs provide onchocerciasis control in 30 endemic countries in Africa. (OCP — Onchocerciasis Control Program — initial area of vector control; APOC — African Program for Onchocerciasis Control — World Bank and WHO supported ivermectin distribution; OPEA — Onchocerciasis Elimination Program for the Americas — ivermectin distribution in Latin America). Reprinted from Reference 19 with permission. 2: Onchocerciasis fact file Cause Onchocerca volvulus, a filarial worm. Transmission Various biting black flies. Main African vector is Simulum damnosum. The flies breed along the river banks and in the rapids and fast-flowing streams. A female fly bites an infected person to take a blood meal, and becomes infected with a tiny microscopic worm – a microfilaria – that is less than a third of a millimetre long. Over a week or so, these microfilariae develop into infective larvae and can be transmitted when the fly bites another person. Life stages After entering the body, the infective larvae grow to become adult male or female worms. The males are only 5 cm or so long, but the females may be up to a metre long. The adult worms are wrapped together in a nodule like a ball of string. The worms reproduce sexually and the female releases tens of thousands of microfilariae every day. As the female can live for 10 years or so, she literally releases millions and millions of microfilariae. The microfilariae migrate throughout the host’s body, especially to the skin and the eye. In the skin they wait to be taken up by another black fly to continue the life cycle. If this does not occur within 18 months or so, the microfilariae die. There is no inflammatory response to live microfilariae, but dead or dying microfilariae provoke an intense local response. Disease manifestations Subcutaneous nodules (adult worms often attach to bones or joints) Skin changes: severe pruritus and rash, maculopustular reaction, pigmentary changes, atrophy Eye changes: microfilaria in cornea, anterior chamber and retina; uveitis; sclerosing keratitis; chorioretinal atrophy Liberian rubber tappers from one of the early onchocerciasis drug studies. Bruce Green (left) and Hugh Taylor standing at the back.

Hugh R Taylor AC, MD, FRANZCO

Clinical records Patient 1 A 51-year-old woman was transferred to the Royal Brisbane Hospital from a country hospital, where she had presented with fever, sweats and an increasingly painful swelling of the jaw 5 days after removal of a wisdom tooth. The tooth had been removed by a general dentist, after a complaint of pain and swelling associated with it. The following day she had noticed an intraoral swelling that progressed over the week to become apparent extraorally. At presentation, she had difficulty swallowing and speaking. Although alert and oriented, she was febrile, had a “husky” voice and was starting to drool. Examination revealed a large sublingual, brawny mass extending bilaterally, bilateral submandibular swelling, and a swollen, protruded tongue. An emergency nasal fibreoptic intubation was performed in the operating theatre, where incision and drainage produced a large amount of purulent material. Cultures of this material grew Streptococcus milleri sensitive to penicillin, and the patient continued to receive intravenous ampicillin. An orthopantomogram (OPG) revealed a tooth root in situ after the extraction. The woman was discharged on Day 7 postoperatively with a diagnosis of Ludwig’s angina secondary to an infected extraction socket. Patient 2 A 48-year-old woman presented to the emergency department (ED) with headache and left-sided weakness, initially diagnosed from a computed tomography (CT) scan as a right parietal stroke. Magnetic resonance imaging (MRI) showed a parietal mass consistent with a tumour (Box 1, A). Using stereotactic craniotomy, purulent material was drained from the lesion, and S. milleri and Actinobacillus actinomycetemcomitans were grown on culture. Further investigation by the maxillofacial surgery team revealed two right maxillary premolars that were tender to percussion and radiolucencies at the root apexes on the OPG. The two teeth were removed and the sockets were cleaned by curettage and irrigation. Transthoracic and transoesophageal echocardiography excluded infective endocarditis as a complication. After 8 weeks’ treatment with intravenous benzylpenicillin, ceftriaxone and metronidazole, the woman’s neurological deficits resolved and an MRI scan showed scar tissue in the right parietal lobe without reaccumulation of pus. Patient 3 A 42-year-old woman presented to the ED with a 3-day history of constant right submental pain (no worse with eating) and swelling. She was given analgesia and sent home, but returned the next day with worsening symptoms. She was referred to the oral and maxillofacial surgery service. The patient gave a history of a “partial” right submandibular gland removal 10 years previously after recurrent sialoadenitis. She looked well, had no dysphagia or difficulty breathing, was afebrile and had no respiratory distress. There was a right submandibular scar consistent with her past history, moderate submandibular swelling and submandibular and deep cervical lymphadenopathy. A hard lump was felt in the floor of the mouth, but the tongue and floor of the mouth were not elevated. An OPG demonstrated a right-sided oval-shaped radio-opaque structure, confirmed on axial CT to be in soft tissue on the lingual side of the mandible. No odontogenic lesions were seen. The patient was diagnosed with infection secondary to a retained submandibular duct stone. She was admitted and given intravenous ampicillin and metronidazole. While she was awaiting surgery for removal of the stone, the swelling rapidly progressed over 12 hours, resulting in elevation of the tongue and difficulty in swallowing. Emergency awake fibreoptic nasal intubation and surgery were performed. No abscess was found, but two calculi were removed from the remaining portion of the submandibular duct. The patient, still intubated to protect her airway, was transferred to the intensive care unit. As the swelling of the tongue and floor of the mouth worsened postoperatively, she remained intubated for 3 days. When she became febrile (38.2°C), ampicillin and metronidazole were discontinued and she began treatment with intravenous ticarcillin and clavulanic acid. She was discharged on postoperative Day 4, with instructions to take oral amoxicillin 750 mg with clavulanic acid twice daily for 5 days. She made an uneventful recovery. Patient 4 A 28-year-old man presented to the ED of a regional hospital with left submandibular pain and swelling after having a dental filling 10 days previously in the lower left second molar. The patient was given analgesia and sent home. After a few days, the patient presented to another regional hospital with worsening symptoms. He was given oral amoxycillin and metronidazole and discharged. But the swelling and pain progressed until an inability to swallow saliva prompted him to return to the second hospital. On examination, the patient had difficulty breathing through the mouth. Marked left submandibular swelling, severe trismus and halitosis were noted. He was afebrile, but had a white cell count of 16.3 x 109/L (normal range, 4.0–11.0 x 109/L), neutrophilia of 13.1 x 106/L (normal range, 2.0–7.5 x 109/L) and a serum C-reactive protein level of 207 mg/L (normal range, < 10 mg/L). An OPG revealed a deep dental filling of the lower left second molar and a carious lower left wisdom tooth. He was admitted for airway observation and given intravenous benzylpenicillin and metronidazole. The next day he was unable to completely open his mouth. After awake fibreoptic intubation, the two teeth were removed and the abscess drained. (The clinical and radiological findings for a patient with a similar diagnosis are shown in Box 1, B–D.) Still intubated for airway protection, the patient was transferred to an intensive care unit at a tertiary hospital. His condition deteriorated and pericarditis and mediastinitis were diagnosed, necessitating transfer to an intensive care unit at a specialist chest hospital. After intensive medical treatment, the patient made a complete recovery. Numerous complications are attributed to maxillofacial infections, including Ludwig’s angina, mediastinitis, cerebral abscess, maxillary sinusitis, chronic fistulous tracts and infective endocarditis. These may result from a delay in adequate treatment of the original focus of infection, and may turn a minor problem into one with dangerous complications. Infections in the sublingual or submandibular space are not contained by any anatomical barriers and may spread to the mediastinum or diaphragm via the contiguous fascial spaces of the neck.1 Ludwig’s angina is defined as bilateral cellulitis of the submandibular and sublingual spaces.2 The adult mortality rate from the disease is reported to be between 4% and 10%.3 Ludwig’s angina has the potential to spread rapidly, resulting in mediastinitis and airway obstruction.2,4 Common clinical features of odontogenic infections (which may progress to cause significant maxillofacial infections) are summarised in Box 2. An OPG may reveal evidence of odontogenic infection. Other investigations, such as CT scans of the jaws and neck and blood investigations (eg, full blood count, electrolytes/urea/creatinine levels, procalcitonin level [an indicator of infectious processes] and blood cultures), may be ordered if clinically indicated. Clinical signs warranting prompt hospital referral include dysphagia, difficulty with or pain on moving the tongue, stridor, trismus, elevation of the tongue, and fever. It is inadvisable to treat these patients only with analgesia and antibiotics, as surgical drainage of the abscess or removal of the focus of infection is also required.5 An otherwise well patient with no systemic signs of infection, cellulitis or airway compromise does not require antibiotics once the source of the infection has been eliminated. With respect to odontogenic abscesses, this may involve extraction of the offending tooth or teeth, with drainage via the extraction socket, or may require intraoral and/or extraoral drainage. If the patient’s medical condition allows it, and if dentally suitable, the responsible tooth or teeth may be endodontically treated, allowing the patient to retain the tooth. Options for airway management include awake fibreoptic intubation, creating a surgical airway (tracheostomy or cricothyroidotomy), inhalational induction with blind nasal intubation under deep anaesthesia, and awake blind nasal intubation.6 When indicated, antibiotics that cover the expected mixed anaerobic and aerobic nature of oral infections should be chosen. Suitable choices include intravenous ampicillin (1 g four times a day) together with metronidazole (500 mg three times a day).5 For patients allergic to penicillin, clindamycin is a possible alternative. The regimen should be modified in response to culture and sensitivity results. Suppurative salivary gland infections are often caused by Staphylococcus aureus, for which treatment with dicloxacillin or flucloxacillin is appropriate. Lessons from practice Early management of odontogenic/maxillofacial infections may prevent serious complications Signs of severe infection include fever, stridor, protrusion or elevation of the tongue, dysphagia and trismus. These warrant prompt referral to an oral and maxillofacial surgeon In advanced presentations, airway control is imperative to prevent airway obstruction by soft-tissue swelling Surgical drainage of any collection of pus is mandatory Antibiotics are not indicated unless systemic signs, cellulitis or airway compromise are present, and should be viewed as an adjunct to treatment 1: Manifestations and complications of maxillofacial infections A: Magnetic resonance image (coronal view) of right parietal abscess (Patient 2). B: Right submandibular swelling secondary to an abscess of the lower right second molar tooth (case not described here but similar to Patient 4). C: Computed tomography scan (coronal view) of Patient in B, showing a collection (thick arrow) adjacent to the medial surface of the right mandible (a gas bubble [thin arrow] is also visible). D: Aspiration of pus from Patient in B. 2: Clinical features of odontogenic infections Toothache Dental pain exacerbated by hot or cold foods Intraoral or extraoral swelling Erythematous or inflamed gingiva Carious or broken tooth/teeth Intraoral or extraoral seepage of purulent material

Peter J Aquilina MB BS(Hons), BDS(Hons), FRACDS · Anthony Lynham BMed(Hons), FRACDS(OMS), FRCS

Lloyd K Morgan Retired General Practitioner, PO Box 150, Lorne, VIC 3232. To the Editor: New imaging and pathology investigations continually improve diagnostic accuracy. But tests must be used because they supplement clinical deduction, not because they are available, and the constellation of clinical features should not be ignored. The case report by Chatterjee and colleagues is valuable for describing delayed diagnosis of meningitis, based on imaging which suggested subarachnoid haemorrhage and aspiration pneumonia.1 The 4-day history, examination (raised respiratory and heart rates, high fever) and results of initial investigations (neutrophilia, raised C-reactive protein level, lung consolidation) suggested a primary respiratory infection. The absence of a typical history of onset of subarachnoid haemorrhage is excused by the 5.5- hour hiatus before the patient was found semicomatose. Subarachnoid haemorrhage was diagnosed because of density in the subarachnoid space on computed tomography (CT). The authors noted a 1980 report of this appearance in a patient with bacterial meningitis.2 They also noted only one previous report of purulent meningitis mimicking subarachnoid haemorrhage on CT scan (in 1994),3 but there is reluctance to publish “negative” outcomes. Aspiration as the cause of upper-lobe consolidation was unlikely. Bacterial pneumonia and chemical pneumonitis affect the lower lobe.4 Clinical findings were not consistent with subarachnoid haemorrhage, and meningitis was the differential diagnosis, so only the overweighted CT results prevented lumbar puncture on Day 0, which would have resulted in earlier, broader antibiotic therapy and possibly resumption of warfarin. By Day 1, it was too late to prevent permanent blindness (it was possibly too late on Day 0, but pupils were reactive at that time). Even on Day 1, repeat cranial CT showed infarction but less evidence of bleeding; “a disparity between the amount of [alleged] subarachnoid blood and the patient’s clinical condition” was followed by magnetic resonance imaging then angiography and venography, instead of lumbar puncture as suggested by hindsight in the last sentence of the report. Shadows do not always equate with pathology. Compare an article on the clinical diagnosis of meningococcaemia.5 Holistic care of Chatterjee et al’s patient included anticoagulation therapy. “It probably could have recommenced earlier” than after “a large pulmonary embolus” on Day 13 — perhaps, given the presence of long-term indications (lupus inhibitor, anticardiolipin antibody and previous thrombosis) and cerebral vessel inflammation causing infarction, on Day 1. The main lesson, which we were all taught as students but needs career-long reinforcement, is in the penultimate sentence of the case report: “Investigations should not be interpreted in isolation from the clinical picture”.

Lloyd K Morgan

Taposh Chatterjee,* John R Gowardman,† Tony D Goh‡ * Registrar, † Intensivist (corresponding author), ‡ Radiologist, The Canberra Hospital, PO Box 11, Woden, ACT 2605. John.gowardmanATact.gov.au In reply: We agree with Morgan that the symptoms, signs and laboratory investigations in our case report, although non-specific, supported a diagnosis of infection.1 The C-reactive protein level was not available for 24 hours. The unwitnessed drop in level of consciousness that occurred between 09:00 and 14:30 could have been secondary to meningitis or an acute cerebral event, and, while it is true that the lower lobes are predominantly involved in aspiration, they are not solely involved. Consolidation in other gravity-dependent segments, including the posterior segments of the upper lobes, can occur.2 The suggestion that “permanent blindness” could have been prevented is not supported. Fortuitously, an appropriate antibiotic to which the organism was fully sensitive was given from Day 0 (ceftriaxone). Adjunctive supportive care was quickly provided. In retrospect, anti-coagulation therapy could have recommenced earlier, but this remained a difficult decision in the context of the computed tomography findings. It remains unclear how this would have modulated the meningeal process, but it possibly contributed to the complication of pulmonary embolism. We agree that there is a reluctance to publish what may be perceived as “negative” outcomes, but, educationally, these may be the most rewarding. This case was an uncommon presentation of a common disease, and we considered it sufficiently important to notify other practitioners. Of most importance in this era when technology in medicine advances exponentially, any investigation must be considered only an adjunct to, and not a replacement for, thorough clinical evaluation.

Taposh Chatterjee · John R Gowardman · Tony D Goh

Clinical record In 2001, a young man was admitted to hospital with a 3-day history of gradual-onset headache, nausea, vomiting, neck stiffness and photophobia. Three weeks earlier he had experienced a gastrointestinal illness (nausea, abdominal cramps, diarrhoea, myalgia and fever) that persisted for 1 week. On examination, he had a low-grade fever and meningism. A cerebral computed tomography scan showed no abnormality. Peripheral blood eosinophilia (1.6 x 109/L; reference range [RR], < 0.44 x 109/L) was noted, and examination of cerebrospinal fluid (CSF) showed 530 x 106/L monocytes (RR, < 5 x 106/L), 22 x 106/L red cells (RR, < 1 x 106/L), no eosinophils on routine staining, a raised protein level of 1.07 g/L (RR, < 0.45 g/L) and a normal glucose level. He was treated with intravenous aciclovir for 6 days. A CSF polymerase chain reaction test for herpes simplex virus-1 (HSV-1) and HSV-2 subsequently gave negative results. Serological tests for Strongyloides and Angiostrongylus were negative. CSF and blood cultures showed no growth. Twelve days after admission, he was discharged from hospital with resolving meningism. Five days later, increasing headache and drowsiness prompted his admission to another hospital. He was afebrile, drowsy and irritable, with gross bilateral papilloedema. He described mild paraesthesiae in both hands. He had peripheral blood eosinophilia (3.1 x 109/L). Magnetic resonance imaging of the brain with gadolinium contrast showed multiple focal enhancing lesions in the deep white matter of both cerebral hemispheres, including the corpus callosum (Figure A). CSF from cisternal puncture was cloudy, under high pressure and, on routine toluidine blue staining, had 1008 x 106/L polymorphonuclear cells (RR, < 5 x 106/L), 186 x 106/L monocytes and 21 x 106/L red cells. Further staining to detect eosinophils was requested, and 90% of the polymorphonuclear cells were found to be eosinophils (Figure B). His CSF protein level was elevated at 0.8 g/L and glucose level 2.6 mmol/L (50% serum glucose). India ink, Ziehl–Neelsen and Gram stains were negative. Repeated questioning revealed that the patient had ingested, 5 weeks earlier, for a dare, two slugs from a garden in a Sydney suburb. Repeat Angiostrongylus immunoglobulin G (IgG) enzyme-linked immunosorbent assay (ELISA), tested in parallel with the first specimen, was positive, confirming seroconversion. Several leopard slugs, Limax maximus (Figure C), taken from the Sydney garden were dissected without finding larvae (Figure D), but no rats from the vicinity were examined for this infection. Treatment comprised measures to reduce intracranial pressure with repeated CSF drainage, acetazolamide and dexamethasone, initially given intravenously, and then orally. CSF drainage consisted of one cisterna magna puncture and two lumbar punctures. Specific anthelmintic agents were not given. No ocular larvae were seen on regular formal ophthalmological review. He improved gradually and, after 17 days in hospital, was discharged with instructions to take a reducing dose of dexamethasone over 4 weeks. His final lumbar puncture 1 month after admission showed an almost normal CSF protein level (0.5 g/L) and a reduction in CSF white cell count (107 x 106/L; 8% eosinophils). After 5 months, he successfully returned to full-time studies and competitive sport. A: Magnetic resonance image of the brain, showing multiple focal enhancing lesions in the deep white matter (arrows). B: Spun-down cerebrospinal fluid cells (Romanowsky stain: original magnification x400). C: Limax maximus, the leopard slug, an intermediate host for Angiostrongylus cantonensis. D: Adult female Angiostrongylus cantonensis from the lungs of Rattus norvegicus. This is the first reported case of human eosinophilic meningitis due to Angiostrongylus cantonensis acquired in Sydney. The first A. cantonensis infection in humans reported in Australia was from Brisbane in 1971.1 More recently, a fatal case occurred in a child who ingested molluscs in a suburban Brisbane garden.2 Over the past 10 years, Angiostrongylus has been isolated from dogs, flying foxes, marsupials and zoo primates in Sydney.3 Angiostrongylus cantonensis, also known as Parastrongylus cantonensis, is the commonest infectious cause of eosinophilic meningitis worldwide and is endemic in South-East Asia and the Pacific Basin.4 The other, rarer parasitic causes of eosinophilic meningitis are not endemic to Australia.5 Non-infectious causes of eosinophilic meningitis include haematological malignancies, antibiotics (ciprofloxacin, intraventricular gentamicin or vancomycin) and idiopathic hypereosinophilic syndrome.6 The lifecycle of the parasite from the adult stage in the definitive rat host through the intermediate mollusc host has been described previously.2 Humans become accidental hosts when they ingest the larval stage in raw or undercooked molluscs or crustaceans or in fresh vegetables contaminated by infected molluscs.5 The diagnosis of angiostrongyliasis in a patient with acute eosinophilic meningoencephalitis is supported by a history of mollusc ingestion, but eliciting this may require specific questioning. Symptoms occur 2–45 days after ingestion.7 The most common symptom is headache. Paraesthesiae are frequently reported.6 In our patient, the acute febrile gastrointestinal illness 6 days after consuming the slugs may have been caused by invasion of the parasite through the intestinal wall. Initial entry into the meninges, and subsequent migration through brain parenchyma, caused the clinical picture of meningitis followed by encephalitis. Seizures or other focal neurological symptoms may occur. Peripheral blood and CSF eosinophilia strongly support a diagnosis of Angiostrongylus meningoencephalitis, but may appear only later in the course of the illness, or, in a minority of cases, not at all.4,7,8 It is important to emphasise that eosinophils may not easily be differentiated from neutrophils on routine microbiological staining, such as with toluidine blue wet films. In aseptic meningitis, particularly associated with peripheral eosinophilia, specific Romanowsky stains, such as May–Grünwald–Giemsa or Wright stains, should be performed. An ELISA measuring total IgG can be diagnostic. The ELISA used to demonstrate seroconversion in this case utilised somatic antigens from adult A. cantonensis. The ELISA can be performed on serum or CSF. The Institute for Clinical Pathology and Medical Research at Westmead Hospital is the only centre in New South Wales performing the assay. As parasitologically proven cases are rare, it is difficult to determine the sensitivity and specificity of this assay. Angiostrongylus meningitis is usually mild and resolves spontaneously over 6 weeks. Occasionally, cases are severe and may have chronic sequelae.5,6,8 No randomised controlled studies have assessed optimal management, but repeated CSF drainage may give symptomatic relief.8,9 Steroid treatment appears to be beneficial, presumably reducing CSF pressure and inflammatory response. Regimens reportedly of benefit include prednisolone 30–60 mg/day for 5 days,8 prednisolone 40–60 mg/day with weaning over a few weeks,9 and prednisolone 60 mg/day for 2 weeks.10 The use of anthelmintic agents is controversial. Generally, avoidance of anthelmintic agents has been recommended on the (theoretical) basis of their potential for harm owing to the inflammatory response provoked by antigen release after parasite death.4,8 A. cantonensis should be considered as a cause of aseptic meningitis in patients with paraesthesiae and peripheral eosinophilia, and a history of exposure to undercooked molluscs or crustaceans. This report highlights the wider distribution of this parasite in Australia and, in particular, its close proximity to urban populations. Lessons from practice Angiostrongylus cantonensis should be considered as a cause of aseptic meningitis in patients with paraesthesiae and peripheral eosinophilia, and a history of exposure to undercooked molluscs or crustaceans. It is important to specifically request tests for eosinophils in cerebrospinal fluid (CSF) when their presence is suspected, particularly if there is peripheral eosinophilia. Eosinophilia in peripheral blood and CSF supports a diagnosis of Angiostrongylus meningoencephalitis, but absence of eosinophilia does not exclude it, particularly early in the course of the illness.

Don S Pryor MD, FRACP · Pam Konecny MD, DTM · Sanjaya N Senanayake MB BS(Hons) · John Walker PhD

Donna B Mak,* Eleanor M Platt,† Christopher H Heath‡ * Public Health Medical Officer (currently, Adjunct Research Fellow, School of Population Health, University of Western Australia, Nedlands, WA 6009); † Senior Public Health Nurse, Kimberley Public Health Unit, Derby, WA; ‡ Infectious Diseases Physician and Clinical Microbiologist, Royal Perth Hospital, Perth, WA, and Clinical Senior Lecturer in Medicine, University of Western Australia. makhoATbigpond.com To the Editor: The World Health Organization has established the Global Alliance for the Elimination of Leprosy, which aims to eliminate leprosy from every country by 2005.1 Elimination is defined as reducing the disease prevalence to below one case per 10 000 population. Australia has met this goal. Nevertheless, leprosy transmission still occurs in parts of Australia. Between 1986 and 2002, 28 new cases of leprosy were notified to the Kimberley Public Health Unit (KPHU). All patients except one were Indigenous. At diagnosis their ages ranged from 8 to 63 years. In several recent cases, diagnosis was delayed despite multiple presentations to primary healthcare staff and medical specialists. Eleven patients (39%), including the most recently diagnosed case, had multibacillary disease (WHO classifies leprosy as paucibacillary [< 6 skin lesions with no bacilli on skin smears] or multibacillary [≥ 6 skin lesions and/or positive skin smears]2). People with multibacillary leprosy can transmit the disease. This epidemiological pattern is also seen in Australia’s Northern Territory, where a third of the 236 new cases of leprosy between 1970 and 1997 were multibacillary.3 In leprosy-endemic countries, the proportion of cases that are multibacillary ranges from 32% in Guinea to 84% in Egypt.4 The long incubation period of leprosy (usually 2–5 years, but possibly decades) makes it likely that new cases will occur in Australia over the next few decades. Management of patients in the Kimberley region is challenging, not only because of remoteness, patient mobility and the prolonged treatment and follow-up required, but because adverse reactions to leprosy treatment are common, and may occur weeks to months after starting therapy with antileprotic agents. With all presentations of leprosy, the KPHU informs patients and relevant health professionals about these reactions, including how to recognise them and where to seek specialist advice. The region’s frequent turnover of healthcare professionals and its increasing reliance on short-term and overseas-trained doctors makes this a time-consuming undertaking. With increasing movement of people into and out of leprosy-endemic areas like the Kimberley, or leprosy-endemic countries, Indigenous Australians who have not yet been exposed to leprosy may now be at greater risk of encountering and acquiring the disease. In addition, Indigenous Australians from leprosy-endemic areas may develop symptoms of leprosy when they are no longer in leprosy-endemic areas, and may attend health professionals unfamiliar with leprosy, resulting in delayed diagnosis.5 In the 21st century, the medical community still needs to be alert to the possibility of leprosy in patients with chronic dermatological or neurological conditions, and needs to enquire about exposure to leprosy (eg, living in a leprosy-endemic area, history of leprosy in relatives — both by blood and by marriage). Otherwise, we will fail to diagnose and appropriately manage this disease, risking further outbreaks of leprosy in Indigenous Australian populations.

Donna B Mak · Eleanor M Platt · Christopher H Heath

Re: “Nocardia asteroides pneumonia with bacteraemia”, a letter by Figgis PA, Glanville AR, Harkness JL, in the 4 August 2003 issue of the Journal (Med J Aust 2003; 179: 171-172). The image in Box 3 should have shown the histological appearance of a liver biopsy, not the published lung biopsy. The correct image appears in the Box. The html and pdf versions of this article published on the eMJA website were corrected on 20 October 2003. 3: Liver biopsy in a patient with Nocardia asteroides pneumonia Core biopsy of liver, showing a granuloma within the central portal triad (arrow); the portal ducts are expanded and fibrosed with a patchy lymphocytic infiltrate (original magnification x 40; haematoxylin and eosin stain).

Patricia A Figgis · John L Harkness · Allan R Glanville

Objectives: To compare the effectiveness of ototopical ciprofloxacin (0.3%; CIP) with framycetin (0.5%), gramicidin, dexamethasone (FGD) eardrops (5 drops twice daily for 9 days) together with povidone-iodine (0.5%) ear cleaning as treatments for chronic suppurative otitis media (CSOM) in Aboriginal children.Design and participants: Aboriginal community-controlled, community-based, multicentre, double-blind, randomised controlled trial in eight Aboriginal Community Controlled Health Services across northern Australia, involving 147 Aboriginal children with CSOM.Main outcome measures: Resolution of otorrhoea (clinical cure), proportion of children with healed perforated tympanic membrane (TM) and improved hearing, 10–21 days after starting treatment.Results: 111 children aged 1–14 years (CIP, 55; FGD, 56) completed treatment. CSOM cures occurred in 64% (CIP, 76.4%; FGD, 51.8%), with a significantly higher rate in the ciprofloxacin group (P = 0.009, absolute difference of 24.6% [95% CI, 15.8%–33.4%]). TM perforation size and the level of hearing impairment did not change. Pseudomonas aeruginosa was the most common bacterial pathogen (in 47.6%), while respiratory pathogens were rare (in 5.7%).Conclusions: Twice-daily ear cleaning and topical ciprofloxacin is effective at community-level in achieving cure for CSOM. Healthcare providers to Aboriginal children with CSOM should be given special access to provide ototopical ciprofloxacin as first-line treatment.

Sophie Couzos FRACGP, FACRRM, FAFPHM · Traven Lea MAEIH, DipPHTM · Margaret Culbong · Reinhold Mueller MSc, PhD · Richard Murray FRACGP, MPH

Objective: To assess the reported rate of local reactions after administration of acellular pertussis vaccine (DTPa) according to dose number and type of pertussis vaccine (whole-cell or acellular) used for the primary course, and to document the severity and outcome of fourth-dose local reactions.Design and setting: Retrospective review. Reports of adverse events after vaccination in South Australia between 1 January 1997 and 31 December 2000 were reviewed, and a questionnaire administered to all parents who reported a local reaction after the fourth dose of DTPa.Main outcome measures: The number, and rate per 100 000 administered doses, of local reactions following the primary and booster doses of DTPa, and of local reactions after the fourth-dose in cohorts of children whose primary vaccinations were with either DTPw or DTPa. Redness and/or swelling at the injection site as reported by parents.Results: Of 581 reported adverse events after vaccination, 138 were local reactions after a pertussis-containing vaccine. Primary vaccinations with DTPa was a significant risk factor for a fourth-dose local reaction (relative risk, 6.7; 95% CI, 2.4–18.5). Parental questionnaires were completed for 45 of the 71 children (63%) with reported local reactions after the fourth dose of DTPa; extensive limb swelling was reported in 8 children (18%) and all except one child had recovered by the time of review.Conclusions: Parents should be informed that children receiving booster doses of DTPa vaccine, after primary doses with DTPa, are at increased risk of local reactions (which tend to resolve spontaneously) but not of systemic effects. Studies should be initiated to investigate the pathogenesis and the risk of recurrence of local reactions to further improve vaccination schedules.

Michael S Gold MD, FRACP · Sara Noonan RN · Maggi Osbourn RN · Stella Precepa RN · Ann E Kempe RN, MPH, BSc

The increasing rate of hepatitis C virus (HCV) infection in the community means that there is increased risk of occupational exposure for healthcare workers. In metropolitan hospitals in Victoria, we found that 80–150 healthcare workers have occupational exposures from HCV-infected patients annually. As there is a 1.8%–3% risk of transmission of HCV from a needlestick injury, two to five healthcare workers are likely to acquire HCV each year in Victoria. These needlestick injuries pose a personal, legal and professional risk to healthcare workers and their patients. Recent information shows that early antiviral treatment of acute HCV infection has high cure rates. Current local and international protocols for management of healthcare workers exposed to HCV do not address these issues. We propose a management protocol after needlestick injury that is stratified according to the likelihood of HCV acquisition and potential risk of staff-to-patient transmission, and that is consistent with the current legal and clinical context of HCV infection in Australia.

Patrick GP Charles MB BS · M Lindsay Grayson MD, FRACP, FAFPHM · Peter W Angus MD, FRACP · Joseph J Sasadeusz PhD, FRACP

Clinical record At 03:00 on a Friday in 2002, a clinical staff member in the intensive care unit sustained a needlestick injury involving a suture needle through a glove. An unrelated cardiac arrest occurred soon after, causing a delay in reporting of the injury. At 07:00 (4 hours after the injury), the staff member (recipient) reported the injury, using the paging arrangement and occupational exposure protocol at the time (ie, a message was left for the staff health nurse, as no designated person was on-call for occupational exposures overnight). At 10:00 (7 hours), the recipient received a response to the report from the staff health nurse who initiated action in accordance with the protocol in place at the time. The source patient had a recently recorded negative HIV antibody result by enzyme-linked immunosorbent assay (ELISA). At 10:30 (7.5 hours), a further blood sample was collected from the source patient, along with a baseline blood sample from the recipient. These were processed at 12:30 (9.5 hours). At 13:00 (10 hours), the source patient’s ELISA test gave a positive result for HIV antibody. However, because of the previous negative result, this was assumed to be a false positive. On Sunday, a repeat (western blot) HIV test was performed for confirmation and was again positive for HIV antibody. On Monday at 10:00 (79 hours), the infectious diseases unit was notified of the positive HIV antibody result. At 15:00 (84 hours), the recipient was counselled by an infectious diseases physician and commenced post-exposure prophylaxis. The laboratory subsequently tested stored serum samples from the source patient; all four samples were positive for HIV antibody. Investigation of the previous negative result revealed that the test specimen was not from the source patient, but from another patient with the same surname in the same ward. This report documents a multifactorial failure of the system of reporting and responding to occupational exposures, which led to a substantial delay in instituting prophylaxis for HIV exposure. About half the percutaneous sharps injuries sustained by healthcare workers in the United States go unreported.1 At our 621-bed institution, 66 needlestick injuries were reported in 2001–2002, translating to a rate of 10.6 per 100 beds per year. As data from the US Exposure Prevention Information Network suggest that hospital healthcare workers incur about 30 needlestick injuries per 100 beds per year,2 our rate of 10.6 probably reflects significant underreporting. Increased staff confidence in the quality and confidentiality of follow-up for occupational exposures may help increase reporting.3 The average risk of HIV transmission for healthcare workers after percutaneous exposure to HIV-infected blood is about 0.3%.4 However, post-exposure prophylaxis with zidovudine has been shown in a retrospective case–control study of healthcare personnel to reduce transmission by about 81%.4 The Department of Human Services (Victoria) recommended in 1997 that post-exposure prophylaxis be initiated promptly, preferably within 1–2 hours of exposure (based on 1996 recommendations from the US Centers for Disease Control and Prevention).5 The US Department of Health and Human Services recommends that employers protect healthcare workers from needlestick injuries by providing a safe working environment with effective programs and safer needle devices, notwithstanding additional costs. This includes a combination of prevention strategies for reducing needlestick injuries, and involving workers in the effort.6 Improving response to occupational exposuresAt Southern Health, the occupational exposure protocol was under review before this incident occurred. Root-cause analysis of the incident led to the following changes to occupational exposure and pathology protocols: A uniform system of notification that was under development was implemented across all sites in the Southern Health service of Melbourne. Changes included: A dedicated pager number, operating 24 hours a day 7 days a week, was provided at each site for reporting of occupational exposures and was advertised by posters displayed prominently in clinical areas. Previously, there were different contact numbers for different times of the day, and cover was not around the clock. Occupational exposure coordinators were appointed (one per shift at each site) and attended inservice education about occupational exposure, provided by the infection control unit. Staff were informed of the new pager number and notification process through a memorandum sent to all nursing and clinical support staff and an internal flyer sent to all senior medical staff from the Chair of the Infection Control Advisory Committee for Southern Health; the latter highlighted the urgency in reporting exposures. The new notification process is described in the orientation material for new staff. The pathology department implemented a streamlined testing protocol for all specimens related to occupational exposures; these are processed urgently, and all results are reported to the occupational exposure coordinator. The pathology department also reviewed protocols for blood collection and reception; use of informal “norms” rather than strict adherence to protocol was deemed unacceptable, and inservice education and review were conducted in all areas. All high-risk exposures are discussed by the occupational exposure coordinator with the on-call infectious diseases physician to develop an action plan. Future quality assurance activities will include surveys of staff awareness of the notification process and training status of occupational exposure coordinators. Outcome of measures to improve responseTen weeks after this adverse event, 58 health service staff had been trained as occupational exposure coordinators. The senior infection control practitioner conducted nine education sessions for these coordinators, providing course notes and contact details for troubleshooting or general enquiries. An infectious diseases physician discussed issues of informed consent for testing for bloodborne viruses at each session. Initially, reports of occupational exposures increased threefold, from 1 every 48 hours before implementation of the new protocol to 3 per 48 hours after implementation. Within 4 weeks of implementation, reporting returned to the previous level. The posters displayed in clinical areas appeared to prompt reporting; some exposures occurred before implementation of the new protocol but were reported only after the posters were displayed. The time from occupational exposure to reporting of HIV results for source patients decreased from a range of 7.5–192 hours to 1.1–23 hours (including any delay in reporting by healthcare workers, as well as laboratory processing time). This report demonstrates the importance of effective mechanisms for reporting exposures, accurate specimen labelling, urgent processing of pathology tests and accurate reporting of results with appropriate follow-up, in achieving timely and appropriate action after an occupational exposure. Recognition of the system failure in this incident led to a system change at our institution designed to minimise future incidents and improve quality of care. The education and reporting systems have been revised to be efficient and robust and to achieve long-term effectiveness in reducing morbidity from occupational exposure. Lessons from practice The system for staff to report an occupational exposure needs to be simple and available 24 hours per day, 7 days per week. Testing after an occupational exposure needs to be prioritised and processed urgently to ensure results are available as soon as possible. High-risk exposures need to be discussed with the on-call infectious diseases physician to develop an action plan. All serum should be collected with strict adherence to blood collection and labelling protocols. Serum from the source patient should be collected and tested at the time of the incident to confirm HIV status, even if a recent negative result is known.

Elizabeth E Cooper BN, MPubHlth(Melb) · Stephen L Blamey FACS FRACS

Three young men aged between 19 and 30 years presented at different times with lumps over the deltoid area at the site of Q fever vaccination (Q-Vax, CSL), which had been administered 3–8 months previously. Mandatory pre-vaccination testing had shown that all three subjects were non-immune. Clinically, the lumps (of which two were tender) were considered to be either subcutaneous abscesses or lipomata. Sarcoidosis was excluded clinically and biochemically. The lesions were excised and were macroscopically similar, being 20–47 mm in size and resembling indurated fat. Histologically, the appearances were of sarcoidal granulomatous panniculitis (Box). No aetiology for the granulomata was identified. DiscussionQ fever, a serious zoonosis caused by a rickettsial organism, Coxiella burnetii, is spread to humans by body fluids of infected animals (principally cattle, sheep or goats). A vaccine, Q-Vax, produced by Commonwealth Serum Laboratories, is composed of a killed suspension of virulent phase 1 organisms. The vaccine, limited to Australia, was shown to be effective in trials between 1981 and 1994, and a national vaccination program, aimed at high-risk groups, commenced in 2001. The cases we describe here are examples of a rare idiosyncratic reaction to the vaccine (probably the result of enhanced delayed hypersensitivity) that may be confused with subcutaneous sarcoidosis. This has not, to our knowledge, been previously reported. Histological section of one of the lesions Non-caseating epithelioid cell granulomata (arrows), surrounded by a dense lymphocytic reaction. Immunostaining disclosed that more than 80% of lymphocytes were T cells and less than 20% were B cells, mainly arranged as follicular aggregates (H & E stain; size reduced by half from x100).

Alan E Mills MB ChB FRCPA · Vince Murdolo MB BS FRCPA · Stephen P Webb MB ChB

Patricia A Figgis,* Allan R Glanville,† John L Harkness‡ * Thoracic Registrar (currently, Senior Registrar, General Intensive Care, Royal Prince Alfred Hospital, Missenden Road, Camperdown, NSW, 2050); † Head of Thoracic Medicine, ‡ Director of Microbiology, St Vincent's Hospital, Darlinghurst, NSW. patriciafiggisAThotmail.com To the Editor: A previously well 57-year-old man presented to the emergency department with a 3-day history of severe dyspnoea. Six weeks earlier he had noticed coryzal symptoms with subsequent lethargy, reduced appetite with weight loss, and a non-productive cough. He then developed ankle swelling and increasing abdominal girth. He had a background of excessive alcohol consumption, but had abstained for 10 years. On examination, he was febrile and in respiratory distress, with a respiratory rate of 35 per minute, pulse rate of 130 bpm, and blood pressure of 130/85 mmHg. Chest auscultation revealed bilateral diffuse coarse crackles. The chest x-ray is shown in Box 1, and results of additional investigations in Box 2. Despite treatment with broad-spectrum antibiotics (intravenous ceftriaxone, dicloxacillin and erythromycin), the patient’s condition deteriorated rapidly, and he required intubation within 24 hours of presentation. Trap sputa contained abundant thin, partially acid-fast, beaded, branching filaments, suggesting Nocardia asteroides, which was later confirmed on culture using conventional biochemical testing. Several blood cultures taken on admission also grew N. asteroides. All cultures for mycobacteria were negative. The patient was treated with intravenous trimethoprim–sulfamethoxazole for a total of 5 weeks and oral minocycline for 14 weeks. He spent 6 weeks in hospital. Liver biopsy, performed because of persistently abnormal hepatic function at follow-up 8 weeks after hospital discharge, showed central fibrosis and non-caseating granulomatous hepatitis (Box 3). The patientn received no further treatment and remained well 18 months later, with almost normal hepatic function and a clear chest x-ray. Nocardia bacteraemia is rare, although the incidence appears to be increasing in the immunosuppressed. Nocardia spp. are seldom isolated in blood cultures, with one study finding that blood was the source of only 8% of all Nocardia isolates.1 Up to 30% of patients with Nocardia bacteraemia have coexistent infection with gram-negative bacteria.1,2 There has been one previous report of Nocardia pneumonia associated with positive blood cultures and liver disease. However, this patient had documented end-stage chronic liver disease at presentation, was taking prednisolone, and developed nocardiosis after prolonged hospitalisation with gram-negative sepsis.1 Granulomatous reactions are well described in Nocardia infection. Although granulomatous hepatitis is also described in sarcoidosis, it is rare and usually presents with itch and obstructive abnormalities of liver function.4 In our patient, acute N. asteroides infection was the most likely cause of both the pulmonary infiltrate and the granulomatous hepatitis. Not only were results of modified acid-fast stains consistent with Nocardia spp., but cultures from multiple trap sputa and blood specimens also grew N. asteroides, suggesting a large load of this organism. No other organisms were isolated despite prolonged incubation of cultures, and the patient recovered after specific treatment directed at Nocardia spp. Furthermore, he remained well with no further treatment at 18-month follow-up, with near-normal hepatic function and no new abnormalities. We conclude that N. asteroides infection can present as a fulminant community-acquired pneumonia with bacteraemia in the absence of immunosuppression or coexistent infection. Our case illustrates the potential hepatic sequelae of Nocardia bacteraemia. 1: Chest x-ray of a patient with Nocardia asteroides pneumonia Chest x-ray taken on admission to hospital, showing widespread non-symmetrical interstitial and airspace infiltrates. 2: Results of investigations Result Reference range At presentation Arterial blood gases* pH 7.37 7.35 –7.45 pCO2 (mmHg) 43 35 – 45 pO2 (mmHg) 60 75 –105 Bicarbonate (mmol/L) 24 24 – 31 Base excess 0 − 3 to 3 White cell count Total (x 109/L) 31.5† 4 –11 Neutrophils (x 109/L) 30.2 2 – 7.5 Lymphocytes (x 109/L) 0.7 2 – 4 Follow-up at 8 weeks Liver function tests‡ Bilirubin (μmol/L) 9 < 18 Alkaline phosphatase (U/L) 124 30 –100 γ-Glutamyl transferase (U/L) 153 < 35 Iron studies Serum ferritin (μg/L) 446 30 – 400 Serum iron (μmol/L) < 3 10 – 30 Transferrin (g/L) 1.9 2.0 – 3.5 Transferrin saturation < 6% 15%–50% Vitamin B12 (pmol/L) 376 > 126 Immunological tests HIV antibodies Negative Hepatitis B and C§ Negative Autoantibody screen¶ Negative Complement C3 (g/L) 1.07 0.82 –1.45 Complement C4 (g/L) 0.25 0.15–0.45 * Breathing 10 L/min oxygen. † Occasional myelocytes, toxic granulation. ‡ Levels of alanine and aspartate aminotransferase were in the reference range. § Including hepatitis B surface antigen and hepatitis C antibody. ¶ Including antinuclear, extractable nuclear antigen, double-stranded DNA and antineutrophil cytoplasmic antibodies. 3: Liver biopsy in a patient with Nocardia asteroides pneumonia Core biopsy of liver, showing a granuloma within the central portal triad (arrow); the portal ducts are expanded and fibrosed with a patchy lymphocytic infiltrate (original magnification x 40; haematoxylin and eosin stain).

Patricia A Figgis · Allan R Glanville · John L Harkness

Andrew G Marsden Occupational Physician, Unit 6, 125 Melville Parade, Como, WA 6152. To the Editor: Modern air travel lends itself to aerosol transmission of viral infection. Infected individuals in modern aircraft represent a significant risk for other travellers during long journeys. In September 1999, a person with an influenza-like illness joined other workers returning by aircraft to an isolated mine in north-western Australia. He was identified as unwell by a mine supervisor in the airport lounge but was allowed to board the BAe 146 aircraft (a 75-seat passenger jet aircraft). The flight lasted 3 hours 20 minutes. On landing in the evening, most workers were transported to their quarters in a 10-minute bus trip, but some, including the affected worker, travelled independently. They then went to their individual rooms. The next day, the affected worker reported sick immediately on going to his work site and did not work for 4 days. The other workers undertook 12-hour shifts operating machinery or in offices, relatively isolated from other people. However, they may have mixed socially. Over the next 3–4 days, 15 other workers presented with an acute influenza-like illness, with fever, cough, nasal congestion, anorexia and prostration. No serological tests were undertaken because of the remoteness of the mine. All other workers on the flight were contacted by telephone 6 days after the flight. Five more were identified who had significant upper respiratory tract symptoms and were taking simple analgesics, but had continued to work. The airline reported that no staff from the aircraft had reported sick over the next week or so. The seating positions of the affected workers on the aircraft, which was full, are shown in the Box. The index patient sat in seat 11G. Most of the other affected workers appeared to sit in a “plume” around him. The only affected workers who sat further away were the supervisor who assessed the index patient in the airport lounge (seat 3A) and a person who conducted a raffle during the flight and walked the length of the aircraft collecting money and ticket stubs (seat 1F). In aircraft such as the BAe 146, air is circulated and filtered, entering the passenger compartment through continuous vents just beneath the overhead lockers, circulating downwards and exiting from continuous vents under the seats. Air therefore tends to flow in two contrarotating circles, from ceiling to floor on either side of the aircraft. Infection could well have been transmitted by aerosol droplets to passengers behind the index patient, as he coughed and sneezed throughout the flight. The immunisation status of the passengers was not recorded; most were aged 20–45 years. This outbreak was relatively confined, as the passengers were in an isolated community, and those affected were managed in their rooms. However, the implications for the spread of airborne infection in passenger aircraft and into the wider community are obvious. It must be stressed to the travelling public that people with this type of illness should not fly. Airport authorities at passenger check-ins should be encouraged to identify and formally assess potentially infected individuals, and should have the authority to take precautions against spread. Aircraft seat allocations of index patient and affected passengers I = index patient. F = passenger developed influenza-like illness. M = passenger developed mild upper respiratory tract illness.

Andrew G Marsden

Peter J Collignon*, Dianne E Dreimanis† and Wendy D Beckingham† *Director, Infectious Diseases Unit and Microbiology Department; †Clinical Nurse Consultants, Infection Control; The Canberra Hospital, PO Box 11, Woden, ACT 2606. peter.collignonATact.gov.au To the Editor: Single-use devices (SUDs) are in common use, and many are reprocessed.1-7 When examined, these devices are frequently not clean and have residual biological material on or within them.2-4,6 This material may contain viruses or other infectious agents. SUDs are usually made from plastics or other heat-sensitive materials resulting in less effective means being used for sterilisation than can be used for more robust materials — chemical disinfectants can be ineffective in the presence of organic material, and have poor penetration compared with heat (eg, an autoclave). In 1994 we found that, of 168 Australian hospitals reviewed, 68% were reprocessing SUDs used in sterile sites.1 We repeated this survey (using a similar questionnaire) in 2001, in acute-care hospitals with more than 45 beds. The questionnaire was sent to 461 hospitals — 181 private hospitals (117 with fewer than 100 beds, 59 with 100–300 beds, and five with more than 300 beds) and 286 public hospitals (115 with fewer than 100 beds, 116 with 100–300 beds and 55 with more than 300 beds). Responses were received from 189 (see Box 1). Not all respondents answered all questions and many responded anonymously. Reuse of SUDs still occurred in all states and territories, but compared with 1994 the rate had dropped to 15% (28 hospitals). Large hospitals reused more often than smaller hospitals (see Box 1). Reuse was slightly lower in private hospitals than in public hospitals (13% v 16%). Rural hospitals reused SUDs less often than metropolitan hospitals (12% v 16%). The commonest SUDs reused were diathermy pencils. Given their low cost ($5), the labour costs of reprocessing would exceed the cost of replacement. Diathermy pencils (Box 2) have spring-loaded buttons, which inevitably become contaminated with blood during surgical procedures. Thus, the potential exists to contaminate the surgeon's fingers during subsequent procedures. We believe that reusing such relatively inexpensive items is inappropriate from both financial and infection control perspectives. An Australian National Health and Medical Research Council (NHMRC) report stated that, after reprocessing and packaging in hospitals, almost all SUDs were contaminated with foreign material (including blood), and several pacing electrodes had damaged insulation.6 Other studies have shown that blood persists on cardiac ablation catheters when structural abnormalities (which occurr frequently and early) are present.3 The reuse of these devices has been reviewed by the NHMRC and important changes have been recommended.6 Reuse of SUDs has been common in many countries. In the United States, reprocessing is frequent (eg, 2.5 million devices by one commercial reprocesser).5 In 2000, the US Food and Drug Administration issued a policy that, for practical purposes, should abolish the practice of reprocessing SUDs in hospitals.4 In Australia, the Therapeutic Goods Administration recently announced that reprocessing of SUDs will be regulated.7 This should have a similar effect. As the methods and response rates of our two surveys were similar, we believe that the reuse rate has decreased. However, proportionately, fewer large public hospitals responded (only 13 of 55, or 24%, compared with 41% overall), even though they have the highest reuse rate (54%). Therefore, we are likely to have underestimated the actual rate of reuse. Also, those who are reusing may be less likely to admit to this practice, and thus less likely to respond. Reuse of SUDs in sterile sites remains common practice in Australian hospitals (although the rate is lower than it was in 1994). Most SUDs appear to be unsuitable for reuse as they cannot be adequately cleaned and sterilised. We strongly advise against further reuse of these items. 1: Number and types of hospitals reusing single-use medical devices Number reusing devices / Number respondents Bed numbers Type of hospital Unknown < 100 100–300 > 300 Total respondents Unknown 0/1 0/2 1/4 1/1 2/8 (25%) Public 0/1 5/41 4/44 7/13 16/99 (16%) Private 4/40 6/36 0/2 10/78 (13%) Combined public and private 0/2 0/2 0/4 Total respondents 0/2 9/85 (11%) 11/86 (13%) 8/16 (50%) 28/189 (15%) 2: A diathermy pencil

Peter J Collignon · Dianne E Dreimanis · Wendy D Beckingham

Clifford F Hughes Head, Department of Cardiothoracic Surgery, Royal Prince Alfred Hospital, Suite 304, 100 Carillon Avenue, Newtown, NSW 2042 clifford.hughesATemail.cs.nsw.gov.au Comment: The letter by Collignon, Dreimanis and Beckingham about reuse of single-use medical devices (SUDs) in Australian hospitals again brings in to stark contrast the issue of safety and quality of medical devices and the pressing need to provide affordable services to the Australian public. Seven years ago, Collignon and colleagues showed an unacceptably high reuse of SUDs in Australia, especially in public healthcare institutions.1 Since then, the National Health and Medical Research Council (NHMRC) has produced an expert panel report on these devices2 and the Therapeutic Goods Administration has promulgated detailed device regulations.3 There has been continued debate in both the scientific literature and lay press, and the United States Food and Drug Administration has had extensive comments published on this matter.4,5 Given the intensity of this debate, it is surprising that so few hospitals completed the questionnaire. It is also surprising that, despite the overall reduction in the reuse of SUDs, there has been no apparent reduction in their use in large public institutions, 50% of which continue the practice. Collignon and colleagues have not investigated the quality control mechanisms in place in these hospitals. That could well be a subject for further research. Not so obvious to the casual user is the effect of resterilisation on the materials of the device. The authors allude to the potential for degradation during sterilisation. There is inevitable pressure to use less effective (chemical) means for re-sterilisation. On the other hand, the waste of an enormous resource that, if safe, could be readily reused must be recognised. The costs of devices are easy to quantify. The costs of resterilisation, not to mention quality control, less so. Collignon et al suggest one example of false economy in the reuse of a low budget but commonly used item — diathermy pencils. They make a strong case for mandated reporting of resterilisation protocols for all single-use items. Informed consent must be a prerequisite. Tracking systems could well provide beneficial information on the safety and efficacy of procedures for particular devices. Furthermore, clinical audit would provide an early warning mechanism should resterilisation prove inadequate. These are among the main recommendations of the Report of the NHMRC Panel.2 Extensive regulations and controls have been applied to the use of biological products such as dura mater, heterograft and cardiac valves, among others. There is, however, reluctance to apply similar stringent controls to devices which may be contaminated by more pervasive but less obvious biological hazards. There are only three options: cease this practice wherever a viable alternative is available until there is incontrovertible proof of the safety of reuse; mandate detailed protocols which include audit and surveillance mechanisms coupled with appropriate informed consent whenever SUDs are reused;2 and develop a research and evidence base for improvements in design and materi-al technology so that the "cost efficiencies" of single-use devices could be translated to "nondisposable items". All three must be adopted.

Clifford F Hughes