Infectious diseases

Clinical record A 33-year-old woman presented to the emergency department with a 10-day history of vesicular rash, 2 days of cough and fever, and 12 hours of dyspnoea, malaise and facial swelling. Her three children were recovering uneventfully from chickenpox. She had no past history of varicella infection or vaccination. She was a non-smoker, had no pre-existing medical conditions and was not known to be pregnant at the time of presentation. On presentation, the patient was in respiratory distress, with a respiratory rate of 36 per minute, pulse of 140 bpm, and oxygen saturation of 72% in room air. Subcutaneous emphysema was noted over the upper chest wall. Multiple healing and healed vesicles were present. The provisional clinical diagnosis was pneumonia, in the presence of resolving varicella. Results of blood tests on admission are shown in Box 1. Blood film demonstrated neutrophilia with toxic changes. Chest x-ray revealed pneumomediastinum and subcutaneous emphysema, while computed tomography showed pneumomediastinum and consolidation in the left upper lobe with cavitation (Box 2A). Electrocardiography revealed sinus tachycardia with paroxysmal atrial fibrillation. The patient was admitted to the intensive care unit with acute respiratory failure. Antimicrobial therapy was begun with ceftriaxone, flucloxacillin and aciclovir based on the clinical diagnosis of pneumonia with cavitation in a patient with active varicella. Blood cultures revealed gram-positive cocci in chains after 24 hours of incubation; intravenous clindamycin was added to the antibiotic regimen. The next morning cultures of blood and bronchoalveolar fluid confirmed the presence of Streptococcus pyogenes (group A streptococcus). Uncontrolled sepsis progressed within hours to multiorgan failure, precipitated by an overwhelming systemic inflammatory response syndrome. Clinical features were consistent with streptococcal toxic shock syndrome, with the primary streptococcal infection being pneumonia. Intensive care management included haemofiltration for acute renal failure; inotropic support for septic shock; invasive lung ventilation for respiratory failure (acute respiratory distress syndrome); activated protein C for the systemic inflammatory response syndrome; and infusion of intravenous gamma globulin for toxic shock syndrome, and fresh frozen plasma and platelets for coagulation dysfunction and thrombocytopenia. Despite maximal support, the patient died 44 hours after presentation. An autopsy confined to the chest and abdomen showed interstitial emphysema involving the mediastinum, pericardium and left upper lobe of the lung, and extensive necrotising left bronchopneumonia with abscess formation, but no signs of pneumothorax (Box 2B). Numerous gram-positive cocci consistent with streptococci were evident on microscopy of lung sections. Varicella zoster virus DNA was detected by polymerase chain reaction in one of three tissue samples tested, but no viral cytopathic changes were seen, and no virus was detected by culture. Varicella (chickenpox) is a highly infectious disease caused by varicella zoster virus. Monthly notifications in Australia fluctuate from 40 to 180, with three to four deaths yearly.1 Varicella zoster pneumonia with interstitial pneumonitis and respiratory distress syndrome is a well recognised complication which occurs more frequently in adults than children (particularly smokers, pregnant women and those who are immunocompromised). Despite the presence of varicella zoster virus DNA, there was no histological evidence that varicella pneumonia predisposed to the development of secondary group A streptococcal pneumonia in this case. In children, varicella is a well recognised predisposing condition for invasive group A streptococcal infection, preceding 15% of recorded cases of this infection in a recent Canadian study.2 The most common manifestation of invasive group A streptococcal infection is necrotising fasciitis, a serious but rare infection of the deeper layers of skin and fatty subcutaneous tissues. This is one of the fastest-spreading infections known, consuming tissue at a rate of up to 3 cm per hour.3 Pneumonia is a less common manifestation but has a higher fatality rate (38% versus 12% for necrotising fasciitis), with a reported median survival of 2 days.4 In adults, varicella is less common as a predisposing condition for invasive group A streptococcal infection, but cases have been reported of varicella gangrenosum with limb-necrotising fasciitis and toxic shock syndrome5 and of septic arthritis6 secondary to group A streptococcal infection after chickenpox. The speed of the patient’s demise and the presence of streptococcal bacteraemia and streptococci in postmortem lung tissue supports S. pyogenes as the pathogen causing death in this patient. Pneumomediastinum has many causes, particularly barotrauma and other forms of trauma, but is rare secondary to pneumonia and pulmonary abscess. We believe that this is the first case of group A streptococcal pneumonia with mediastinal gas leakage recorded in Australia. Pneumomediastinum occurring ultimately as a complication of varicella has similarly not been reported previously in this country. Primary vaccination of children is now recommended,7 but is not federally funded. Vaccination of adolescents and adults should also be strongly considered, as these age groups are more at risk of severe or lethal complications, including overwhelming secondary infection. Once invasive group A streptococcal infection is clinically suspected, it can be confirmed bacteriologically by culture of blood or affected tissue. Early medical treatment with intravenous penicillin and clindamycin is indicated. When infection is associated with streptococcal toxic shock syndrome, normal human immunoglobulin reduces organ failure and possibly mortality.8 Aggressive surgical debridement is critical for invasive fasciitis or myositis. However, in our patient, surgical debridement of affected pulmonary and mediastinal tissue was not an option. The prognosis was clearly extremely poor at presentation. The illness could have been prevented by varicella vaccination. Lessons from practice Varicella in adults is potentially serious, with a significant risk of very severe secondary bacterial infection. Varicella zoster pneumonia with interstitial pneumonitis and respiratory distress syndrome is a well recognised complication of varicella, and is more common in adults than children, particularly smokers, pregnant women and those who are immunocompromised. Varicella vaccination, although not federally funded, is recommended for children and should be strongly considered in adolescents and adults because of their higher risk of severe and lethal complications. Invasive group A streptococcal infection spreads rapidly and is often fatal; if suspected clinically, treatment should be begun urgently with intravenous penicillin and clindamycin; the addition of intravenous immunoglobulin for toxic shock should be considered, and surgical debridement for invasive fasciitis or myositis. 1 Results of blood tests in a patient with complications from varicella Test Result Normal range On admission Serum sodium (mmol/L) 121 135–145 Serum potassium (mmol/L) 3.4 3.2–4.5 Serum chloride (mmol/L) 79 100–110 Urea (mmol/L) 47.7 3.0–8.0 Creatinine (mmol/L) 0.48 0.05–0.10 Albumin (g/L) 21 33–47 Globulins (g/L) 50 25–45 Bilirubin (μmol/L) 31 < 20 Alkaline phosphatase (U/L) 144 30–120 γ-Glutamyl transferase (U/L) 308 < 50 Aspartate aminotransferase (U/L) 89 < 40 Lactate dehydrogenase (U/L) 425 110–250 Prothrombin time (s) 19 8–14 Fibrinogen (g/L) 9.9 1.5–4.0 Haemoglobin (g/L) 127 110–165 White blood cell count (cells/L) 17.3 x 109 3.5–11.0 x 109 Neutrophils (cells/L) 16.2 x 109 2.0–8.0 x 109 Platelets (cells/L) 113 x 109 140–400 x 109 6 h after admission* pH 7.01 7.35–7.45 pco2 (mmHg) 54 35–45 po2 (mmHg) 87 75–100 * After intubation and ventilation. 2 Appearance of the lungs in a patient with group A streptococcal pneumonia A: Computed tomography of the chest on admission showed subcutaneous emphysema, pneumomediastinum and consolidation in the left upper lobe with cavitation. B: Postmortem examination showed extensive necrotising left bronchopneumonia with abscess formation.

Peter JO Stride FRACP, FRCP · Matthys JJ Campher FANZCA · Janice M Geary RN, GradDipInfectionControl, GradCertHealthManagement · Christopher Coulter FRACP, FRCPA · Edwina E Duhig BMedSci, FRCPA

Ronan J Murray,* Kishore Sieunarine,† Peter B Ward,‡ John W Pearman§ * Senior Microbiology Registrar, § Clinical Microbiologist, † Vascular Surgeon, Royal Perth Hospital, Perth, WA; ‡ Senior Scientist, Department of Microbiology, Austin Repatriation Medical Centre, Heidelberg, VIC. ronan.murrayAThealth.wa.gov.au To the Editor: Previous articles in the Journal have described the emergence of Staphylococcus aureus with reduced susceptibility to vancomycin (also known as heteroresistant vancomycin-intermediate Staphylococcus aureus, or hVISA) in populations where methicillin-resistant S. aureus (MRSA) is endemic in healthcare settings.1,2 We describe a case of infection caused by hVISA from a region where healthcare-associated MRSA infection is relatively uncommon.3 A 79-year-old woman with an extensive medical history, including type 2 diabetes mellitus and multiple bypass procedures for lower-limb ischaemia, presented with critical ischaemia of the right lower leg. After above-knee amputation, she developed a discharge from the stump wound from which multiresistant MRSA was cultured. Despite receiving several courses of intravenous vancomycin (a total of 25 days of therapy over 5 months), the infection did not resolve. Extensive debridement surgery, with removal of multiple grossly infected vascular grafts, was performed, and MRSA was cultured from the graft material. Subsequently, the patient developed a discharging sinus from which MRSA with reduced susceptibility to glycopeptide antibiotics was cultured (vancomycin minimal inhibitory concentration [MIC], 8 mg/L; teicoplanin MIC, 24 mg/L). This isolate was shown to be hVISA by population analysis profiling (PAP). When the original MRSA isolate was subsequently tested by PAP, heterogenous subpopulations of bacteria with reduced susceptibility to vancomycin were present which had not been detected by routine susceptibility testing (ie, the isolate was already hVISA). Review of the patient’s medical records from other Perth healthcare institutions revealed no evidence of vancomycin administration before the initial isolation of MRSA, or contact with known MRSA-colonised patients or healthcare workers. Multilocus sequence typing and staphylococcal cassette chromosome mec allotyping identified the MRSA strain as ST239-MRSA-III, a multiresistant “international” MRSA clone frequently isolated in Australia, mainly on the east coast.4 Despite further surgery and institution of alternative antimicrobial therapy (initially rifampicin and fusidic acid and subsequently linezolid), the patient died of ongoing ischaemia and uncontrolled infection. Prolonged or repeated use of vancomycin in patients with implanted prostheses that are infected with MRSA should be discouraged, not only because it is commonly futile, but also because it may promote the emergence of subpopulations of S. aureus with reduced susceptibility to vancomycin, as occurred in this case. The fact that these resistant subpopulations were detected in an isolate before the commencement of vancomycin therapy (and then only with specialised testing) reinforces our recommendation.

Ronan J Murray · Kishore Sieunarine · Peter B Ward · John W Pearman

Subhash C Arya,* Nirmala Agarwal† * Clinical Microbiologist; † Chief of Gynaecology and Obstetrics, Sant Parmanand Hospital, 18 Alipore Road, Delhi-110054, India. subhashjiAThotmail.com To the Editor: The recent editorial by Burgess and McIntyre on the recommended vaccination schedules in Australia1 points to the fiscal constraints on offering the new, costlier vaccines. Overcoming these constraints would not be insurmountable if vaccinations were to be linked with annual festivals and celebrations in the life of individuals and the community. Birthday celebrations are important for infants and preschool children. Rather than giving conventional birthday gifts, varicella vaccine, costing $40, would be most appropriate. For those in the sixth or higher decades of life, gifts of influenza vaccine, 23-valent pneumococcal polysaccharide vaccine or the adult formulation of the diphtheria–tetanus vaccine would be memorable on Mother’s Day or Father’s Day and silver, golden or platinum wedding anniversaries. Similarly, slight adjustments to the allocation of funds for celebrating festivals such as Christmas and New Year, Dewali or Eid could make costly vaccines available to all. Vaccine producers, like department stores, could gear up for a Christmas vaccine sale. The public should be motivated to consider vaccines the most appropriate gifts. This is bound to address any poor coverage of costlier vaccines, such as varicella or the pneumococcal polysaccharide vaccine.

Subhash C Arya · Nirmala Agarwal

James D Kidd Retired General Practitioner, The Medical Centre, 125 River Road, Emu Plains, NSW 2750. To the Editor: Although I am retired, I wish to make some comment on the controversy about the use of ciprofloxacin in the treatment of chronic suppurative otitis media.1 I still feel uneasy when there is mention of the topical use of an antibiotic that may be used either orally or parenterally. Many years ago, when I had a large practice, including paediatric patients, chronic suppurative otitis media was common, although most cases responded to the classical ear drops. However, some persisted and, not infrequently, a new patient would present with this problem. As mentioned, most were the result of a pseudomonas infection. Pseudomonas was then a common problem in chronic leg ulcer of the elderly, and I had found that treatment with Burrow’s solution (aluminium sulfate [2.25 g], acetic acid [33%], tartaric acid [0.45 g], calcium carbonate [1 g], purified water [7.5 mL]) was very successful and continued to be successful right up to my retirement, even in new cases which had been treated unsuccessfully with ciprofloxacin. Before the advent of ciprofloxacin, I used Burrow’s solution ear drops in many adult cases of chronic suppurative otitis media with great success. As the number of children with this problem grew, I attempted to get advice on the use and any toxicity of Burrow’s solution ear drops in children. I could not find anyone at the Children’s Hospital with any experience, but the consensus was that it was unlikely to be toxic. Although at first I had difficulty in getting the chemist to make up ear drops for adults, by this time there was little problem getting them made for children, and the results were dramatic. There were recurrences, but these responded as well as they did the first time they were treated. Advice on correct aural hygiene after swimming and bathing was important. Burrow’s solution kills pseudomonas. Am I too old fashioned?

James D Kidd

There is currently no need to panic At a recent forum of the Australian Health Policy Institute in Sydney, the Editor of the Journal expressed concerns about Australia’s ability to cope with avian flu, and asked whether he could sleep soundly in his bed. We attempt to answer his concerns. Influenza is justifiably feared. In 1918–1919, 40 to 50 million people (2%–3% of the world’s population) died in the “Spanish” influenza pandemic.1 Subsequent influenza pandemics occurred in 1957 and 1968. Although the mortality of the later pandemics was far less, the potential for another major pandemic is ever present. Annual influenza outbreaks have caused more deaths overall than pandemics, but gentle antigenic “drift”, caused by minor mutations in the viral genome, allows the annual development of a new influenza vaccine, matched as closely as possible with predicted circulating strains. Pandemic strains caused by antigenic “shift” are, by definition, unpredictable, and unlikely to be prevented in the short term by vaccines. In 1999, stimulated by human infections caused by avian influenza in Hong Kong, the World Health Organization (WHO) published a pandemic preparedness plan, and urged countries to make their own plans.2 How well prepared is Australia? The origin of pandemics: The segmented genome of the influenza A virus favours genetic reassortment, which can lead to antigenic shift to a new, potentially pandemic, strain. Pandemic strains arise when a new type of haemagglutinin is introduced into humans. Pigs may act as a mixing vessel for reassortment by supporting growth of both avian and human viruses, or a human might be co-infected with both avian and human strains. Pandemic influenza spreads rapidly and affects children and young adults, causing enormous social disruption.1 Avian influenza: Birds, particularly aquatic and migratory species, are natural hosts of all 15 haemagglutinin subtypes of influenza A virus, whereas only a few of these viruses have established transmissible infections in humans, pigs and other mammals.1 Avian influenza strains readily infect domestic poultry and are highly pathogenic to birds.3 Since mid-December 2003, there has been a catastrophic outbreak of avian influenza in Asia, caused by a highly pathogenic H5N1 strain. Eight countries have confirmed outbreaks, mostly in commercial poultry, although wild birds have been infected. In 2 months, over 100 million birds in Asia died or were culled.3 There was great alarm when human infections with this avian strain were reported, with high mortality in both adults and children. However, despite the extent of the outbreak in birds, very few human cases have been reported. By 24 March 2004, 57 cases had been notified from Vietnam (37) and Thailand (20), of which 23 (40%) were fatal. All cases followed exposure to infected poultry. The number of unreported human cases is uncertain, but the absence of documented human-to-human spread is reassuring.3 The greatest concern is that there will be reassortment between the current avian H5N1 strain and circulating human or porcine influenza viruses, producing a novel, virulent human strain. Pandemic planning: Australia has been actively planning action to cope with an influenza pandemic since 1997. The framework for a pandemic plan was published in 1999,4 and an action plan was published in 2003.5 A National Influenza Pandemic Action Committee (NIPAC), formed in 2003, continues to plan for future pandemics and has closely monitored the avian influenza situation. Although NIPAC is an anagram of “panic”, the message so far is that there is no need to panic. A major concern of the audience at the health policy forum was the large number of different agencies involved in planning for a pandemic — a veritable “spaghetti junction”. Who should coordinate these agencies? Given the complexity of pandemic planning, we believe it is entirely appropriate that there are many different players, coordinated, as is now the case, by the Australian Department of Health and Ageing.6 Planning for pandemic influenza overlaps to an extent with planning for outbreaks of other viral infections. Australian pandemic planning has benefited from the need to develop plans to cope with a potential epidemic of SARS (severe acute respiratory syndrome)7 and possible bioterrorist attack with smallpox virus.8 NIPAC is addressing many facets of planning, including: Border protection. Although Australia is an island, modern air travel and the high infectivity of influenza preclude total exclusion of a pandemic. Because influenza can be transmitted before symptoms appear, screening incoming passengers for reported symptoms, as was done for SARS, would be less effective, but might delay widespread introduction of influenza. Even weeks of delay could be invaluable for vaccine development and distribution. Immunisation. It would probably take at least 6 months after the onset of a pandemic for significant quantities of vaccines specific to the pandemic strain to become available.9 WHO is currently developing H5N1 viruses suitable for vaccine production as rapidly as possible. Antivirals. The H5N1 virus is resistant to amantadine, but sensitive to the neuraminidase inhibitors oseltamivir and zanamavir, which can be used for both treatment and prophylaxis. It has been suggested that countries should stockpile antivirals.10 There was some evidence of their benefit in humans during the 2003 outbreak of highly pathogenic avian H7N7 influenza A in Dutch poultry farms.1 However, antivirals are very expensive and in short supply, and realistically could only be used as a stop-gap measure to “buy time” by treating early cases and protecting essential staff. Laboratory diagnosis. Influenza is difficult to differentiate clinically from “influenza-like illnesses”, necessitating laboratory testing of appropriate respiratory samples for confirmation. However, testing is not often done routinely (at least in adults). SARS and the threat of avian influenza suggest testing should be more widely available to facilitate decisions about infection control, but few laboratories provide rapid viral diagnosis. The network of WHO influenza and other public-health laboratories in Australia is actively developing rapid tests to detect H5N1 influenza. Infection control measures to limit spread. Children are at high risk of contracting and dying of influenza,1 and are an important source of infection for the elderly.11 In a pandemic, it would almost certainly be necessary to close schools, childcare centres and public gatherings to reduce spread. Respiratory hygiene. Simple respiratory hygiene, such as covering the nose and mouth when sneezing, and disposing of used tissues promptly in “no-touch” receptacles, is as important as the use of masks.12 Communication. The level of public concern and, in many countries, panic during the SARS outbreak vividly illustrates the importance of effective public communication. It is vital that authorities do not leave the dissemination of information about outbreaks to the popular press. There is currently no need to panic about avian influenza, as human cases are extremely rare and have followed close exposure to birds. Human-to-human spread of avian influenza has not been described. While Australia is well prepared to cope if an influenza pandemic started tomorrow, the unpredictability of these pandemics, their rapid spread and high attack rates mean it is impossible to be totally reassuring. Like the rest of us, the Editor of the Journal, if he wants to sleep soundly, will just have to cope with uncertainty.

David Isaacs MD, FRACP, FRCPCH · Dominic E Dwyer MD, FRACP, FRCPA · Alan W Hampson MSc, MASM

Sebastiaan J M van Hal,* Jeffrey J Post† * Advanced Trainee, † Infectious Diseases Physician, Prince of Wales Hospital, Barker Street, Randwick, NSW 2031. j.postATunsw.edu.au To the Editor: Community-acquired methicillin-resistant Staphylococcus aureus (CAMRSA) infection is an increasingly recognised cause of skin and soft tissue infection, as well as more serious manifestations, including necrotising pneumonia, endocarditis, osteomyelitis and severe sepsis.1,2 We report another serious manifestation of CAMRSA infection. A 24-year-old Australian-born white, HIV-negative, male prison inmate was transferred to hospital. He had previously injected drugs, but not for more than 2 years. He reported a 10-day history of cervical neck pain, left-sided pleuritic chest pain and a 2-cm occipital carbuncle, which developed after a laceration on the scalp from a close haircut with barber’s shears. Examination revealed a temperature of 37.9°C, sinus tachycardia, profound neck stiffness and signs of left basal consolidation with a left pleural effusion. There were no focal neurological signs or other signs of meningism. Investigations revealed a neutrophil leukocytosis of 22.7 × 109/L (reference range, 1.7–7.0 × 109/L) with mild elevation of hepatic transaminases and hypoalbuminaemia. CAMRSA was isolated from blood cultures and a swab of the occipital carbuncle. The organism was susceptible to erythromycin, vancomycin, rifampicin and fusidic acid. A chest radiograph showed extensive left-sided consolidation consistent with pneumonia. A magnetic resonance imaging scan of the entire spine revealed asymmetric thickening and enhancement of the epidural tissue from C2 to C5, with no discrete abscess, osteomyelitis or discitis. The patient made a full recovery after 4 weeks of intravenous therapy with vancomycin (1 g every 12 hours) and clindamycin (600 mg every 6 hours). This is the first reported case of epidural tissue infection (epiduritis) caused by CAMRSA, and adds to the spectrum of potential clinical manifestations. In addition, this is the first reported case of CAMRSA infection occurring in an Australian prison inmate. There have been several reported outbreaks of CAMRSA in US correctional facilities.3,4 Although no similar outbreaks have been described in Australia, clinicians should be aware that correctional facilities may contribute to the spread of CAMRSA. The most common manifestations of CAMRSA infection in the prison setting in the United States are skin and soft tissue infections, with invasive infection occurring in 1.7% of patients.4 Clinicians providing care to inmates should be aware that strategies have been identified to reduce the incidence of CAMRSA infection.5 Clinicians need to be aware of the increasing incidence of CAMRSA infection, the diverse and potentially severe manifestations, and the treatment and preventive strategies available.

Sebastiaan J M van Hal · Jeffrey J Post

Donald M Clark Obstetrician, PO Box 503, Mount Lawley, WA 6929. To the Editor: Giles et al1 have “poisoned the well” for future research by attacking the obstetricians who took the trouble to help them with their study on management of hepatitis B virus (HBV), hepatitis C virus (HCV) and HIV. Many of the discrepancies noted between current practice and the recommendations/guidelines are easy to explain: Failure to screen. Many obstetricians were told that it is discriminatory to screen for HIV and HCV without extensive pretest counselling. The advice is obsolete, but old habits die slowly. Failure to recommend caesarean section for women with HIV. Many obstetricians have never seen a case of HIV and would most certainly phone for advice if the situation arose. Failure to promote breastfeeding. Many obstetricians leave advice on breastfeeding to the midwives and paediatricians. However, the article does concede that mother-to-baby transmission is a theoretical risk, so patients are entitled to be informed. Failure to adhere to guidelines. Many obstetricians regard guidelines issued by the Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG) as just that — guidelines, not gospel.

Donald M Clark

Objective: To investigate the source and risk factors associated with Australia’s largest outbreak of Legionnaires’ disease.Design and setting: Epidemiological and environmental investigation of cases of Legionnaires’ disease associated with visits to the Melbourne Aquarium; two case–control studies to confirm the outbreak source and to investigate risk factors for infection, respectively.Participants: Patients with confirmed Legionnaires’ disease who visited the Melbourne Aquarium between 11 and 27 April 2000 were compared (i) with control participants from the community, and (ii) with control participants selected from other visitors to the Aquarium during this period.Main outcome measures: Risk factors for acquiring Legionnaires’ disease.Results: There were 125 confirmed cases of Legionnaires’ disease caused by Legionella pneumophila serogroup 1 associated with the Aquarium; 76% of patients were hospitalised, and four (3.2%) died. The Aquarium cooling towers were contaminated with this organism. Visiting the Aquarium was significantly associated with disease (odds ratio [OR], 207; 95% CI, 73–630). The case–control study indicated that current smoking was a dose-dependent risk (multivariable OR for currently smoking > 70 cigarettes/week, 13.5; 95% CI, 5–36), but chronic illness and duration of exposure at the site were not significant risks.Conclusions: This study showed an association between poorly disinfected cooling towers at the Aquarium and Legionnaires’ disease in visitors, and confirmed current smoking as a critical risk factor. The rapid response, publicity, and widespread urinary antigen testing may have resulted in detection of milder cases and contributed to the relatively low apparent morbidity and mortality rates. The urinary antigen test allows rapid identification of cases and may be changing the severity of illness recognised as Legionnaires’ disease and altering who is considered at risk.

Jane E Greig PhD, MAppEpid · John A Carnie FAFPHM, MPH · Graham F Tallis FAFPHM, MPH · Bernard Zwolak MAppSc, BEd · William G Hart MB BS(Hons), FAFPHM · Charles S Guest PhD, FAFPHM · Norbert J Ryan PhD, BAgrSc · Jennie A Leydon BAppSc · Agnes G Tan BTech(Food)Hons, MHlthAdmin · Ian R Gordon PhD, AStat

John R Gowardman,* Maria Brosnan,† Joy Whiting,‡ Peter Collignon§ * Intensive Care Physician, † Medical Student, ‡ Data Manager, Intensive Care Unit, § Director, Infectious Diseases Unit and Microbiology Department, The Canberra Hospital, PO Box 11, Woden, ACT 2607. peter.collignonATact.gov.au To the Editor: In most serious infections associated with intravascular devices, the device is a central venous catheter (CVC).1,2 Good clinical practice dictates that these devices should be removed when no longer needed.3 Our intensive care unit maintains a clinical practice of prompt removal of CVCs once they are no longer required. In addition, CVCs are to be removed before patients are discharged from the unit (for “general” patients) or within 24 hours (for cardiothoracic surgical patients). We conducted an audit to determine how often this practice was followed and whether it had unintended adverse clinical consequences (eg, need to reinsert a CVC). The audit was conducted over 8 weeks in 2001 and included 126 CVCs in 103 patients. Fifty-eight CVCs (46%) were removed by the predetermined time, and 68 (53%) were retained past this time (Box). The data demonstrated: Low removal rates, with 31% (23/74) of CVCs removed in general patients, but higher rates in cardiothoracic surgical patients (67%; 35/52). APACHE II scores, ventilation times and lengths of stay in the intensive care unit were similar in the group who had the CVC removed and the group who retained the CVC, implying that severity of illness was not a factor biasing retention. Among patients who had a CVC removed, none had another CVC reinserted; cannulation rates with short peripheral catheters were low and acceptable. Retention of the CVC past the predetermined time resulted in significant prolongation of CVC in-situ time (eg, general patients 7.0 v 3.2 days). The reason given for CVC retention in general patients was antibiotic administration for 37/40 (93%) (vancomycin, 6; β-lactams, 20; aminoglycosides, 9; and quinolones, 2), while total parenteral nutrition and poor peripheral access were factors in only seven (18%). In the 13 cardiothoracic surgical patients, the reason given was inotrope infusion in four (30%) and amiodarone infusion in four; no reason could be ascertained in the other five. Two issues emerge from this audit. Firstly, there did not appear to be good reasons for retaining many of these CVCs. Drug therapy was most often quoted, but many of these drugs (antibiotics and amiodarone) could have been safely administered via a short peripheral intravenous cannula, with markedly lower risk of infection.2-5 We believe that when a patient left the intensive care unit with a CVC, it most likely remained in place as a “convenience” factor for busy nursing and junior medical staff on the wards. However, this was at the cost of a significant increase in CVC in-situ times, increasing the risk of both mechanical and infectious complications. Secondly, implementation of predetermined CVC removal appears safe in our hospital. Although removal rates were lower than expected, nearly half of all CVCs inserted over the 8-week study period were removed as per “clinical practice”, without any need for CVC reinsertions. We have now further refined our clinical practice and introduced a formal written policy that: All CVCs should be removed and replaced with a suitable alternative before patient discharge from the intensive care unit, unless there is a specific indication for retention. Retention of a CVC should be based on simple guidelines, such as need for total parenteral nutrition, poor peripheral venous access, or use of drugs that require central access. We recommend implementation of this simple policy in other intensive care units. Characteristics of patients and central venous catheters (CVCs) in the audit General ICU patients Cardiothoracic patients CVC removed CVC retained P CVC removed CVC retained P Number of patients 20 40 30 13 Number of CVCs 23 51 35 17 APACHE II score (mean [SD]) 14 (3) 16 (6) 0.13 13 (4) 13 (2) 1.00 Length of ICU stay (d) (mean [SD]) 3.9 (5.4) 2.4 (3.5) 0.2 1 (0) 2.1 (3.7) 0.1 Ventilation time (h) (mean [SD]) 61 (86) 47 (51) 0.5 17 (3.5) 20 (15.6) 0.3 % Of patients ventilated* 60% 41% 100%‡ 100%‡ CVC in-situ time (d) (mean [SD]) 3.2 (3.2) 7.0 (5.6) 0.003 2.1 (0.25) 4.5 (3.8) 0.001 Number of peripheral IV catheters† (mean [SD]) 1.8 (1) 0.6 (0.6) < 0.001 0 0.07‡ Number of CVCs reinserted 0 na 0 na ICU = intensive care unit. IV = intravenous. na = not applicable. * Mechanically ventilated in the intensive care unit. † At 7-day follow up. ‡ Only one peripheral catheter was inserted in one patient.

John R Gowardman · Maria Brosnan · Joy Whiting · Peter Collignon

Jennifer H Barralet,* Neil R Parker† * Epidemiologist, Communicable Diseases Unit, † Public Health Physician, Darling Downs Public Health Unit, Queensland Health, GPO Box 48, Brisbane, QLD 4001. Neil_ParkerAThealth.qld.gov.au To the Editor: Queensland has a small but increasing number of Q fever notifications in children. This is of concern to public health services in the Darling Downs and south-west Queensland where most Q fever notifications originate (Box). Little is known about Q fever in children, especially in Australia, as the disease is primarily diagnosed in adults following occupational exposure to Coxiella burnetii. Here we report a case series examining clinical presentation, exposure to risk factors and disease outcomes in children. Twenty-one children aged 3–14 years notified with Q fever from the Darling Downs and south-west Queensland in 2001 and 2002 were followed up. In acute cases the febrile illness was similar to that in adults from the same region. The one child with chronic Q fever had no known acute illness and presented with osteomyelitis of the wrist. All the children recovered, although relapsing symptoms were reported in two children and three reported persisting fatigue for 3 months or more after diagnosis. All but one patient reported contact with cattle, sheep or goats (13 lived on a farm and 7 had visited a farm). The single exception reported contact with kangaroos and feral pigs through hunting. Prolonged exposure to animals or the farm environment was not necessary for infection. Twelve of the children had high risk exposure to C. burnetii (contact with animal births, newborn animals, or animal carcasses). With increasing age, exposure of children from rural properties approaches that of their parents as they participate in the same activities. An effective vaccine is available,1 but use in people younger than 15 years is not recommended because of the lack of safety and efficacy data. Although avoidance of high risk situations such as shearing, animal births or on-farm butchering will decrease the chance of infection, these measures may be impractical for rural children. Realising this, some practitioners choose to vaccinate younger children who assist with animal births and butchering. Increasing notifications in children may reflect increased awareness that Q fever is not confined to adults with occupational exposures. Increased awareness leading to recognition of infection would give children access to effective treatment and may contribute to prevention of chronic disease. However, much remains unknown about Q fever in children, including how often the infection is asymptomatic, the spectrum and outcome of disease, and if there are effective preventive strategies. As many rural children cannot avoid potential exposure to Q fever, our study highlights the need for a safe and effective vaccine for children. Q fever notifications in children aged 0–14 years, 1997–2002

Jennifer H Barralet · Neil R Parker

The impact of a computer-based infectious diseases electronic antibiotic advice and approval system (“IDEA3S”) was assessed as an alternative to a labour-intensive, phone-based approval system. IDEA3S-based approvals replaced 48% of all approvals for the most frequently requested antimicrobial agents (ceftriaxone/cefotaxime, vancomycin) and were associated with stable overall rates of antimicrobial use. Antibiotic prescribing for community-acquired pneumonia was 76% concordant with IDEA3S recommendations, and clinical acceptance of IDEA3S was excellent. Successful implementation required a coordinated, evidence-based approach between clinicians, pharmacists and hospital administration, together with ongoing staff education and feedback of results. IDEA3S is a useful new adjunct to routine clinician consultation to support appropriate antibiotic prescribing for a number of common indications in hospitals.

M Lindsay Grayson MD, FRACP, FAFPHM · Sharmila Melvani BPharm · Sue W Kirsa BPharm, GradDipHospPharm · Stephen Cheung BPharm, GradDipInfoSys · M Kent Garrett BPharm, GradDipHospPharm · Anthony M Korman MB BS, FRACP · William A Thomson BPharm, MSc, FSHPA

Stephanie L Jones,* Eugene Athan,† Daniel O’Brien,† Stephen R Graves,‡ Chelsea Nguyen,§ John Stenos¶ * Infectious Diseases Registrar, † Infectious Diseases Physician, Geelong Hospital, Ryrie St, Geelong, VIC 3220; ‡ Medical Microbiologist, § Scientist, ¶ Senior Scientist, Australian Rickettsial Reference Laboratory, Barwon Health, Geelong, VIC. StephljonesATyahoo.com To the Editor: Murine typhus (caused by Rickettsia typhi) has not been previously described in the state of Victoria, although it is well known in Western Australia, Queensland and South Australia. In 2002, a 49-year-old man presented to Geelong Hospital, Victoria, with a 10-day history of fever, myalgia, rigors, headache, rash, sore throat, dry cough and pleuritic chest pain. On examination, he had a fever (temperature, 39.2°C), hypoxia (oxygen saturation, 91% in room air), tachycardia, a central maculopapular rash and conjunctivitis. Blood tests revealed hyponatraemia, thrombocytopenia, white cell count in the reference range, with left-shifted neutrophil change (toxic granulation and increased immature forms) and a C-reactive protein level of 377 mg/L (reference range, < 10 mg/L). The patient lived on a hobby farm close to Geelong. Two weeks before becoming unwell, he had cleaned out the contents of a shearing shed, including two rotten sheepskins in which rats had been nesting. He reported generating a lot of dust and debris in the air. He had not noticed any tick, flea or other insect bites. Serological testing was performed for rickettsia. Baseline serum, taken 10 days after symptom onset, showed antibodies to the typhus group of rickettsiae, R. typhi (murine typhus) and R. prowazekii (epidemic typhus), with a titre of 2000. The titre rose over the following 4 days to 64 000, a fivefold increase, diagnostic of typhus group infection. Antibody titre to the spotted fever group of rickettsiae was significantly lower (peak titre, 8000). The patient was treated with oral doxycycline and recovered completely. Murine typhus was first described in Adelaide in 19221 and is now considered endemic in parts of Western Australia and Queensland.2,3 A possible case reported from Melbourne4 was, in retrospect, probably Brill–Zinsser disease (relapsed epidemic typhus). Murine typhus has an incubation period of 8–16 days and is generally self-limiting, although fatalities have occurred.1 The disease typically presents with fevers, prominent myalgia, a central rash, nausea, conjunctivitis, and often significant pulmonary involvement. Unlike the tick-borne spotted fever group of rickettsiae, R. typhi is transmitted by rodent fleas. Transmission occurs either by aerosolisation and inhalation of infected flea faeces, often during demolition or cleaning of rat-infested environments, or, less commonly, by inoculation of faeces into a fleabite. Murine typhus is usually diagnosed retrospectively by serological testing using microimmunofluorescence. Antibodies are usually detectable 7 to 9 days after disease onset, and IgG may persist for years. Cross-reactivity is seen between R. typhi and R. prowazekii; it is not possible to identify the pathogen by serological testing alone.5 Specific diagnosis is based on known local epidemiology and, as epidemic typhus does not occur in Australia, we believe this was a case of murine typhus, the first described in Victoria.

Stephanie L Jones · Eugene Athan · Daniel O’Brien · Stephen R Graves · Chelsea Nguyen · John Stenos

Kirsty L Buising,* Karin A Thursky,† James F Black,‡ Graham V Brown§ * Clinical Research Fellow, † Infectious Diseases Physician, ‡ Head of Epidemiology, § Head, Victorian Infectious Diseases Service, Royal Melbourne Hospital, Grattan Street, Parkville, VIC 3050. Kirsty.buisingATmh.org.au To the Editor: The 2003 Australian guidelines on antibiotic therapy suggest that the Pneumonia Severity Index (PSI) may be used to triage site of care and antibiotic selection for patients with community-acquired pneumonia.1,2 The PSI was developed as a mortality prediction tool, using data from over 14 000 patients with community-acquired pneumonia.3 The antibiotic guidelines suggest specifically that PSI classes I and II represent patients suitable for outpatient therapy, and that class V can identify patients likely to require intensive care and broad-spectrum antibiotic therapy. We believe this is beyond the previously recommended applications of the PSI and advise caution about its use to identify patients with severe pneumonia. In the cohort used to validate the PSI, only 32% of patients with severe pneumonia (requiring intensive care) were in class V, indicating that the PSI has poor sensitivity for severe pneumonia.3 This finding has been reflected in other studies.4 The strength of the PSI lies in its ability to identify low-risk patients, as the title of the validating article suggests.3 The PSI is so heavily weighted by age and comorbidities that younger patients needing intensive care are unlikely to accumulate enough points to reach class V. This is important, as early identification of patients with severe pneumonia and initiation of broad-spectrum antibiotic therapy and intensive-care support improves outcomes. We are concerned that the PSI may be widely accepted for a purpose for which it was not intended and has not been validated. In underestimating the severity of illness in two-thirds of patients with “severe pneumonia”, the guidelines may provide false reassurance, while clinicians may lose confidence in the PSI if they find it “misses” most patients requiring intensive care. Current evidence does support use of the PSI to guide decisions about inpatient or outpatient therapy. However, the modified British Thoracic Society (BTS) Severity Score is a simpler, better-validated tool to identify patients with “severe pneumonia” who are likely to need intensive care assessment5 (Box). This tool is useful for junior staff to “flag” patients with potentially severe pneumonia and ensure that they are discussed with a senior clinician. As always, the final management and antibiotic selection should be guided by clinical judgement. We believe that the antibiotic guidelines are valuable to encourage appropriate antibiotic use; our aim is to promote discussion of their content relating to this particular condition. Suggested alternative approach to assessing patients with community-acquired pneumonia Step 1: Does the patient need admission to hospital? Assess with the Pneumonia Severity Index (PSI). Class I or II: consider outpatient management (but also need to consider comorbidities, social supports, likelihood of compliance). Class III-V: likely to need inpatient management. Step 2: Does the patient need admission to the intensive care unit? Assess with the modified British Thoracic Society (BTS) Severity Score. Class as severe if two or more of the following features are present on initial assessment or within 24 hours of presentation (and are not attributable to another cause): Confusion (acute onset) Serum urea level > 7 mmol/L Respiratory rate ≥ 30 breaths/minute Systolic blood pressure < 90 mmHg or diastolic blood pressure ≤ 60 mmHg If severe, discuss the case with a senior clinician and consider intensive-care review and aggressive broad-spectrum antibiotics.

Kirsty L Buising · Karin A Thursky · James F Black · Graham V Brown

Wenbiao Hu,* Anthony J McMichael,† Shilu Tong‡ * PhD candidate, Centre for Health Research, Queensland University of Technology; † Director, National Centre for Epidemiology and Population Health, Australian National University, Canberra; ‡ NHMRC Senior Research Fellow, School of Public Health, and Centre for Health Research, Queensland University of Technology, Kelvin Grove, QLD 4059. s.tongATqut.edu.au To the Editor: We examined the possible association between the Southern Oscillation Index (SOI) and the occurrence of hepatitis A in Australia using a Seasonal AutoRegressive Integrated Moving Average (SARIMA) regression model.1 Our results indicate that the SOI is statistically significantly associated with the transmission of hepatitis A. We obtained data on the monthly counts of hepatitis A cases in Australia and the monthly SOI between 1 January 1991 and 31 December 2000 from the Commonwealth Department of Health and Ageing and the Australian Bureau of Meteorology, respectively. Data on population sizes were obtained from the Australian Bureau of Statistics. Cross-correlations were used to compute a series of correlations between SOI and the incidence of hepatitis A over a range of time lags (defined as the time span between the SOI and the incidence of hepatitis A). A SARIMA model was used to estimate the independent contribution of SOI in our study. We adjusted for seasonality by “seasonally differencing” (ie, replacing each observation by the difference between it and the observation from the previous year). In the modelling process, attention was paid to observations well outside the main body of the data (outliers) and the only outlier was excluded in the final SARIMA model. We used the SARIMA [1,0,0] [1,1,0]12 model (ie, first-order autoregressive combined, first-order seasonal autoregressive, after adjustment for first-order seasonal integration) to assess the association between SOI and the incidence of hepatitis A. We found that a decrease in the SOI (ie, warmer and drier conditions) was statistically significantly associated, at a lag of 1 month, with an increase in the monthly incidence of hepatitis A (β = − 0.01; P = 0.001). Two El Niño events (1991–92 and 1997–98) were also clearly associated with an increased incidence of hepatitis A (Box). The results suggest that there was an increase of about 360 cases per year in Australia for an, on average, interquartile range decrease in the SOI. The residuals in the model fluctuated randomly around zero, and there was no apparent autocorrelation between residuals at different lag times (data are available from the corresponding author). These results indicate that the model fitted the data well, with no violation of assumptions. The significant association between SOI and the incidence of hepatitis A remained when the outlier was included in the model (β = − 0.013; P = 0.001). El Niño Southern Oscillation (ENSO) has been found to be related to various health outcomes, including waterborne disease, vectorborne disease, and natural disaster-related deaths (eg, floods, bushfires and cyclones).2-4 Our study adds further evidence of ENSO-related health effects. Infectious diseases are, in general, sensitive to climate variability, as climate can influence the development and transmissibility of pathogens, and can also affect people’s behaviour.3,5 If the relationship between ENSO and hepatitis A is confirmed by other studies, these findings may facilitate the development of early warning systems for controlling and preventing this widespread communicable disease. Incidence of hepatitis A in Australia and the Southern Oscillation Index between January 1991 and December 2000 Negative values of the SOI are associated with El Niño conditions (dry and warm in Australia), and positive values with La Niña conditions (wet and less warm in Australia).

Wenbiao Hu · Anthony J McMichael · Shilu Tong

Objective: To assess obstetricians’ current antenatal screening practices for blood-borne viruses (hepatitis B, hepatitis C and HIV) and how they manage pregnant women infected with a blood-borne virus.Design and participants: National cross-sectional survey conducted between September 2002 and January 2003. All obstetricians (n = 767) registered with the Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG) were mailed a questionnaire assessing their antenatal screening practices and knowledge of management of women potentially infected with a blood-borne virus.Outcome measures: Concordance of clinical practice with RANZCOG recommendations and current evidence-based guidelines.Results: 523 obstetricians (68% response rate) completed the questionnaire. Fifty-one per cent of respondents said they would always offer HIV screening and 60% would always offer HCV screening. For HIV-infected women, 36% of obstetricians would always recommend elective caesarean section and 33% would always avoid rupture of membranes. Despite a lack of evidence, 34% of obstetricians advise patients that the risk of HBV transmission is increased with breastfeeding, and 47% give the same advice about HCV transmission.Conclusion: There is some discordance between the RANZCOG antenatal screening recommendations for HCV and HIV and current practice. Knowledge about the management of HIV-infected women could be improved, and more obstetricians need to be aware that current evidence suggests there is no increased risk of transmission of HBV or HCV with breastfeeding.

Michelle L Giles MB BS · Suzanne M Garland MB BS, FRCPA, FRANZCOG · Joseph J Sasadeusz MB BS, FRACP, PhD · Sonia R Grover MB BS, FRANZCOG · Margaret E Hellard MB BS, FRACP, PhD

Andie S Lee,* John R Dyer† * Registrar, † Senior Infectious Diseases Physician, Department of Microbiology and Infectious Diseases, Flinders Medical Centre, Flinders Drive, Bedford Park, SA 5042. John.dyerATfmc.sa.gov.au A 79-year-old man presented with 5 days of right-leg pain, high fever, severe headache and deteriorating conscious state. He was previously fit and healthy and took no medications. The patient appeared unwell, had a temperature of 39.5°C, moderate irritability and depressed conscious state. There was marked neck stiffness and his left wrist and right knee joints appeared swollen and inflamed. There was a cardiac systolic murmur, but no stigmata of bacterial endocarditis. Aspirates of the left wrist and right knee yielded purulent fluid containing numerous gram-positive cocci. The patient was admitted to the intensive care unit and treated with high dose benzylpenicillin plus vancomycin. A cerebral computed tomography scan was normal; lumbar puncture was not performed. The affected joints were washed out within 24 hours. All cultures of blood and synovial fluid yielded a Lancefield Group C β-haemolytic streptococcus, identified further using the ID 32 Strep strip (BioMerieux, Marcy l’Etoile, France) as Streptococcus equi subspecies zooepidemicus (S. zooepidemicus) based on its ability to ferment sorbitol and not trehalose. This isolate was shown to be sensitive to penicillin (minimum inhibitory concentration, < 0.1 mg/L). Intravenous penicillin therapy was continued. Transoesophageal echocardiography showed echodensities close to the aortic valve which suggested vegetations. The patient’s condition improved steadily, and he ultimately received intravenous antibiotics for 6 weeks. Further history revealed that the patient collected fresh horse manure for his garden daily from a local paddock. He reported no direct contact with animals or ingestion of unpasteurised dairy products. S. zooepidemicus could not be cultured from a single specimen of horse manure collected from the paddock, and it was not possible to collect clinical specimens directly from any of the horses that used the paddock. Human infection with S. zooepidemicus can usually be traced to an animal source.1 Outbreaks associated with ingestion of unpasteurised milk and cheese have also been described.2,3 Likely entry routes include the respiratory or gastrointestinal tract and skin.1 Severe sequelae of S. zooepidemicus infection include endovascular infection, meningitis, septic arthritis, and epidemic post-infectious glomerulonephritis. Our patient’s clinical picture indicated multifocal sepsis, with polyarthritis, endocarditis, and probable meningitis. In a recently reported case of S. zooepidemicus meningitis, pulsed-field gel electrophoresis showed molecular identity between patient isolates and a throat swab isolate from a horse with which the patient had been in close contact.4 Our patient was most likely infected via the respiratory or cutaneous routes, or by ingestion after contact with respiratory secretions of horses deposited in the environment. Exposures in the garden can lead to a variety of severe infections.5 This is the first reported case where S. zooepidemicus infection appears to have been acquired through gardening. Severe disease with this organism can be a particular hazard in elderly gardeners with comorbid conditions.1

Andie S Lee · John R Dyer

Compassion for those with hepatitis C and accurate information about preventing its transmission will also benefit the wider community My GP’s rooms were the last place I would have expected to feel like a leper because I was sick, but that’s my story, and unfortunately it’s a fairly common one among people living with hepatitis C (HCV).1 Discrimination against people who are HCV-positive is not confined to healthcare settings, but this is where it is most often reported,2 partly because it’s the context in which affected people are most likely to disclose their condition. Discrimination also rears its ugly head at home, in social situations, at work, school, in the media and when we attempt to access services, such as insurance. It even clings to people beyond death, with families of people with HCV sometimes being refused viewings of their loved ones’ bodies, even though this is inconsistent with public health regulations. Several Australian government reports and a growing body of social research identify hepatitis C-related discrimination as an epidemic in its own right,3 and show that stigmatisation has detrimental effects on people’s health and quality of life,1 as well as significant social and economic costs.4 When the NSW Anti-Discrimination Board announced its world-first enquiry into hepatitis C-related discrimination in 2001, I decided to make a submission about my experience of being diagnosed with HCV. The Hepatitis C Council of NSW knew my story and that, as a journalist, I would be comfortable dealing with my colleagues, so I was asked if I would talk to the media to raise awareness of the enquiry and the issues it was investigating. Although there are an estimated 225 000 people in Australia with hepatitis C,5 many fear the consequences of disclosure in their daily lives, so very few are prepared to publicly identify themselves as HCV-positive. Since agreeing to talk to the media, I have been invited to tell my story many times. It is always rewarding work, because, as HIV/AIDS-positive speakers throughout the world have demonstrated,6 presenting a personal experience of living with an infection like HCV not only educates audiences about the disease and prevention strategies, but also challenges negative stereotypes that result in discrimination. I was diagnosed in March 2000 by the GP I had consulted for 7 years. She was used to me complaining of extreme tiredness, for which she diagnosed “some sort of virus” and recommended a few days off work. However, in January 2000, I felt as if I had aged 60 years in a couple of months. Vomiting after lunch was becoming routine. I had three weeks off work, but it made little difference to how I felt. I went back to the doctor in March to request a hepatitis C test because I had met a woman who was HCV-positive. She had described the debilitating symptoms that had forced her to give up her career as a medical practitioner, and I identified with them all, so I knew I had to be tested. Back in 1985, before hepatitis C got its name and before there was a test for it, I took heroin for a few months. When I sought help, my drug use was treated in a non-judgemental way by my family, a fabulous GP and a psychiatrist. I received excellent care and emerged with my self-respect intact and my body in good shape. Or so I had thought for 15 years. In 2000, my doctor’s response to my request for an HCV test was “you wouldn’t have that”. My subsequent admission of injecting drug use all those years ago was met with silence, but she ordered the test. When I went back for the results it seemed that she didn’t want to know about me or my illness, despite the fact that I was very sick. She offered almost no information at all about the virus, explaining that she “just doesn’t see it” in her surgery, and handed me a brochure produced in 1991, which said there was little in the way of treatment, that the prognosis was not good, and that the highest risk group was homosexual men. All of this was simply untrue in 2000, but I did not know that then. I felt that my GP’s diagnosis was not that I had a serious liver disease, but an untreatable moral malady. If I had been one of the many people who are diagnosed before they experience any symptoms, I would have left her rooms, not told a soul and tried to forget all about it. I didn’t go home filled with righteous indignation and contempt for my doctor that day. I was consumed with self-loathing — I felt like a piece of human debris, unclean and totally unworthy. But the gods were smiling on me. It was 27 March 2000 — the day the New South Wales Health Department launched the world’s first hepatitis C mass media public awareness campaign. On the news, doctors were talking about treatment and there was some discussion about discrimination. I rang the Hepatitis C Council of NSW helpline the next day and received accurate information, support, and referral to my local liver clinic. I was on the road to recovery, but the shame I felt about my positive status was hard to overcome. After my experience with my GP, I was wary of people finding out about my illness. Sometimes I still am. In the past four years I’ve met lots of people with hepatitis C, and many of them express shame and fear because they have had such negative experiences when they disclosed their HCV status. There were people in my treatment support group who expressed the medieval notion that their illness was direct punishment for their “sins” and that they deserved to suffer and to be treated poorly because they had injected drugs in the past. The NSW Anti-Discrimination Board enquiry into hepatitis C-related discrimination in 2001 found two reasons for discrimination.2 It heard evidence of many cases of stigmatisation as a result of ignorance about the virus and how it is transmitted, but it was the close association between injecting drug use and HCV infection that was found to be the main reason why people with hepatitis C were treated in a discriminatory manner. Its report, C-change, says much more needs to be done to educate the general community, and especially healthcare workers, about what hepatitis C is, how it is contracted and who contracts it. This requires the political will to change things, but is not an insurmountable problem. However, the enquiry found that the perception of people with hepatitis C as being “somehow deviant and automatically engaged in illegal or criminal behaviour” is far more difficult to tackle.2 It is acceptable to vilify very few groups within society these days, but people seem to feel it is quite reasonable to denigrate injecting drug users because their behaviour is illegal and highly stigmatised. In his introduction to the NSW Anti-Discrimination Board report, former president Chris Puplick comments: “Were this nexus to be severed, either by means of legislative change or by changes in perceptions, attitudes and responses, then most of the problems identified in the C-change report would be more easily resolved”.2 There is little hope of this vision being realised in the short term. I believe the Australian Government’s proposed Disability Discrimination Amendment Bill7-9 aims to overturn a Federal Court decision in 2000 that found addiction to a prohibited drug could be regarded as a disability.10 If the bill becomes law, illicit drug users (and their families) could, in some circumstances, face legalised and institutionalised discrimination. Healthcare workers have voiced concerns that such an amendment may result in the increased spread of bloodborne viruses, such as hepatitis C, and limit access to drug treatment programs.7 The illegal status of injecting drug use already results in negative health outcomes for many people with hepatitis C, especially if they are current injecting drug users.11 Quite simply, many do not attempt to seek medical treatment unless they absolutely have to, and, when they do, they sometimes report receiving very shoddy treatment. The Disability Discrimination Amendment Bill and the Federal Government’s rejection of evidence-based recommendations, such as harm minimisation, for combating the HCV epidemic stand in stark contrast to Australia’s highly successful response to HIV/AIDS. This response depended to a large extent on legislative action by Australian governments, in particular the repeal of laws that made homosexuality illegal and discrimination acceptable. A recent study has found that discrimination against people who are already vulnerable because they are ill can be “a profoundly negative experience”.11 This is so not only for the person with hepatitis C, but for the wider community as well, because access to information about preventing transmission is compromised when people are afraid of dealing with healthcare services.11 Around 40% of the relatively small number of people who undergo treatment become free of the virus.12 I consider myself extremely fortunate to count myself as one of them. The side effects of treatment12 were extremely difficult during my 48 weeks of therapy, but it was worth it. I have been free of the virus since 2001, and feel better than I have for many years. It’s wonderful to have a happy ending to share when I talk publicly about living with hepatitis C, but I hope the audience understands that it was not just the medicine that made me better. Love, understanding and compassion are great healers that many with hepatitis C just don’t experience.

Lisa Waller BA

Clinical recordA 56-year-old woman presented to her general practitioner a fortnight after a trip to Bali. She had a 2-week history of profuse loose brown stools, lethargy, weakness, nausea and some dyspeptic symptoms. The diarrhoea had initially settled with loperamide, but then recurred. A faecal specimen was collected for microscopy, culture and testing for enteric viruses, all of which gave negative results. Routine blood tests showed mild iron deficiency with no anaemia. Serum levels of vitamin B12 and folate were in the reference ranges. Serological testing for Toxoplasma and Cytomegalovirus showed no evidence of recent infection. An initial course of metronidazole for presumed Giardia infection was unhelpful, and she was referred for further gastroenterological evaluation. At the time of review by the gastroenterologist, she had had persistent diarrhoea for nearly 4 weeks. Thyroid, respiratory, abdominal and cardiovascular examination gave unremarkable results. A faecal enzyme-linked immunoassay analysis for Giardia antigens gave negative results. Gastroscopy showed mild diffuse gastritis, and a rapid urease test for Helicobacter pylori was negative. The duodenum appeared normal, and small-bowel biopsy specimens were sent for disaccharidase testing and histopathological examination. No abnormalities were seen on colonoscopy. Faecal fluid was collected and sent in formalin for saline–acid fixation faecal testing. Examination of small-bowel biopsy specimens showed moderate villous blunting with increased intraepithelial and lamina propria lymphocytes and no evidence of dysplasia or malignancy, no granulomas or parasites. The report concluded that this appearance was very suggestive of coeliac disease. (Figure 1). However, examination of the faecal specimen in saline–acid fixative revealed oocytes of Cyclospora cayetanensis (Figure 2). 1: Small-bowel biopsy specimens taken before and after treatment with trimethoprim–sulfamethoxazole, showing moderate villous blunting before treatment (left) and normal architecture after treatment (right) (original magnification, x 50). 2: Oocysts of Cyclospora cayetanensis (left) and Cryptosporidium parvum (right), showing size difference (original magnification, x 1000). A diagnosis was made of small intestinal villous atrophy secondary to C. cayetanensis infection. The patient was treated with trimethoprim–sulfamethoxazole (800 mg/160 mg twice daily for 5 days). Her symptoms resolved within days. Serological tests and a repeat small-bowel biopsy were undertaken to exclude latent coeliac disease. Serological testing was negative for antigliadin and antiendomysial antibodies, and there was no evidence of residual villous atrophy in the biopsy specimen (Figure 1). The patient remained well on follow-up after completing the course of antibiotics. This case of protracted diarrhoea in an Australian traveller initially appeared consistent with coeliac disease. Further analysis revealed infection with Cyclospora cayetanensis, which was successfully treated with antibiotics. The increasing number of documented outbreaks of Cyclospora infection,1 and the need for special preparation of stool samples for their detection,2 highlight the importance of a high degree of suspicion in cases of traveller’s diarrhoea. C. cayetanensis is a protozoan which was first recognised as a human intestinal parasite in the early 1990s.3 In 1994, Butcher et al described the first case in an Australian traveller of explosive diarrhoea caused by a large acid-fast spherical organism that had only recently been classified as a member of the genus Cyclospora.4 Since then, reports of outbreaks of Cyclospora infection have increased,1 presumably due to greater awareness of this parasite. Outbreaks have been reported from many parts of the world, including North, Central and South America, Europe, South East Asia, India, South Africa, and the Caribbean Islands.5,6 The mode of transmission is thought to be faecal–oral, or via ingestion of contaminated water. The mechanism by which the protozoan causes villous atrophy is not well understood, but organisms have been found at the site of inflammatory changes. Like Cryptosporidium spp. (which are morphologically similar [Figure 2]), Cyclospora spp. cause nausea, profuse diarrhoea and weight loss, as well as profound fatigue. Abdominal pain and bloating can manifest as “indigestion” or “heartburn”. If untreated, symptoms last for 6 weeks to 3 months (longer in the immunocompromised), and can be mistaken for irritable-bowel syndrome. The treatment of choice is trimethoprim–sulfamethoxazole, with ongoing prophylaxis for patients with AIDS.7 Clinicians need to be aware that the histopathological appearance of the small intestine in C. cayetanensis infection is similar to that in coeliac disease. Other causes of small-intestine villous atrophy include viral enteritis, giardiasis, and cows’ milk allergy. Hence, diagnosis of coeliac disease should not be based purely on the finding of villous atrophy. Investigations that we used to test the diagnosis in this patient included a highly specific immunoassay for giardia antigens, as well as testing for antiendomysial and antigliadin antibodies to disprove coeliac disease definitively. However, the clinical history (particularly onset and duration of illness) needs to be considered before requesting these tests. In the setting of recent travel or a community outbreak, a high index of suspicion for infectious causes of villous blunting is warranted. Despite the increasing knowledge about the genus Cyclospora, many infections are missed, as the parasite can be difficult to detect in human faecal samples. Clinicians need to be aware that acid-fast staining is required, and that this requires preservation of the faecal specimen in formalin.3 It is also important to realise that Cyclospora oocysts are usually shed in low numbers, even when the patient is very ill. In addition, faecal specimens sent to pathology laboratories for examination for ova and parasites are commonly not examined for Cyclospora spp. Hence, Cyclospora testing must be specifically requested.2 Finally, laboratory investigators need to be aware that Cyclospora cysts are morphologically similar to cysts of Cryptosporidium parvum. The most obvious difference is size, as Cyclospora cysts are larger (8–10 μm) than Cryptosporidium cysts (4–6 μm) (Figure 2). It is important to differentiate the two, as Cyclospora infection can be treated with antibiotic therapy, whereas management of Cryptosporidium infection is largely supportive.5 Dialogue between the clinician and pathologist can help to avoid confounding diagnoses. Newer techniques, such as polymerase chain reaction (PCR) testing for parasite DNA, are currently being developed, but are expensive and may not be available in a routine laboratory. Lessons from practice Cyclospora cayetanensis was relatively recently recognised as an intestinal parasite that causes protracted diarrhoea. Beware of histological and clinical overlap with other conditions, including coeliac disease, cryptosporidiosis and irritable-bowel syndrome. Cyclospora organisms can be difficult to detect: faecal specimens need to be transported in a saline–acid fixative, and examination for Cyclospora needs to be specifically requested. Treatment is a 7–10-day course of trimethoprim–sulfamethoxazole.

Vidyut Pinge-Suttor BSc(Med), MB BS · Chris Douglas FRCPA(App) · Antony Wettstein FRACP

Objective: To assess the effectiveness of the Australian border entry screening program to detect arriving travellers with symptoms of severe acute respiratory syndrome (SARS).Design and setting: Descriptive study of outcomes of screening at Australian airports and seaports between 5 April 2003 and 16 June 2003. To determine the number of international travellers who were symptomatic on arrival in Australia but missed by screening, data were obtained on the number of arrivals screened and the number with symptoms (from the Australian Quarantine and Inspection Service [AQIS]), as well as the number of people investigated for SARS (from the Australian SARS Case Register).Results: There were 1.84 million arrivals into Australia during the study period, and 794 were referred for screening to AQIS staff. Of these, the findings in four travellers were consistent with the World Health Organization case definition for SARS, and they were referred by the Chief Quarantine Officers to designated hospitals for further investigation. None of these people was confirmed to have SARS. One person reported as a probable SARS case acknowledged being symptomatic on arrival, but had been missed by border screening.Conclusions: The low identification rate was attributed to the low prevalence of SARS, the use of exit screening by affected countries, and the subjective measures used in the screening process. With current knowledge about SARS, border screening should focus on educating incoming travellers, especially groups at high risk of transmitting the disease (the elderly and those with underlying chronic illnesses). Objective screening measures should be used during SARS outbreaks to prevent importation of the disease.

Gina Samaan BPsych(Hons) · Jenean Spencer PhD, MAppEpid · Leslee Roberts MB BS, PhD, MAppEpid · Mahomed Patel MB BCh, FRACP, FAFPHM

Sanjaya N Senanayake,* Mark J Ferson,† Susan J Botham,‡ Roslyn T Belinfante§ * Infectious Diseases Physician, † Director and Medical Officer of Health, ‡ Infectious Diseases Team Coordinator, § Environmental Health Officer, South Eastern Sydney Public Health Unit, Locked Bag 88, Randwick, NSW 2031. djayaATbigpond.com To the Editor: Keeping fish as pets, as with other animals, carries the risk of zoonotic infections. A 2000 review of bacterial zoonoses that can be acquired topically from fish commented on infection with Aeromonas hydrophila, Edwardsiella tarda, Erysipelothrix rhusiopathiae, Mycobacterium marinum, Streptococcus iniae, Vibrio vulnificus and Vibrio damsela.1 Our public health unit was recently notified of a case of Salmonella infection acquired from a fish tank. In October 2003, a 14-month-old boy was admitted to hospital with a 2-day history of fever, vomiting and diarrhoea. Culture of three stool specimens revealed a Salmonella isolate. This was identified by serotyping (at the Institute of Medical and Veterinary Science, Adelaide, South Australia) and phage typing (at the Microbiological Diagnostic Unit, Melbourne, Victoria) as Salmonella enterica serotype Paratyphi B var Java phage type Dundee. The child had no recent history of overseas travel or overseas visitors. Other family members were well, and their stool specimens were negative for Salmonella spp. However, the family kept a tropical fish tank, and the child’s parents reported that he would place his hands in the water to help feed the fish. Culture of water from the tank revealed a Salmonella isolate identical to that in the stool specimens. We believe that the boy became infected after touching the water while feeding the fish. The fish tank contained red-eyed tetras, bala sharks, silver dollars and angel fish, which had been purchased from three local aquariums several years previously. None appeared sick at the time of the child’s illness. It is important for clinicians to recognise that Salmonella infections are not always foodborne in origin. Salmonellosis is a well-known zoonosis that can be found in a variety of pets, including cats, dogs, birds, rodents and even reptiles.2 In fact, an estimated 90% of all reptiles shed Salmonella spp. in their faeces.3 Salmonella spp. have been isolated from tropical fish aquariums previously; unusual Salmonella serotypes were found in eight of 100 tropical aquariums sampled in Wales.4 Fish can excrete Salmonella without appearing unwell.5 Our patient was a 14-month-old child. In a Canadian outbreak of S. enterica serotype Paratyphi B linked to aquariums, five of seven cases were also in children aged under 10 years.5 This may reflect a combination of immature immunity and behaviour — young children may not wash their hands properly (or at all) before eating or touching their mouths. This case highlights the importance of good handwashing at all times after contact with an aquarium, regardless of the appearance of the fish. It may also be worthwhile recommending close supervision of children under 5 years of age around aquariums.

Sanjaya N Senanayake · Mark J Ferson · Susan J Botham · Roslyn T Belinfante

Although infectiousness is a feature of Creutzfeldt–Jakob disease (CJD), only a small proportion of cases are linked to transmission through healthcare provision. As of January 2003, over 120 cases of CJD associated with use of human cadaveric dura mater had been recognised worldwide; almost all were associated with the commercial product Lyodura. Most cases (97) have occurred in Japan, giving an overall risk estimate of around 1 per 2268 patients treated with Lyodura (0.04%) in that country. In Australia, five cases of CJD have so far been linked to Lyodura, but, given the protracted tails of previous epidemics of transmissible spongiform encephalopathies, further cases are possible. Results of surveys of Lyodura use in Australia are incomplete, but information from the manufacturer suggests that 2208–2478 sheets of Lyodura may have been used here. This use translates to a relatively high incidence of Lyodura-associated CJD, with current overall rates appearing around five times higher than those reported in Japan; reasons for this difference are unclear.

Fiona J Brooke BA(Hons) · Alison Boyd PostGradDipGenCoun · Genevieve M Klug BSc(Hons), PostGradDipEpiBiostat · Colin L Masters FRCPA · Steven J Collins FRACP

Stacey L Emmett,* Adam J O’Brien,† Joseph E Ibrahim† * Research Officer, † Consultant Physician, Clinical Liaison Service, Victorian Institute of Forensic Medicine and the State Coroner’s Office, 57-83 Kavanagh St, Southbank, VIC 3006. staceyeATvifm.org To the Editor: Root-cause analysis is an established, retrospective, structured investigative technique1 that was first introduced into wide clinical practice in public hospitals in Victoria in 2001.2 It is usually reserved for investigating infrequent and significant adverse events and explores the nature and causes of organisational systems failures.1 It is important for all healthcare professionals to understand this technique, as it is used increasingly by healthcare organisations. Cooper and Blamey’s Lesson from Practice described the outcome of an investigation using root-cause analysis of an occupational exposure to HIV from a needlestick injury.3 We commend the analyses that identified multiple failures of the system for reporting and responding to occupational exposures to hazardous material. The practice changes that ensued at Southern Health demonstrate the value of root-cause analysis. However, more information and analysis is required about the mistaken use of the stored serum samples. As the authors explain, the initial information was that the source patient tested negative for HIV antibodies. Some time later, it was discovered that the specimen tested was not from the source patient but from a patient of the same surname in the same ward. This caused a 3-day delay between the initial test and the Infectious Diseases Unit being notified that the source patient had twice tested positive for HIV antibodies. We contend this is an important and common systems failure that usually makes headlines of the form “Wrong site, wrong procedure, wrong person surgery”. The Joint Commission on Accreditation of Healthcare Organisations developed a universal protocol with the intention of highlighting the causative systems failures and minimising the frequency of recurrences of wrong-site surgery.4 The information given by Cooper and Blamey does not clearly explain why (ie, the root cause) the incorrect specimen was tested initially. The pathology department’s review identified the presence of unacceptable “informal norms” in the practice of blood collection and labelling. The suggested remedy that “all serum should be collected with strict adherence to blood collection and labelling protocols” is unlikely to prevent a recurrence. Exhortation to do better rarely solves the underlying problem. It is therefore important to understand why health professionals violate procedures and protocols.5 The experiences of Cooper and Blamey demonstrate that some of the limitations and benefits of root-cause analysis depend on the depth of the investigation. The early and unquestioning acceptance that strict adherence to an existing protocol will prevent another “wrong person” error is not convincing. This contrasts with the well-conducted inquiry and subsequent management of occupational exposure to needlestick injuries.

Stacey L Emmett · Adam J O’Brien · Joseph E Ibrahim

Elizabeth E Cooper,* Stephen L Blamey† * Sterilisation and Infection Control Coordinator, Southern Health Infection Control and Epidemiology, Southern Health, Locked Bag 29, Clayton, VIC 3168; † Head, Department of GastrointestinaI Surgery, Monash Medical Centre, Melbourne, VIC. elizabeth.cooperATsouthernhealth.org.au In reply: Emmett and colleagues request more information and analysis about the mistaken use of stored serum samples. The pathology staff member correctly labelled the specimen of the patient being bled but did not follow the protocol in identifying that the patient was the same as on the request slip. It had not been highlighted that there were two patients with the same surname (but different first names) in the ward, and blood was collected from one patient with a request slip labelled for another. At specimen reception, the protocols were again not followed, as the staff did not check that the minimum identifiers on the specimen label and request form matched. It is recognised that violations of procedures are not root causes and are not directly manageable. The cause of the procedural violation must be managed.1 The collection and labelling of blood protocols were reviewed after this incident and found to be appropriate. The root-cause analysis identified that the protocols were not followed and that unacceptable “informal norms” had become practice in the collection and labelling of specimens. Staff training was examined and revised to ensure that staff were aware of the content of the protocols and that they followed them accordingly. All staff members were counselled about the importance of following correct procedures and the consequences of not doing so. Up to 1000 specimens are received at specimen reception each weekday. New “front end processing” technology is to be introduced at the end of 2003. This electronically scans the specimen and request slip to ensure details match. In the interim, in recognition that mislabelling will occur, all specimens relating to occupational exposures are collected at the time of the incident. Previously available results and serum stored in the laboratory are not relied on.

Elizabeth E Cooper · Stephen L Blamey

Nicola Magnavita Researcher, Italian Study Group on Hazardous Workers and Institute of Occupational Medicine, Catholic University School of Medicine, Largo Gemelli 8, Rome, 00168, Italy. magnavitaATrm.unicatt.it To the Editor: The article by Charles and colleagues1 is an interesting contribution to the development of Australian protocols for healthcare workers infected with hepatitis C virus (HCV). To date, most European countries have no national policy for HCV-infected healthcare workers, and existing guidelines are advisory in nature and poorly enforced. A panel of European and American experts recently failed to reach consensus on management of HCV-infected healthcare workers who perform exposure-prone procedures, and concluded that screening for HCV infection and restricting infected healthcare workers is not justified, based on current published data.2 Today, the effectiveness of guidelines relies solely on self-assessment of HCV status from healthcare workers. However, collaboration of healthcare workers might be problematic if management criteria are not defined, and workers’ rights are not guaranteed. Issues such as practice restriction, disclosure of serological status to patients, privacy and discrimination need to be resolved. Given the risk of HCV transmission from healthcare workers to patients is not clear, the burden of uncertainty rests entirely with healthcare workers. Because of the fear of discrimination, needlestick injuries may be under-reported, and infected workers may not seek diagnosis and treatment because they have greater legal protection if they can honestly say that they did not know their serological status.3 Moreover, the largely asymptomatic nature of HCV infection may leave healthcare workers unaware of their infective status. The results of Charles and colleagues suggest up to tenfold underreporting of occupational injuries with blood exposure in Australian healthcare workers.1 With this number of unreported exposures, there may be two or three new cases of HCV infection in healthcare workers in metropolitan hospitals in Melbourne each year — a figure similar to the prevalence of occupational HCV infection from notified injuries. Paradoxically, the prevalence of HCV infection in healthcare workers and the transmission risk for patients cannot be assessed without compulsory testing of healthcare workers, but without risk assessment there is no reason for this compulsory testing. Overcoming this Catch-22 with well-targeted epidemiological studies may help create broad consensus about policies for HCV-infected workers.

Nicola Magnavita