Environmental health

To the Editor: Contact burns in children caused by hair-straightening devices are increasingly common. Although the dangers of hair dryers and other similar devices are well known,1 there is less awareness of the risks associated with hair straighteners. The relevant Australian Standard does not mention hair straighteners.2 Four recent studies from the United Kingdom have reported on this problem,3-6 but there is no readily identifiable published information from Australia. Hair straighteners consist of two opposing ceramic plates that are held apart when not in use. The plates are reported to reach average temperatures of 169.5°C within 4 minutes 20 seconds of being switched on. They can cause burns (temperature > 66°C) on short-term contact (10 seconds) for a period of up to 9 minutes 20 seconds after being switched off,3 and can take 30 minutes to cool to below 50°C, at which temperature they can cause superficial burns on prolonged contact. Using data collected by the Stuart Pegg Paediatric Burns Centre at the Royal Children’s Hospital, Brisbane, and the Queensland Injury Surveillance Unit, we identified 22 patients treated for hair-straightener injuries between January 2004 and June 2009. Sixteen of these were treated within the past 2 years. The median age of patients was 43.4 months (range, 9 months to 14 years). A mean of 1% of total body surface area was involved. Injuries were to the forearm and hands (16 patients) (Box), foot and lower leg (five patients), and the back (one patient). The burns were significant, with 19 partial-thickness burns, and three full-thickness burns requiring surgery. Nine of the 22 children (41%) required long-term scar management. We observed two typical patterns of injury. In toddlers (16 patients aged 9–48 months), the main mechanism of injury was grasping or pulling down a hair straightener that was either turned on or cooling, with inadequate supervision a common factor. An early-teen group (three patients) had self-inflicted burns from accidental contact or misuse, including one patient who misguidedly used the device in an attempt to remove leg hair, sustaining full-thickness burns requiring skin grafting. Increased awareness of the potential dangers of hair straighteners might help prevent burns. We suggest four precautions: Hair straighteners should be placed out of reach of children during use and storage; Children should be supervised while the device is warming or cooling; Manufacturers should label the device to warn of potential dangers; and Manufacturers should either redesign the device so that plates are not exposed, or provide a cool-touch cover. Burns to a toddler’s hand caused by contact with a hair-straightening device

Zoe M Poiner · Michael D Kerr · Belinda A Wallis · Roy M Kimble

Objective: To describe the planning and execution of a statewide campaign aimed at improving compliance with hand hygiene practices in New South Wales public hospitals.Design and setting: The campaign was conducted in all area health services (AHSs) in NSW (covering 208 public hospitals) between February 2006 and February 2007. Clinical practice improvement methods and campaign strategies were used to improve the availability and use of alcohol-based hand rub (AHR) at the point of patient care, using staff champions and local leaders, engaging patients and families, and measuring compliance. Staff were given regular feedback on their performance. Project officers funded by the Clinical Excellence Commission (CEC) provided local project management support and implemented the campaign in a standardised format orchestrated by the CEC.Main outcome measures: Proportion of available beds with secured and unsecured AHR containers nearby; amount of AHR used (based on purchasing patterns).Results: Hospital visits before the campaign identified a lack of appropriately placed AHR at the point of care. The number of AHR containers per available bed in near-patient locations increased to 13 280/18 951 (70%) after the campaign. The quantity of AHR purchased per month across NSW public hospitals increased from 1477 L to 5568 L (a 377% increase).Conclusion: The CEC was successful in systematising the placement of AHR in all NSW public hospitals at the point of patient care. Although the use of AHR increased substantially, some staff were resistant to changing their hand hygiene practices.

Annette C Pantle MB BS, MPH, FRACMA · Kimberley R Fitzpatrick BHSM · Mary-Louise McLaws DipTropPublHlth, MPH, PhD · Clifford F Hughes MB BS, FRACS, FACS

Objective: To present the results of surveys of staff, patients and visitors about their perceptions of hand hygiene behaviour before and after implementation of the Clean hands save lives campaign in New South Wales public hospitals.Design and setting: Pre- and post-campaign questionnaires, disseminated through project officers in each health authority, were completed by selected staff and patients/visitors in all 208 public hospitals in NSW. Combined, de-identified results for each health authority were forwarded to the NSW Clinical Excellence Commission for analysis.Main outcome measures: Awareness of campaign material; staff perceptions about their ability to maintain a high level of hand hygiene compliance before and after contact with patients; compliance self-reported by staff compared with compliance perceived by patients/visitors and compliance assessed by overt observation.Results: Most staff and patients/visitors were aware of campaign materials. Eighty-six per cent of staff respondents (495/578) believed that placement of alcohol-based hand rub (AHR) close to the point of patient care had improved hand hygiene compliance, and 76% (510/671) believed they could sustain their level of compliance. Only 1 in 4 patients or visitors (106/397) were willing to question health care workers who appeared not to be complying with hand hygiene practices.Conclusion: As the first coordinated statewide campaign to modify hand hygiene culture, the Clean hands save lives campaign successfully engendered positive attitudes and dispelled negative perceptions about the onerous nature of before- and after-patient-contact hand hygiene compliance.

Kimberley R Fitzpatrick BHSM · Annette C Pantle MB BS, MPH, FRACMA · Mary-Louise McLaws DipTropPublHlth, MPH, PhD · Clifford F Hughes MB BS, FRACS, FACS

Objective: To examine whether improved hand hygiene compliance in health care workers after a statewide hand hygiene campaign in New South Wales hospitals was associated with a fall in rates of infection with multiresistant organisms.Design and setting: Data on rates of new methicillin-resistant Staphylococcus aureus (MRSA) infections (expressed as four clinical indicators) are reported by some Australian hospitals to the Australian Council on Healthcare Standards (ACHS) for accreditation purposes and are mandatorily reported by all NSW hospitals to the NSW Department of Health. Infections are classified according to whether they are acquired in the intensive care unit (ICU) or other wards and whether they are from sterile sites (blood cultures) or non-sterile sites. The clinical indicators reflect four different site categories (ICU sterile site, ICU non-sterile site, non-ICU sterile site and non-ICU non-sterile site) and are expressed as the number of new health care-associated infections per 10 000 acute care bed-days. Clinical indicator rates were examined for any decline between the pre-campaign period (July–December 2005) and post-campaign period (January–July 2007), and were compared with trends over a similar period in states without a hand hygiene campaign.Main outcome measures: Pre-campaign and post-campaign rates for four MRSA clinical indicators.Results: Between the pre- and post-campaign periods, there was a 25% fall in MRSA non-ICU sterile site infections, from 0.60/10 000 bed-days to 0.45/10 000 bed-days (P = 0.027), and a 16% fall in ICU non-sterile site infections, from 36.36/10 000 bed-days to 30.43/10 000 bed-days (P = 0.037). The pre- and post-campaign rates of MRSA infection from ICU sterile sites (5.28/10 000 bed-days v 4.80/10 000 bed-days; P = 0.664) and non-ICU non-sterile sites (5.92/10 000 bed-days v 5.66/10 000 bed-days; P = 0.207) remained stable. Australia-wide MRSA data reported to the ACHS showed a 45% decline in infections from ICU non-sterile sites, from 25.89/10 000 bed-days to 14.30/10 000 bed-days (P < 0.001), and a 46% decline in infections from non-ICU non-sterile sites, from 3.70/10 000 bed-days to 1.99/10 000 bed-days (P < 0.001) over the period 2005–2006.Conclusion: Two out of four clinical indicators of MRSA infection remained unchanged despite significant improvements in hand hygiene compliance in NSW hospitals. The reduction in MRSA infections from ICU non-sterile sites in NSW hospitals was mirrored in ACHS data for other Australian states and cannot be assumed to be the result of improved hand hygiene compliance. Concurrent clinical and infection control practices possibly influence MRSA infection rates and may modify the effects of hand hygiene compliance. More sensitive measurements of hand hygiene compliance are needed.

Mary-Louise McLaws DipTropPublHlth, MPH, PhD · Annette C Pantle MB BS, MPH, FRACMA · Kimberley R Fitzpatrick BHSM · Clifford F Hughes MB BS, FRACS, FACS

Standard and Droplet Precautions are considered adequate to control the transmission of influenza in most health care situations. Vaccination of health care staff, carers and vulnerable patients against seasonal and, eventually, pandemic influenza strains is an essential protective strategy. Management principles include: performance of hand hygiene before and after every patient contact or contact with the patient environment, in accord with the national 5 Moments for Hand Hygiene Standard; disinfection of the patient environment; early identification and isolation of patients with suspected or proven influenza; adoption of a greater minimum distance of patient separation (2 metres) than previously recommended; use of a surgical mask and eye protection for personal protection on entry to infectious areas or within 2 metres of an infectious patient; contact tracing for patient and health care staff and restriction of prophylactic antivirals mainly to those at high risk of severe disease; in high aerosol-risk settings, use of particulate mask, eye protection, impervious long-sleeved gown, and gloves donned in that sequence and removed in reverse sequence, avoiding self-contamination; exclusion of symptomatic staff from the workplace until criteria for non-infectious status are met; reserving negative-pressure ventilation rooms (if available) for intensive care patients, especially those receiving non-invasive ventilation; ensuring that infectious postpartum women wear surgical masks when caring for their newborn infants and practise strict hand hygiene; and implementation of special arrangements for potentially infected newborns who require nursery or intensive care.

Rhonda L Stuart FRACP, PhD · Allen C Cheng FRACP, MPH, PhD · Caroline L Marshall FRACP, PhD, GradDipClinEpi · John K Ferguson FRACP, FRCPA, DTMH

To the Editor: Roe and McDermott recently noted that the health benefits of swimming pools demonstrated by Silva and colleagues1 may be more modest than reported.2 Our initial observations from a remote South Australian Aboriginal community support this observation, but there are also many difficulties with study implementation that may introduce biases. A swimming pool was constructed during 2007 as a result of a community-led initiative. With ethics approval, trachoma screening was performed before the pool opening (November 2007) and 6 and 18 months after the pool was opened. Rates of middle ear infections, skin infections and antibiotic prescriptions among children aged 1–15 years were assessed using a retrospective analysis of clinic records between May 2007 and April 2009. A questionnaire regarding the benefits of and barriers to swimming pool use in the community was administered to key persons, such as community health workers and school teachers in April 2009. We aimed to examine every child in the community aged 1–10 years; 45/56 (80%), 46/62 (74%) and 59/64 (92%) children were examined at each of the three visits. The proportion of children with follicular trachomatous inflammation remained low and unchanged at the three time points (7%, 7% and 8%). The clinic records of 166 children showed a trend of increasing rates of infection and antibiotic prescriptions for the period. With hypoendemic rates of trachoma and possible confounding factors, including a small sample size, population mobility, reporting bias and a high turnover of health personnel, we were unable to demonstrate health benefits of pool usage. Our findings highlight the importance of avoiding complacency once a single intervention, such as a swimming pool, has been put in place. Long-term maintenance and supervision are needed to ensure efficacy of a pool. Aspects such as housing, sanitation, nutrition, education and substance misuse should also be high priorities when trying to address health conditions for which low socioeconomic conditions are major risks.3,4 Although we found no specific health benefits of having a pool, interviewees reported that the pool benefited the community in other ways, including providing an opportunity for exercise and recreational activity for otherwise unoccupied children, and creating an incentive to attend school, owing to a “no school, no pool” policy. The pool is a “public good”2 that cannot be denied based on lack of health benefits. Ongoing investigation is planned to monitor the effects of the pool in this community, and it may be too early to draw final conclusions concerning the health benefits of swimming pool use.

Anu A Mathew · Collin J McDonnell · Jill Benson · Hugh R Taylor

To the Editor: Eslick and Eslick believe that the television program The Simpsons causes children to smoke.1 What they gloss over is that in this show, only “losers” smoke. The characters Patty and Selma are old, ugly, mean-tempered, sexually frustrated sisters working in deadening jobs at the motor vehicle licensing office. They don’t just smoke, they chain-smoke — a well established television trope for sleaze and disease — and then they cough, hack, and wheeze. Krusty the Clown, if the name doesn’t tell you already, is a beaten-up, ageing, balding guy. He’s nasty, neurotic, and estranged from his father for abandoning his orthodox Jewish roots for the sinful life of television. Mrs Krabappel, the schoolteacher, is old, divorced, ugly, hates her job, hates her life, and hates children. It may be that children watch The Simpsons. I don’t know, and Eslick and Eslick cite no data that show they do. The questions, though, are: Do children understand what a loser is? Do they emulate losers, or shun them? Eslick and Eslick cite studies showing that any portrayal of smoking causes children to smoke.1 If this is so, why bother to differentiate between “neutral”, “positive” and “negative” portrayals of smoking? And what, precisely, do these labels mean? If, as they say, the “most notable characters” who smoke are these four loser characters, it is strange that they have coded most smoking instances as neutral rather than negative. Even if the authors have a valid labelling system, and even if neutral portrayals cause children to smoke, the question then becomes: is this effect greater than any countervailing effects, such as, perhaps, that of discouraging adults (and adults who are parents) from smoking, or that of creating a broad cultural association between smoking, social failure, and sickness? The logic of the argument put by Eslick and Eslick is that smoking should not be depicted at all in television programs that children watch. Given that children see people smoking in real life, and presumably look around them for some guidance as to whether they should do it too, it seems to me that it is actually commendable to tell them that only losers smoke. Strong evidence and argument that this approach does more harm than good would be very valuable.

Nicholas Jefferson-Lenskyj

To the Editor: The article by Eslick and Eslick1 caught my attention, as the sophisticated parodying of the tobacco industry on The Simpsons has been a much discussed topic among my tobacco-control colleagues. In the introduction to the article, the authors ask if the smoking and tobacco industry portrayals in this program are “just satire, or does the repetitive nature of characters smoking on The Simpsons have an influence on young children watching?” The study design employed cannot answer this question. I was surprised then that the authors concluded that the portrayals of smoking on The Simpsons negatively influence young children. The study results indicate that positive portrayals of smoking on the show are, in fact, extremely rare. It could equally be the case that the more numerous negative portrayals of smoking on this popular and subversive comedy reach young viewers in a way no government-sanctioned health promotion campaign can. Health education messages presented through social satire may not be politically correct, but this does not mean they are ineffective in communicating antismoking sentiments.2 The two most prominent smokers in The Simpsons, Patty and Selma Bouvier, are not characters that any teenager would aspire to be like — disgruntled, middle-aged sisters who live together, work in depressing jobs at the local Department of Motor Vehicles, Selma constantly bemoaning her lack of a husband and fantasising about 1980s heart-throb MacGyver, and Patty best known for her utter joylessness and cynicism. Surely these grim stereotypes would cause most young people to turn away from smoking, and not towards it? Tobacco-control policies themselves were recently lampooned in The Simpsons, with the Simpson family opening a pub in Ireland that illegally allowed patrons to smoke. Much mayhem ensues, and the Simpsons are eventually deported back to the United States for breaking the Irish antismoking laws.3 I am delighted that tobacco control has such universal momentum that it can be parodied on a pop-culture phenomenon like The Simpsons.

Becky Freeman

Objective: To describe demographic and clinical characteristics of patients residing in Victoria who were diagnosed with multidrug-resistant tuberculosis (MDR-TB) during the period 1 January 1998 to 31 December 2007.Design, setting and patients: Retrospective review of Victorian Department of Health data on laboratory-confirmed cases of MDR-TB for the period 1998–2007.Main outcome measures: Age, sex, country of birth, time between arrival in Australia and notification of TB, residency status, site of disease, and treatment period and outcome.Results: From 1998 to 2007, 31 patients who resided in Victoria were diagnosed with MDR-TB. The median age of patients was 27 years, most patients were born overseas, and more than half were full-time students. The median time between arrival in Australia and notification of TB was 2 years, and 24 patients were notified to the Department within 5 years of arrival. Twenty patients had pulmonary disease; in 12 of these patients, sputum was smear-positive for acid-fast bacilli. The median treatment period for patients who completed treatment was 22 months.Conclusions: The number of patients diagnosed with MDR-TB per year increased during the period 1998–2007. If sustained, this increase will have important implications for public health policy and planning.

Caroline J Lavender BA, BSc(Hons) · Lynne K Brown DipAppSci · Paul D R Johnson MB BS, PhD, FRACP

Objective: Design, setting and participants: Cross-sectional survey of Sydney residents during WHO Phase 5 of pandemic (H1N1) 2009. Members of the public were approached in shopping and pedestrian malls in seven areas of Sydney between 2 May and 29 May 2009 to undertake the survey. The survey was also made available by email.Main outcome measures: Perceived personal risk and seriousness of the disease, opinion on the government and health authorities’ response, feelings about quarantine and infection control methods, and potential compliance with antiviral prophylaxis.Results: Of 620 respondents, 596 (96%) were aware of pandemic (H1N1) 2009, but 44% (273/620) felt they did not have enough information about the situation. More than a third (38%; 235/620) ranked their risk of catching influenza during a pandemic as low. When asked how they felt pandemic influenza would affect their health if they were infected, only a third (33%; 206/620) said “very seriously”. Just over half of the respondents (58%; 360/620) believed the pandemic would be over within a year. Respondents rated quarantine and vaccination with a pandemic vaccine as more effective than hand hygiene for the prevention of pandemic influenza.Conclusions: Emphasising the efficacy of recommended actions (such as hand hygiene), risks from the disease and the possible duration of the outbreak may help to promote compliance with official advice.

Holly Seale BSc, PhD · Mary-Louise McLaws DipTropPH, MPH, PhD · Anita E Heywood BSc, MPH · Kirsten F Ward BHthSci(Public Health) · Chris P Lowbridge RN, BAppSci, MPH · Debbie Van · Jan Gralton BSc · C Raina MacIntyre MB BS, PhD, FRACP

To the Editor: Grayson and Johnson’s editorial of 17 June1 and Eizenberg’s viewpoint article of 1 July2 both betray blind spots regarding Victoria’s laboratory response to pandemic influenza (H1N1) 2009 (“swine flu”) and the role of the Victorian Infectious Diseases Reference Laboratory (VIDRL). Grayson and Johnson incorrectly suggest that Victoria’s swine flu infection case definition represented a barrier to laboratory testing and detection of disease spread. Between 18 April 2009 (when the second case was identified in the United States) and 18 May 2009 (when the first case was identified in Victoria), VIDRL tested more than 500 specimens for respiratory viruses. All 16 influenza viruses detected were seasonal influenza strains. Swine flu testing was appropriately reserved for cases with a high pre-test probability of being positive, and even in this at-risk population, no positive cases were detected. The same authors highlight VIDRL’s prominent role in public hospital testing for viral diseases, but mistakenly conflate this with public health laboratory support of infectious disease outbreaks, as if concentration of diagnostic virology at VIDRL were a matter of policy. VIDRL’s diagnostic service is available to Victorian health care institutions for as long as they elect to refer specimens. There is no barrier to decentralising this capacity through access to appropriate new technology and scientific expertise. Nevertheless, centralisation of laboratory capability with optimised specimen transport and reporting offers an arguably more efficient model, and is widely used for this reason. On the other hand, VIDRL’s public health role in supporting the Victorian Department of Human Services’ (DHS’s) outbreak response capability represents a deliberate centralisation of capacity — for good reasons. Public health laboratory testing needs enormous surge capacity — on 1 June 2009, for example, we processed 1004 specimens requiring 1401 swine flu polymerase chain reaction (PCR) tests in a laboratory normally doing 100 respiratory tests daily. Public health laboratories also require expertise to develop, validate and perform essential tests during the early high-pressure phase of an outbreak, while also working closely with the DHS to manage the large patient data flows that underpin public health actions. There is nothing visionary about frittering away this crucial response capacity by devolving responsibility to a series of small nodes, each below critical mass. Both Grayson and Johnson and Eizenberg make misleading generalisations about test turnaround times and refer to non-existent backlogs. On 1 June, the most demanding day of the swine flu outbreak, the mean turnaround time for the 1401 PCR tests performed was 24 hours, with 90% of samples being tested within 32 hours of receipt. There are several reasons outside VIDRL’s control why occasional delays might have occurred. Firstly, transport from point of collection to VIDRL was often slow (1–3 days, with few if any public hospitals achieving faster times). Secondly, more than 10% of samples arrived with missing or incorrect information regarding addresses for reports. Eizenberg should note the high number of general practitioners completing a private pathology provider’s request form but sending the specimen directly to VIDRL, causing delay while results went to the apparent referring laboratory. More than 200 specimens arrived with no request forms at all. Finally, many organisations had no mechanism in place for receipt of large numbers of test results late in the evening, when VIDRL was continuing to work. With Victoria’s move to the “Sustain” phase of the pandemic influenza plan on 3 June, test capacity was directed to defined clinically at-risk patients.3 Many hundreds of samples not meeting the criteria for testing continued to arrive each day. Between 5 and 16 June, these were stored but not tested, and an immediate report went to the sender saying so, and explaining why. Although the capacity to test approved samples was never under threat, stocks of key PCR reagents were transiently sufficiently limited in Australia to preclude testing of samples classified as not meriting a laboratory test in the first place. It may be this scenario that Eizenberg tries inaccurately to describe. It is disappointing to be drawn into exchanging correspondence in these pages rather than having a constructive debriefing together at the end of this outbreak. No criticism by us of laboratory colleagues is intended, as we know there is a shared sense of the logistic challenges with which we have grappled, and can improve together. However, the record still needs to be put straight for a small number of physicians with a more limited grasp of the issues.

Michael G Catton · Julian D Druce · Chris J Birch

To the Editor: The increasing overcrowding on public transport, particularly trains, in many Australian cities makes for considerable discomfort. As the problem deteriorates, concerns about attributable illness and even death have been raised.1 Overcrowding on public transport also contributes to the spread of respiratory diseases such as influenza (pandemic or otherwise).2 The risk of contracting influenza is greatest for people who are within 1 m of an infectious person, through exposure to respiratory droplets, particularly for periods of more than 15 minutes.3,4 Seasonal influenza, which infects millions of Australians annually — resulting in an estimated 2000 deaths and 10 000 hospitalisations5 — is a major health concern. As a resident of Melbourne and regular train commuter, personal observation supports recent claims of severe overcrowding,1 with the average number of people sitting or standing within 1 m of another person on Melbourne trains during peak periods having increased markedly over the past few years. If an average peak commuter is now placed within 1 m of 10 people for a prolonged period twice a day (a conservative estimate), at least 100 infectious influenza contacts potentially occur each week. With annual attack rates for seasonal influenza of 5%–10%,5 the likelihood of contracting infection while crammed into under-resourced train networks is significant. In the context of an influenza pandemic, with higher attack rates, the risk is even greater. Substantial community resources have appropriately been invested in pandemic planning and mitigation strategies. Perhaps we should devote some of these resources to public transport services to reduce overcrowding. Our national pandemic plan advises that A very simple way of reducing the chances of being infected or passing on infection is to stand or sit back from other people in public or in the workplace. Where possible, you should try to maintain a distance of at least a metre, which is about a large step.4 Such advice is impossible to follow on peak-period train services, certainly in Melbourne. Investment in train services to reduce the spread of infections would not only help delay the onset of the next influenza pandemic, but would also reduce seasonal influenza and other respiratory virus transmission. Furthermore, it could avert injuries and illness due to crushing and overheating/dehydration, and could conceivably reduce the road toll by taking cars off roads during peak hours. Few pandemic influenza planning investments could deliver such diverse public health dividends while we ride out the latest influenza pandemic and await the inevitable next one.

Benjamin C Cowie

To the Editor: A 79-year-old man from Gatton, 80 km west of Brisbane (Box 1), presented in July 2008 with an extensive area of cellulitis on the right knee surrounding a central ulcer 2 cm in diameter (Box 2). Gram staining of swabs taken from the ulcer showed polymorphs and gram-negative bacilli. An oxidase-positive, gentamicin-resistant, gram-negative bacillus was cultured. It had the biochemical profile and characteristic colonial morphology of Burkholderia pseudomallei, the causative organism of melioidosis. The identity of the organism was confirmed by polymerase chain reaction. Blood and urine cultures were negative, and a chest x-ray was normal. The patient was treated with intravenous ceftazidime 2 g four times a day for 10 days, as well as oral cotrimoxazole 320/1600 mg twice a day for 6 months. The infection appeared to be localised, and the patient made a successful recovery. Melioidosis can have a wide spectrum of clinical manifestations.1 Skin and soft tissue infections, as seen in our patient, may lead to fulminating systemic infections if treatment is inadequate.1 There were also several factors that predisposed our patient to melioidosis, including type 2 diabetes, renal impairment, and concurrent steroid treatment (for persistent sinusitis). The patient had a history of recent local exposure to floodwaters and soil: he had spent several hours kneeling in wet mud repairing a burst water pipe. Within a few days, an abrasion on the knee had developed into the presenting lesion. The patient denied visiting any areas where tropical melioidosis was endemic. In Australia, melioidosis is generally considered endemic in areas north of 20°S. In subtropical Australia, below 20°S, sporadic endemic infections in domestic animals and humans have occurred in south-eastern Queensland2-6 and south-western Western Australia.7 Three fatal human cases have been reported from the Brisbane River valley (two in 1996, near a reservoir 20 km north of Gatton;4 one in 1999, 5 km from Ipswich city centre5). All three patients were exposed to floodwaters, two had infected skin lesions, and all three progressed to fulminating pneumonia. All three also had alcohol-associated pathology, a recognised comorbidity.1 There were also two less well documented (but apparently local) human cases from the Brisbane region in 19676 and 1974.4 Recent molecular typing of five strains of B. pseudomallei isolated from south-eastern Queensland showed them to be genetically distinct from each other and from isolates obtained from tropical Australia, suggesting that this subtropical focus is most likely a natural phenomenon from ancient times.5 The reticulated water supply to our patient’s house was sourced from the Wivenhoe Dam. The source of the bacteria was most likely the local soil, which is of a heavy clay type suitable for this organism. The Brisbane River valley appears to be a subtropical endemic area for melioidosis, and further sporadic cases can be expected. 1 Location of melioidosis cases reported in Queensland 2 Area of cellulitis around a central ulcer on the patient’s right knee

Roger W Guard · Peter J Morero · Win Yi · Maureen J Mackay

To the Editor: Sikic and colleagues state that the 1990 legislation making helmets compulsory for bicyclists in Victoria was associated with a decrease in non-fatal head injuries and fatalities.1 However, of the three citations given to support this statement (references 8–10 in Sikic et al),1 one is a study performed before the helmet law was introduced, another is an editorial, and the third makes the common error of attributing to helmet use the effects of economic recession and road safety campaigns. These together reduced all road deaths in Australia by about a third.2 Careful analysis takes account of such factors. Western Australia and New Zealand offer good datasets of injuries to cyclists and control groups through the period of increasing helmet use and enforcement: neither dataset shows evidence that mass helmet use reduced the occurrence of serious head injuries to cyclists.3 With fewer serious crashes, there were fewer serious head injuries, and a general reduction in severity of injury in road accidents for all road users. These observations make it hard to accept that cycle helmets reliably confer significant protection. Sikic et al further state that “Wearing an approved safety helmet substantially reduces the risk of serious head injury in cyclists who fall or are involved in collisions with motor vehicles”,1 citing case–control studies. Such studies are known to have serious weaknesses when applied to voluntary behaviour in a socially disparate population.4,5 Risk assessments do not justify helmet laws for cyclists alone. Analysis of Australian Government data (1988–1990) showed that cyclists faced a lower risk of death per hour than car occupants (0.41 v 0.46 fatalities per million hours of use).6 Wider risk assessment based on European data confirms that cycling risks are in the same range as for walking and driving.7 Sikic et al ask for further research to identify factors other than helmet wearing that contribute to preventing cycling injuries. One important factor is already well known: an increase in cyclists on the roads means less risk per cyclist.8 Considerable experience is now available to show that mass helmet use has not been effective in preventing serious head injuries in cycling populations.3 Enforced helmet laws in Australia may deter people from cycling9 and getting the major health benefits of moderate exercise.10

Malcolm J Wardlaw

In reply: The main conclusion of our population-based study1 was that a consistent increase in bicycle-related injuries occurred over the study period. Our study was not designed to analyse the effect of helmet wearing. The potential benefits of helmet wearing were identified in the discussion as a means of reducing the increasing burden of injury. There has been opposition to legislation enforcing helmet wearing in Australia.2 The response to this opposition has been adequately addressed by Canadian researchers.3,4 In addition, a number of Cochrane systematic reviews have arrived at different conclusions to Wardlaw.5,6 Although there are no randomised controlled trials, the weight of evidence would suggest that wearing helmets reduces head injuries in the bicycle-riding population and the imposition is worth the inconvenience to bicycle riders.

Antonina A Mikocka-Walus · Francis T McDermott · Peter A Cameron

West Nile virus is an arbovirus that has caused large outbreaks of febrile illness, meningitis and encephalitis in Europe, North America and the Middle East. We describe the first laboratory-confirmed human case of West Nile virus infection in Australia, in a 58-year-old tourist who was almost certainly infected in Israel. The case is a reminder of the need to consider exotic pathogens in travellers and of the risk of introducing new pathogens into Australia. Clinical recordA 58-year-old man presented to the emergency department of our hospital with chills, malaise, myalgia and epigastric pain. He was a tourist from Israel who had arrived in Australia with his family 3 days previously to visit relatives. The family flew directly from Tel Aviv to Melbourne, with a brief transit stop in Hong Kong airport. The patient reported a 5-day history of low-grade fevers, malaise, headache and epigastric discomfort, which started before he left Israel. He was previously well with no significant past medical history. He resided on a large cooperative farm in the southern district of Israel but worked in administration, with minimal contact with farm animals. He was not taking any regular medications, consumed alcohol infrequently and was a non-smoker. On examination, he had a temperature of 37.8°C and a diffuse erythematous macular rash. He was diagnosed with “viral illness”, treated symptomatically and discharged from the emergency department. On Day 7 of the illness, the patient re-presented to the emergency department increasingly unwell. Symptoms now included rigors, headache, dizziness and ear pain. On examination, he had a fever (temperature, 39.6°C), but no neck stiffness, photophobia or focal neurological deficit. After investigation and stabilisation in the emergency department, he was transferred to a ward for ongoing investigation by the infectious diseases team. Supportive care was instituted. Over the next 24 hours, the patient’s condition deteriorated with ongoing fevers and the onset of mild delirium and ataxia. A presumptive diagnosis of encephalitis was made, and diagnostic investigations were undertaken. Acyclovir was commenced empirically for herpes simplex encephalitis until this diagnosis was excluded. The patient’s fever began to resolve by Day 10 of the illness, and he was discharged after 18 days in hospital with mild ataxia. At outpatient review 2 weeks after discharge, he had persisting lethargy and mild ataxia. He returned to Israel with his family, where he underwent outpatient rehabilitation. InvestigationsExtensive investigations were undertaken to diagnose the aetiology of the encephalitis. Cerebrospinal fluid (CSF) sampled on Day 10 of the illness showed leukocytosis (polymorphs, 2 × 106/L; lymphocytes, 75 × 106/L; unidentified cells 12 × 106/L; and erythrocytes, 90 × 106/L), raised protein level (0.84 g/L; reference range [RR], 0.15–0.4 g/L), but a glucose level in the reference range (3.7 mmol/L; RR, 2.5–4.5 mmol/L). However, culture and polymerase chain reaction (PCR) tests for common viral and mycobacterial pathogens gave negative results. Serological testing of acute and convalescent blood samples for common viral and bacterial causes of encephalitis showed no acute infection. Appearance of the brain on magnetic resonance imaging (MRI) was unremarkable. Diagnosis of West Nile virusPaired sera from Day 9 and Day 31 of the illness were tested in parallel in a flavivirus group-reactive enzyme-linked immunosorbent assay (ELISA) for IgG and IgM. This showed a fourfold rise in IgG titre, and IgM seroconversion. The sera were then tested against a panel of flaviviruses for total antibody (by neutralisation) and for IgG and IgM (by immunofluorescence). The strongest reaction by immunofluorescence was against the New York 99 strain of West Nile virus (WNV; Box 1); seroconversion to this virus was confirmed by neutralisation (“gold standard”) tests (Box 2). A stored CSF sample tested positive for IgM against WNV by immunofluorescence. Flavivirus RNA was not detected in CSF or serum by PCR testing. DiscussionThis is the first report of a laboratory-confirmed human importation of WNV infection in Australia. The only previously diagnosed case of acute WNV infection in Australia was in a horse imported for the breeding season, which acquired the infection overseas but became symptomatic on arrival (unpublished data, Arbovirus Emerging Diseases Unit, CIDMLS, Westmead Hospital, Sydney, NSW). WNV transmission has not been recorded in Australia. WNV is a single-stranded RNA flavivirus that was first isolated in 1937 from a patient with fever in the West Nile District of Uganda.1 The virus exists in a bird–mosquito–bird cycle, with wild birds as the amplifying host and reservoir.2 It has been isolated from 43 species of mosquito, mostly bird-feeding members of the Culex genus. Humans and other mammals are incidental hosts, when bitten by infected mosquitoes. Since first described, WNV has spread widely, with an associated dramatic increase in disease severity.3,4 It is found in Africa, Europe and the Middle East, with large outbreaks identified during the past decade in Romania, North America and Israel.5-7 About 80% of patients with WNV infection are asymptomatic. The incubation period for symptomatic disease is 2–14 days. “West Nile fever” is a non-specific febrile illness that includes headache, myalgia, and occasional gastrointestinal symptoms and usually resolves spontaneously in less than a week.8 Acute neurological illness is uncommon, occurring in fewer than 1% of infections, and can present with meningitis, encephalitis or a poliomyelitis-like acute flaccid paralysis.9 Our patient was almost certainly infected in Israel, where WNV is endemic, with episodic outbreaks reported since the 1950s, most recently in 2000.7 Israel is the likely origin of the WNV strain now circulating widely in North America.6 In Australia, WNV is not routinely considered in locally acquired encephalitis but was investigated in our patient because of the country where he acquired the illness. Close communication was needed with the testing laboratory to convey a more detailed history and clinical description than is usual on a standard request form. The most frequent arboviral cause of encephalitis in Australia is Murray Valley encephalitis virus, which is endemic in northern Western Australia, the Northern Territory and northern Queensland, and has epidemic activity in southern Australia.10 Less common arboviral causes of locally acquired encephalitis include Japanese encephalitis virus and Kunjin virus.11 The latter shares 80% of its genome with WNV and has been classified as a subtype of WNV.12 It is endemic in northern tropical regions of Australia,13 and the usual presentation is as a febrile illness; it is a rare cause of encephalitis.11 There have been no reports of locally acquired flavivirus in Melbourne, Victoria, where our patient resided while in Australia. Infection with WNV was diagnosed retrospectively in our patient based on serological testing of acute and convalescent sera. WNV IgM concentration was then measured in a stored CSF sample. The initial low-positive serological results for flavivirus group IgG suggested the patient had previously been infected with another member of the flavivirus family. The fourfold rise in IgG titre and new detection of IgM antibodies to WNV indicated this presentation was a new infection. The strongest reaction was to the New York 99 strain of WNV, which is closely related to strains isolated in Israel. Reactions to the Sarafend strain of WNV and the closely related Kunjin virus were significantly weaker. Negative PCR results are common in WNV infection because of the low-level transient viraemia of WNV.8 Similarly, only about 30% of patients have abnormal MRI findings.8 Our patient’s presentation illustrates the common clinical features of encephalitis. Fever, headache, personality change or delirium and altered conscious state are typical, and focal neurological deficits and seizures may also occur.14 The onset can be gradual. In this case, encephalitis was diagnosed on Day 9 of the illness. Initially, headache and dizziness were attributed to systemic infection until further neurological symptoms became apparent. The CSF findings were also typical of encephalitis, with an elevated white cell count and protein concentration, and glucose concentration in the reference range.14 The likelihood of WNV causing encephalitis rather than an isolated febrile illness or meningitis increases with advanced age.9 From a public health perspective, this case raises the question of whether WNV could be introduced into Australia. Culex mosquitoes are distributed widely throughout the country, and recent research has confirmed that Australian Culex mosquitoes can be infected with, and transmit, the North American strain of WNV.15 However, because of the similarity between WNV and Kunjin virus, antibodies to the latter in vertebrate hosts may limit the infectivity and establishment of WNV in the Australian environment, depending on the geographic distribution of Kunjin virus.16 The type of animal harbouring, and thus importing, WNV is also important. Some research shows humans are likely to be “dead end hosts”, with a level of viraemia that is too low to transmit to an uninfected mosquito.17 This suggests the risk of secondary cases from our patient was very low. The inadvertent or illegal importation of infected mosquitoes or birds would pose a far greater risk of introducing WNV into Australia. This is the first human case of laboratory-confirmed WNV infection recorded in Australia. It highlights the importance of considering the geographic origin of illness in travellers and is a reminder of the various arboviral causes of encephalitis. It is also a reminder of the possibility of international travellers, human or otherwise, introducing new infective agents. Fortunately, spread of the virus beyond the index patient was unlikely in this case. We urge vigilance regarding the possible introduction of new pathogens to the Australian environment. Any concern should be reported promptly to the relevant state or territory authorities. 1 West Nile virus Transmission electron micrograph of the West Nile virus (from another case). (Original image, Cynthia Goldsmith, Centers for Disease Control and Prevention, Atlanta, Ga, USA.) 2 Antibody titres against a range of flaviviruses* in the patient’s acute (Day 9) and convalescent (Day 31) sera Antibody assay Day 9 Day 31 Enzyme-linked immunosorbent assay Flavivirus group IgG 100 400 IgM < 100 800 Immunofluorescence test West Nile virus (New York 99) IgG < 10 640 IgM < 10 40 West Nile virus (Sarafend) IgG < 10 20 IgM < 10 < 10 Kunjin virus IgG < 10 20 IgM < 10 < 10 Murray Valley encephalitis virus IgG < 10 < 10 IgM < 10 < 10 Neutralisation test West Nile virus (New York 99) < 10 2560 West Nile virus (Sarafend) < 10 40 Kunjin virus < 10 80 * Sera were tested against representatives of a range of West Nile virus groups: New York 99 (Lineage 1, Clade 1a); Kunjin (Lineage 1, Clade 1b), and Sarafend (Lineage 2).

Benjamin A Rogers MB BS · Linda Hueston MSc · Irani Ratnam MB BS, FRACP

To the Editor: Recycling water from sewage into drinking water was recently discussed in the Journal.1 Although this is technically feasible, we need to be very wary. Such recycling is associated with very high ongoing monetary and energy costs, but, most importantly from a health perspective, is a “very high-risk”2 proposal that reverses 150 years of good public health policy of striving to keep sewage out of our drinking water supplies. When we need to recycle water from highly contaminated sources, it is much safer to do so for industrial purposes using separated pipelines (as is done in Singapore and Brisbane). The most extensive scientific review on this issue concluded that putting it into drinking water should be a “last resort”, that should be adopted only if other measures — including other water sources, nonpotable reuse, and water conservation — have been evaluated and rejected as technically or economically infeasible.3 Sewage contains very high concentrations of pathogens and drugs. Viruses (the most difficult pathogens to remove) can occur in concentrations higher than 106 per litre — orders of magnitude higher than in even the most polluted rivers. The technical and human performance needed to remove viruses safely will have to be proportionately higher than current practice — difficult to achieve, as we already have skills shortages. We would also need to ensure that the system will work all the time. Reverse osmosis (RO) is the most effective way to remove viruses and drugs from sewage, and should remove virtually all viruses and drugs. Surprisingly, few in-use data are available to check this. RO membranes seem to leak. One study found that RO only removed 92% of antibiotics.4 Recent safety reviews, including an Australian review5 (based on the previous study3), showed viruses were still detected post-treatment at three of seven sites on some occasions. The calculated virus removal ranged from 87% to > 99.995%, which equates to a “log reduction” of 1 to 5. However, to produce safe drinking water from sewage, we need a consistent 9.5-log reduction for enteroviruses.2 Even Giardia was not always removed. This less than optimal performance was when the system was not known to be malfunctioning; lowered performance might occur as often as 5 days a year.6 Current surrogate testing (eg, organic carbon) can only detect a membrane leak (or bypass) of at least 1%, which is well short of meeting the 9.5-log reduction we need for virus removal and reasonable safety.2 We need real-time tests to show that there is adequate virus removal, rather than none at all or only becoming aware of a problem after processed but contaminated water is already in our reservoirs.

Peter J Collignon

In reply: We agree that augmentation of drinking water sources with recycled sewage goes against the traditional policy of separating the two, and that many factors including cost and energy use need consideration in securing future water supplies. Our editorial1 was not written to promote potable recycling, which ultimately is a political and societal decision, but rather to point out that the carefully considered Australian guidelines for water recycling2 have been developed to ensure that, if this form of recycling is contemplated, it is done in a manner that safeguards public health. Main messages in the recycling guidelines include the importance of risk assessment for each individual scheme; avoidance of complete reliance on any single technical step (including reverse osmosis) for removal of contaminants, via a “multiple barrier” approach; adequate operational and water quality verification monitoring; and optimising training and skills management within water treatment facilities. Importantly, credits given for “log removal” for each treatment step are based on verifiable on-line performance, not theoretical values.2 These practical messages are also fundamental to the way we manage our conventional drinking water supplies.3 Consequently, discussions about recycling help reinforce the importance of continual assessment of water management, regardless of the source, and help ensure we do not become complacent.

Karin S Leder · Joanne E O’Toole · Martha I Sinclair

To the Editor: The recent withdrawal of faulty faecal occult blood testing (FOBT) kits by the government highlights the flaws in the National Bowel Cancer Screening Program (NBCSP), with 475 000 kits needing to be replaced. In their recent editorial,1 Ee and Olynyk attempted to persuade us that the NBCSP, which has now temporarily suspended the issuing of new invitations to participate, is both rational and appropriate for an affluent country such as Australia. The facts about bowel cancer mortality are not disputed — it is second only to lung cancer, equating to about 12 Australian deaths per day from a potentially preventable cancer. There are only two serious contenders for bowel cancer screening: FOBT and colonoscopy. Annual FOBT has the potential to reduce mortality by 15% (realistic) to 33% (optimistic).2 Colonoscopy is both diagnostic and preventive, with a predicted reduction in mortality of 76% (realistic) to 90% (optimistic).3 Recent United States guidelines advocate colonoscopy at 10-yearly intervals as the test of choice.3 Cost and potential mortality are two major issues raised by proponents of FOBT versus colonoscopy. However, Australian data using all costs, including infrastructure, colonoscopy, surgery, pathology, anaesthesia, chemotherapy and disinfection, have shown that 10-yearly colonoscopy is of equal cost–benefit to annual FOBT.4 A recent publication from Germany highlights some important facts.5 In a study of 269 144 colonoscopies, the completion rate (ie, reaching the caecum) was high, at 97.3%. The perforation rate was low (0.02%), as was the incidence of bleeding (0.16%), though this was predictably greater in those requiring polypectomy (0.8%). There were no deaths attributable to perforation or bleeding. Colonoscopy is therefore a rational option for screening, with the potential for prevention — a feature not shared by FOBT. The NBCSP’s letter of invitation and FOBT kit are sent only to individuals aged 50, 55 and 65 years. It ignores other age groups and gives no educational advice about alternative strategies such as colonoscopy. Ee and Olynyk1 clearly believe that centrally organised government screening programs are to be preferred, and they disapprove of colonoscopy screening “driven by patients”. Recent case series show colonoscopy to be safe and to have a higher completion rate than older series.5 Current initiatives in Australian colonoscopy training programs should improve safety and completion rates further. For those with no active interest in their health, centralised, directive programs are likely to be the most effective. For the informed, however, discussion about lifestyle changes, screening programs and healthy dietary alternatives should be their right.

Terry D Bolin · Melvyn G Korman · Alistair E Cowen

Targeted post-exposure prophylaxis represents a more efficient use of the stockpile than treatment alone With the emergence of H1N1 influenza 09 (novel human swine influenza A[H1N1] 2009), efforts to control the spread and mitigate the impact of this virus have been implemented. The Australian health management plan for pandemic influenza (2008)1 (AHMPPI) outlines a range of strategies aimed at eliminating an outbreak where possible (the “Contain” response), or reducing transmission sufficiently to allow distribution of a targeted vaccine (the “Sustain” response). Following evidence of sustained transmission within Victoria in May 2009, state and territory health departments began implementing the Contain response, with a switch to a modified Sustain response in Victoria within weeks. The AHMPPI recommends liberal distribution of the stockpile of neuraminidase inhibitors (oseltamivir, zanamivir) to constrain influenza transmission.1 This policy was based on modelling studies synthesising the best available evidence, including clear demonstration of the efficacy of antiviral drugs to prevent secondary infection in randomised controlled trials.2,3 Notwithstanding revision of the AHMPPI on 17 June 2009 to incorporate the present “Protect” phase, understanding the rationale for and defining the operational implications of the initial recommendations for antiviral drug use are priorities. Translation of evidence from epidemiological trials into pandemic policy is challenging, given the complexity of real-world factors that influence intervention effectiveness. For example, as has been observed with many vaccines, drug effects on transmission have far greater impact when implemented across a whole population. The chosen antiviral deployment strategy needs to take into account not only the direct effects benefiting the treated individual, but also indirect effects due to changes in subsequent transmission. In a rapidly growing epidemic, these secondary effects are critical to determining the optimal deployment strategy. Mathematical modelling provides a way to systematically investigate these issues. Using a diverse set of assumptions and frameworks, models consistently demonstrate that for a country with a sufficiently large stockpile of antiviral drugs, augmenting a patient treatment policy with targeted post-exposure prophylaxis represents a more efficient use of the stockpile than treatment alone.4-6 Modelling performed in the Australian context, where the number of stockpiled antiviral drug courses is 40% of the population size, has demonstrated that extensive drug distribution for preventive purposes does not compromise the ability to treat infected patients.6 It was therefore recommended in the AHMPPI that prophylaxis should be provided to as many readily identifiable contacts as possible during the Contain response, with continued provision to household contacts during the Sustain response. Provision of continuous pre-exposure prophylaxis to health care workers was also recommended, as this additive burden on the stockpile would not substantially impede efforts to delay the pandemic. Lessons learned so far in the effort to implement these recommendations have highlighted the importance of clear case definitions to guide treatment, particularly when disease is mild. Delays in confirming infection, associated with finite laboratory resources, posed significant challenges for front-line health care workers. This practical issue must be addressed should deployment of existing stockpile reserves be recommended in coming years, as potentially more virulent variants of the present pandemic strain arise. Meanwhile, further research and policy development are required on a largely unaddressed issue. A transmissible drug-resistant variant of the pandemic strain may arise either by de-novo mutation or by reassortment with drug-resistant seasonal strains (eg, the oseltamivir-resistant 2008 seasonal H1N1 strain carrying the H274Y mutation [histidine-to-tyrosine mutation at codon 274]), and its spread would be favoured by widespread antiviral use. The effort to delay the appearance of such a variant might stimulate a change to the recommended strategies for antiviral deployment. To date, novel H1N1 viruses demonstrating oseltamivir resistance have been isolated from individuals in Denmark and Japan.7 Several published models have been used to investigate the potential consequences of antiviral drug resistance and all demonstrate that emergence of a transmissible drug-resistant variant will reduce the effectiveness of antiviral distribution strategies, with obvious consequences for their utility in “buying time” before a targeted vaccine becomes available. Two recent studies have investigated strategies for reducing the negative impact of drug resistance.8,9 Both considered the case where the main stockpile (ie, oseltamivir) is supplemented with a smaller secondary stockpile of another drug (eg, zanamivir). One study considered four strategies for antiviral drug distribution when both drugs are available for treatment and prophylaxis.8 It was concluded that a strategy whereby the smaller stockpile (drug B) is reserved for treatment, while the main stockpile (drug A) is used for prophylaxis, will most effectively delay the peak of the epidemic and result in the lowest overall level of drug resistance. Alternative strategies of random allocation of drug A or drug B to each individual who is prescribed an antiviral drug, or use of drug B followed by drug A, were also shown to have significant benefits over a single-drug policy. Cycling between one drug and the other over a period of weeks or months was shown to be a high-risk strategy and cannot be recommended. Treatment strategies were also considered in the other study, which demonstrated that using a small amount of drug B followed by drug A will reduce the overall attack and greatly reduce the resistant attack rate.9 In addition, the global implications of a two-drug strategy were considered, taking into account regular entry of infectious individuals into countries and regions over the course of a pandemic. It was shown that if the primary source country implements a strategic two-drug distribution policy, any country into which strains are subsequently introduced will gain a significant benefit from implementing a similar policy. Both these studies provide strong evidence for jurisdictions to consider acquisition of a secondary drug to supplement their primary drug stockpile. Whether the stockpiles are deployed in order (drug B, then drug A) or separated for use as treatment only and prophylaxis only would largely depend on logistical constraints and overall feasibility of the alternative strategies. Either strategy is likely to provide significant benefits compared with deployment of a single drug. In a climate of great uncertainty surrounding characteristics of the current influenza outbreak,10 the challenge worldwide is for jurisdictions to implement flexible evidence-based policies for antiviral stockpile distribution that maximise their effectiveness.

James M McCaw BSc, PhD · James G Wood BSc, PhD · Emma S McBryde MB BS, PhD, FRACP · Terry M Nolan MB BS, PhD, FRACP · Joseph T Wu PhD · Marc Lipsitch DPhil · Jodie McVernon BMedSc, MB BS, PhD

In 6 weeks, swine influenza A(H1N1) virus has spread from 10 to 74 countries. Australia has the fifth highest number of cases and the third highest rate of infection among the top five affected nations. People who are hospitalised with or die from this novel virus are more likely to have predisposing risk factors. There is a predilection for younger age groups and sparing of older age groups. This may be a property of influenza A viruses in general rather than being specific to swine influenza A. If unchecked, the sheer number of cases may lead to much higher numbers of deaths and hospitalised patients than would normally be attributed to a standard influenza season. Paradoxically, the low case-fatality rate of the virus raises the question of how best to approach management of this outbreak. It is uncertain how an expected vaccine against the novel virus will be used.

Sanjaya N Senanayake MB BS, FRACP, MAppEpid

The median age of patients with pandemic influenza H1N1 2009 infection was reported as 20–25 years in initial case series from Europe and the United States. This has been lowered to 13 years in the US after testing of more patients, but this may reflect differential increased testing of school-aged children as part of the pandemic response. The median age of patients with seasonal influenza A(H1N1) infection identified through sentinel surveillance in Western Australia and Victoria in 2007–2008 was 18 and 22 years, respectively. For pandemic influenza H1N1 2009 infection, the median age of the first 244 patients identified in WA was 22 years, and median age of the first 135 patients identified through sentinel surveillance in Victoria was 21 years. Other comparisons of the epidemiological features of pandemic and seasonal influenza are difficult because much less laboratory testing is done for seasonal than for pandemic influenza. While early surveillance data indicated co-circulation of both pandemic and seasonal strains in WA and Victoria, more recent data from both states indicate an increasing predominance of pandemic influenza. If the evolving pandemic allows, we should take advantage of the increased testing being conducted for pandemic influenza to learn more about the real impact of laboratory-confirmed seasonal influenza.

Heath A Kelly BSc, MB BS, MPH · Kristina A Grant BSc · Simon Williams BSc(Hons) · James Fielding BSc(Hons), MAppEpidemiol · David Smith MB BS, FRCPA, FACPM

Objective: To assess the impact of introducing a publicly funded infant rotavirus vaccination program on disease notifications and on laboratory testing and results.Design and setting: Retrospective analysis of routinely collected data (rotavirus notifications [2006–2008] and laboratory rotavirus testing data from Queensland Health laboratories [2000–2008]) to monitor rotavirus trends before and after the introduction of a publicly funded infant rotavirus vaccination program in Queensland in July 2007.Main outcome measures: Age group-specific rotavirus notification trends; number of rotavirus tests performed and the proportion positive.Results: In the less than 2 years age group, rotavirus notifications declined by 53% (2007) and 65% (2008); the number of laboratory tests performed declined by 3% (2007) and 15% (2008); and the proportion of tests positive declined by 45% (2007) and 43% (2008) compared with data collected before introduction of the vaccination program. An indirect effect of infant vaccination was seen: notifications and the proportion of tests positive for rotavirus declined in older age groups as well.Conclusions: The publicly funded rotavirus vaccination program in Queensland is having an early impact, direct and indirect, on rotavirus disease as assessed using routinely collected data. Further observational studies are required to assess vaccine effectiveness. Parents and immunisation providers should ensure that all Australian children receive the recommended rotavirus vaccine doses in the required timeframe.

Stephen B Lambert MB BS, MAppEpid, FAFPHM · Cassandra E Faux MSc(ClinMicro) · Lisa Hall BTech(BiomedSc)(Hons), PhD · Frances A Birrell MPH, MAppEpid, GCSc(Stats) · Karen V Peterson DipT, BEd, MHlthSc · Christine E Selvey MB BS, MSc · Theo P Sloots BSc, GradCertMgt, PhD · Michael D Nissen BMedSc, FRACP, FRCPA · Keith Grimwood MD, FRACP

To the Editor: Australia’s world-leading government-funded National Human Papillomavirus (HPV) Vaccination Program for women aged 12–26 years is made up of two components: an ongoing school-based program and a time-limited catch-up program delivered through schools, general practices and community vaccination services. The catch-up program started in April 2007 and was due to finish by July 2009, but has been extended to 31 December 2009 to allow women to complete the three-dose schedule. Assessing the coverage achieved by the National HPV Vaccination Program will be an important measure of the Program’s success, particularly in terms of ensuring equity in vaccine uptake — so that the current gap in cervical cancer incidence and mortality between Indigenous and non-Indigenous women is reduced, not widened.1 Vaccination coverage data are also needed to monitor vaccine effectiveness in preventing cervical lesions and cancer. Accordingly, an integral part of the Program was the establishment, enabled by legislation passed in August 2007, of Australia’s first national adult vaccine register — the National HPV Vaccination Program Register. The Register began collecting data in mid 2008 and is currently uploading notifications of the 5 million doses of HPV vaccine distributed in Australia to date. Initial coverage estimates from the Register will be published by the end of the year, with all notifications from the catch-up program due to be submitted to the Register by March 2010. General practitioner incentive payments of $6 per notification will be available until that time. Interim coverage data provided by various jurisdictions are encouraging; school-based program data for 2007 from New South Wales and Victoria estimate one-dose coverage of more than 80% and three-dose coverage of approximately 70%.2 Unfortunately, there are no routine systems in place to provisionally estimate coverage in women vaccinated outside of schools. In a small population-based telephone survey that was conducted by the Cancer Council Victoria 3 months after the Program commenced, 35 of 90 women aged 18–26 years (39%) had received HPV vaccine. Australian women are taking advantage of Australia’s most expensive vaccination program to date. We encourage vaccination providers to notify the Register3 of doses administered to ensure that this facet of Australian women’s health can be followed into the future. Although we anticipate complete notification of vaccinations given at schools, the accuracy and completeness of total coverage data will depend on GPs notifying the Register.

Julia M L Brotherton · Robyn M Mullins

To the Editor: The relationship between population, climate warming and environmental impact has been little discussed in the Australian medical media and often ignored in the wider Australian media. All doctors should have a good working knowledge of the science of climate change and its correlation with increased human activity. Six billion humans (circa 2000 ad) have a greater environmental impact than one billion humans (circa 1800 ad), and this increase correlates with deterioration in nature’s “free goods”, such as clean air and water. Globally, demand for food is outstripping supply, resulting in malnutrition and starvation for the world’s poorest. Nationally, changes in the Australian climate have the potential for increased prevalence of tropical diseases, and extreme weather events can cause damage to infrastructure (including health facilities), social dislocation, injury and death. Guillebaud and Hayes argue that doctors must lead the discussion on population growth and climate change.1 They point out that the global population increase of 1.5 million each week equates to a huge new city ... which destroys wildlife habitats and augments world fossil fuel consumption. Every person born adds to greenhouse gas emissions ...1 Those who insist on the right to a large family must also consider the wider social implications of population growth,2 although there is little to be gained by recriminations against those who have already formed large families. We should take the perspective of retired physician Bryan Furnass: address the problems — population, pollution and poverty — with the solutions — ecology, education and ethics.3 Those doctors who understand the methods used by the tobacco industry to subvert the community’s appreciation of the risks of smoking will also understand that similar tactics can and are being employed by those with vested interests in high carbon-emitting industries. Their arguments are based on a belief that technology can solve all problems, while hiding the relationship between increased total consumption, profit and population growth. We need to understand and lead the community’s discussions on global overpopulation and health reduction. Australian doctors are lagging behind in this. British doctors are already publishing on this topic,4 and the Australian Parliament has commenced discussion on the need for a population policy.5 It is time for Australian doctors to read, discuss, research, write and, following the lead of Walters,6 publish constructively on population growth and its impact.

Robin I W Collin