Volume 191 Issue 3

If there is one issue that preoccupies our society, it is health. The mainstream media continually run stories on the health of individuals, society in general, or institutions, as well as exposés of both the failure of health care provision and its spiralling cost. The famed American researcher, physician and author Lewis Thomas vividly captured this fixation on health: “As a people, we have become obsessed with Health. There is something fundamentally, radically unhealthy about all this. We do not seem to be seeking more exuberance in living as much as staving off failure, putting off dying.” Of late, there has been an emerging debate as to what is meant by health, focusing on the World Health Organization declarations dating back to its foundation in 1948. At that time, its lofty goal was “the attainment by all peoples of the highest possible level of health”, which was defined as “a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity”. Some commentators have declared this to be simply a bad definition. Richard Smith, previous editor of the BMJ, opines: “It’s a ludicrous definition that would leave most of us unhealthy most of the time”. The Lancet has also weighed into the debate with its own definition, namely that health is “the ability to adapt”. Quite appropriate, perhaps, in the year celebrating Charles Darwin’s contributions to the theory of evolution! Interestingly, this concept has been borrowed from the French physician Georges Canguilhem, who in 1943 described health not as something defined statistically or mechanistically, but rather as the ability to adapt to one’s environment. This begs the question: is this debate about the definition of health simply academic hot air and obfuscation? The average citizen would certainly have no difficulty understanding what health means: a state of wellbeing. The rest is simply superfluous.

Martin B Van Der Weyden

Australia is in a unique position to assess the impact of two different rotavirus vaccines In 1973, Ruth Bishop and her colleagues in Melbourne were the first to identify rotavirus gastroenteritis in infants. Rotavirus has since been recognised as the most frequent cause of severe childhood gastroenteritis worldwide. In temperate climates, infection occurs predominantly in winter and spring. The spectrum of disease ranges from severe gastroenteritis to mild or clinically inapparent infection. Reinfection is common. In Australia, the peak age of hospitalisation for rotavirus infection is 6–24 months; however, in Indigenous children, infection occurs earlier and is more severe.1 About half of the 20 000 annual hospitalisations for acute gastroenteritis in Australian children under 5 years of age are attributed to rotavirus.2 The first rotavirus vaccine licensed in the United States (RotaShield [Wyeth, Madison, NJ, USA]) was withdrawn from use in 1999, after barely 9 months, due to an increased occurrence of intussusception after vaccination (attributable risk, one case per 10 000 vaccine recipients). Two other live attenuated oral vaccines (RotaTeq [Merck, Whitehouse Station, NJ, USA], a pentavalent human–bovine reassortant vaccine; and Rotarix [GlaxoSmithKline, Rixensart, Belgium], a human monovalent vaccine) have recently been approved for use in many countries after extensive clinical trials showed them to be effective against the most common circulating strains, and found no evidence of an association with intussusception.3,4 The RotaTeq vaccine was introduced into the US vaccination schedule in February 2006. A report from a national network of sentinel laboratories, published in June 20085 and updated in October 2008,6,7 shows that the 2007–2008 US rotavirus season was significantly delayed, shortened and diminished compared with the 2000–2006 seasons. Only 4% of children aged under 3 years who were hospitalised with acute gastroenteritis had rotavirus-positive stools in 2008 compared with 56% in 2006, and only 9% of emergency room patients with acute gastroenteritis tested positive for rotavirus compared with 58% in 2006. Reductions in hospitalisation of up to 85% for rotavirus gastroenteritis and 56% for all-cause diarrhoea in young children were also reported, suggesting very large savings in hospital costs.6 Although these findings need confirmation over future seasons, this rapid vaccine impact is particularly striking given that, at the time, the estimated vaccine coverage was just 56% for one dose in infants aged 3 months and 34% for three doses by age 13 months.5 Reassuringly, preliminary data from surveillance in the US over the first 19 months of its rotavirus program, when over 9 million doses of vaccine were distributed, do not indicate any association of RotaTeq with intussusception or other serious adverse events.8 In Australia, rotavirus vaccination commenced in the Northern Territory in October 2006 and in the remaining jurisdictions in July 2007. Rotarix is used in the NT, New South Wales, Tasmania and the Australian Capital Territory, and was used in Western Australia until May 2009. RotaTeq is used in Victoria, South Australia and Queensland. This geographical split results in about half of the birth cohort receiving Rotarix (two-dose schedule) and half receiving RotaTeq (three-dose schedule). Program implementation has been faster in Australia than in the US, with an estimated coverage, by December 2008, of 87% for at least one dose of vaccine received by 4 months of age, and 84% for a full vaccine course (either two or three doses) received by 13 months of age (Mr Brynley Hull, Epidemiologist, National Centre for Immunisation Research and Surveillance, personal communication). Australia is in a unique position to assess the impact of the two vaccines because of the geographical split. However, it is important to recognise that the prevailing strains of rotavirus vary by region and change unpredictably from year to year.9 As the composition of the two licensed vaccines differs, effectiveness against certain strains, such as those not contained in the vaccines, may vary. An early study during a rotavirus outbreak in the NT showed that Rotarix was effective against the lately emerged G9 strain.10 Although Australia has an established national strain surveillance system,9 it needs to be enhanced, as samples for strain typing have not always been representative of all geographical areas or accompanied by clinical data. National disease notification using laboratory-confirmed cases needs to be implemented, and further studies of field effectiveness should be undertaken. Adverse events following vaccination in Australia are reported and reviewed nationally. The vaccines have not been associated with an excess of serious adverse events during the first 6 months of the program.11 Additionally, all cases of any-cause intussusception are reported by paediatricians to the Australian Paediatric Surveillance Unit, with enhanced active surveillance for intussusception being undertaken in a pilot program. Although efficacy of both vaccines persisted in clinical trials for 2 years,12,13 the full extent and duration of vaccine effectiveness, the degree of herd immunity, and whether a shift in disease incidence to older age groups has occurred, are yet to be determined. Identifying the emergence of new strains of rotavirus, either spontaneously or under vaccine pressure, will also be essential. Successful implementation of rotavirus vaccination in developing countries — where more than 95% of the world’s annual rotavirus deaths occur — is also much anticipated, possibly using new, less costly vaccines.7 In this issue of the Journal, Lambert and colleagues14 report on rotavirus notifications and laboratory tests performed in Queensland before and after the introduction of an infant rotavirus vaccination program. This is the first published evidence of a substantial population-based decline in rotavirus disease activity in Australia since introduction of the vaccine. Furthermore, laboratory-confirmed rotavirus infection appears to have declined not only in the cohort eligible for vaccination (infants aged under 2 years), but also in older children and in adults, suggesting a herd immunity effect, as has been observed in preliminary data from the US.7 Much points to the potential for Australia’s rotavirus vaccine program to have a substantial impact on acute childhood gastroenteritis, both in terms of health care utilisation and broader social and economic effects. It is important to document this with well targeted research and surveillance.

Kristine K Macartney MB BS, MD, FRACP · Margaret A Burgess MD, FRACP, FAFPHM

The Therapeutic Goods Administration is strengthening pharmacovigilance, but strategies to encourage the conduct of pharmacoepidemiological research in Australia are needed For four decades, spontaneous reporting has been the main mechanism by which adverse drug reactions are identified after a medicine is released onto the market, and the Australian program has been exceptionally effective. However, spontaneous reporting programs are limited in their ability to identify an association between a drug and an outcome that is common among the users independent of drug use, and they are not sufficiently sensitive to detect a small increase in the risk of certain rare events. In particular, the increasing long-term use of medication for prevention and control of chronic disease in otherwise healthy individuals presents a challenge to which current postmarketing surveillance mechanisms cannot effectively respond. For example, spontaneous reporting cannot detect an increased rate of myocardial infarction associated with hormone replacement therapy, rosiglitazone or rofecoxib; demonstration of these associations requires large, long-term randomised controlled trials. In recognition of these limitations, the Therapeutic Goods Administration (TGA) recently announced administrative changes that involve a strengthening of pharmacovigilance.1-3 As part of the pre-approval process for a medicine, sponsors will be required to present postmarketing pharmacovigilance and risk minimisation plans. In some cases, the pharmacovigilance plan may simply describe routine passive pharmacovigilance activities. In other cases, where there are important gaps in safety data (eg, groups of potential users for whom documented exposure is inadequate) or where data suggest potentially significant safety issues, the plan will propose studies that specifically address these matters. Studies may use any of the full gamut of epidemiological approaches, including randomised controlled trials, registries of new drug users, and data-linkage and case–control studies. Risk minimisation plans will outline practical steps that will be undertaken to reduce the risk of known safety hazards during the postmarketing period. Possible steps include a small pack size, second-line use only, and advice given in the product information; these measures were available options in the past, but they will now be listed in a single document. Pharmacovigilance and risk minimisation plans may be updated at any time during the postmarketing period, if a need to do so is identified. In addition, sponsors of medicines that are already registered when the new measures are implemented may also be required to draw up suitable plans on a case-by-case basis. These changes bring Australia into line with overseas initiatives, particularly those in the United States and Europe, and involve adoption of guidelines prepared by the European Medicines Agency.4,5 The result has been termed a “whole-of-lifecycle” approach, where active investigation of the safety of a medicine may continue for as long as it is in clinical use.1 A newly constituted medicines safety committee will have responsibility for providing advice on pharmacovigilance and risk minimisation plans, and overseeing the spontaneous reporting program. Medicines prescribed over a long period for disease prevention have typically been approved on the basis of a measured response to a surrogate marker for efficacy, such as improved glucose control, decreased cholesterol level or lowered blood pressure. However, the critical measures of the benefits of such responses to medicines are changes in risk of hard end points, such as myocardial infarction, renal failure and death. These end points are outcomes of the multidimensional effects of medicines — beneficial and adverse — on body systems. Marketing approval of medicines has rarely, if ever, required demonstration of such hypothesised benefits. Under the administrative changes, promising new medicines may still be approved on the basis of surrogate data, but consideration will be given to pharmacovigilance plans that include long-term studies with cohorts that are large enough to determine differences in hard clinical end points and identify any serious adverse effects that may offset benefits. In 2004, Merck Sharp and Dohme precipitately removed rofecoxib from the market worldwide, because evidence of a significantly higher rate of myocardial infarction than with placebo was an incidental outcome of a randomised controlled trial. There had been prior evidence of this association in the VIGOR (Vioxx Gastrointestinal Outcomes Research) study published in 2000.6 At that time, the manufacturer made a small protocol change to the already commenced APPROVe (Adenomatous Polyp Prevention on Vioxx) study, to allow participants to take low-dose aspirin,7 but apparently took no action to verify the association before 2002.8 Under the new procedures, it will be a routine matter for medicine regulators, including the TGA, to ensure that the sponsor conducts suitable studies to clarify safety concerns such as those raised in the VIGOR study. Of critical importance to the success of the expanded approach to pharmacovigilance is the level of resourcing at the TGA. Consideration of requirements must include capacity to: evaluate the suitability of pharmacovigilance plans that are included in applications for marketing approval of medicines; review pharmacovigilance plan updates that are submitted by sponsors; identify areas that require further investigation during the lifecycle of a medicine; and prepare reports for the medicines safety committee. It is disappointing that the initiatives do not include provisions for the TGA to fund, commission or conduct active safety investigations. The US Food and Drug Administration has received a substantial injection of funding for this purpose,4 and Medsafe, the New Zealand medicines authority, is funding product vigilance research through a joint initiative with the Health Research Council of New Zealand.9 Commissioned studies could address questions that sponsors could not reasonably be required to ask, such as those related to genetic markers for hypersensitivity reactions. They could also provide an alternative source of data in cases where the manufacturer chooses not to be transparent about safety matters, as allegedly occurred with rofecoxib10 and cerivastatin.11 As these changes in pharmacovigilance and drug regulation are occurring internationally, in general the TGA will be requiring postmarketing studies in concert with other regulators. In the absence of local initiatives or leadership from the TGA or other federal agencies that encourage the conduct of pharmacovigilance research in this country, Australia may not do much better than to achieve high-level observer status. Linkage of de-identified data from the Pharmaceutical Benefits Scheme and National Cancer Statistics Clearing House, as well as morbidity and mortality data from the Australian Institute of Health and Welfare, would provide a platform for epidemiological studies. Studies using this platform would need to be ones that do not require data on disease severity, concurrent disease, non-subsidised medication or lifestyle factors to control for confounding. While studies using more time-intensive means of data collection should also be encouraged in Australia, the years of inaction with regard to advancing this data linkage cannot be justified.12 The new approach being implemented by the TGA is welcome. Supplementing passive spontaneous reporting with evidence from active pharmacovigilance, in the form of studies designed to address important safety issues associated with medicines, will lead to more timely elucidation of adverse effects, together with reassurance for prescribers and patients. But the failure to include, as an essential part of the proposed changes, a package to ensure that active pharmacovigilance occurs in this country is baffling. This deficiency needs to be addressed urgently, and the matter would benefit from being taken up at a high level of government.

Kathlyn J Ronaldson BSc, MSc, DPhil

Results are promising but long-term safety remains uncertain Hypoactive sexual desire disorder (HSDD; loss of desire that causes personal distress)1 is common, with proposed prevalences ranging between 8% and 50% (wide variation is due to differences among populations surveyed and questionnaires used).2,3 Women with HSDD have been observed to experience poor sexual self-image, feelings of unattractiveness, fear of disappointing their partners, depression, anxiety and diminished quality of life.4,5 The effect of HSDD on quality of life has been reported as similar in magnitude to the effect of other common chronic conditions, such as diabetes and back pain.5 Furthermore, both men and women reporting a discrepancy between their own and their partner’s sexual desire have lower relationship satisfaction,6 and individuals in sexually inactive marriages report less marital happiness.7 Thus, HSDD merits recognition and intervention. In many cases, counselling and general sex education are helpful. However, the proportion of postmenopausal women who continue to experience HSDD despite good clinical care are left with few options, as there are no approved therapies presently available for this condition. APHRODITE is the most recent of a series of randomised controlled trials (RCTs) evaluating the efficacy and safety of transdermal testosterone patch therapy in postmenopausal women with HSDD.8 This large, multinational study, involving women with either natural or surgical menopause, differed from preceding studies in that participants were not receiving concurrent oestrogen therapy. The study was conducted and financed by Procter and Gamble Pharmaceuticals. However, it was instigated by the investigators, who were concerned that women may resort to off-label use of the testosterone patch Intrinsa (Procter and Gamble), when it becomes available, in the wake of the findings of the Women’s Health Initiative Studies (these findings initially raised concerns about the safety of postmenopausal oestrogen therapy). As effects of testosterone use without concurrent treatment with systemic oestrogen are unknown, the investigators believed this study would provide much-needed data. In this 52-week trial, 814 women with HSDD were randomly assigned to receive a patch delivering 150 μg or 300 μg of testosterone per day, or placebo. The primary end point was the number of self-reported sexually satisfactory events per month. The findings were interesting on several fronts. At baseline, women reported engaging in sexual activity on average 5 times per month, with half these events reported as unsatisfying. Participants had low sexual desire and a high level of personal distress measured by validated scales. By 24 weeks, women treated with the testosterone 300 μg patch reported a mean of 4.5 satisfactory events per month compared with 3.2 satisfactory events per month for women in the placebo group. Sexual desire increased and distress diminished substantially for both groups of women receiving active therapy. These findings have been interpreted by some as representing very little gain.9 However, women treated with the 300 μg testosterone patch reported enjoying nearly all of their sexual encounters, whereas those who received the placebo experienced pleasure 65% of the time. It is worth noting that women treated with testosterone did not report a significant increase in total sexual activity; this may be an effect of strongly established relationship patterns, including interest and availability of partners. In line with previous studies of transdermal testosterone therapy in postmenopausal and premenopausal women, efficacy did not manifest until after 8 weeks of therapy.10,11 Although women who received testosterone were more likely to report increased hair growth (20% of women receiving testosterone 300 μg v 10.5% of those receiving placebo), withdrawal from the study due to androgenic effects did not differ between the groups, and women treated with placebo were more likely to withdraw (19% of women receiving placebo v 14% of those receiving testosterone 300 μg). No significant adverse metabolic or endometrial effects were detected. The main concern arising from this study was the finding of breast cancer in four women treated with testosterone and none in the placebo group; the ratio of participants receiving testosterone to those receiving placebo was 2:1. The relationship between these findings and testosterone use is unclear, with two of the cancers likely to have been pre-existing (one diagnosed within 4 months of randomisation and another in a woman who recalled symptoms before randomisation when diagnosed after 7 months of treatment). A third woman diagnosed with breast cancer had previously been treated with hormone replacement therapy for 25 years and had a sister with breast cancer. The fourth was diagnosed after completion of 24 months of the study. The literature regarding the breast cancer risk of exogenous testosterone does not illuminate this issue. No other RCTs have been large enough or long enough to provide meaningful data. Observational data for oral methyltestosterone suggesting an increase in breast cancer risk12 have major limitations — the data are from the 1990s when testosterone was commonly prescribed for mastalgia in postmenopausal women receiving oestrogen therapy and the comparator group comprised non-hormone users, such that any apparent risk may have been the risk of oestrogen or oestrogen plus progestin use. A subsequent study in fact suggests the latter may well be the case.13 Two independent observational Australian studies have not found an increase in breast cancer risk with therapeutic testosterone use.14,15 Available data indicate transdermal testosterone can be useful for the treatment of HSDD in postmenopausal women. Short-term use appears to be safe, yet the effects of long-term use remain uncertain. Ideally, long-term safety should be evaluated in large longitudinal studies; however, as 70% of women who elect to use testosterone for HSDD do so for less than 3 years,15 retention of women in such studies will be a challenge.

Susan R Davis MB BS, FRACP, PhD

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 complete, up-to-date guidelines can be found at: http://www.mja.com.au/ public/rop/cheng/che10661_fm.html Since the initial reports of H1N1 influenza (human swine influenza; caused by influenza A/2009/H1N1/swl) in Mexico and the United States in mid April 2009, many thousands of cases have been reported worldwide. At the time of writing, community transmission is becoming established in many areas in Australia, but the number of reported cases is likely to be an underestimate of the true incidence due to policies for testing. These guidelines provide advice to clinicians on the use of antiviral agents for this newly emerged influenza virus. A full version of these guidelines, including all references, has been previously published online (http://www.mja.com.au/public/rop/cheng/che10661_fm.html). Recommendations for diagnosis of influenzaIn areas with established community transmission, patients presenting with an acute febrile respiratory illness (fever with cough and/or sore throat) are considered to have H1N1 influenza 09 and testing is generally not recommended. Early in the course of the pandemic, timely influenza diagnostic tests can be used to enable targeted antiviral treatment, but will be less useful once community transmission is widespread. Health care workers performing nose swabs or other high-risk aerosol-generating procedures (eg, suctioning, bronchoscopy or intubation) should use a particulate respirator (N95, P2 mask or equivalent), eye protection, impervious gowns, gloves, and, where possible, carry out the procedure in a negative pressure room. The use of nasopharyngeal aspirates are not recommended because of the risk to staff. The use of a combined nose–throat swab is recommended for diagnosis. Specimens for viral nucleic acid detection and culture at reference laboratories should be taken for epidemiological surveillance and to monitor for drug resistance. Once the pandemic is established, this is best facilitated through existing sentinel surveillance systems. Recommendations for treatment using antiviral agentsAntiviral treatment has been shown to reduce the duration of symptoms and may also reduce the incidence of lower respiratory tract infection. Neuraminidase inhibitors (oseltamivir and zanamivir) are the antiviral agents of choice for H1N1 influenza 09. Dose recommendations for treatment and prophylaxis are provided in Box 1 and Box 2, respectively. The decision to treat an individual patient, particularly before the results of confirmatory testing are available, depends on three factors: An assessment of the likelihood of influenza, based on the known prevalence of infection in the region, a history of contact and the characteristics of the illness. An assessment of the likely benefits of treatment (Box 3), based on the presence of established complications, comorbidities and risk factors (Box 4), and the time since onset of the illness. The phase of the pandemic and the public health policies regarding distribution of the national stockpile (Box 5). Recommendations for treatment in adultsAntiviral treatment should only be given to patients with confirmed or suspected influenza within 48 hours of symptom onset, except in cases of severe influenza. Treatment should be prioritised for patients with risk factors for poor outcomes, such as the morbidly obese, pregnant women, those with chronic disease (including asthma, cardiorespiratory disease, diabetes and renal failure) or immunosuppression, and those presenting with severe disease. Recommendations for treatment in childrenAntiviral treatment can be given to children as young as 1 year. Parents should be warned of the possibility of rare neuropsychiatric symptoms related to oseltamivir use in children and adolescents. There is a concern regarding central nervous system accumulation of neuraminidase inhibitors in infants aged under 1 year, based on animal data; a treatment decision must balance the potential benefits of treatment with potential toxicity. Recommendations for treatment in pregnant womenAntiviral treatment should be offered to pregnant women with suspected or confirmed influenza because of the risk of severe disease in this group. Oseltamivir and zanamivir are in the Australian Drug Evaluation Committee category B1, with limited evidence suggesting safety. Recommendations for treatment of severe influenzaAntiviral treatment should be given to hospitalised patients with severe influenza infection (especially pneumonia), even if commenced more than 48 hours after the onset of symptoms. Antibiotic treatment should not be given routinely for influenza-like illness, but antibiotic treatment should follow established national guidelines for treatment of community-acquired pneumonia. Recommendations for prophylaxis with antiviral agentsLong-term prophylaxis can be given to first-responder health care workers for up to 6 weeks for oseltamivir and up to 4 weeks for zanamivir. Use of antiviral prophylaxis for these groups should be in the context of agreement to use the national stockpile. Antiviral prophylaxis can be given to health care workers and close contacts of patients with influenza following exposure, and to residents of institutions to terminate outbreaks. Contacts not provided with prophylaxis should have access to early treatment with antiviral agents, where indicated. Updated informationWe acknowledge that the evidence on which these recommendations are based is rapidly changing. In particular, estimates of disease severity and case fatality, and risk factors for severity are poorly defined at present and may influence clinical decision making. We therefore include some resources for further information. Updates to these clinical guidelines will be posted on the websites of the Australasian Society for Infectious Diseases (ASID) (http://www.asid.net.au), the Thoracic Society of Australia and New Zealand (TSANZ) (http://www.thoracic.org.au) and the MJA (http://www.mja.com.au). Australian resources for pandemic influenza, including links to clinical and infection control guidelines (http://www.flupandemic.gov.au) and current information on the H1N1 outbreak (http://www.healthemergency.gov.au and http://www.influenza specialistgroup.org.au). For information on accessing personal protective equipment and antiviral medication, see links below: http://www.emergency.health.nsw.gov.au/swineflu/professionals/index.asp (New South Wales) http://humanswineflu.health.vic.gov.au/practitioners/index.htm (Victoria) http://www.health.qld.gov.au/swineflu/html/hc_resources.asp (Queensland) http://flu.sa.gov.au/Swineflu/InformationforGPs.aspx (South Australia) http://www.public.health.wa.gov.au/3/952/3/human_swine_flu_health_providers.pm (Western Australia) http://www.pandemic.tas.gov.au/what_does_it_mean_to_you/health_sector (Tasmania) http://www.health.nt.gov.au/H1N1_Influenza/General_Information_Resources/index.aspx (Northern Territory) http://health.act.gov.au/c/health?a=da&did=11044035&pid=1242181681 (Australian Capital Territory). 1 Dose recommendations for treatment of influenza Treatment Dose, interval, duration Oseltamivir Adults; children > 13 years 75 mg, twice daily orally, 5 days Renal impairment* 75 mg, daily orally, 5 days Children aged 1–13 years < 15 kg 30 mg, twice daily, 5 days 15–23 kg 45 mg, twice daily, 5 days 23–40 kg 60 mg, twice daily, 5 days > 40 kg 75 mg, twice daily, 5 days Zanamivir Adults 10 mg (2 inhalations), twice daily, 5 days Children > 5 years 10 mg (2 inhalations), twice daily, 5 days * Creatinine clearance, 10–30 mL/min. 2 Dose recommendations for prophylaxis against influenza Prophylaxis Dose, interval, duration Oseltamivir Adults; children > 13 years 75 mg, daily, 10 days Renal impairment* 75 mg, alternate days, 10 days Children aged 1–13 years < 15 kg 30 mg, daily, 10 days 15–23 kg 45 mg, daily, 10 days 23–40 kg 60 mg, daily, 10 days > 40 kg 75 mg, daily, 10 days Zanamivir Adults 10 mg (2 inhalations), daily, 10 days Children > 5 years 10 mg (2 inhalations), daily, 10 days * Creatinine clearance, 10–30 mL/min. 3 Factors to consider in deciding on likely benefits of treatment for H1N1 influenza 09 (human swine influenza) infection Established complications Hospitalised patients Patients with respiratory compromise Patients with pneumonitis or secondary bacterial pneumonia High risk of complications Pregnant women Patients with morbid obesity Indigenous Australians Patients with chronic respiratory disease; other comorbidities (see Box 4) Potential for transmission to others Health care workers and first responders (eg, paramedics) Household contact or carer of high-risk patient Low risk of complications Healthy adults Low likelihood of benefit Presentation > 48 hours after onset of illness High prevalence of circulating influenza strains with resistance to neuraminidase inhibitors Potential risks of treatment Infants < 1 year 4 Patients at risk of complications from influenza infection* Pregnant women Indigenous Australians Patients with: chronic respiratory disease (including asthma and chronic obstructive pulmonary disease); cardiac disease; morbid obesity; chronic diseases (eg, diabetes, chronic metabolic diseases, chronic renal failure, haemoglobinopathies); chronic neurological disorders; or impaired immunity, including HIV infection Homeless people Residents of nursing homes and long-term care facilities Children aged 6 months – 10 years on long-term aspirin therapy Older people (> 65 years) Children < 5 years * Adapted from the Australian immunisation handbook.1 5 Indications for antiviral treatment and prophylaxis for H1N1 influenza 09 (human swine influenza) infection, depending on likelihood of benefit and stage of pandemic Pandemic phase Delay Contain Sustain Protect Epidemiological setting Little or no community transmission; cases identifiable via exposure history Limited community transmission; cases not identifiable via exposure history Community transmission in some regions Widespread community transmission Treatment Patients with established complications Clinically presumed or laboratory-confirmed Clinically presumed or laboratory-confirmed Clinically presumed or laboratory-confirmed Clinically presumed or laboratory-confirmed Groups at risk of complications* Clinically presumed or laboratory-confirmed. Consider treatment > 48 h after onset if severe or not improving Clinically presumed or laboratory-confirmed. Consider treatment > 48 h after onset if severe or not improving Clinically presumed or laboratory-confirmed. Consider treatment > 48 h after onset if severe or not improving Clinically presumed or laboratory-confirmed. Consider treatment > 48 h after onset if severe or not improving Health care workers, carers for patients at risk of complications within 48 h of onset of illness Clinically presumed or laboratory-confirmed Clinically presumed (if appropriate exposure history) or laboratory-confirmed Clinically presumed or laboratory-confirmed Clinically presumed or laboratory-confirmed Otherwise healthy adults and children > 5 y within 48 h of onset of illness Clinically presumed or laboratory-confirmed Laboratory-confirmed Clinically presumed (depending on rationing policy and virulence) Not generally indicated Infants < 1 y Depends on clinical scenario Depends on clinical scenario Depends on clinical scenario Depends on clinical scenario Low likelihood of benefit (> 48 h after presentation, known high prevalence of resistance) Not indicated, unless severe infection present. Consider zanamivir if oseltamivir-resistant Not indicated, unless severe infection present. Consider zanamivir if oseltamivir-resistant Not indicated, unless severe infection present. Consider zanamivir if oseltamivir-resistant Not indicated, unless severe infection present Prophylaxis following exposure Groups at risk of complications* Indicated Indicated Indicated (depending on rationing policies) Not generally indicated, except immunosuppressed patients and closed communities Health care workers, carers for patients with comorbidities Indicated Indicated Indicated (depending on policy for national stockpile) Not generally indicated (depending on hospital policy) Healthy adults and children > 5 y within 48 h of exposure Indicated Indicated Not indicated (depending on rationing policy and virulence) Not indicated Children < 1 y Not generally indicated Not generally indicated Not generally indicated Not generally indicated Low likelihood of benefit (> 48 h after exposure) Consider up to 7 days after exposure to prevent transmission Depends on observed incubation period and public health policy Consider early treatment if symptoms develop Not indicated * Such as pregnant women, patients with comorbidities or immunosuppression, and Indigenous Australians (Box 4).

Allen C Cheng FRACP, MPH, PhD · Dominic E Dwyer MD, FRACP, FRCPA · A Thomas C Kotsimbos MB BS, FRACP, MD · Mike Starr MB BS, FRACP · Tony M Korman MB BS, FRACP · Jim P Buttery MB BS, MSc, FRACP · Christine R Jenkins MD, FRACP · Vicki L Krause MD, FAFPHM, DTM · Paul D R Johnson MB BS, PhD, FRACP

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

What lessons can be learnt from Australia’s initial response to the outbreak? Given all the detailed planning and preparation that has gone into the Australian Health Management Plan for Pandemic Influenza (AHMPPI)1 over the past 4 years, Australians may be wondering how well the plan has performed in Victoria during the recent H1N1 (swine) influenza outbreak. As clinicians working in one of the main affected hospitals, we would like to offer four key observations. Firstly, the AHMPPI is a carefully developed medical and social management plan that was primarily designed to deal with a serious new strain of influenza, such as avian influenza, in which the case mortality (death rate) was expected to be up to 40%.2 It was developed by experts in virology, epidemiology and health policy based on computer modelling that used assumptions about disease transmission rates (infectiousness), disease severity and the likely effectiveness of a single drug — oseltamivir. In planning, there was only limited input from clinicians, and practical issues — such as the adequacy of the protective mask stockpile or the means of rapidly distributing drugs and equipment to the “front line” — do not appear to have been planned in detail.3 In reality, the severity of the 2009 swine flu outbreak has fallen well short of the worst-case scenario: instead of resulting in high mortality, swine flu has been associated with only a 1%–2% hospital admission rate and zero mortality in Australia (so far); early experience has shown that the clinical case definition (fundamental to accurate disease modelling) was not an accurate model for the swine flu epidemic; and drug and mask distribution has been extremely slow, especially to general practitioners, who are crucial to effective disease management and containment. But the AHMPPI has lagged in adapting to these circumstances. Instead of being flexible and responding to feedback from the medical front line in Victoria, the AHMPPI has continued to be rigidly based on past assumptions. The process has tended to focus on managing data and information flow, rather than managing the sick patients. Secondly, initial laboratory testing to confirm a case of swine flu was only allowed if a sick patient fitted the specific case definition — namely, the patient had to be a recently returned traveller from Mexico or North America, or a close contact of a proven case. Tests on all other patients who had a clinical illness suspected of being swine flu were initially refused or given low laboratory priority. This is the opposite of what should have occurred. To understand the full extent of disease spread, widespread testing without assumptions needs to occur so that the accuracy of the proposed case definition can be tested. The case definition should be used to guide clinicians, not the laboratory testing strategy. Otherwise it simply becomes self-confirming and does not identify the real extent of disease spread until it is too late — as has occurred in Victoria. Thirdly, public hospital testing capacity for viral diseases has been primarily concentrated, over the past three decades, on just one centre in Victoria — the Victorian Infectious Diseases Reference Laboratory. Although initially this made sense given the complexity of viral testing, technology has developed so rapidly in recent years that most public hospital laboratories now have molecular testing equipment available to accurately test for swine flu and other viruses. Thus, the present approach needs to change to reduce the current bottleneck whereby swine flu test results often take 3–5 days to come through. Meanwhile, the patient is not in quarantine and is generally not receiving antiviral therapy. If all hospitals had testing capacity and the rules for testing were not based on preconceived assumptions, the current influenza situation might have been different. Of course, confirmation of positive results by a reference laboratory would still be required, but its workload would be manageable (about 10%–20% of current levels). Finally, the AHMPPI depends on faith in oseltamivir — that it is totally safe and that its use will reduce disease severity and spread. However, to be effective, the drug should be commenced within 48 hours of disease onset.4 With laboratory results taking days to return, the only clinical solution would be to commence oseltamivir immediately influenza is suspected — in which case, at Austin Health we would be treating up to 80% of patients for a disease they do not have. Already it is known that the main seasonal influenza strain in the United States in 2008 was resistant to oseltamivir. The real nightmare scenario will be if the current swine flu strain also develops resistance in the face of widespread use of oseltamivir, leaving us with few treatment options. We are currently wasting oseltamivir on a mild illness when we are likely to need it next year, when the current strain could become more aggressive. Of course, some good things have come from the current outbreak. It is possible (but not certain) that people who caught swine flu this year may have some protection for next year’s possibly more aggressive strain. Secondly, the Acting Chief Health Officer in Victoria has done a great job in establishing new communication links with front-line clinicians and injecting some common sense into the AHMPPI debate. Finally, it has given Australia a chance to test its AHMPPI — what we need now is to critically evaluate its practical strengths and weaknesses.

M Lindsay Grayson MD, MSc, FRACP · Paul D R Johnson MB BS, FRACP, PhD

The swine influenza (H1N1 09) outbreak in Victoria has provided an excellent opportunity to review the Australian Health Management Plan for Pandemic Influenza (AHMPPI) and to assess its performance in practice. General practitioners play a major role in seasonal flu management, and it was expected that the AHMPPI would enable GPs on the front line to maintain this central role during the swine flu pandemic. The role of front-line GPs has been made extremely difficult by deficiencies in implementation of the AHMPPI, including resource supply failures, time-consuming administrative burdens, delays in receiving laboratory test results and approval for provision of oseltamivir to patients, and a lack of clear communication about policy changes as the situation progressed. We must use this experience to ensure timely and appropriate review of the AHMPPI and the way it is implemented. Better consultation with front-line clinicians, particularly GPs, is crucial and must occur as a matter of urgent priority.

Peter Eizenberg MB BS

We present the first six cases of H1N1 influenza 09 (confirmed by a polymerase chain reaction test from nasopharyngeal swabs) in patients requiring admission to intensive care in Australia (in three hospitals in the north-western suburbs of Melbourne). These cases highlight the small but significant risk of life-threatening respiratory failure associated with H1N1 influenza 09 infection. Clinical recordsPatient 1A 28-year-old obese woman (body mass index [BMI], 57 kg/m2) presented to the emergency department (ED) with a history of 5 days of sore throat, lethargy and myalgias, and a clear chest x-ray, followed by 2 days of dyspnoea, productive cough, and pleuritic chest pain. She was febrile (40°C), and had tachypnoea (respiratory rate, 36 breaths/min) and hypoxia (oxygen saturation measured by pulse oximetry [Spo2], 87% on 15 L/min oxygen via face mask). Her admission chest x-ray showed widespread alveolar infiltrates. She had a normal white cell count (WCC) of 6.3 × 109/L, but an elevated serum C-reactive protein (CRP) level of 221 mg/L (reference ranges shown in Box 1). She was admitted to the intensive care unit (ICU) and, after a brief trial of non-invasive ventilation (NIV), was intubated and treated with mechanical ventilation (MV) with a fraction of inspired oxygen (Fio2) of 1.0 and positive end-expiratory pressure (PEEP) of 20 cm H2O for the first 24 hours to maintain an Spo2 > 89%. She was treated with inotropes for septic shock and with renal replacement therapy for acute renal failure. Therapy with oseltamivir in addition to empiric broad-spectrum antibiotics was commenced. Bacterial cultures of blood, urine and tracheal aspirate were negative. The result of a test for urine pneumococcal antigen was negative. The patient was successfully weaned from ventilatory support on Day 14. Patient 2A previously well 24-year-old man (BMI, 22 kg/m2) was admitted to a regional hospital with a 1-week history of dry cough, fever, headache, abdominal pain, and vomiting. Thirty-six hours later, he was transferred to a metropolitan hospital because of worsening dyspnoea and hypoxia (Spo2, 88% on 15 L/min oxygen via face mask). He had tachycardia (110 beats/min), tachypnoea (respiratory rate, 34 breaths/min) and was febrile (39.9°C). He had a normal WCC (4.2 × 109/L) but an elevated CRP level (256 mg/L). A chest x-ray showed unilateral lobar consolidation. He was transferred to the ICU and treated with oseltamivir, broad-spectrum antibiotics, and NIV with an Fio2 of 1.0. After 96 hours, his hypoxia remained severe (partial pressure of arterial oxygen [Pao2] to Fio2 ratio, < 100), another chest x-ray showed bilateral alveolar infiltrates, and he was intubated and MV was commenced with an Fio2 of 1.0 and high-level PEEP (20 cm H2O) for several days. Bacterial cultures and urine pneumococcal antigen test results were negative. Oseltamivir therapy was continued for 7 days, and MV for 15 days. Patient 3A 26-year-old obese man (BMI, > 40 kg/m2) with a history of mild asthma presented after 2 days of nausea without vomiting, and no fever or cough. On the day of admission, he developed shortness of breath. He was found to be hypoxic (Spo2, 90% on an Fio2 of 1.0) with bilateral pulmonary infiltrates showing on a chest x-ray. His WCC was 5.6 × 109/L and CRP level was 137 mg/L. Therapy with broad-spectrum antibiotics and oseltamivir was commenced. He was intubated, and MV was commenced with an Fio2 of > 0.6 and high-level PEEP (15 cm H2O); the patient was successfully extubated after 10 days. Patient 4A previously well 41-year-old man (BMI, 30 kg/m2) presented with a 7-day history of cough, coryza, malaise, back pains and rigors. On the day of presentation, he became febrile (39.6°C) and developed tachypnoea (respiratory rate, 45 breaths/min) and severe hypoxia (Spo2, 84% on 10 L/min oxygen via face mask). His chest x-ray showed widespread pulmonary infiltrates. He had a WCC of 4.4 × 109/L and a CRP level of 166 mg/L. He was intubated in the ED and MV was commenced, and he was given oseltamivir and broad-spectrum antibiotics. He remained severely hypoxic (requiring an Fio2 of > 0.8) for 10 days, and was treated with MV in the prone position and inhaled nitric oxide. His condition gradually improved, and he was extubated on Day 13. Patient 5A 60-year-old man presented to hospital with an exacerbation of his severe chronic obstructive pulmonary disease (COPD). He also had severe peripheral and coronary vascular disease. On examination, he had tachypnoea (respiratory rate, 36 breaths/min) but no fever. He had no prodrome of coryza or myalgias, and a chest x-ray showed mild bibasal opacities. His WCC was elevated (11.4 × 109/L), but his CRP level was 12 mg/L. He was admitted to the respiratory ward and treated with oseltamivir, broad-spectrum antibiotics, and NIV. Two days later he was intubated, and MV was commenced for hypercapnic respiratory failure. Bacterial cultures were negative. His hypoxia was mild (requiring an Fio2 of < 0.5), but he required MV for 14 days. Patient 6An 18-year-old pregnant woman presented with a 4-day history of cough, fever, and persistent vomiting without diarrhoea. Oseltamivir therapy for possible H1N1 influenza infection was discussed with the patient, but not administered. After intravenous rehydration, she was discharged home, but she returned several hours later in premature labour. Her WCC was 8.2 × 109/L but her CRP level was high (90 mg/L). She was given steroids for fetal lung immaturity and transferred to a tertiary obstetric/neonatal hospital. Twenty-four hours after delivering a 26-week live infant, she developed hypoxic respiratory failure with tachypnoea (respiratory rate, 35 breaths/min) and bilateral pulmonary infiltrates. She required a high level of inspired oxygen therapy (Fio2, 0.6) by face mask, and monitoring in the ICU. The mother, but not her baby, had a positive polymerase chain reaction (PCR) test result for H1N1 influenza 09, and both were treated with broad-spectrum antibiotics and oseltamivir. DiscussionSince the emergence of the novel H1N1 influenza 09 (human swine influenza) in North America and Mexico in mid April, the number of confirmed cases has increased to over 55 000 across 105 countries.1 While most individuals will experience a mild clinical illness (coryza, fever, cough and myalgias), there have been 238 reported deaths (0.4%).2 A Centers for Disease Control and Prevention (CDC) report in May provided details of the 30 patients who were hospitalised in California, of whom six required admission to an ICU and four required MV.3 At the time of writing, there have been 3912 confirmed cases of H1N1 influenza 09 in Australia.2 Most reported illness has been mild, but 268 patients (6.9%) have been hospitalised, over 25 (0.6%) have been admitted to ICUs, and five deaths (0.1%) have been reported. Here, we presented the first six cases of H1N1 influenza 09 (confirmed by PCR test from nasopharyngeal swabs) in which patients required admission to intensive care in Australia. Admissions were to three hospitals in the north-western suburbs of Melbourne. These cases highlight the small but significant risk of life-threatening respiratory failure associated with H1N1 influenza 09 infection. All patients experienced a rapid (but reversible) decline in respiratory function, with most requiring complex respiratory support. The age distribution of these patients is consistent with other reports, and lower than that seen in previous influenza seasons.4,5 Four of the six cases we report had risk factors, including asthma, chronic lung disease, smoking, obesity, and pregnancy; these risk factors were similar to those identified in the CDC reports.3 Patients 2 and 4 had no identifiable risk factors. There are several possible explanations for the acute respiratory failure observed in these patients. Early onset of respiratory failure with widespread pulmonary infiltrates (Patient 3) suggests primary viral pneumonitis, whereas the delayed onset of fever with lobar signs (Patient 2) and pleurisy (Patient 1) suggest secondary bacterial pneumonia. A cytokine-mediated acute lung injury may also explain the late appearance of diffuse pulmonary infiltrates (Patients 4 and 6). The absence of a severe prodrome in Patient 5 suggests an exacerbation of the patient’s COPD. With the number of cases of H1N1 influenza 09 infection likely to increase, it is anticipated that further cases of severe respiratory failure associated with this influenza will be seen. Based on the cases reported here and other reports, we offer the recommendations shown in Box 2. A high index of suspicion that respiratory failure may ensue is warranted in patients who have risk factors5 or present with tachypnoea (respiratory rate, > 24 breaths/min) and/or hypoxia (Spo2, < 95% on supplemental oxygen), and early referral to hospital is warranted. Youth and prior good health do not preclude the possibility of severe respiratory failure. The Victorian Department of Human Services currently recommends nasopharyngeal swabs for a PCR test for influenza A in patients admitted to hospital with suspected influenza. Empiric therapy with antiviral agents (oseltamivir or zanamivir)5 should be considered in addition to antibiotic treatment for community-acquired pneumonia pathogens, in consultation with an infectious diseases specialist. Patients with suspected H1N1 infection should be isolated, preferably in a negative pressure isolation room.6,7 Where possible, antiviral filters applied to the expiratory limb of the ventilator circuit may further reduce the risk to health care staff. Oseltamivir (Tamiflu) and zanamivir (Relenza) reduce viral replication and shedding, and may reduce the risk of more severe illness. Their safety in pregnancy has not been investigated (Category B1 for use in pregnancy), but without treatment there may be a greater risk of premature labour (Patient 6).5,8 Increasing resistance to oseltamivir has been reported in other strains of currently circulating influenza A viruses, but, as yet, not in the H1N1 influenza 09 lineage.9,10 Any patient with respiratory distress or severe hypoxia (requiring an Fio2 of > 0.5) and pulmonary infiltrates on chest x-ray should be referred to an intensive care specialist for further assessment. Mechanical ventilation for these patients is complex, and requires expertise and specialised equipment. We used restrictive tidal volumes (6 mL/kg ideal body weight), high PEEP (15–20 cm H2O), pressure-limited modes of ventilation, alveolar recruitment manoeuvres, inhaled nitric oxide, and restrictive fluid therapy with apparent success. This is consistent with ventilation strategies used by others,11 and in keeping with strategies described by the Acute Respiratory Distress Syndrome (ARDS) Clinical Network.12 Extracorporeal oxygenation therapy has recently been used in other cases (G J D, personal communication). Based on the available data, we would not recommend NIV as the mainstay of respiratory support. The four patients who were given a trial of NIV in this series all required intubation and MV. This is consistent with published data for ARDS and pneumonia.13 NIV temporarily improves oxygenation and reduces the work of breathing, but does not necessarily alter the course of the disease.14 The need for NIV is an indication of severe disease and the likelihood of intubation and MV. For the most part, H1N1 influenza 09 is a benign disease, but it may lead to severe respiratory complications in a small proportion of patients. In our series, prompt diagnosis and intensive therapy was associated with favourable outcomes. 1 Reference ranges for white cell count and C-reactive protein level Reference range White cell count (WCC) 4–11 ×109/L C-reactive protein (CRP) < 5 mg/L 2 Summary of clinical recommendations for managing patients with possible H1N1 influenza 09 infection Maintain a high index of suspicion of possible respiratory failure in patients with risk factors such as asthma, smoking, pregnancy, obesity or chronic medical conditions.2,4 Refer patients to hospital if they have hypoxia (oxygen saturation measured by pulse oximetry [Spo2], < 95%) and/or tachypnoea (respiratory rate, > 24 breaths/min) or pulmonary infiltrates. Institute respiratory and contact precautions, including personal protective equipment.2,4-6 Conduct polymerase chain reaction tests for H1N1 influenza A in patients admitted to hospital with suspected influenza. Start antiviral therapy early; its benefits in pregnant mothers may outweigh the risks.4,7 Refer patients for intensive care unit assessment if a fraction of inspired oxygen (Fio2) of > 0.5 or oxygen at a rate of > 10 L/min is required to maintain the Spo2 at > 92%. Non-invasive ventilation is unlikely to improve the outcome; consider intubation and mechanical ventilation. Complex mechanical ventilation strategies are often required.

Melissa A Kaufman MB BS · Graeme J Duke MD, FJFICM, FANZCA · Forbes McGain FJFICM, FANZCA · Craig French FJFICM, FANZCA · Craig Aboltins MB BS, FRACP · Gary Lane FRACP, MMed(ClinEpi), MQIHC · Geoff A Gutteridge FJFICM, FANZCA

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

Objectives: To examine the levels and predictors of injection of buprenorphine–naloxone (BNX) — a combination of a partial opioid agonist and an opioid antagonist for treating opioid dependence — which was specifically developed to limit injecting. Comparison was made with injecting of two other opioid substitution treatment medications, methadone and buprenorphine (BPN); severe harms have been documented after injection of the latter.Design and participants: Injecting was studied in regular injecting drug users (“IDUs”) and current opioid substitution treatment clients (“clients”). Regular IDUs are interviewed annually in each Australian capital city (about 900 per year) and data for 2003–2007 were used; 399 clients were interviewed in 2007. Data on injection of opioid substitution treatment medications between 2003 and 2007 were adjusted for availability of medications (from national sales data for methadone, BPN and BNX). Predictors of injecting were analysed by multiple regression analyses.Setting: Capital cities of all Australian states and territories.Main outcome measure: Injection of opioid substitution treatment medications among individuals both in and out of treatment.Results: In the year after its introduction in Australia, BNX was injected less frequently and by fewer regular IDUs and clients compared with BPN, particularly when differences in the availability of medications were taken into account. Some individuals did nonetheless regularly inject BNX. Injection of methadone, BPN and BNX was more likely to occur among those injecting other pharmaceutical opioids.Conclusions: A partial opioid agonist–antagonist combination appears to be less commonly and less frequently injected by clients in treatment and IDUs who are not. Further studies are needed to evaluate longer-term trends in use and harms.

Louisa Degenhardt PhD, MPsych(Clinical) · Briony K Larance BSc(Psych)(Hons) · James R Bell FRACP, MD, FAChAM · Adam R Winstock MSc, MRCPsych, FAChAM · Nicholas Lintzeris MB BS, PhD, FAChAM · Robert L Ali MB BS, FFPHM, FAChAM · Nicolas Scheuer PGDipEconometrics, BAppEconometrics · Richard P Mattick PhD, MPsych(Clinical)

Australia’s achievement in tobacco control has been remarkable, but relies on indirect estimates of tobacco-attributed mortality, and on using relative risks from Western countries to calculate tobacco’s impact. To accelerate the decline in smoking, more precise measures of tobacco’s relative importance among different population subgroups are required. We propose that more direct and accurate measures of tobacco-attributed mortality are needed, which could be achieved by adding a small set of voluntary questions about the smoking status of the deceased to a revised death notification form. Ideally, this form should also record the smoking status of the next-of-kin or family informant, as this would help establish a living control group. Such information will provide data on tobacco-attributed deaths with incomparable precision, allowing accurate monitoring of the current state of the smoking epidemic, and its evolution over time. This is particularly pertinent for sections of the population in which tobacco control measures have been less successful. A number of practical concerns have been raised, but we do not believe these are insurmountable.

Freddy Sitas MSc(Med), MSc(Epidemiol), DPhil · Dianne L O’Connell BMaths(Hons), PhD · Konrad Jamrozik DPhil, FAFPHM · Alan D Lopez MS, PhD, HonFAFPHM

Demand for medical education is increasing, and clinicians are struggling to maintain involvement in teaching and research activities. The settings of clinical training are changing and diversifying. The traditional model of medical education and the sustainability of academic medicine are under strain. Better support is required to ensure continued integration of research and education with clinical activities. Better coordination is required to overcome fragmentation within the medical education system, to ensure appropriate recognition for teaching and research across all clinical settings.

Catherine M Joyce BA(Hons), MPsych, PhD · Leon Piterman MB BS, MEdSt, FRACGP · Steven L Wesselingh BM BS, FRACP, PhD

Clinical records Patient 1 A 73-year-old woman presented to a Western Australian metropolitan hospital in September 2007. She described having a dry mouth, lethargy and difficulty mobilising about an hour after eating two scones prepared with lupin flour. On arrival at hospital, her condition was much improved, and lethargy and dry mucous membranes were the only symptoms recorded. However, the treating doctor was not aware of the potential for anticholinergic effects, and may not have been looking for specific anticholinergic features. The patient was discharged several hours after presenting; her symptoms were attributed to a presumed allergic reaction. Patient 2 A 66-year-old woman presented to the same hospital 3 days later in September 2007. This patient had developed symptoms 15 minutes after eating pancakes prepared with lupin flour. She reported more typical anticholinergic features of blurred vision, dry mouth, lethargy and light-headedness. On examination she was found to have a sinus tachycardia of 100 beats/min, mildly dilated pupils, dry mouth, blurred vision and a residual bladder volume of 590 mL after voiding, indicating a moderate degree of urinary retention. Anticholinergic syndrome after ingesting lupins was diagnosed. She was kept in hospital overnight and her symptoms had resolved by morning. Recognition of a possible link After Patient 2 was diagnosed with anticholinergic syndrome caused by eating lupins, consulting physicians recalled that Patient 1 had also reported lupin consumption. After reviewing the clinical notes from Patient 1, it was recognised that this patient also had anticholinergic symptoms and that the two cases might be linked. Case investigation The two patients were interviewed in regard to their food consumption before becoming ill. Patient 1 had purchased lupin flour from a specialty grocery chain and made scones with the flour. She remarked that the two scones she ate tasted very bitter. Patient 2 had purchased both lupin flour and lupin beans from a different store of the same grocery chain as that reported by Patient 1. She also remarked on the bitterness of the pancakes she had made with the flour. In addition, she reported soaking lupin beans she had purchased overnight, boiling them and eating one lupin bean, which tasted bitter. The store identified by Patient 2 was inspected 2 days after she had bought the lupin flour. Questioning revealed that after the normal supply of sweet lupin flour was exhausted, a storeman had had 125 kg of bitter lupin beans (Lupinus albus) milled into flour. He was unaware of the danger associated with consuming untreated bitter lupins. It was this flour that was purchased and consumed by the two patients. The bitter lupin flour was distributed to a number of stores within the grocery chain. Further investigation revealed another two complaints of bitter-tasting bread made from the lupin flour, but no other cases of anticholinergic syndrome were reported. Following the investigation, the proprietor removed the bitter lupin flour from sale. Samples of both bitter lupin beans and the bitter lupin flour were submitted for chemical analysis. The total alkaloid levels for the bitter lupin beans and flour were 1.92% and 2.01%, respectively. This was about 100 times the permissible alkaloid level for flour of 0.02%, or 200 mg/kg, as detailed in the Australia New Zealand Food Standards Code.1 No standard exists in the code for allowable alkaloid levels in whole lupin beans. Lupins (Lupinus spp) are legumes, otherwise known as pulses. There are about 450 Lupinus species, with L. angustifolius and L. albus being the main species cultivated in Australia. While lupins have been predominantly used for animal feed, recent research has shown that eating them can provide health benefits for humans. The addition of sweet lupin flour to bread has been shown to reduce its glycaemic index, reduce energy intake and increase satiety of study participants compared with those who consumed standard white bread.2,3 The addition of sweet lupin flour to sausages was shown to decrease fat intake and increase satiety in study participants when compared with those who consumed full-fat sausages.4 Lessons from practice Anticholinergic syndromes vary in their severity, but any combination of blurred vision; mydriasis; tachycardia; dry, flushed skin; dry mucous membranes; urinary retention; ileus; or delirium should raise suspicion of this diagnosis. Most anticholinergic syndromes are caused by medications used therapeutically or in the misuse setting. However, naturally occurring toxins from foods or plants should be considered where appropriate. Clinicians should question patients who present with symptoms of anticholinergic syndrome about their recent food consumption, particularly consumption of lupin-containing products. With increasing community interest in foods with a low glycaemic index, it is important that lupin flour suppliers understand the importance of distinguishing between sweet and bitter lupins in flour preparation. Adverse consequences of eating lupins can be divided into toxic and allergic reactions. Studies have identified both serological and clinical cross-reactivity between peanut and lupin, although lupin allergy can also occur without allergy to other legumes.5,6 Lupins are separated into sweet varieties, which have an alkaloid content of approximately 130–150 mg/kg,7 and bitter varieties, which need to undergo a debittering process to remove potent alkaloids before consumption (these are left with an alkaloid content of approximately 500 mg/kg after debittering).7 The debittering process involves soaking beans in repeated changes of water. The alkaloids leach from the beans into the water, which is then discarded. Solvents can also be used for debittering. Failure to remove, or incomplete removal of, alkaloids can result in lupin toxicity, manifesting as anticholinergic syndrome. Anticholinergic syndrome can also be caused by various drugs, including some antihistamines, antipsychotics, antispasmodics and antidepressants, as well as by eating some mushrooms and plants.8,9 Plants known to cause anticholinergic syndrome when ingested include Datura spp (jimson weed, angel’s trumpet), Salvia divinorum (diviner’s sage), Atropa belladonna (deadly nightshade), Hyoscyamus niger (black henbane) and Mandragora officinarum (mandrake).9,10 Fatal cases of lupin poisoning have been reported, with the lethal dose calculated as about 30 mg/kg bodyweight.7 Bitter lupins are commonly eaten by people of Mediterranean origin, and these traditional users are aware of the need to debitter the lupins before consumption. There are relatively few published reports of acute lupin toxicity overseas,9-12 and only one in Australia,13 which involved a Mediterranean woman who had eaten lupin beans that had not been sufficiently debittered. In light of the increasing consumption of lupin products, we recommend that information be provided to food suppliers and consumers about the dangers of selling and eating products containing bitter lupins that have not been appropriately pretreated to remove toxic alkaloids. Clinicians should question patients who present with symptoms of anticholinergic syndrome about their recent food consumption, particularly consumption of lupin-containing products.

Nevada M Pingault BSc(Hons), MASM, MAIMS · Robyn A Gibbs BSc, PhD · Alexander M Barclay MAIFST, MAIEH · Mark Monaghan MB BS, FACEM

Aboriginal protocol usually links the right to tell a story with a declaration of involvement or connection to the story.1 Iam Aboriginal . . . I am a woman, daughter, sister, aunty and wife. I am also a mother to three beautiful children aged 6, 4 and 2 years. To my children at this point in their lives, I am their provider, nurturer, teacher, cook, taxi driver, mediator, stylist, Elder, slave, and expert on all there is to know in the world. Being the centre of the universe to three impressionable young minds is a role that I cherish deeply, and I take the responsibilities of it very seriously. I love the job of parenting. As any parent would agree, it is the most challenging and difficult job of all, but the opportunity to bring a life into the world and shape and mould a little person into a big person brings rewards that no career can. The story I share here is of a professional journey I travelled within my own community in coordinating an Indigenous early years intervention. I simply cannot tell this story without acknowledging and declaring my connections as a mother first. It is through my identities as a mother and an Aboriginal person that this journey was experienced, and therefore it is through these eyes that this story is told. An Indigenous early years interventionAfter the birth of my third child, I returned to the workforce in a part-time capacity with the Inala Indigenous Health Service. Through a partnership with Mission Australia’s Communities for Children initiative (funded by the Australian Government Department of Families, Housing, Community Services and Indigenous Affairs Stronger Families and Communities Strategy), I was given the brief to develop an intervention that would improve the lives of Indigenous children aged 5 years and under and their families in the Inala to Goodna region. In recent times, the term “intervention” seems to have become a kind of dirty word within Indigenous communities. Within the context of Indigenous social policy, intervention seems to imply swift action and necessary interference. However, for a number of Indigenous communities (and many Indigenous parents) in the Northern Territory and Far North Queensland, the idea of intervention has meant forced, punitive social controls and surveillance over everyday living and family decision making. These interventions are justified through the premise that Indigenous parents in these communities just don’t have the capacity or desire to raise their children right. For some people, the policy of intervention in Indigenous communities invokes imagery of incompetent parents; for others, it invokes images of incompetent politicians and policymakers. I recognise that I have no first-hand involvement with or connection to the intervention experience in the NT or the family income management schemes in Cape York. But the common experience I share with the parents in these places (and all parents, for that matter) is the desire to raise happy, healthy children who will grow to be physically strong, culturally wise and always walk with their heads held high. The community that my children call home and the site of this intervention is an outer-western suburb of Brisbane called Inala. It is home to one of the largest Indigenous communities in south-eastern Queensland, and has a high density of public housing.2 Every socioeconomic indicator strongly suggests that Inala is a disadvantaged community, which commonly implies that Inala must be a “bad” community. “Bad” communities, of course, are composed of “bad” families, as evidenced by a statement from the Queensland Government Family Responsibilities Commissioner, David Glasgow, in which he suggested extending the Cape York welfare reforms to “places like Inala, Redbank and places of that nature where children are not looked after properly”.3 As parents (who happen to be Aboriginal), my husband and I know that we are far from perfect. Inasmuch as we love our children, we are just as convinced that we will make mistakes — that is part of life, no doubt. Yet, the challenges of parenthood are made more difficult by the stigmas attached to parents who happen to be Aboriginal or younger than average, or who reside in disadvantaged neighbourhoods. When my husband and I venture out with our children into the predominantly white spaces of neighbouring suburbs, we cannot help but notice how people are “reading” us. As Aboriginal parents, we are aware that the public gaze is transfixed on the horrors of physical and sexual abuse and neglect of Indigenous children and families, to the extent that it makes it difficult for some people to see us beyond those depictions. I can attest that the stigma of stereotyping is a heavy burden to shoulder, and is one that we are loath for our children to inherit. Given these experiences, I was determined that this intervention would not be grounded in those kind of assumptions. Of course, there are Aboriginal parents who are abusive and neglectful of their duties. However, it would be unthinkable to allow the worst cases of parental abuse and neglect within the non-Indigenous community to be used as the yardstick for driving family and social policy for the rest of Australian society. So my starting point for the Indigenous Early Years Intervention in Inala was the premise that all parents love their children and only want what’s best for them. Therefore, our intervention would not necessitate forced or punitive controls and surveillance to effect positive social change. I believe it is for precisely this reason that this initiative achieved a wide range of positive outcomes for Indigenous families in our community. Within just 12 months, the Indigenous Early Years Intervention was successful in developing local Indigenous health promotion resources, establishing an Indigenous playgroup within the community, and improved literacy awareness among Indigenous parents and carers, as well as providing opportunities for skill development for local Indigenous parents and workers. The intervention also focused on building the capacity of the Indigenous sector to support Indigenous children and their families beyond the lifespan of the project. The Box lists some of our major accomplishments. It is kind of ironic that these kinds of outputs could be achieved, given what we supposedly know about Indigenous parents and “places like Inala”. The critical success factors for this intervention don’t lie in romanticised assumptions about families in Inala or Aboriginality. The success achieved is a product of age-old processes that our mob has used in the doing of our everyday business. The failure to recognise the strengths of Indigenous parents in Indigenous social policy is simply reflective of a broader failure to recognise the strengths of Aboriginal culture, processes and protocols. As a health professional working in Indigenous communities, I’ve always been guided by the principles I’ve been taught as an Aboriginal person. Mapping country — seeing strengthFor many Aboriginal people, the importance of knowing one’s country is inherent to our sense of Aboriginality and sense of wellbeing. This requires an intimate knowledge of traditional lands and the dreaming stories contained within. These lands are identified by geographical boundaries, and landmarks such as lakes, rivers, mountains, trees and rocks. Tom Dystra articulates this distinct relationship: We cultivated our land, but in a different way from the white man. We endeavoured to live with the land; they seemed to live off it. I was taught to preserve, never to destroy.4 As an Aboriginal person working within my own community, it is imperative that I know my country too. I must know the landmarks and identifiers of the country and community that I live in and call home. However, the landmarks that I’m looking for here are not so much about the physical landscape, but instead are features of the social landscape. Mapping country is about taking the time to explore and identify the existing energies, strengths, and skills of the community, its members and the service sector. Importantly, our attention here is drawn to what is already present in a community and not in what is lacking. White fellas call this process “asset mapping” — we call it mapping country. Recognising a community’s strengths or assets sets the platform for possibilities. Charting a community’s deficits only seems to deepen the despair. Admittedly, some strengths may be small — they may be only seeds that have just been planted. But that is our role as custodians of our land, community and culture — to nurture and grow, and preserve, not destroy. Perhaps that is what is so offensive about the other intervention experiences inflicted upon Aboriginal people. Before the circus of armies, institutes, researchers and bureaucrats rolled into town, not one person cared to take the time to look and see what was already there. Yarning up — hearing hopeOur Aboriginal culture is steeped in oral tradition. Consequently, the act of yarning and storytelling is one of utmost importance. As a child, and the youngest of four, the rules of narrating and witnessing stories were impressed upon me from early on. My father always would remind me as a child to “know my place” and the importance of being quiet and listening. Working within a community, the task of respecting the knowledge and wisdom of those who have gone before you is another fundamental. In developing this intervention, the obvious next step was to listen and learn from our community. White fellas call this consultation — we call it yarning. There are several important points to this yarning process that are integral to its effectiveness in informing community practice within an Indigenous context. Firstly, we yarned with people about what they thought was necessary to make their community better. The question wasn’t “what is wrong with your family and community?” Instead we asked, “how can the community better support you and your family?” This is important, because our communities have become so accustomed to recounting stories of dysfunction and horror, it can be far too easy to be drawn back to community weakness and need. The yarning process must be empowering. When we talked to people, we spoke with both big fellas and little fellas because Eldership and leadership are not determined solely by the number of breaths one has taken. We went to our mob — we didn’t expect them to come to us. We went to sporting festivals and community gatherings, and engaged in conversations wherever they could be had. As a result, we yarned with over 100 people. The development of this intervention grew out of the dialogue between the service sector and the community in question, and not external spectators, voyeurs, commentators and public opinion. It seems glaringly obvious that community ownership and control is the perfect antidote to passivity and dependency, but such ownership can only be facilitated by engaging our mob in the yarning process from the very beginning. Creating new dreaming storiesThese processes must culminate in a “joining of the dots”, so to speak. Through mapping the landscape and collecting knowledge stories, a new dreaming can be found. For our intervention, this meaning-making occurred through a collaborative process between our community workers and organisations. What emerged through the efforts of the Indigenous Early Years Partnership Group was a 12-month plan of possibility and opportunity. It was precisely because the initiatives stemmed from community strengths, knowledge and desires that very little investment was required to engage Indigenous parents in the activities and opportunities created. Not one person had to be transported to an activity or initiative; food and gifts were not brandished in the faces of parents to entice their interest; and, most importantly, no one’s welfare payments were threatened in order to enlist collaboration or compliance. We shifted ideologically in our thinking of our community, from negative assumptions to endless opportunities. We refrained from drawing assumptions around notions of “good” and “bad” communities or families — we simply started from strengths. We did not assume that nothing was being done in our community — we simply asked “what can we do better?” Through this process, we uncovered endless examples of Indigenous workers, organisations, parents and children embracing opportunities to grow stronger. Unless and until current Indigenous social policy and interventions are premised upon the possibility that Indigenous parents, families and communities possess strength and capabilities, there will never be the opportunity for our children, families, community and culture to grow stronger. Indigenous Early Years Intervention — highlights Consultations undertaken with over 100 local Indigenous community members. More than 10 local community organisations and government agencies involved in steering the initiative via the Indigenous Early Years Partnership Group (met bimonthly). The development of an Indigenous child health promotion resource, in partnership with eight local agencies and 90 community members and children, with a distribution of 16 000 units within our community and across the state. The establishment of an Indigenous playgroup in partnership with six local agencies, attracting over 133 children, 75 parents and carers, and 56 volunteers within a 7-month period. The delivery of Let’s Read resources to more than 70 Indigenous children and their families. Support provided to four local Indigenous community festivals to become more child-friendly (involving reviewing site layout, provision of infrastructure and activities for children under 5 years of age). Engaged over 80 volunteers. Supported 50 people to participate in early years training opportunities within our community. Supported over 20 organisations and initiatives with resource support (eg, grant-writing support, health resources and information, health promotion stalls and activities, committee membership, in-service training to early years sector).

Chelsea Bond PhD

Extracorporeal membrane oxygenation (ECMO) is a technique that involves oxygenation of blood outside the body, and provides support to selected patients with severe respiratory or cardiac failure. The two major ECMO modalities are venoarterial and venovenous. Data from several randomised trials support the use of ECMO in neonatal respiratory failure, and a recent randomised controlled trial of ECMO in adults has produced encouraging results. The evidence base for ECMO use in cardiac disease is developing, but progress has been slowed by considerations of clinical equipoise and evolving indications for ECMO. Advancing ECMO technology and increasing experience with ECMO techniques have improved patient outcomes, reduced complications and expanded the potential applications of ECMO. Awareness of the indications and implications of ECMO among doctors managing patients with severe but potentially reversible respiratory or cardiac failure may help facilitate better communication between health care teams and improve patient recovery.

Steven J Lindstrom MB BS(Hons), BMedSc(Hons) · Vincent A Pellegrino MB BS, FRACP, FJFICM · W Warwick Butt MB BS, FRACP, FJFICM

Objective: To describe demographic, geographical and clinical features of envenoming by the rough-scaled snake (RSS) (Tropidechis carinatus).Design, setting and participants: Prospective cohort study of RSS snakebite victims, recruited between January 2004 and December 2008, as part of the Australian Snakebite Project. RSS envenoming cases were confirmed by snake identification and/or venom-specific enzyme immunoassay.Main outcome measures: Clinical and laboratory features of envenoming.Results: There were 24 confirmed cases of RSS envenoming, nearly all occurring in coastal areas between northern New South Wales and south-eastern Queensland. Twenty-three patients had local bite-site effects and 17 had at least three non-specific systemic effects (eg, nausea, headache). All 24 had venom-induced consumption coagulopathy (VICC), and 19 had an international normalised ratio > 3.0. Six had bleeding from the bite site or intravenous cannula site, 10 had blood detected on urinalysis, and one had a major intra-abdominal haemorrhage. Mild neurotoxicity developed in two patients, and one patient developed myotoxicity with generalised myalgia, myoglobinuria and a peak creatine kinase level of 59 700 IU/L. Twenty-three patients were treated with antivenom (21 with tiger snake antivenom, two with polyvalent antivenom). Free venom was undetectable in 19 of 20 blood samples taken after antivenom administration.Conclusion: RSS envenoming occurs predominantly in coastal areas of northern NSW and southern Queensland, and within this range, most envenoming is due to the RSS rather than tiger snakes. Clinically it is characterised by VICC, with mild neurotoxicity and myotoxicity in some cases. Tiger snake antivenom appears to be effective against RSS envenoming.

Melissa Gan MB BS · Margaret A O’Leary PhD · Simon G A Brown MB BS, FACEM, PhD · Tamara Jacoby BSc · David Spain MB BS, FACEM · Alan Tankel FACEM · Chris Gavaghan MB BS, FACEM · Peter Garrett MB BS, FACEM · Geoffrey K Isbister BSc, FACEM, MD

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: Over a third of women seeking a termination of pregnancy (TOP) in Melbourne are aged 30 years or over.1 Between 1996 and 2006, there was a 29% increase in the number of women aged 30–50 years having a TOP.2 Possible reasons for this trend are not immediately apparent. We audited the files of 50 consecutive women aged 35 years and over attending a private termination service in metropolitan Melbourne in February 2007 to determine reasons for deciding on a TOP and the women’s prior and intended contraceptive use. Of the 50 women, 38 were working in paid employment, 28 had private health insurance, 39 had at least one child, 22 had had at least one previous TOP, and 43 were in an ongoing relationship. Sixteen separate reasons for TOP were elicited (Box), with nearly three-quarters of the women citing more than three reasons for terminating their pregnancy. Over a third of the women cited financial pressures, a focus on career or studies, having dependent children, or emotional unpreparedness for children as reasons for having a TOP. Contraceptive methods used by the 29 women who indicated their prior contraceptive practice were as follows: none (9), condoms (8), natural family planning (NFP) (4), the combined oral contraceptive pill (COCP) (4), withdrawal (3), and the mini pill (1). After the TOP, contraceptive methods chosen were the COCP (11), vasectomy (10), an intrauterine device (10), condoms (8), the mini pill (5), an etonogestrel implant (4) and NFP (1). Although ours was a small retrospective audit, the contraceptive findings and reasons given for TOP in our study were similar to those of other studies.1-4 However, some of the reasons given for TOP in this age group have not previously been described — for example, having ageing parents to care for, recent migration to Australia, and ambivalence towards parenting. Furthermore, although recent Australian studies have reported a high level of contraceptive use,2,5 women in our study often relied on less effective forms of contraception or no contraception at all. Further qualitative research is needed in women of this age group to explore their understanding of fertility and pregnancy risk, barriers to effective contraceptive use, and additional supports and interventions that could prevent unplanned pregnancy in these women. Reasons for termination of pregnancy among 50 women aged ≥ 35 years Reason Number citing reason Already have dependent children 17 Focus on career or studies 17 Emotionally unprepared for a child 16 Financial pressures 16 Completed family 15 Relationship factors 14 Too old to raise a child 10 Partner factors, including partner not wanting children 9 Physical or psychological health issues 8 Concerns about congenital anomalies 7 Does not want single parenthood 6 Bad timing (recent job change, move home, move to Australia) 4 Uncertain of wanting children or does not want children 4 Exposure to medications or agents that might harm fetus 1 Pregnancy from sexual assault 1 Other factors (other life plans, uncertain paternity, poor social supports, aged dependent parents) 9

Wendy Lee · Danielle Mazza

To the Editor: We agree with Stockigt that clinical accountability is needed in the production of consumer medicines information (CMI).1 However, providing CMI is a great deal more complex. The ways in which consumers access and absorb medical information are still largely unknown, and the most important issue is potentially that consumers are not receiving CMI. The benefits of involving consumers in shaping health research and medical policy are widely acknowledged.2,3 We recently completed a study funded by the National Health and Medical Research Council (NHMRC) on improving medication safety and chronic disease outcomes in people aged over 65 years, which was accepted for presentation at the national General Practice and Primary Health Care Research Conference in Melbourne, July 2009. Three community forums co-facilitated by the Health Consumers’ Council of Western Australia raised key issues around the safe use of medicines, and an expert panel of consumers aged over 65 years was convened to guide the study. The safe use of medicines was then qualitatively explored in a series of focus groups and individual interviews. Our findings add to those of Vitry and colleagues,4 and suggest that campaigns urging consumers to request CMI may fall short of what is required to make a difference. We found that most study participants did not know they could ask for a CMI printout at the pharmacy. They noted that if the pharmacist was busy, they would not ask for advice or CMI, even if they were uncertain of dosages or potential side effects or interactions. Given that medication side effects and interactions were the greatest concerns for this age group, it is troubling that CMI is not getting to those who need it. In addition, it was noted that participants were not selective in accessing alternative web-based information about medicines, believing it to be reliable because it is “written by medical professionals”. A further issue raised by participants was a perception of undue influence of pharmaceutical companies on the prescribing choices of general practitioners, leading to mistrust of medicines information provided by doctors. Clearly, there is still more to be done to ensure consumers receive the right information at the right time about their medicines.

Caroline E Bulsara · Anne McKenzie

To the Editor: We share Millar’s concerns about the conflicts of interest that influence the genesis and adoption of clinical guidelines1 specifically, and the lack of independent assessment regarding information provided by the pharmaceutical industry generally. Iain Chalmers puts it succinctly: I do not blame industry for trying to get away with anything that is normally considered to be its primary purpose, which is to make profits and look after its shareholders’ interests. It is our profession that has colluded in all of this and been prepared to go along with it — we are the people to blame because we need not have stood for it.2 We believe the reasons behind this acquiescence are complex, but worthy of discussion. A strong and viable pharmaceutical industry is essential for clinical improvement. Similarly, clinical involvement in industry research is necessary. We would not debate either of these statements, but we are concerned about the failure of our profession to stand back and exercise careful scrutiny of data. Classic examples are thalidomide in the 1960s and, more recently, the cyclooxygenase-2 (COX-2) inhibitors, but many less dramatic examples can be found, such as gatifloxacin or rosiglitazone. This failure on our part harms both patients and the standing of our profession. A recent article in this Journal suggested this failure of physician leadership may in part be due to the comfortable position we cultivate with industry,3 relationships that go beyond the business transaction of providing independent medical advice for a consulting fee. Further, the role of “key opinion leaders”, cultivated by industry, is reinforced by criteria for hospital accreditation and university promotion, leading to disproportionate value being placed on service to company boards (which is often paid and of modest time commitment) compared with service on hospital, state and national regulatory and quality committees (which is usually time-consuming and unpaid). The presupposition in this discrepancy is that physicians on the company circuit are better physicians than those who are not. We should all support the recommendations of Millar,1 Olver and Haines,3 and Van Der Weyden,4 including those for true independence and transparency of guideline development and dissemination, strengthening ethical administrative structures and placing appropriate value on public service. Upskilling of clinicians in epidemiology and critical analysis is thus urgently needed so the incremental benefit and costs of new therapies can be objectively examined.

Jennifer H Martin · Christopher Beer · Raymond G Morris · Matthew P Doogue

To the Editor: Articles by Olver and Haines1,2 have catalysed robust discussion about the relationship between the pharmaceutical and device industries and the medical profession.3 These authors advocate changes in the direction of clinical cancer research and in health policy.2 In an era in which research into medicines is dominated by industry, they argue for greater scrutiny of data in a resource-constrained environment, and for fundamental changes in the collection, interpretation and ownership of data. We find their arguments sound and equally applicable to other areas of medicines research and health policy. Their primary recommendation is for “. . . a system to follow up and evaluate the outcomes of all treatments . . .” That is, that we exercise our duty to patients by monitoring and analysing existing clinical data to inform health care policy. There is a great deal of valuable clinical data collected that are not readily accessible because of ownership or privacy issues. For example, much business involving public health dollars is labelled “commercial in confidence”, and laboratory data held in many pathology databases are not accessible at all. The likely benefits to patients and society of transparency and data linkage in health care are greater than possible benefits to individuals of secrecy and privacy. Quality use of medicines (QUM) is one of the central objectives of Australia’s national medicines policy. QUM means selecting management options wisely; choosing suitable medicines if a medicine is considered necessary; and using medicines safely and effectively.4 Olver and Haines also identify issues relating to quality use of research. Quality use of research might include: supporting research into monitoring clinical outcomes related to drug use; supporting research into better use of existing drugs; and supporting truly independent guideline development. There continue to be advances. For example, registration of trials in public databases, such as the Australian New Zealand Clinical Trials Registry, should reduce publication bias.5 However, the decline of independent public sector clinical drug research and the marketing-based design of phase III and, increasingly, phase II industry-funded studies contribute additional bias to the available information. Olver and Haines’ arguments apply to all therapeutics, and particularly to all drug therapies. We strongly support their proposals for health data linkage and for quality use of research. These fit within existing health policy, and our continued failure to make full use of clinical data is an ethically compelling reason for improved political and clinical governance.

Matthew P Doogue · Kathleen M Knights

To the Editor: The expert working party that developed the Australian Medical Council (AMC) draft code of professional conduct referred to by Komesaroff and Kerridge1 was chaired by Joanna Flynn, past President of the Victorian Medical Practitioners Board (MPB [Vic]). Herein lies the crunch. The AMC is surely meant to be an independent and objective body — yet if it is aligned with the MPB (Vic), how can this be the case? Komesaroff and Kerridge state that the appendices to the AMC’s draft code “quote extensively (without attribution) the conclusions of guidelines developed by the Royal Australasian College of Physicians” and that “in the AMC’s version, the evidence, context and argumentation are omitted and the recommendations are presented as legally binding”.1 If this is the case, there is cause to question the integrity of the drafters of the code, to fear the code’s implications, and to request “that the whole process that gave rise to it be rigorously reconsidered”.1 Plagiarism cannot be condoned. To attribute honestly and give credit where credit is due is central to ethical practice, scientific discovery, education, accountability and learning. Similarly, context matters. In my opinion, integrity, the basis of ethics and morality, is measured by the extent to which context is valued and conceded. Ethical conduct demands both honesty and integrity. Doctors and the public, and government surely, place their trust in the AMC to objectively evaluate governing practices, laws and regulations, such as the Health Professions Registration Act 2005 (Vic) (“the HPR Act”), under which the MPB (Vic) operates, as well as professional conduct. Yet the authors of the AMC draft code fail to address the issue of the accountability of regulatory bodies and the fact that the HPR Act contains no benchmark for excellence: because context is omitted from the Act, “unprofessional conduct” cannot be defined and becomes relative. This leaves it open for any third party, including members of the regulatory authority itself, to abuse doctors and patients by being dismissive of the patient’s view (and thus, context), while claiming to protect patients and guide doctors. By contrast, the Medical Treatment Act 1988 (Vic), which is not mentioned in the AMC draft code, provides a benchmark for excellence in clinical practice with reference to both doctors and patients. This Act specifies (a) that the wishes of the patient to refuse treatment be respected, and (b) that medical practitioners who act in good faith in accordance with the patient’s expressed wishes be protected from any civil or criminal liability or disciplinary action by the regulatory board.2 As doctors, we are the naturally appointed advocates of our patients’ health preferences and wellbeing. Ensuring that choices are made for the patient’s benefit requires honesty and integrity at all levels of government.1,3,4 When a failure occurs in the system, it is imperative to have avenues of awareness, transparency, protection and evaluation available through public action and professional debate.1,3,5

John B Myers

In reply: The debate about the proposed national code of conduct (“the Code”) has raised a number of important issues, including those highlighted by Myers. The original draft aroused serious concern in the community about the potential role of a centralised bureaucracy with the power to enforce a set of precepts derived from a narrow, largely discredited, philosophical perspective. Although the revised draft now circulated for public comment is admittedly less objectionable than its predecessor, significant concerns remain relating to both its form and its content. The main issues are still the purpose and role of the Code and the confusion between ethical and legal discourses on which it is based. In a multicultural society in which pluralism and diversity are themselves regarded as inherently valuable, the very concept of a unitary set of criteria that define good practice is questionable. In this setting, the proper roles of codes of conduct and of ethics are not to enforce particular kinds of outcomes, but rather to inform and enrich practice. If the Code were devised as an educational process to stimulate clinicians to reflect critically on their existing practices and underlying values, it would be much more likely to change behaviour and increase community wellbeing.

Paul A Komesaroff · Ian H Kerridge

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

To the Editor: On my way to Canberra for the Charles Darwin exhibition at the National Museum of Australia, I diverted to Pambula, on the far south coast of New South Wales, for two reasons. Pambula is part of the Australian connection with Darwin through Syms Covington, who, at the age of 15, sailed as a cabin boy on the Beagle in 1831. Darwin soon came to rely on Covington to collect specimens, excavate fossils and act as his personal assistant. During the Beagle’s brief visit to Sydney, Covington was impressed by the colony. In 1840, after a period of employment with Darwin in England, he returned to Australia and eventually became a wealthy man. At first he lived in Sydney, but by 1854 had moved to Pambula, where he became postmaster. His entrepreneurial activities included buying large tracts of land around the Pambula River and the little township of Pambula. On a large block, he built a house of solid sandstone bricks with cedar woodwork throughout — “Covington’s Retreat”. Covington continued to correspond with Darwin and, at the latter’s request, collected specimens for him. He died in 1861. The house, at 28 Quondola Street, still stands and has been listed by the National Trust of Australia (NSW) in Heritage Council File HC32549. After being used for various purposes, including as an inn and as a police station, it became the residence of the local doctor, probably around the start of the 20th century — hence my second reason for visiting Pambula. The subsequent careers of some of the Pambula general practitioners, all of whom lived in the house, are of considerable interest. All came to Pambula from outside the area. Grace Cuthbert (later Cuthbert Browne), MBE, left Pambula in 1929. She was Director of the Division of Maternal and Baby Welfare of the NSW Department of Public Health (1937–1965) and, among many other positions, President of the Australian Federation of Medical Women. Naomi Wing, CBE, and her husband Lindon practised in Pambula from 1929 to 1936. She was an early advocate of rehabilitation medicine as a medical discipline and became President of the Australian Association of Physical and Rehabilitation Medicine. The Naomi Wing Rehabilitation Centre in Zetland, Sydney, was named in her honour. Her husband, Lindon Worlledge Wing, KStJ, was an early practitioner of occupational medicine in Sydney. Their son, Emeritus Professor Lindon Michael Harper Wing, was Dean of the Medical School at Flinders University, Adelaide, from 1998 to 2007. From 1936 to 1945, the house was owned by Keith Jones, who went to World War II from Pambula and whose name is on the town’s war memorial. After the war, he became a surgeon and, over the years, undertook a wide range of community activities. He was President of the Australian Medical Association (1973–1976), Chairman of the Australasian Medical Publishing Company Limited (1976–1982) and, for a time, Acting Editor of the Medical Journal of Australia. He was knighted in 1980. Covington’s Retreat is now a Thai restaurant called “Covingtons Thai”.

George D Repin

The opening session of the Australian Medical Association’s national conference this year was once again the venue for the presentation of the Medical Journal of Australia’s two annual awards, the MJA/Wyeth Prize and the Dr Ross Ingram Memorial Essay Prize. In an MJA “first”, the 2008 MJA/Wyeth Award was presented to a familiar face. Dr Lindsay Grayson and colleagues won the 2005 MJA/Wyeth Award for their report of a multifaceted hand hygiene program at Austin Health in Melbourne, which increased hand hygiene compliance by hospital staff and reduced the rates of methicillin-resistant Staphylococcus aureus infection. Following their initial success, they were able to expand the program to several other Victorian hospitals and eventually to roll it out statewide. They described and evaluated this process in a report entitled “Significant reductions in methicillin-resistant Staphylococcus aureus bacteraemia and clinical isolates associated with a multisite, hand hygiene culture-change program and subsequent successful statewide roll-out” (published in the 2 June 2008 issue), which was assessed by the Journal’s Content Review Committee as being the year’s best research report. In presenting the $10 000 prize, Dr Michael Lee, Medical Director of Wyeth Australia, reaffirmed his company’s commitment to preventive care, and congratulated the authors for their ability to build on their earlier findings to promulgate a widely beneficial intervention. Improving the health of Aboriginal people in prison was the subject of the winning essay in this year’s Dr Ross Ingram Memorial Essay Competition and, indeed, is its recipient’s life work. Beverley Spiers, a Justice Health Aboriginal health worker and education officer based at Cessnock Correctional Centre in New South Wales, has worked in the criminal justice system for over 20 years and believes that all Aboriginal offenders should be encouraged into the caring hands of Aboriginal health workers. Her prize-winning essay, “Antecedents of chronic kidney disease in Aboriginal offenders in New South Wales prisons” (published in the 18 May 2009 issue), describes a single day at the Centre, in which she and a Justice Health nurse screened 88 Aboriginal offenders for markers of kidney disease. In accepting her $5000 prize, donated by the Australasian Medical Publishing Company, Beverley reminded the conference about the real human stories behind the gap in life expectancy between Indigenous and non-Indigenous Australians, and called for more funding for Aboriginal health workers in all areas where Indigenous Australians require access to medical care. From left: Rosanna Capolingua, Ruth Armstrong, Beverley Spiers, Martin Van Der Weyden, Lindsay Grayson, Michael Lee. Dr Ruth Armstrong, MJA

Ruth Armstrong

Tom Wills. His spectacular rise and tragic fall. Greg de Moore. Sydney: Allen & Unwin, 2008 (xvi + 336 pp). ISBN 978 1 74175 499 5. Greg de Moore, a Sydney psychiatrist, has undertaken an amazing amount of research in compiling this account of the interesting life of one of Victoria’s sporting identities of the 19th century. Born on a sheep run on the Molonglo River in 1835, Tom Wills was sent in 1850 to England for education at Rugby, where he was no great scholar but excelled in cricket, football, athletics and other sporting activities. On returning to the colony, Wills soon established himself as the best batsman and bowler in the colony of Victoria and achieved celebrity status. He was later described by the English doyen of cricket, Dr W G Grace, as “the greatest cricketer in the land”. At that time, cricketers were given such prominence that the sitting times of Parliament were adjusted to facilitate members watching the match. Employers were expected to release workers for the same reason. Football was a winter game played after the cricket season was completed and was virtually a free-for-all without rules. In a hotel on 17 May 1859, Wills and three others wrote the first rules of the Australian Football Code (a copy of the original hand-written document is reproduced in the book). Wills’ family, and later Wills himself, moved to a cattle station in Queensland. His father was later killed there by Aboriginal people. To the surprise of many, years on, Wills coached the well known all-Aboriginal cricket team. Unfortunately, Wills was a heavy drinker, and ultimately suicided.1 De Moore has located original records held by numerous organisations, including Rugby school. In addition to the details of Wills’ life, he gives an interesting insight into Victorian society as it was in Australia. His book is well priced and worthwhile reading for anyone interested in sport or sporting history. 1 de Moore GM. The suicide of Thomas Wentworth Wills. Med J Aust 1999; 171: 656-658.

Michael C Kennedy

Incorrect author affiliation: In the letter “Avoiding the tragedy of another balcony collapse” in the 1 June 2009 issue of the Journal (Med J Aust 2009; 190: 651-652), James W Nixon was incorrectly described as a paediatrician at the Royal Children’s Hospital, Brisbane. James W Nixon is Chair of Kidsafe Queensland, Brisbane, QLD. The html and pdf versions of the article published online were corrected on 5 June 2009.

Shinichiro Sakata · Craig A McBride · James W Nixon · Roy M Kimble

Pump up the volume Technological improvements in MP3 music player technology may make for a better listening experience, but they are also likely to lead to greater hearing loss in teenagers. Better sound quality without distortion at higher volumes, minimal sound leakage from better earphones, and the increased volume delivered by earbud-style earphones all contribute, along with newer music recordings being made with much stronger compression (which makes the average sound level closer to the maximal output level). A study of 1687 Dutch secondary school students showed that 90% used MP3 players with earphones to listen to music, 33% used them for more than an hour every day and 48% used high-volume settings. Frequent users were more likely to listen at higher volumes, and overall, teenagers were unlikely to engage in any protective actions such as taking breaks, reducing the volume, using noise limiters or heeding warnings about potential hearing loss. Pediatrics 2009; 123: e953-e958 Wedded bliss beats brain decline Although some long-term partners may beg to differ, being married in mid life appears to protect people from developing cognitive impairment, say Swedish and Finnish researchers. The population-based study examined 2000 participants for cognitive impairment and other signs of dementia in mid life (mean age of 50.4 years) and again around 21 years later. People who lived with a partner in mid life were less likely, when compared with single, separated or widowed participants, to show cognitive impairment later in life. People who were widowed or divorced in mid life and still in the same situation at follow-up had three times the risk for Alzheimer’s disease. Those who were widowed or divorced in mid life and at follow-up and who carried the apolipoprotein E e4 allele, a genetic marker for Alzheimer’s disease, showed the highest incidence. BMJ 2009; 339: b2462 Salt stumps diabetes drugs Australian researchers have come closer to solving the puzzle of why anti-diabetes drugs are successful in some patients and not others. The answer appears to lie in the effect of high salt intake on people with type 2 diabetes. The drug telmisartan acts by protecting the kidneys from excessive protein loss. In a randomised controlled trial, the effects of sodium chloride (NaCl) supplementation on the antialbuminuric action of telmisartan ± hydrochlorothiazide were studied. Patients in the trial had type 2 diabetes and were hypertensive at baseline. A significant decrease (75%) in the antialbuminuric effect of the drugs was seen in patients who had a habitually low dietary salt intake and who were given high doses of NaCl by supplementation during the trial. The authors comment that the high levels of dietary sodium consumption in industrialised countries are a potential target of public health campaigns that could maximise the effects of anti-diabetes therapy. Diabetes Care 2009; 23 Jun [Epub ahead of print] HPV vaccine The vaccine against human papillomavirus (HPV-16/18 AS04-adjuvanted vaccine) shows high efficacy against cervical intraepithelial neoplasia 2+ associated with HPV types 16/18, according to the results of a multinational trial involving over 18 000 women aged between 15 and 25 years. Participants, who were seronegative at baseline, were followed up for a mean of 34.9 months after the third dose of vaccine. Cross-protection against non-vaccine oncogenic HPV types was also noted, giving coverage against the five types of HPV that are responsible for over 80% of all cervical cancers. The authors comment that the results are encouraging, and that the vaccination has been shown to potentially reduce the incidence of cervical pre-cancer and cancer in the target population. Lancet 2009; 7 Jul [Epub ahead of print]

Tanya Grassi