Volume 185 Issue 3

Clinically useful CAP management guidelines are still elusive Community-acquired pneumonia (CAP) continues to generate controversy. Although CAP is common and generally mild, it can be life-threatening. For the treating clinician there are many questions. How much effort should be directed to establishing the aetiology, given that the responsible pathogen is infrequently diagnosed? Should the patient be managed in hospital or at home? Should one choose older, established antibiotics that work most of the time or broad-spectrum therapy that treats all imaginable pathogens but is probably unnecessary, has a less established safety record and is likely to contribute to increased cost of treatment and the emergence of resistance? To help clinicians with these questions, international guidelines for managing CAP have been published.1-5 However, their clinical usefulness in the Australian health care context is questionable, as they are not based on particularly robust evidence and there is marked disagreement between Europeans and North Americans on the correct approach. The North Americans recommend that extensive investigations should be avoided, many patients should be treated at home, and broad-spectrum antibiotics should be used.1-3 The British and European guidelines are less focused on treating patients at home, suggest the use of cheaper, narrow-spectrum agents, and do not recommend dual therapy to treat both “typical” (eg, pneumococcus) and “atypical” (eg, Mycoplasma, Chlamydophila or Legionella) pathogens, except in patients with more severe illness.4,5 In comparison, the Australian antibiotic guidelines6 steer a middle course, suggesting the use of the Pneumonia Severity Index (PSI)7 to guide the decision regarding the need for hospital admission but then also using the PSI as a tool to assist with empirical antibiotic selection. This latter feature is somewhat unique and is based on local (as yet, unpublished) data. Some authors have suggested that investigations for CAP aetiology are not cost-effective.8 However, these opinions are often based on studies in which sputum samples were of poor quality or were collected after antibiotics were commenced. In most cases, such investigations won’t affect choice of therapy if the doctor treats for both “typical” and “atypical” agents. However, not performing these tests will mean missing the occasional unusual cause of CAP (such as Staphylococcus aureus, Legionella, community-acquired methicillin-resistant S. aureus and gram-negative organisms such as Pseudomonas). Furthermore, for hospitalised patients, the cost of these investigations is minimal compared with the cost of inpatient stay. Neglecting these investigations could lead to inappropriate management of patients who are initially thought to have CAP but who turn out to have an illness such as urinary sepsis or endocarditis. For patients who are sufficiently ill to require admission to hospital, we recommend that at least blood cultures and sputum Gram stain and cultures be performed. Apart from clinical acumen, what other tools can be used to assess the severity of CAP in an individual patient and hence guide the decision on site of care? The two most commonly used CAP severity scoring systems are the PSI7 and CURB-65 (Confusion, elevated Urea, elevated Respiratory rate, low Blood pressure and age at least 65).9 The key purpose of the PSI is to identify CAP patients who could be safely managed at home. However, it is reasonably complex, requiring input of 20 features of patient demographics, premorbid illnesses, initial vital signs and investigation results to calculate the PSI score. In addition, the PSI gives high weighting to patient age and past history but lower weighting to potentially important clinical features such as hypoxia. Thus, young, previously well patients can be classed as having mild CAP (PSI classes I–III), despite being hypoxic and having clinically severe disease. Despite these criticisms, the PSI has been validated on over 40 000 patients and appears to be accurate for predicting 30-day mortality both in the United States and Australia.7,10 For this reason it has been recommended in the current Australian antibiotic guidelines, but its uptake by Australian doctors has been limited.11 CURB-65 has the advantage of being simpler and more focused on the severity of the episode of CAP rather than the patient’s past history. However, a disadvantage is that it appears less useful for determining who is safe to be treated at home.12,13 Neither the PSI nor CURB-65 appears particularly useful for predicting accurately whether an individual patient will require admission to an intensive care unit.14 A recent Australian study suggested a modified version of CURB-65 as being more accurate for this purpose, but this is yet to be validated.15 Given these limitations, clinicians should be mindful that features such as hypoxia, vomiting, poor social circumstances, unstable comorbid conditions and empyema often indicate the need for hospital admission regardless of the PSI or CURB-65 score. Australian recommendations for empirical therapy are much closer to those of the UK and European guidelines than the North American guidelines, promoting the use of cheaper, narrow-spectrum agents such as penicillin and doxycycline.6 It is notable that penicillin is not mentioned at all in the North American guidelines.1-3 The Australian guidelines are supported by the fact that, even in an era in which penicillin resistance appears to be increasing among some Streptococcus pneumoniae isolates, there have been no documented failures of high-dose penicillin in treating pneumococcal pneumonia or bacteraemia. In comparison, there are documented cases of treatment failure with fluoroquinolones, and the widespread use of these agents has been clearly associated with increased levels of resistance to quinolones in S. pneumoniae and other previously susceptible bacteria.16 Given the importance of these issues, a large Australian, multi-state study of CAP is currently under way, with results to be made available in the next 12 months, to better guide clinicians. In the meantime, clinicians may find our general approach to patients with CAP useful (Box). Approach to managing the patient with community-acquired pneumonia (CAP) confirmed by chest x-ray PSI = Pneumonia Severity Index. * Abnormal vital signs are respiratory rate ≥ 30 breaths/minute, heart rate ≥ 125 beats/minute, systolic blood pressure < 90 mmHg. Young patients are less likely to be tachypnoeic. † Hypoxia is defined as partial pressure of oxygen (Pao2) < 60 mmHg or oxygen saturation measured by pulse oximetry (Spo2) ≤ 90% (in patients aged ≤ 40 years, use Pao2 < 70 mmHg or Spo2 ≤ 93%). ‡ Approximate costs: sputum testing, $34; blood culture, $31; Legionella urinary antigen testing, $29.

Patrick G P Charles MB BS, FRACP · Paul D R Johnson MB BS, FRACP, PhD · M Lindsay Grayson FRACP, MD, FAFPHM

We need to know if and when this organism arrives in Australia There is world-wide concern about a new infectious diseases threat following the recent emergence, in Canada,1 the United States,2 and now Europe,3 of a highly virulent strain of Clostridium difficile (called PCR ribotype 027 in Europe and NAP1 in the US). Rates of detection of C. difficile have risen dramatically: at the Centre Hospitalier Universitaire de Sherbrooke in Quebec Province (population, 7.5 million in 2003) in Canada, the incidence among patients aged ≥ 65 years increased from 102 per 100 000 population in 1991 to 867 per 100 000 in 2003.4 C. difficile disease has been more severe, with the proportion of complicated cases in Sherbrooke increasing from 7.1% (12/169) in 1991–92 to 18.2% (71/390) in 2003,4 suggesting a more virulent strain of the organism is emerging. The Quebec Health Ministry reported a total of 7004 cases of C. difficile infection between 1 April 2003 and 31 March 2004, with 1270 deaths (a crude mortality rate of 18%).5 Loo and colleagues1 reported an attributable mortality of greater than 10% in those aged over 60 years — a remarkably high figure. C. difficile is the most commonly diagnosed cause of infectious hospital-acquired diarrhoea in developed countries. Most patients with C. difficile-associated diarrhoea have been exposed to antimicrobials that reduce “colonisation resistance” of the large intestine, allowing subsequent infection with C. difficile. Acquisition of C. difficile is facilitated by its ability to form spores that are resistant to many disinfectants, so that it remains viable in the hospital environment for long periods of time. Toxigenic isolates of C. difficile usually produce two toxins, toxin A (tcdA, an enterotoxin) and toxin B (tcdB, a cytotoxin), which are considered the major virulence factors.6 Some strains of C. difficile produce an additional toxin called binary toxin (CDT). This was first reported in 1988 but not considered important until now.1,2,7 Binary toxin producers make up the majority of the C. difficile strains isolated in the recent large outbreaks of the disease overseas.1,2 A correlation between binary toxin production and severity of diarrhoea has been demonstrated,7 and more community-acquired C. difficile-associated diarrhoea was found to be caused by binary toxin producers. To determine the effects of binary toxin alone, researchers have characterised C. difficile strains that only produce binary toxin (ie, tcdA– tcdB– CDT+ strains). Although supernatants from tcdA– tcdB– CDT+ strains of C. difficile caused fluid accumulation in a rabbit ileal loop after concentration and trypsinisation, challenge of clindamycin-treated hamsters with these strains resulted in colonisation but not diarrhoea or death, suggesting that binary toxin by itself may not cause disease.8 The significance of binary toxin clearly needs further investigation. A second important feature of this “new” organism is that it produces more toxin A and B than other strains. Production of these toxins in C. difficile is encoded by the tcdA and tcdB genes, respectively. These two genes form part of a highly stable pathogenicity locus (PaLoc), a region of the chromosome that also includes the genes tcdC, tcdR and tcdE. Toxin A variant strains fail to produce toxin A detectable by enzyme immunoassay because of a deletion in the tcdA gene. The tcdC gene is a down-regulator of toxin A and B production. The PCR ribotype 027/NAP1 strain has a deletion in the tcdC gene resulting in it no longer down-regulating, and strains produce toxin throughout the log phase of growth instead of just in the stationary phase.9 Non-toxigenic strains lack the PaLoc. The third important feature of these strains is that they are resistant to fluoroquinolone antibiotics, and excessive fluoroquinolone use appears to be a contributing factor in the recent outbreaks.10 C. difficile develops resistance to quinolones soon after exposure.11 Both the newer fluoroquinolones, such as gatifloxacin and levofloxacin, and, somewhat surprisingly, the older one, ciprofloxacin, have been implicated.10 Ciprofloxacin has always been thought of as a low-risk antimicrobial for inciting C. difficile-associated diarrhoea.12 However, once C. difficile becomes resistant to the later fluoroquinolones, it is also resistant to ciprofloxacin, and the resistance trait may become more important for initiation of disease. Another significant finding from the outbreaks reported overseas is the marked variation in C. difficile-associated diarrhoea rates among different age groups. While older people have always been at increased risk, due primarily to decreased host defences, rates in those ≥ 65 years of age have increased dramatically since 2000.13 One possible novel risk factor is exposure to gastric acid suppressants, such as histamine-2 receptor inhibitors or proton pump inhibitors. These agents have been more commonly prescribed in recent years and may be linked with the increased rates of C. difficile-associated diarrhoea in the community,14 although some case–control studies with hospital patients show no association.1,10 The importance of community onset C. difficile-associated diarrhoea was highlighted recently by a report of severe cases in previously healthy people and peripartum women.15 Is this organism in Australia yet? We do not really know because molecular typing is required to distinguish the outbreak strain from others, and this is rarely done. However, it is probably not here — there have been no reports of more severe C. difficile disease, and Australia uses less of the most incriminated fluoroquinolones than other parts of the world. A major problem is that many laboratories in Australia have moved away from culturing for C. difficile, and to save money and time are using enzyme immunoassay kits. C. difficile toxin A enzyme immunoassay kits will not detect strains that don’t produce toxin A, and toxin A + B kits will not detect binary toxin producers. This diagnostic problem is compounded by the fact that laboratories servicing general practitioners often do not examine faecal samples for C. difficile because of the continuing misconception that C. difficile-associated diarrhoea is a hospital problem only. Given the high mortality rate in recent C. difficile-associated diarrhoea cases overseas, it is important that we know if and when this organism arrives in Australia. How could this be achieved? Should C. difficile-associated diarrhoea become a notifiable disease in Australia, as happened in Canada in response to the outbreak there? This is unlikely to be particularly helpful without molecular typing to distinguish the outbreak strain. Targeted surveillance, with one or two laboratories being funded periodically to type a representative sample of isolates of C. difficile from a variety of Australian hospitals, would seem a more reasonable approach. Finally, the value of sensible policies regarding antibiotic use, and good infection control staff and procedures, cannot be over-emphasised. Antibiotic restriction can be effective in reducing C. difficile-associated diarrhoea.16 In response to the outbreak in Canada, the Quebec government recently provided CA$20 million to hospitals in the province to buy additional equipment and hire infection control staff.17 In the long term, such initiatives are likely to have an impact not only on C. difficile-associated diarrhoea but also on other infection control problem organisms, such as methicillin-resistant Staphylococcus aureus and vancomycin-resistant Enterococcus spp.

Thomas V Riley PhD, FRCPath, FASM

Objective: To compare the survival rate from out-of-hospital cardiac arrest in rural and urban areas of Victoria, and to investigate the factors associated with these differences.Design: Retrospective case series using data from the Victorian Ambulance Cardiac Arrest Registry.Setting: All out-of-hospital cardiac arrests occurring in Victoria that were attended by Rural Ambulance Victoria or the Metropolitan Ambulance Service.Participants: 1790 people who suffered a bystander-witnessed cardiac arrest between January 2002 and December 2003.Results: Bystander cardiopulmonary resuscitation was more likely in rural (65.7%) than urban areas (48.4%) (P = 0.001). Urban patients with bystander-witnessed cardiac arrest were more likely to arrive at an emergency department with a cardiac output (odds ratio [OR], 2.92; 95% CI, 1.65–5.17; P < 0.001), and to be discharged from hospital alive than rural patients (urban, 125/1685 [7.4%]; rural, 2/105 [1.9%]; OR, 4.13; 95% CI, 1.09–34.91). Major factors associated with survival to hospital admission were distance of cardiac arrest from the closest ambulance branch (OR, 0.87; 95% CI, 0.82–0.92), endotracheal intubation (OR, 3.46; 95% CI, 2.49–4.80), and the presence of asystole (OR, 0.50; 95% CI, 0.38–0.67) or pulseless electrical activity (OR, 0.73; 95% CI, 0.56–0.95) on arrival of the first ambulance crew.Conclusions: Survival rates differ between urban and rural cardiac arrest patients. This is largely due to a difference in ambulance response time. As it is impractical to substantially decrease response times in rural areas, other strategies that may improve outcome after cardiac arrest require investigation.

Paul A Jennings BN, MClinEpi · Peter Cameron MB BS, MD · Tony Walker BParamedStud, GDipEd · Stephen Bernard MB BS, FACEM · Karen Smith BSc(Hons), PhD

Objective: To estimate the frequency of chronic kidney disease (CKD) in a clinic-based sample of patients with type 2 diabetes in the setting of Australian primary care.Design, setting and participants: Expressions of interest were invited from all registered general practitioners in Australia: 500 GP investigators were randomly selected from each stratum (state and urban versus rural location), proportional to the census population, and asked to recruit and provide data for 10–15 consecutively presenting adults with type 2 diabetes between April and September 2005.Main outcome measures: Estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73 m2 and evidence of kidney damage on urinalysis (eg, microalbuminuria).Results: 348 GP investigators submitted data for 3893 individuals with type 2 diabetes (52% men; median age, 66 years). Almost one in every four patients consulting their GPs had an eGFR < 60 mL/min/1.73 m2 (23.1%; 95% CI, 21.8%–24.5%). More than one in three had an elevated urinary albumin–creatinine ratio (ACR) (34.6%; 95% CI, 33.3%–35.9%). There was an overlap of 10.4% of patients with both an eGFR < 60 mL/min/1.73 m2 and an elevated urinary ACR, meaning that almost one in two patients with type 2 diabetes consulting their GPs (47.1%; 95% CI, 45.8%–48.4%) had CKD. CKD was significantly more common in women, in older people, and in individuals with established macrovascular disease.Conclusion: CKD is a common complication of type 2 diabetes, found in about half of all patients with type 2 diabetes consulting their GPs. Efforts to increase the recognition of CKD will lead to improved care, and possibly survival, of patients with type 2 diabetes.

Merlin C Thomas PhD, FRACP · Andrew J Weekes MD · Olivia J Broadley BSc, BCA · Mark E Cooper MB BS, PhD · Tim H Mathew PhD, FRACP

Objective: To examine trends in Northern Territory Indigenous mortality from chronic diseases other than cancer.Design: A comparison of trends in rates of mortality from six chronic diseases (ischaemic heart disease [IHD], chronic obstructive pulmonary disease [COPD], cerebrovascular disease [CVD], diabetes mellitus [DM], renal failure [RF] and rheumatic heart disease [RHD]) in the NT Indigenous population with those of the total Australian population.Participants: NT Indigenous and total Australian populations, 1977–2001.Main outcome measures: Estimated average annual change in chronic disease mortality rates and in mortality rate ratios.Results: Death rates from IHD and DM among NT Indigenous peoples increased between 1977 and 2001, but this increase slowed after 1990. Death rates from COPD rose before 1990, but fell thereafter. There were non-significant declines in death rates from CVD and RHD. Mortality rates from RF rose in those aged ≥ 50 years. The ratios of mortality rates for NT Indigenous to total Australian populations from these chronic diseases increased throughout the period.Conclusions: Mortality rates from IHD and DM in the NT Indigenous population have been increasing since 1977, but there is evidence of a slower rise (or even a fall) in death rates in the 1990s. These early small changes give reason to hope that some improvements (possibly in medical care) have been putting the brakes on chronic disease mortality among Aboriginal and Torres Strait Islander peoples.

David P Thomas MMedSc, PhD, FAFPHM · John R Condon MPH, PhD, FAFPHM · Ian P Anderson MB BS, FAFPHM · Shu Q Li MB, MPH · Stephen Halpin BSc, MSc · Joan Cunningham ScD · Steven L Guthridge MB BS, MTH, FAFPHM

The 2006 Dr Ross Ingram Memorial Essay Prize was presented to Dennis McDermott, Koori psychologist, academic and poet, at the AMA National Conference in Adelaide in May 2006. This year we were honoured by the presence of Ross Ingram’s wife, Julie Neville, who joined MJA editorial staff and federal AMA president, Dr Mukesh Haikerwal, in presenting the prize named in her late husband’s memory. Dennis McDermott is Conjoint Senior Lecturer in Indigenous Health at the Muru Marri Indigenous Health Unit of the School of Public Health and Community Medicine, University of New South Wales. He won the prize of $5000 for his essay, Unknown family at the taxi stand, which was published in the 15 May 2006 issue of the MJA (http://www.mja.com.au/public/issues/184_10_150506/mcd10107_fm.html). In presenting the prize, MJA Deputy Editor Dr Ruth Armstrong commented that Dennis had combined the stories of his Aboriginal family, the insights of a psychologist, the analytical abilities of an academic and the beautiful, layered writing style of a poet to produce an elegant and thought-provoking essay that emerged as a clear winner with the external panel of judges. Dennis McDermott thanked the Journal for providing a platform for the voices of Indigenous people to be heard, noting that the complexities of Indigenous health were not being adequately represented in current media debates. He urged the doctors present to be bold in supporting initiatives to improve the health of Aboriginal and Torres Strait Islander peoples and to resist measures that are counterproductive. Entries for the 2007 Dr Ross Ingram Memorial Essay Competition close on 15 January 2007. The competition is open to any Aboriginal or Torres Strait Islander person who is working, researching or training in a health-related field. See the eMJA for details (http://www.mja.com.au/public/issues/180_10_170504/arm10277_fm.html). The runner-up essay, A journey of Indigenous identity, by Dr Marshall Watson, is published in this issue of the Journal (A journey of Indigenous identity). From left: Mukesh Haikerwal, Dennis McDermott, Ruth Armstrong, Martin Van Der Weyden and Julie Neville.

Ruth M Armstrong

Tearing down the road on a mountain bike that was three sizes too big (or at least that’s what it felt like) on another 40-God-knows-what degrees Celsius day in Karratha, the heat reflecting off the road, I was stopped by a familiar voice booming from the weatherboard house on the corner. “Hey Esme, what you doin’? You wanna come fishin’?” It was Ritchie, a Torres Strait Islander bloke my age, and a good mate. “Nah, mate, goin’ to mow lawns — besides, don’t have a rod, unless you got a spare”, I replied. Ritchie smiled. “What you want a rod for? It’s much better this way”, and held up a fishing spear. * An Australian television drama series. “Well, if you change your mind I’ll be down the back beach” he added, and I continued on my way. I had Ritchie to thank for the nickname “Esme”, after Esme Watson of A Country Practice* — he liked it so much he even named his dog Esme. Now I didn’t liken myself to my namesake at all, and could not be stuffed with gossip, but the name stuck like mud. Ritchie was part of a big Torres Strait Islander family in town and had rellies around Karratha, Roebourne and Wickham. His dad had a bloody good reputation as being one of the best trades assistants around. Ritchie was not the academic type, and went to school if and when he liked. When I look back, I realise he taught me a lot about Indigenous identity and I have a lot to thank him and his family for. My family moved to Karratha from Perth when I was 12, as my dad Noel got a job with Hamersley Iron. Even though Noel is not my biological dad, nor is he Aboriginal, he always said to me, from when I was a young age, “You’re Aboriginal ya know, and it’s something to be proud of”. I had no idea what being Aboriginal meant. All I’d learnt about Aboriginal people was what I’d seen on TV and snippets from other family and friends, neither of which were positive. I always knew I was different, but couldn’t define how. Growing up is hard enough, but growing up in a country town during adolescence and trying to find your identity as an Indigenous Australian is even harder. This is where it gets a little complex, but follow as you can. I knew who my biological father was, and it was his brother and his family that I grew up around in my younger years in Perth. However, I was like the secret, the “black sheep” of the family, if you will — the one who was not spoken about in a family that denounced their Aboriginality. Just as my biological dad was not spoken about when mum was around. So how did this young kid — who knew he was Aboriginal, knew his family was Aboriginal and knew they did not accept it — have a hope in hell of figuring out his place in the world? I didn’t know where to start; all I had to go by was what I’d heard from my family, such as “you’re only part Aboriginal”, and sneaking in looks at photos of my grandmother (because I was too afraid to ask any questions). The only Indigenous family I had contact with was Ritchie’s. This is how it remained for several years. † Tertiary Entrance Examination. During my university years I found it tough going at times. Don’t get me wrong — I have some great memories of my uni days. It was funny that while all the white mob were discussing TEE† scores, the Aboriginal mob were more interested in where you were from and who your mob were. But still I didn’t know much more about my Aboriginal family and in some ways I felt isolated and sad, but my stubbornness and anger at my biological dad held me back. There were those who accepted and understood my viewpoint and others who did not. Occasionally I was called a “coconut” (black on the outside and white on the inside) because I hadn’t found my family. Of those who knew my pain and helped me over the years, two stand out. Both are Indigenous, one a doctor and the other soon to graduate in medicine. Furthermore, it was another friend’s mother who gave me hope. When I mentioned my Aboriginal grandmother’s name, she replied, “Edith Oldridge, I remember her from the AMS [Aboriginal Medical Service]. She was a Holmes.” Jackpot! I had a connection and it all seemed to steamroll from there for a short time. Although I found out that the Holmes were related to the Williams, any other information that I wanted to get required me to go through the Department of Indigenous Affairs, and to do that I would need to get the permission of my biological dad. This I was still not ready to do. I became scared that, if I didn’t find my family, all the elders would die and I’d be forgotten and I wouldn’t find my country — a fear that would make me cry and keep me awake at night. But what I was to learn in the years to come was that I was not forgotten. As people do not forget, neither does country, and I was to discover that returning to your country is both embracing and healing. I visited the mission at New Norcia recently; this was where my great grandmother was in her younger years. To walk the same ground as my ancestors was a very restorative experience, even if it had been a mission. I met the Aboriginal woman who would become my wife several years ago and moved to Adelaide from Melbourne to be with her. It was coming to know her and her family, whom I absolutely adore, that made me truly understand the fundamental nature of Aboriginal family. Nobody was perfect but everybody was loved, and all efforts were made to locate family members who were lost. It was from this that the fire to find my roots was rekindled. I was no longer angry, just bloody curious and had had a gutful. I wanted to know about my family and I wanted to know yesterday! In January 2005, I made contact with Alan, my biological dad. He and I both had lots of questions, so we organised a meeting. It was emotional, but when we met I learned more from him about my family in the first 10 minutes than I had in the previous 30 years — he knew it all. Being Aboriginal, however, did not mean a great deal to him at this time. He grew up as the youngest of 10 children and remembers being taken away to Sister Kate’s (Parkerville) Children’s Home with his other three youngest siblings. Eventually he returned to the family, but as a matter of survival the family denounced their Aboriginality, claiming that they were either Afghan or Tahitian. For reasons that are another story altogether, dad became separated from the family and, over the years, joined the army and then became a member of the Patriots Bikers Club. This may make some uncomfortable, but the core business of the club was raising money for children’s charities. The point is that both of these became the extended family that my dad didn’t have but yearned for. Since I have known him over the past year, he has come out of his shell, to say the least. He has embraced his Aboriginality and is on his own journey of identity. He has returned to Parkerville Children’s Home to face his demons, met people who remember him from his early years, and met cousins that he never knew he had. As a result of this, he has changed as a person and is much more at peace with himself now that he has found his place — unlike his brothers and sisters, who are not yet ready to do this. My sister, who until a year ago was unaware that she had an older brother, is now also on her own journey of identity. Many Aboriginal and Torres Strait Islander peoples are unaware of their family relationships, their kinship structures, that are the strength of Aboriginal society and that place them in the context of their family, their country and their culture. This is a result of the process of colonisation and assimilation policies. Current understanding of the determinants of Indigenous health highlights the negative effects of the denial of sovereignty, cultural dislocation, dispossession and disempowerment, particularly in relation to social and emotional wellbeing.1 Our children need to have a nurturing and loving environment to grow up in, with family on all sides; our adolescents need to be able to learn how to be young adults and parents; our young adults need to be active members of the community, rearing children and caring for others; and our elders need to be able to pass on family stories and traditions to educate the younger generations. All of this has to occur in a society that, in many instances, has been unjust to Indigenous Australians. As an Indigenous health professional, and because my people are the “statistics”, I know all too well the reality of Aboriginal and Torres Strait Islander health. It is not all bad, however — we are a resilient mob. What keeps us going is our love and respect for one another and our land. The titbits of information I had when I was young were precious to me and sustained me through difficult times. I lament for those Aboriginal and Torres Strait Islander people who know nothing of their history. I know I am not the first — nor will I be the last — Aboriginal person with a story about discovering identity. As health professionals we need to be aware of its significance for social and emotional wellbeing, recognise the effects of “missing” or “lost” identity, and understand how the smallest amount of knowing can heal.2 In response to loss, all humans grieve. Aboriginal and Torres Strait Islander peoples have been deprived of their normal grieving processes, and this has resulted in an overwhelming burden of grief, both recognised and unrecognised. A reconnection with identity is one pathway to resolving some of this burden.3 Finding the self and coming to terms with individual loss is a prelude to communities finding their collective value in the richness of culture and reconciliation. I am first and foremost an Aboriginal man, then a son, brother, husband, father-to-be and doctor. This all started with a young Aboriginal bloke wanting to know more about himself. There’s no rocket science in it, just a hunger for identity. It’s fortunate that my children will grow up from Day 1 knowing about their history, family, connections to country, and place within the world. So, what about Ritchie? As I remember him, he was a proud man and, in hindsight, someone who was (and I hope still is) looking out for family, especially his nieces and nephews. He came from a strong family who loved and supported him in the way that Indigenous families do. I’m sure that many outsiders would not have seen his family’s dynamics as their cup of tea, but, looking back on it, I realise that none of those kids ever went without food, shelter or clothing, nor love or spirituality. This is my journey to date. Take from it what you will and learn from it. The discovery of identity and the journey of reconnection is one that many Indigenous Australians travel at some point in their lifetime and it is fundamental to our wellbeing. I hope my story gives readers the courage to search for the truth with Aboriginal and Torres Strait Islander people and the strength to be a lifeline for those struggling in the abyss of the unknown.

Marshall R Watson MB BS

Objective: To determine how commonly articles are retracted on the basis of unintentional mistakes, and whether these articles differ from those retracted for scientific misconduct in authorship, funding, type of study, publication, and time to retraction.Data source and study selection: All retractions of English language publications indexed in MEDLINE between 1982 and 2002 were extracted.Data extraction: Two reviewers categorised the reasons for retraction of each article as misconduct (falsification, fabrication, or plagiarism) or unintentional error (mistakes in sampling, procedures, or data analysis; failure to reproduce findings; accidental omission of information about methods or data analysis).Data synthesis: Of the 395 articles retracted between 1982 and 2002, 107 (27.1%) were retracted because of scientific misconduct, 244 (61.8%) because of unintentional errors, and 44 (11.1%) could not be categorised. Compared with articles retracted because of misconduct, articles with unintentional mistakes were more likely to have multiple authors, no reported funding source, and to be published in frequently cited journals. They were more likely to be retracted by the author(s) of the article, and the retraction was more likely to occur more promptly (mean, 2.0 years; 95% CI, 1.8–2.2) than articles withdrawn because of misconduct (mean, 3.3 years; 95% CI, 2.7–3.9) (P < 0.05 for all comparisons).Conclusions: Retractions in the biomedical literature were more than twice as likely to result from unintentional mistakes than from scientific misconduct. The different characteristics of articles retracted for misconduct and for mistakes reflect distinct causes and, potentially, distinct solutions.

Sara B Nath PhD, MSW · Steven C Marcus PhD · Benjamin G Druss MD, MPH

Objective: To determine temporal trends in PubMed publications for Australian authors compared with changes in funding for health and medical research (HMR).Design: Retrospective observational study.Setting: Internet-based bibliometric study that collated Australian HMR expenditure from the Australian Institute of Health and Welfare and Australian (and other) research publications from PubMed.Main outcome measures: Australian expenditure on HMR and numbers of PubMed-cited publications from 1980 to 2004, with subgroup analyses for universities, clinical trials, and genetic and biotechnology research, and comparison with similar results from the United Kingdom and New Zealand.Results: From 1980–81 to 2003–04, Australian HMR expenditure increased from $66 million to $1503 million and total Australian PubMed publications increased from 844 to 13 836. From 1995–96 to 2003–04, Australian publications for university-derived research and for clinical trials increased at a fairly constant rate. Genetic and biotechnology publications increased about fivefold (49 to 277) between 1990–91 and 2003–04. Between 1990 and 2004, total publications increased from 1754 to 3288 for New Zealand and from 12 401 to 19 600 for the UK.Conclusions: There is an association between increased funding for HMR and increased publications, as determined using PubMed, in the past 10 years. Using PubMed may be a simple way to track output from HMR expenditure.

Kumara Mendis MB BS, MSc, MD · Rick McLean MD, FRACP

Insulin resistance is considered a core component in the pathophysiology of the metabolic syndrome. Some clinicians measure serum insulin concentrations in the mistaken belief that they can be used to diagnose insulin resistance. Serum insulin levels are poor measures of insulin resistance. Furthermore, there is no clinical benefit in measuring insulin resistance in clinical practice. Measurements of fasting serum insulin levels should be reserved for large population-based epidemiological studies, where they can provide valuable data on the relationship of insulin sensitivity to risk factors for diabetes and cardiovascular disease. Clinicians should shift from identifying “insulin resistance” to identifying risk factors, such as fasting glucose and lipid levels, hypertension and central obesity. These proven risk factors converge within the metabolic syndrome. Individuals “at risk” of diabetes and atherosclerotic cardiac disease can be identified simply and inexpensively, using classic clinical techniques, such as history-taking, physical examination, and very basic investigations.

Katherine Samaras MB BS, PhD, FRACP · Aidan McElduff MB BS, PhD, FRACP · Stephen M Twigg MB BS, PhD, FRACP · Joseph Proietto MB BS, PhD, FRACP · John B Prins MB BS, PhD, FRACP · Timothy A Welborn MB BS, PhD, FRACP · Paul Zimmet AO, MB BS, MD, FRACP · Donald J Chisholm MB BS, MRACP, FRACP · Lesley V Campbell MRCP, FRCP, FRACP

High patient volume for both hospitals and surgeons is an important determinant of operative mortality and outcome for complex and infrequently performed operations. The 13% of Australia’s population who live in rural and remote areas often choose to have surgery close to home and support networks despite the potentially higher operative mortality and morbidity. Rural patients should be able to make an informed choice about having their surgery locally. Rural and metropolitan surgeons should discuss and reach mutual agreement on where each patient is best treated. A balance must be struck between quality of services that can be provided locally and geographic convenience.

Grant D Stewart BSc(Hons), MB ChB, MRCSEd · Gareth Long MB BS, FRACS · Bruce R Tulloh MS, FRACS, FRCSEd

Setting You have agreed to have Year 1 postgraduate doctors attached to your ambulatory practice. You have had undergraduate students attached before, but you are thinking about how to integrate these new doctors into the practice and how to teach both them and the medical student. Trainee doctors and students are increasingly taught in community and outpatient settings, where most patient care now occurs and the mix of patients is appropriate for learning.1-3 Indeed, trainees learn clinical skills just as well in ambulatory as in inpatient settings,2 and experiences in community settings influence doctors’ decisions regarding their future workplace.1,4 Unique opportunities exist for providing insights into population health, multidisciplinary care and chronic disease management, and for gaining a balanced understanding of health services.1,3-5 The challenges of teaching in ambulatory settings are different from those in inpatient settings. In ambulatory clinics, the pace is rapid, with reduced opportunity for direct observation and the potential for lost income.1,3-6 The focus is often on management, and the learner can end up observing rather than doing, being asked questions of factual recall, being given peremptory post-consultation tutorials, or tackling patients with already defined rather than more challenging undifferentiated problems.2,6,7 However, the problems of ambulatory care teaching — variability, unpredictability, immediacy and lack of continuity3,4 — can be avoided with appropriate planning. Importantly, characteristics of the teacher (clinician) as well as the practice influence learning.6-9 The clinician should: Provide opportunities for learners to assume increasing levels of responsibility (eg, by allowing them to see patients alone); Provide opportunities for learners to practise practical and problem-solving skills; Have an appropriate number and variety of patients; Be enthusiastic, organised and concise, and provide direction; Be willing to answer questions and explore clinical reasoning; and Provide timely feedback. The learner expects: Relevant pre-reading or pre-training; Learning based on patients; Allocation of follow-up activities; and Provision of the necessary resources (eg, computer-based guidelines). The principles of teaching and learning that apply to a single teaching session or clinical attachment apply equally well in an outpatient setting (Box 1) — namely, planning, providing teaching and learning, appraisal, assessment, giving feedback and reflecting on the learner’s experience.10-13 Planning Key factors of teaching and learning in ambulatory settings include: Defining the outcomes (including unique ones available in the community setting).4,11 These may include managing common presentations and understanding the role of the practice nurse. Discussion of outcomes with the learner will allow joint expectations to be explored. Good orientation to the practice, patient care, learning and resources.3,4,13 If this is the learner’s first experience in a community setting, he or she may not be used to exposure to multiple social and often emotional aspects of patients’ lives.4 Orientation helps learners to have the confidence and competence to be involved. LearningTake-home message When teaching in outpatient settings: Remember that planning and orientation are essential. Consider what outcomes are unique to your setting. Ensure the learner has good patient contact, with an adequate number and variety of patients. Ensure the learner has access to you for discussion, feedback and some protected teaching time. Learners should be active members of the team, which means you need to provide them with authentic patient experiences.3,5-7 Trainees initially may value simply watching and learning from role modelling by clinicians, but soon they will want to take responsibility for interaction with patients.3,4 Encourage learners to consider why a particular patient is coming to the clinic, provide guidance as to how long they should spend with a patient, and tell them that interaction needs to be focused rather than extensive. At the same time, ensure they are not missing important aspects of the consultation by focusing too much on one area. Consider what types of patient are appropriate for trainees’ learning needs (eg, in health care assessment, chronic disease management and aged care). Teaching with or in front of patients, such as when the trainee sees the patient alone first and then presents and plans management in front of the patient, doesn’t add much time to the clinician’s work, but significantly increases the time the patient spends with the health care team.2 This requires the use of a second room and flexibility in patient scheduling (eg, “wave” scheduling [see Box 1 footnote]3). In general, clinicians tend to extend their workday by 30–50 minutes per half day to accommodate this type of teaching arrangement, rather than reduce their clinical load.2 Depending on the learner’s level of experience, you may wish to: Jointly review the patient after the initial review or get the learner actively involved during the consultation (when teaching students) (Box 2); or Provide advice outside the door on each patient, and/or follow-up at the end of the clinic (when teaching trainees). Trainees generally prefer to work alone and do not like having the supervising doctor come in and review the patient with them, feeling that it changes the doctor–patient relationship they have established.7 But they do want input. Identify areas of uncertainty for learners, help them find resources, and agree on a time for follow-up. Students and trainees value formalised time for teaching, so set aside an hour a week for that purpose. Appraisal and assessment Learning in clinics can be challenging. In an outpatient setting, learners may find themselves alone with patients, as opposed to a hospital setting, where there are often other people available to give advice. Furthermore, direct observation of trainees in outpatient settings is harder, even though it is important for determining their strengths and areas for improvement. You may wish to sit in with the trainee for a clinic every few months. Gather feedback from others (the receptionist often knows whether patients want to see your trainee again!).3 Finally, self-reflection by the teacher on individual teaching encounters and on the entire attachment will improve subsequent teaching. 1 Cycle of learning in the outpatient setting3,6,7,9-11 Planning Define course outcomes and methods of assessment. Consider organisation of the clinic (eg, having a second room available, “wave” scheduling*). Provide an orientation to: Clinic and community; Patient care — expectations; Learning activities; Resources (people, Internet-based resources); Key personnel (practice nurses, educators and other health professionals). Learning Ensure authentic patient contact. Pre-select patients for review, based on the experience level of the learner. Teach through pre-clinic, post-clinic and “case of the week” discussions. Set aside time for a tutorial. Use other members of the team for teaching (eg, nurse, patient educator). Appraisal and assessment Allow direct observation and give feedback. Use questions to ascertain understanding. Reflection Consider whether the student/trainee experience was optimal. Plan the next session. *An example of “wave” scheduling: the clinician sees patients 1 and 2 while the student sees patient 3, then the clinician joins the student and they jointly see patient 3. In this way, the clinician sees his or her own patients as well as the ones the learner has just seen. 2 Strategies for joint consultation with clinician and student present3-5,10,13,14 Before the observed consultation, give the learner a framework for thinking, and discuss his or her reflections later. Watch the learner take the history or perform the physical examination, and provide feedback. Use structured frameworks for teaching (eg, the “one-minute teacher”, the “SNAPPS” approach*). Ask the learner to look up medications or side effects during the consultation. Get the learner to provide the information on lifestyle changes (eg, smoking cessation). Get the learner to record observations in the patient notes. * SNAPPS: Summarise the case, Narrow the differential diagnosis, Analyse the differential diagnosis, Probe the teacher about areas of uncertainty, Plan management, and Select an issue for self-directed learning.

Fiona R Lake MB BS, FRACP, MD · Alistair W Vickery MB BS, FRACGP

Clinical record A 13-year-old girl with no significant medical history was referred to our tertiary hospital for the management of a left corneal abscess. She had borrowed a girlfriend’s coloured plano contact lenses over the preceding weekend. On Monday, the patient presented to her general practitioner with a red and painful left eye and was subsequently assessed by a community ophthalmologist. Topical chloramphenicol was commenced, but after review 24 hours later the patient was referred to us with deteriorating visual acuity, increasing pain, and purulent ocular discharge. On admission, the patient’s left visual acuity was light perception. A large central necrotic corneal abscess and hypopyon were found on slit-lamp examination. Corneal scrapings were taken and the contact lens case submitted for microscopy, Gram stain and bacterial, fungal and viral culture. Intensive (every 15 minutes) fortified gentamicin and cephalothin were commenced in addition to oral ciprofloxacin. Gentamicin- and tobramycin-sensitive Pseudomonas aeruginosa was isolated 48 hours after admission, and the therapy was changed to gentamicin and tobramycin. The patient’s symptoms, hypopyon, and corneal infiltrate size abated, and the residual ulcer after scraping re-epithelialised. She was discharged after 3 weeks with marked corneal thinning and dense residual scarring (Figure), limiting visual acuity to count fingers at 30 cm. Fluorescein staining of a central corneal scar after Pseudomonas keratitis A: View with the naked eye B: Slit-lamp view Keratitis remains a significant risk of wearing contact lenses, despite advances over the past 10 years such as disposable and silicone hydrogel lenses. The incidence of severe keratitis from extended hydrogel lens wear was estimated at 96.4 (95% CI, 37.5–254.2) per 10 000 lens wearers in a British study.1 Even among users of daily disposable hydrogel lenses, the incidence of severe keratitis was 4.9 (95% CI, 2.5–9.6) per 10 000 lens wearers. Contact lens keratitis is precipitated by microtrauma from lens wear, which allows pathogens (Pseudomonas aeruginosa, Acanthamoeba spp., Streptococcus spp., Staphylococcus spp., Serratia spp., Fusarium spp., Aspergillus spp., Curvularia spp., Herpes simplex virus, and others) to invade the damaged cornea. Pseudomonas aeruginosa is one of the most virulent and common pathogenic organisms. It possesses virulence factors that facilitate survival and growth in the human cornea, including bacterial cell surface adherence factors and secreted cytotoxins that destroy corneal epithelium.2 The host immune response further damages the cornea,3 leading to scarring and loss of visual acuity and function. A Pseudomonas corneal ulcer is usually located centrally, and infection develops and progresses rapidly. Among people with contact lens keratitis, Pseudomonas accounts for the largest mean diameter of corneal ulcers, the highest mean nmber of days in hospital, the greatest mean number of outpatient visits, and the poorest visual acuity outcome.4 Lessons from practice Contact lens keratitis is a potentially vision-destroying infection. Pseudomonas keratitis progresses rapidly and often results in significant scarring and visual loss. Lens wearers presenting with a red eye should be referred early for specialist care. Contact lens wearers need to be properly educated regarding contact lens handling and hygiene and made aware of the serious risk of keratitis. Poor contact lens hygiene is a well known risk factor for keratitis.5,6 However, the importance of contact lens hygiene is still poorly appreciated by the community. In a survey of contact lens keratitis in New South Wales, 40% of keratitis patients reported poor hygiene.7 In a study of contact lens users in Auckland, 81% of cosmetic contact lens cases were contaminated with various pathogens.8 Colour and novelty contact lenses are becoming increasingly popular, and can be purchased from outlets such as beauty shops, markets, surf shops and auction websites. This leads to unsafe practices such as wearing lenses overnight, sharing of lenses, and poor lens hygiene. Contact lens care and hygiene play an important part in the prevention of keratitis, and education regarding contact lens hygiene remains an important task for eye care professionals. Medical practitioners and their patients need to be aware of the hazards associated with contact lens wear. Any contact lens wearer presenting with a red eye not relieved by lens removal may have potentially serious keratitis. The patient should be referred to an ophthalmologist for urgent review and prompt treatment, to prevent serious visual loss.

Yi-Chiao Li MSc(Hons), MB BS, PhD · Alina Zeldovich MB BS · Brian J Chua BSc, MB BS, MPH · Neil J Rowe MB BS, MPH, FRANZCO · Frank J Martin MB BS, FRANZCO, FRACS · Kathleen A McClellan PhD, FRANZCO, FRACS

A 36-year-old man presented to our emergency department with a 6-month history of thoracic back pain. He was born in Ghana and moved to live in the United Kingdom 8 years ago. Over the preceding 3 months, he had gradually developed symmetrical masses on either side of the thoracic spine (A and B). He denied any respiratory symptoms, fever, sweats or weight loss. On examination, he was afebrile and both masses were fluctuant but not tender or inflamed. Spinal movement was unrestricted and no features of spinal cord compression were present. Blood tests showed a normal white cell count and differential, a C-reactive protein level of 180 mg/L (reference range, 0–4 mg/L), and an erythrocyte sedimentation rate of 64 mm/h (reference range, 0–15 mm/h). HIV serology was negative. Magnetic resonance imaging of the thoracic cord showed large, bilateral collections within the rectus spinae muscles extending between T3 and T10, and destruction of the spinous process of T5. There was also high signal in the facet joints at this level, suggesting an infection arising from them (C). About 400 mL of pus was drained percutaneously; auramine staining showed this contained acid-fast bacilli. Fully sensitive Mycobacterium tuberculosis was subsequently cultured. Standard quadruple anti-tuberculous therapy was commenced, and percutaneous aspiration was repeated for re-accumulation of the collections. The masses had resolved on clinical review after 3 months. A B C

Simon Goldenberg · Nicholas Price

CorrectionRe: “Sackings at the Canadian Medical Association Journal and editorial independence”, by Martin B Van Der Weyden, in the 5 June issue of the Journal (Med J Aust 2006; 184: 543-545). References 8, 12 and 13 of this editorial were incorrect. The corrected references are: The html and pdf versions of the article were corrected on 20 June 2006.

Martin B Van Der Weyden

Born in Sydney on 22 April 1920, John Tyrer was appointed the first full-time Professor of Medicine in Queensland at the age of 34 and shaped medical teaching and research in that state for over 30 years. John graduated in medicine from the University of Sydney in 1941 after a distinguished undergraduate career and trained as a physician at the Royal Prince Alfred Hospital, Sydney. There he carried out the experimental studies on the cardiovascular dynamics of artificially perfused sheep for which he was awarded a Doctorate of Medicine. After assuming the Chair of Medicine of the University of Queensland in 1954, John set about building a modern research-based Department of Medicine at the Royal Brisbane Hospital (then the Brisbane General Hospital), an institution whose traditions had been almost wholly clinical. He systematically recruited research-oriented academic clinicians, initially from outside Queensland and then from within. He established several “temporary clinical lectureships” that were filled by aspiring medical registrars who were given the opportunity to combine clinical responsibilities with research. Many people who spent their formative years being nurtured in such positions subsequently went on to become academic leaders in Australia. By the time of John’s retirement, in 1985, his Department of Medicine was one of the largest and most productive in the University of Queensland, spanning three teaching hospitals. John’s main interest lay in neurology and neuropharmacology, in which he collaborated productively with his colleague Mervyn Eadie. However, he remained an astute general physician with superb clinical acumen and skills. Perhaps his greatest legacy lies in the large number of students and junior colleagues whom he influenced and encouraged. His high academic standards, meticulous record keeping and clarity of thought and speech were salutary and refreshing. John authored or co-authored eight books and over 100 articles. After retirement, he wrote a lavishly illustrated book, The history of the Brisbane Hospital — a mammoth undertaking. John was a Francophile and collaborated with French neurologists such as Raymond Garcin and François Lhermitte. He had a special interest in language and was widely read in classical literature, history and philosophy. John died in Brisbane on 6 June 2006 of advanced bladder cancer. He is survived by his wife Patricia and seven children. Lawrie Powell

Lawrie W Powell

To the Editor: Food, medication or insect stings are the major causes of systemic allergic reactions.1 That topical agents can mimic such reactions is not commonly appreciated. I report here a systemic allergic reaction to a topical medication (initially attributed to food). A 7-year-old boy experienced generalised urticaria and facial swelling within an hour of eating a peanut-containing slice. His father recalled applying a topical antiseptic (Medi Creme [Pharmacare]) to a graze over the boy’s right elbow at about the same time. There were no respiratory or cardiovascular symptoms, and the urticaria settled within 2 hours of taking oral promethazine. Six months later, the same cream applied to a graze over the boy’s right chest resulted in a localised 15 cm urticarial welt. Intercurrent problems included atopic dermatitis but no known food or drug hypersensitivity. The active ingredients of Medi Creme are hexamidine isethionate, chlorhexidine acetate, cetrimide and lignocaine hydrochloride. With the assistance of the manufacturer, skin prick tests using a 10% weight/volume suspension of Medi Creme or a 10% suspension of hexamidine isethionate in normal saline produced 5 mm itchy weals at 15 minutes in the patient (but not controls). By contrast, skin prick tests to the other active ingredients, inert vehicles and relevant foods (including peanut, almond, brazil nut, cashew, hazelnut, pecan, walnut, sunflower seed and sesame seed) were negative. Avoidance of hexamidine was advised. The child has eaten peanut products before and since without any adverse reaction. Hexamidine is an aromatic diamidine antiseptic (other members of the group include pentamidine and dibrompropamidine). These drugs have broad antibacterial and antifungal properties and are also used topically to treat corneal infections and some skin infections.2 In Australia, hexamidine is an ingredient of one topical local anaesthetic/antiseptic cream (Medi Creme) and one nappy rash cream, as well as some tinea treatment creams, medicated shampoos, sunscreens and cosmetic facial wipes in other countries. Adverse reactions (such as contact allergic dermatitis and photodermatitis3) are rare — only four reports of localised dermatitis have been reported to Australia’s Adverse Drug Reactions Advisory Committee (ADRAC) in the past 6 years (Dr K Mackay, Acting Director, ADRAC, Adverse Drug Reactions Unit, Therapeutic Goods Administration, personal communication). There have been more reports of systemic allergic reactions (including anaphylaxis) triggered by chlorhexidine or cetrimide,4 with one description of anaphylaxis to hexamidine after patch testing, but none with clinical use.3 Underlying dermatitis is a risk factor for sensitisation to topical agents.5 This case emphasises the importance of documenting exposure to potential allergenic triggers in the setting of a short-lived episode of urticaria (where the search for an avoidable trigger is more likely to be productive) or anaphylaxis. Exposure to stinging insects is usually obvious, whereas exposure to particular foods or medications is often poorly recalled. That topical allergens can also trigger systemic reactions should be considered.

Raymond J Mullins PhD, FRACP, FRCPA

To the Editor: Extended-wear silicone hydrogel contact lenses allow the convenience of 24-hour correction of refractive error and freedom from cleaning solutions and storage containers. However, they are associated with an increase in the risk of microbial keratitis when worn overnight compared with daily wear.1-5 The following cases from a single ophthalmology practice illustrate the risk to contact lens wearers when they use silicone hydrogel contact lenses overnight. A 36-year-old woman presented 11 days after sleeping with her silicone hydrogel contact lenses in overnight. She had increasing right ocular pain and photophobia over the preceding 9 days, which had not resolved with chloramphenicol drops. On examination, visual acuity was 6/18 right and 6/6 left. Corneal cultures grew Acanthamoeba, which responded to polyhexamethylene biguanide and brolene drops hourly. Her final best corrected visual acuity was 6/9 right, 5 weeks later. A 24-year-old woman presented with 2 days of left ocular pain, conjunctival injection, and epiphora following continuous silicone hydrogel contact lens use over the preceding week. On examination, visual acuity was 6/6 right and 6/18 left. A central corneal ulcer with stromal infiltrate and significant anterior chamber activity was present in her left eye (Box). Corneal cultures grew Pseudomonas aeruginosa, which responded to topical gentamicin 1% drops hourly. Her final best corrected visual acuity was 6/5 left, 3 weeks after diagnosis. An 8-year-old girl was seen 2 months after commencing continuous wear of her silicone hydrogel contact lenses for uniocular myopia. She had worn the same lenses for 4 weeks continuously when she presented with a 2-day history of right ocular irritation, photophobia, and conjunctival injection. On examination, visual acuity was 6/36 right and 6/6 left. She was commenced empirically on cephalothin 5% and gentamicin 1% drops hourly. Corneal cultures did not grow any causative organism, and her clinical condition improved significantly over the following 7 days. Her final best corrected visual acuity was 6/9 right. Although microbial keratitis may only affect a small proportion of individuals1,2,5 and our patients did not experience significant reduction in vision following treatment, microbial keratitis is potentially blinding and should not be trivialised. Silicone hydrogel contact lenses have a lower risk of associated microbial keratitis than other lens types, but they do not remove it completely. In view of this, contact lenses should not be worn overnight or for an extended period. Furthermore, a painful red eye in a contact lens wearer should be considered microbial keratitis until proven otherwise, and needs a prompt ophthalmologist referral. Microbial keratitis in a 24-year-old woman

John A Landers · John L Crompton

To the Editor: Uveitis is an intraocular inflammation which potentially leads to permanent loss of vision.1,2 Tuberculosis is considered to be an infrequent infectious cause of uveitis in the developed world. However, its recurrence as a major public health problem raises the possibility that the incidence of tuberculosis-related uveitis in the developed world may rise.3,4 Uveitis in tuberculosis is presumed to result from either direct invasion or a hypersensitivity reaction. At the ophthalmology departments of the Erasmus Medical Center and the Eye Hospital in Rotterdam, The Netherlands, all patients presenting with refractory uveitis undergo investigation for a systemic cause, including tuberculin skin testing. When ocular findings are consistent with intraocular tuberculosis, and the tuberculin skin test is positive, while no other cause of uveitis is suggested by symptoms, signs or ancillary testing, then a diagnosis of presumed intraocular tuberculosis is made. Using these criteria, eight cases of presumed intraocular tuberculosis were identified among 89 people referred with refractory uveitis between January 2002 and January 2004. Characteristics of the eight patients are shown in the Box. One patient (F) withdrew from clinical care, and another (A) later had a positive culture result for tuberculosis on lymph node biopsy. This patient had complete remission of uveitis after tuberculostatic treatment, but was excluded from this study as the aim was to assess whether antituberculosis treatment is warranted based solely on a positive tuberculin skin test. We treated the patients with a complete tuberculostatic regimen (2 months of isoniazid, rifampicin, ethambutol and pyrazinamide, followed by 4 months of isoniazid, rifampicin and ethambutol). All had been previously treated for more than 3 years with immunosuppressive drugs (mainly corticosteroids), either local or systemic, or both, without adequate response. Main outcome measures were visual acuity and degree of intraocular inflammation seen on ophthalmological examination before and on completion of antituberculosis therapy. The predominant clinical finding was blurred vision. Five patients exhibited decreased intraocular inflammation and an increase in visual acuity after antituberculosis treatment, allowing tapering of the corticosteroid treatment. One patient had no response. Improvement as part of the natural history was regarded unlikely. As our department is a tertiary referral centre for patients with uveitis, our patient population is not a representative sample of all patients with uveitis in The Netherlands. Nevertheless, our findings suggest that intraocular tuberculosis should be considered in the differential diagnois of uveitis, even in developed countries. We believe that, given our results, antituberculosis therapy is justified in patients with uveitis even when a positive tuberculin skin test is the only argument for tuberculosis as the cause of the eye disease. An additional argument for antituberculosis treatment is that many patients with uveitis refractory to immunosuppressive therapy can be adequately treated with tumour necrosis factor-α (TNF-α) blocking drugs.5 However, as severe tuberculosis infection has been described after use of these agents, antituberculosis therapy is warranted in any patient with a positive tuberculin skin test who is a candidate for TNF-α blocking therapy. Details of eight patients with presumed intraocular tuberculosis Affected eye Place of birth Visual acuity Uveitis treatment Antituberculosis treatment Patient Sex Age Uveitis Before* After* Response A M 25 Left Anterior Congo NR† NR† NR† NR† NR† B F 40 Both Posterior Cape Verde 1.8/6 (R), 1.2/6 (L) 4.8/6 (both) Local steroids HRZE, HRE Partial response, local steroids continued C F 69 Left Posterior Netherlands‡ 4.8/6 4.8/6 Local steroids HRZE, HRE Complete response, local steroids stopped D M 49 Right Posterior Surinam 0.6/6 0.8/6 Vitrectomy, local steroids HRZE, HRE No response E F 36 Both Anterior Morocco 2.4/6 (R), 3/6 (L) 4.8/6 (R), 6/6 (L) Local steroids HRZE, HRE Complete response, local steroids stopped F F 62 Both Posterior Morocco 0.6/6 (R), 0.6/6 (L) Local steroids — Lost to follow up before treatment G M 54 Right Posterior Surinam 2.4/6 5.5/6 Local and systemic steroids HRZE, HRE Partial response, systemic steroids stopped H F 19 Both Intermediate Netherlands‡ 4.3/6 (R), 1.2/6 (L) 6/6 (R), 6/6 (L) Local steroids HRZE, HRE Complete response, local steroids stopped * Before and after antituberculosis therapy. † NR = no result as patient excluded from the study. ‡ Patient C’s parents were born in The Netherlands, but Patient H’s parents were from Morocco. M = male. F = female. H = isoniazid. R = rifampicin. Z = pyrazinamide. E = ethambutol.

Paul L A van Daele · Marleen Bakker · P Martin van Hagen · G Seerp Baarsma · Robert W A M Kuijpers

To the Editor: Mycobacterium ulcerans is an environmental pathogen with a global geographic distribution and focal disease clusters. The World Health Organization considers M. ulcerans infection to be of increasing global importance, particularly in West Africa. In Australia, the clinical and pathological features were fully described in 1948, when the disease was named Bairnsdale ulcer.1 Since then, the number of cases has increased, and new focal areas continue to emerge around southern coastal Victoria.2 In Queensland, the disease is most frequently reported in the Mossman area (north of Cairns in north Queensland), where it is known as Daintree ulcer.3 However, the organism is probably more widely distributed. We describe four patients recently diagnosed with proven M. ulcerans infection in the Capricorn coast region of central Queensland (Box). The suspected epicentre of infection is around Yeppoon, approximately 1000 km south of Mossman. None of the patients had significant contact with recognised endemic areas in north Queensland or Victoria. Patient 1 had visited Townsville in July 2000, but had minimal contact with the natural environment. She undertook extensive gardening at her home in North Rockhampton, using sugar cane bagasse mulch from north Queensland. The previous occupants of her house had lived in north Queensland and left behind at her home numerous potted plants originally from that area. However, investigation of soil from potted plants, gardens and roses at the home using polymerase chain reaction (PCR) failed to detect any evidence of M. ulcerans. Patient 2 lived near a coffee plantation originally planted with seeds transported from north Queensland. Sampling of plants and soil in the area by PCR revealed no atypical mycobacteria. M. ulcerans is an environmental organism associated with bodies of water, but its specific ecological niche is unknown.4 The organism is difficult to culture from the environment but has been identified by PCR in water, biofilms, aquatic insects, snails and fish. The mode of transmission to humans remains unknown. It has shown a marked propensity for causing intense focal outbreaks in Victoria (Phillip Island and Point Lonsdale) and Queensland (Daintree region). The recognition that M. ulcerans occurs in coastal central Queensland is important, as early diagnosis of M. ulcerans infection minimises the extent of tissue debridement necessary and improves outcomes. The patients we describe had complicated disease requiring multiple debridements and, in one case, amputation. Awareness of the possibility of M. ulcerans infection is critical, as diagnosis by PCR is straightforward once the infection is considered in the differential diagnosis. In 1942, Cilento described possible M. ulcerans infections from around Rockhampton.5 Four other culture-confirmed cases were reported between 1957 and 1962 from the Glass House Mountains (Sunshine Coast)3 and Maryborough (Fraser Coast)6-8 regions in Queensland. Our four cases occurred within a small geographic area centred on Yeppoon and the suburbs of Rockhampton. If the cases previously described by Cilento were truly related to M. ulcerans, then there appears to have been a five-decade gap in identification of M. ulcerans infection in the Capricorn Coast region of central Queensland. Possible explanations for this include low organism numbers resulting in sporadic infection, focal concentrations of the organism with environmental changes, such as development, land clearing and cultivation modifying human contact, or failure to diagnose the condition. Patients who acquired the infection in central Queensland may also have been diagnosed outside the area. The increase in cases in Victoria raises the possibility of a potentially similar dramatic increase in cases in central Queensland. Consideration should be given to making M. ulcerans infection a reportable disease to enable monitoring. Four patients with Mycobacterium ulcerans infection in central Queensland Age/sex Location Presentation Site Clinical features Diagnosis Treatment 47 F North Rockhampton Sep 2000 Fifth finger (left hand) Nodule Histology, PCR Debridement, antimycobacterial antibiotics, amputation 33 F Yeppoon Jun 2003 Left knee Ulcer Histology, culture Debridement 64 M Bungundarra Aug 2004 Right elbow Ulcer Histology, PCR Multiple debridements 18 M Keppel Sands Nov 2004 Right knee Ulcer Histology, culture Multiple debridements, antimycobacterial antibiotics PCR = polymerase chain reaction. F= female. M = male.

Glenn D Francis · Michael Whitby · Marion Woods

To the Editor: “... what a difference can be made and how bureaucracies can stuff things up”. “... systematic testing and treatment of people with high blood pressure and kidney disease dramatically improved blood pressure and resulted in a 50% reduction of deaths”. “... excellent results were achieved by good management and they were lost when intensity of management was relaxed”. The above quotes are from an episode of The health report broadcast late last year on Radio National.1 The episode, which described a deterioration in the health of an Indigenous community after a chronic disease treatment program was handed over to a community health board, caused me to take a closer look at the articles in the Journal by Hoy and colleagues on which the claims were based.2,3 I found several issues of concern. The small numbers of deaths each year in the study community and the analysis and presentation of the death data mean that the conclusions about trends in mortality over time are tenuous. This is highlighted by the discrepancies between the two articles in the terminology used to classify deaths, in the numbers of deaths reported, and in the trends over time. Discrepancies in terminology or numbers of reported deaths are not explained. The declining trend in the number of “natural” deaths described in the 2000 article is not apparent in the “non-renal” deaths in the 2005 article. The rate of “non-renal” death for the period 1996–97 to 1998–99 reported in the 2005 article appears to be increasing rather than declining, as described in the 2000 article (rates for earlier years are not presented in either article). It is clear that, with these small numbers, the reclassification or misclassification of a single death can affect the trends in “renal death” or end-stage renal disease over time, and that the use of “rolling averages” hides the year-to-year variability that would be expected in these data. The trend over time in the key intermediate outcome indicator of blood pressure control does not support the conclusion regarding impact of the “handover” on the program. The data presented in the 2005 article show a decline in control commencing in the third year. An earlier analysis of the same data showed the decline in blood pressure control began as early as the second year after entry into the program.4 Neither analysis shows any clear change in the declining trend in blood pressure control around the time of “handover” of the program. While the discussion of the findings of the 2005 article is circumspect, at the time of interview, Hoy conspicuously did not deny the statement of The health report host that the primary cause of the apparent loss of the early impact of the program was the bureaucracy “stuffing up”. The article makes some important points about the operation of chronic disease programs, but makes no mention of the commonly experienced difficulties of sustaining health programs,5,6 or the research requirements for understanding sustainability.7 These issues raise serious questions about the validity of the conclusions and the simplistic claims arising from the articles.

Ross S Bailie MD, FAFPHM

In reply: I appreciate the feedback on the 2000 and 2005 articles describing the dynamics and outcomes of the “Tiwi treatment program”.1,2 Thorough and timely identification and enumeration of deaths is a problem, especially for people not enrolled in the treatment program. Without a register of such people, systematic checking of their fate was not possible. The additional “non-renal” deaths in the community-at-large presented in our 2005 article, compared with previous articles, seem to have been captured largely by the broad net spread by the Tiwi Health Board when it assumed responsibility for its primary care services, in an attempt to identify all its potential clients. This process identified several hundred more people than expected and captured additional deaths, several dating back years. The precise definition of a community member is also a problem, especially for people living permanently or intermittently elsewhere (eg, in Darwin or other communities). The broadened definition of “renal deaths” in the 2005 article,2 which accommodates people who died with renal failure but did not begin dialysis, more fully represents the impact of renal disease. Conversely, recording only those who began dialysis allows estimates of the impact on health services and potential savings from better management.3 Both approaches have their place. Rolling averages, which indeed have limits, were used in view of the overall small and erratically spaced number of terminal events in any year. The figures we reported in our 2005 article did not show a deterioration in blood pressure at Year 2, either in the treatment group as a whole, or in the smaller cohort followed for a full 6 years.2 An earlier analysis, which largely embraced the active years of the program, also showed that blood pressure at Year 3 was not significantly different from that at Year 2 (systolic blood pressure, P = 0.68) (Box). With time, the number of people who had moved through 3 years of treatment increased, and the timing of their 3-year blood pressure measurements moved from a mix of 1998–1999 to 1999–2002, when, as program dynamics suggest, intensity of management was relaxed, and mean values deteriorated, as we reported in 2005. The blood pressure measurements in the report by Bailie’s group5 were compiled from a review of paper-based medical records, the clinic’s newly implemented Coordinated Care Trial Information System, and the Territory’s Information System (Systematic Health Information Logically Organised), as well our from our treatment program database. Those blood pressures were allocated time definitions in a different way, and the summary data were derived from adjusted predictions from cross-sectional time series modelling, rather than from factual recordings at the stated intervals.5 I did not solicit the interview for The health report, nor determine its directions nor the resulting headlines. However, the under-resourcing of primary care relative to needs in remote Aboriginal settings, and the lack of stability in the organisations in which it is delivered, are very detrimental. I regret that, once the Tiwi Health Board was constituted, it was not mentored and supported through its difficulties. More recently, the fledgling community-controlled Gulf Health Service in the Borroloola region of the Northern Territory met a similar fate. Chronic disease remains underserviced in both these regions, where the people are among the sickest in Australia. Blood pressure measurements (mm Hg) over 3 years of follow-up after enrolment in 123 people who had observations at every interval4 Baseline 6 months 1 year 2 years 3 years Mean systolic BP (SD) 136.2 (21.6) 125.4 (21.6) 123.6 (20.3) 120.6 (21.6) 121.7 (21.5) Mean diastolic BP (SD) 81.9 (13.2) 75.5 (13.7) 76.3 (12.9) 74.5 (13.7) 74.0 (11.0)

Wendy E Hoy

To the Editor: As I have said elsewhere, “The last thing the majority wants is that the tyranny of the majority be applied to it. It is much easier to apply the tyranny of the majority to a minority. In a properly functioning democratic society minorities are not subjected to, but are protected against, the tyranny of the majority. Is the tyranny of the majority being applied through the medium of the Howard government onto the Aboriginal communities of Australia in this matter of ‘shared responsibility agreements’?”1 I note with interest recent articles by Collard and colleagues2 and by Kowal,3 debating “shared responsibility agreements”. The expressions “shared responsibility agreement”3 and “mutual obligation” are variations of the expression “social contract”. The concept of “social contract” underlies the concept of democracy originating in the writings of Thomas Hobbes, John Locke and Jean-Jacques Rousseau. Present-day political scientists discuss social-contract theory in their writings about democracy, and may mention “mutual obligation” or “shared responsibility”. While it is commonplace for aspects of the social contract to apply to subgroups in the population, it is discriminatory to make arrangements that apply only to a particular racial or ethnic group. Even though the agreements are declared to be voluntary, it is likely that Aboriginal communities are under pressure to do as they are told to achieve social contracts with the Australian Government. If Indigenous people must comply with certain conditions before they can achieve social contracts, how might similar conditions be applied to the rest of the Australian population? The “ticking time bombs” of Australian public health are smoking and obesity. If non-Indigenous Australians refuse to stop smoking and refuse to eat less and take more exercise, should access to public hospitals and pharmaceutical benefits be denied them? Should they be denied petrol to force them to walk and to use public transport? Obviously not. These services are not subject to social-contract agreements as thiswould be a clear violation of Australian law. Australian members of parliament in particular, and Australians in general, for the sake of themselves, their families and of Australian health care costs, would benefit from negotiating “shared responsibility agreements” with themselves to stop smoking and to lose weight. In current circumstances, “shared responsibility agreements” with Aboriginal communities represent inequality of sharing the responsibility for health.

John N Burry

To the Editor: Where is the evidence for the claim by Joyce, McNeil and Stoelwinder1 that there was a boom in medical workforce supply in the 1970s? They are perpetuating the accepted macroeconomic myth of there having been a surplus at that time. The microeconomic, marketplace truth was that there was a shortage of general practitioners throughout the 1970s.2 This was so severe that, after battling for some years after 1974 to find a partner for my suburban Sydney practice, I resorted to advertising overseas, finally importing an overseas-trained graduate. It is time for this myth to be laid to rest. There has been a marketplace shortage of GPs since the early 1970s. The truth is that federal governments have baulked at the expansion of payments through Medibank/Medicare. Rather than apply any controls on demand, they have obstinately rationed supply, repeatedly citing dubious statistics and invalid international comparisons to justify a diminution in the supply of GPs.

Peter C Arnold

In reply: Our reference to a boom in medical workforce supply during the 1970s was based on the marked increase in medical workforce entries in that decade. The number of Australian medical graduates rose from 851 in 1970 to 1278 in 1980.1,2 In contrast — and as a result of a shift to a policy of constraint — graduate numbers remained quite static during the 1980s and 1990s, at around 1200–1300 per year (Commonwealth Department of Education, Science and Training custom datasets RFI 03-312, RFI 04-360, 2004). Although the policy shift in the 1980s was based on a perception of surplus, judgements about workforce adequacy were contentious at that time and remain so. We did not intend to imply necessarily that there was a surplus in the medical workforce (or the general practice workforce specifically) during the 1970s. Rather, our historical reference was intended to show the parallels with the large influx that will result from current expansion in medical school intakes, and to highlight the cyclic nature of both medical workforce policy and perceptions of adequacy. We agree with Arnold’s implication that policies which attempt simply to adjust gross supply (up or down) are insufficient to ensure an adequate medical workforce.

Catherine M Joyce · John J McNeil · Johannes U Stoelwinder

To the Editor: We read with interest the letter by Breeze et al on management of abnormalities detected on cervical screening.1 Their study identifies a universal and fundamental feature of the Pap smear — namely, that it is an imperfect predictor of underlying abnormalities in the cervical epithelium. For smears reported as a low-grade squamous intraepithelial lesion (LSIL) (atypical squamous cells of uncertain significance) or possible LSIL, Breeze and colleagues have shown that underestimation of the extent of the underlying abnormality is greater in infrequently screened women than in frequently screened women. They claim that following the latest National Health and Medical Research Council (NHMRC) guidelines for cervical screening2 will put women in rural and remote areas with cytologically detected low-grade lesions at risk of developing high-grade lesions that go undetected through lack of timely follow-up. I contend that following the new NHMRC guidelines presents a significant risk to all women with LSIL or possible LSIL reported on smears, regardless of ethnicity, locality or social class. The risk is merely greater for women living in rural and remote areas. In addition to delays in diagnosis of high-grade lesions, data from cervical cytology registries indicate that there will be delays in diagnosis for the 30–50 women each year whose smears show changes only of LSIL or possible LSIL but who are shown on biopsy to have cervical cancer.3 The problem of women defaulting on clinic appointments or being lost to follow-up is a phenomenon commonly encountered in cervical screening programs in general, but in Far North Queensland the risks of inadequate follow-up are magnified. For these and other reasons, the Royal College of Pathologists of Australasia, other learned societies and individuals have consistently and strenuously opposed the latest NHMRC guidelines during the period of their development and during the consultation period of many months. Rather than advocate a separate set of guidelines for women in rural and remote areas, it would be better to have a universally accepted safe set of guidelines that conforms to international best practice and applies to all Australian women. Using the guidelines that were in use until 20054 and that have served us so well in the past is one option. Another option, which is backed by first class scientific evidence,5 is to use human papillomavirus DNA testing for triage of women with smears reported as possible LSIL.

Stewart Bryant

In reply: In June 2005, the National Health and Medical Research Council (NHMRC) endorsed new guidelines for managing asymptomatic women with screen-detected abnormalities because they were safe for Australian women and were based on the best available Australian and international evidence.1 The NHMRC accepted that new information about the natural history of human papillomavirus (HPV) infection of the cervix and cervical neoplasia demanded a reassessment of our traditional approach to this disease. HPV infection of the cervix and associated, potentially neoplastic precursor lesions are very common, but not all of these have malignant potential. Optimal prevention of cervical cancer will depend on timely diagnosis and treatment of lesions that are most likely to progress. Overdiagnosis and treatment of all incident lesions is unnecessary and potentially results in avoidable morbidity. The approach recommended in the latest guidelines moves away from probabilistic prediction and intensive investigation based on a single cytological specimen to an evidence-based program of intermittent cytological surveillance of this chronic viral infection. Intervention is timed to coincide with evidence of persistent and potentially dangerous infection. Contrary to Bryant’s claim about Australian registry data, there is no evidence that the new guidelines will mean any increase in the diagnosis of cancer, a view that is supported by independent epidemiological expert review (M Clements, Research Fellow, National Centre for Epidemiology and Population Health, Australian National University, personal communication). The experience of Breeze and colleagues in Far North Queensland suggests that the greatest risk factor for any woman to develop cervical cancer is infrequent screening.2 Furthermore, in the unlikely event that the latest guidelines do result in increased cancer incidence, such an increase will immediately be detected by the monitoring program that is integral to the new approach. Bryant advocates increased pathology testing using HPV DNA tests. We are not aware of any population data demonstrating that such an approach would result in improved cancer prevention, nor that such an approach would be cost-effective. Consequently, the Guidelines Review Group did not recommend the use of HPV DNA testing as part of triage of women with abnormal smears. The approach recommended in the guidelines is also consistent with contemporary international experience3 — namely, that the clinical significance of a single incident measurement of HPV status is not established. We believe that the latest NHMRC guidelines1 are safe and acceptable for all Australian women and that all women deserve appropriate investigation and treatment of cervical abnormalities in a manner that will protect them from both cervical cancer and unnecessary, potentially harmful interventions. Finally, to address the concerns of Breeze and colleagues, the guidelines specifically advise that clinical management be tailored to the patient’s individual circumstances.

Gerard V Wain · Ian G Hammond · Penelope I Blomfield · Marion A Saville · Margaret Davy

To the Editor: The National Cancer Control Initiative (NCCI) was established in 1997 jointly by the Department of Health and Ageing and The Cancer Council Australia to “provide timely advice, identify appropriate initiatives, and make specific recommendations to the Commonwealth Government and other key groups regarding the prevention, detection, treatment and palliation of cancer for all Australians”. It has been the only independent group dealing with all aspects of cancer nationally, and incorporating government, non-government, consumer and professional input. On 31 May 2006, it ceased operation due to lack of funding support, and no arrangements have been made to allow continuity between its work and that of a proposed new body, Cancer Australia, which at the time of writing was still not functioning. The NCCI’s contributions include national surveys of colorectal cancer management and of skin cancer incidence and treatment; clinical trials assessing the management of skin lesions in primary care; the first protocols for pilot programs for bowel cancer screening; national programs to promote the implementation of National Health and Medical Research Council guidelines on psychosocial aspects of cancer and on lung and other cancers; programs to improve decision making in prostate cancer screening; a nationally agreed core clinical dataset for cancers; support for cancer registries to include staging and survival information; new methods to establish evidence-based requirements for radiotherapy services; and support for cancer research, for strengthening clinical trials and for consumers’ activities. Since 2000, the small group of NCCI staff has produced seven national workshops, over 30 published reports, and over 60 peer-reviewed articles. These are available online at <http://www.ncci.org.au/> along with current contact details of NCCI staff, and the final report of the NCCI is at <http://www.ncci.org.au/pdf/Final%20 report/NCCI_final_report.pdf>. An independent review in 2004 reported that NCCI’s work was of high quality, well researched, insightful, and cost-efficient, and recommended a considerable increase in funding. A major contribution of NCCI was producing, jointly with The Cancer Council Australia and the Clinical Oncology Society of Australia, the report Optimising cancer care in Australia. The government’s 2004 election policy on cancer (http://www.health.gov.au/internet/budget/publishing.nsf/Content/health-budget2005-hbudget-hfact1.htm) was based partly on this report, and included setting up Cancer Australia, with terms of reference overlapping those of NCCI. The assumption of many policymakers, consumer representatives and cancer experts was that NCCI would become a component of Cancer Australia. This has not happened. Indeed, from 2005, proposals from NCCI for the planned next stages of work on topics including psychosocial aspects of cancer, lung cancer, and primary care in cancer, received no response from the Department of Health and Ageing. With the closure of NCCI, the Director and Deputy Director are relocating overseas, and the highly productive staff members, specifically praised in the independent review, are moving to other roles. The premature demise of the NCCI, before Cancer Australia has started to function, is short-sighted, inefficient, and wastes the experience, resources and staff that NCCI has developed. This finishes a decade-long unique partnership between the Australian Government and non-government national cancer organisations. Cancer Australia will need to develop anew the expertise to identify and address issues in cancer control in Australia, and to link the government and non-government sectors.

J Mark Elwood · Robert C Burton · Michael A Quinn

Ethical choices: case studies for medical practice. 2nd ed. Lois Snyder (editor). Philadelphia: American College of Physicians, 2005 (xvi + 188 pp). ISBN 1 930513 57 7. Ethics teaching is often theoretical, emphasising broad ethical principles, such as autonomy, or normative theories, such as consequentialism. Case studies are used primarily to illustrate these principles and theories. As a case-based text, Ethical choices: case studies for medical practice eschews the theoretical approach to medical ethics, arguing that ethics is “not just about philosophical and other principles, ideals and rigorous arguments, but about the very real aspects of what people do and why”. Through commentaries on 28 cases, divided into four sections (The clinical encounter, Non-clinical dimensions, Medicine’s collective obligations and The business of medicine), Ethical choices illustrates the resolution of a wide variety of dilemmas. Commentators do not argue by analogy with other cases — a finding consistent with the (potentially contestable) assertion that “ethical concerns are raised only when suggested courses of conduct deviate from the norm”. Instead, the emphasis is on the power of “stories” in ethics education, and on the importance of “using individual cases in all their complexity”. This does not mean that the suggested resolutions are complex; indeed, the majority of the commentaries follow a common pattern in which existing regulations and evidence are considered in light of broad ethical principles and duties, and the remaining uncertainty is navigated through relational, discursive and administrative processes. The implicit message seems to be that while principles and duties are useful for clarifying ethical dilemmas, it is processes, such as empathic doctor–patient or doctor–colleague conversations and development of institutional policies, that ultimately provide a resolution to ethical problems. The cases are realistic and topical (such as medical error or direct-to-consumer advertising) and the commentaries are clear, concise and multidisciplinary. Contributors include ethicists, clinicians, lawyers, administrators and public health practitioners. Many of the suggested procedures are refreshingly practical (for instance, the steps involved in negotiating end-of-life care) and conceptually interesting (such as the taxonomy of types of alternative medicine). There is a definite air of optimism in some of the suggested resolutions, implying that compassionate, contextually-sensitive communication procedures are certain to result in acquiescence, if not consensus. But processes do not always result in agreement and it is necessary at times to choose one principle over another, or to accept the necessity of making “tragic choices”. A brief introductory discussion of the theoretical underpinnings and potential drawbacks of relational and process-based ethics would thus be helpful. While the regulation discussed is specific to the United States, and some cases would need to be adapted for use in Australian medical schools, most of the cases are relevant to Australian practice. Those that are not directly relevant, such as the myriad difficulties associated with managed care, provide a timely warning of issues that may emerge locally. In its current US-specific form, Ethical choices would be most useful as a sourcebook for teachers but, if adapted to the Australian setting, could be used as a text for students and junior medical officers. Wendy L LipworthPhD candidate Centre for Values, Ethics and the Law in Medicine, University of Sydney, NSW

Wendy L Lipworth

The vulva and vagina manual. Graeme Dennerstein, James Scurry, John Brenan, et al. Melbourne: Gynederm Publishing, 2005 (300 pp). ISBN 0 646044531 6. Despite an ongoing clinical interest, I usually find books on vulvovaginal disorders instantly soporific. These authors, who have been working together at a dermogynaecology clinic, have done a fine job making this manual readable. The book reflects a collaborative approach from their different specialties: gynaecology, pathology, dermatology, gynaecological oncology, and psychology. A combination of clinicians ideal in management but, unfortunately, not often available. I liked most that the manual is applicable to clinical practice and practical — most of us have evolved our own system of examination and investigation through imperfect instruction and trial and error. The vulva and vagina manual covers the basics with great practical detail, such as which position and speculum to use during examination, and how to do a vulval biopsy. Clinical experience is only acquired over a great period of time and most of us in practice will be confronted by a lesion (or lesions) we’ve never seen before. The most stunning contribution in the manual is the collection of clinical photographs of both common and rare conditions. There is also an extraordinary list of vulvovaginal disorders and their mode of presentation (pruritus, discharge, etc). These should be helpful in sorting out possible diagnoses of conditions when you don’t know what it is you are seeing but you know what it’s not — a common scenario in this field. I would have liked more clinical photographs in the cancer section, which was complete but similar to those in other textbooks. Whether you are a general practitioner with little experience, or a specialist with experience in the area, you will find this book good value and useful. Gregory K DavisObstetrician and gynaecologist St George Hospital, NSW

Gregory K Davis

Investigate always UK study authors say that all patients aged 45 years or older with new onset rectal bleeding should be offered bowel investigation, whether or not they have other symptoms. du Toit and colleagues conducted a 10-year study in a rural UK general practice; 265 patients aged 45 or older reported new rectal bleeding and were all investigated (via rigid sigmoidoscopy with barium enema, flexible sigmoidoscopy or colonoscopy) — 15 had colorectal cancer and 13 had colonic adenoma. That is, about one in 10 had colorectal neoplasia, however, only two of the patients with cancer had had diarrhoea. BMJ 2006; 333: 69-70 Novel anti-smoking agent Varenicline — a nicotinic acetylcholine receptor partial agonist — holds promise for smoking cessation; however, it is definitely not a panacea, say US experts.1 Klesges and colleagues were commenting on three randomised controlled trials conducted by the Varenicline Phase 3 Study Group.2 The trials found that varenicline may be better than bupropion in terms of long-term cessation and may also help in reducing relapse. However, adverse effects such as nausea and abnormal dreams were reported with varenicline; and, after all, most study participants did not quit smoking — even with varenicline. 1. JAMA 2006; 296: 94-952. JAMA 2006; 296: 47-55, 56-63, 64-71 Driving plastered? Queensland authors aimed to answer the question of whether a patient can safely drive a car while wearing an upper limb fracture cast. One of the authors (a young, pain-free man) was assessed by an occupational therapist and an experienced driving instructor in 10 different driving situations — with no cast, and while wearing one of four plasters (a right short arm cast, a right long arm cast, a left short arm cast and a left long arm cast), in both manual and automatic transmission vehicles. The author passed all tests with no cast and failed all tests with a long arm cast. When wearing short arm casts, the author passed with the occupational therapist but failed with the driving instructor To pass a driving test both hands must remain on the steering wheel unless changing gears; in a plaster, this is impossible when executing turns and reverse parking. Thus, these authors do not condone patients driving while wearing any upper limb cast. Aust N Z J Surg 2006; 76: 439-441 MAGIC cancer trial The Medical Research Council Adjuvant Gastric Infusional Chemotherapy (MAGIC) Trial has found that perioperative chemotherapy can improve the odds of survival in patients with resectable gastro-oesophageal cancer. The trial studied survival rates in more than 500 patients with resectable adenocarcinoma of the stomach, oesophagogastric junction or lower oesophagus who were randomised to receive either perioperative chemotherapy and surgery or surgery alone. Chemotherapy involved three pre-operative and three post-operative cycles of intravenous epirubicin, cisplatin and fluorouracil. Five-year survival was higher in the group receiving chemotherapy, 36% v 23%. N Engl J Med 2006; 355: 11-20 Keep your eyes open Doctors worldwide need to be aware of the likelihood of outbreaks of potentially blinding fungal keratitis, say Singapore authors. They reported a recent epidemic of Fusarium keratitis in Singapore, associated with contact lens wear to correct a refractive error, and affecting 66 patients; five patients required corneal transplantation. Most patients reported using the same brand of contact lens cleaning solution — ReNu, Bausch & Lomb; however, poor lens hygiene practices and wearing lenses past their replacement date were also commonly reported. Similar cases were reported in Hong Kong and the United States. On 15 May 2006, Bausch & Lomb announced a permanent worldwide recall of one product — ReNu with MoistureLoc, stating “some aspect of the MoistureLoc formula may be increasing the relative risk of Fusarium infection in unusual circumstances”. JAMA 2006; 295: 2867-2873 ’flu: the hope of history With the emergence of bird ’flu, the Annals of Internal Medicine has republished an essay by Dr Isaac Starr recollecting his experiences as a third year medical student in Philadelphia during the 1918 influenza epidemic. With the First World War raging, many doctors were away in the army, so medical students, including Starr, were co-opted to work in an emergency hospital. At the height of the epidemic, one in five of the total patient population died each night. But after only about 3 weeks the worst was clearly over. A mild febrile disease appeared for a further few weeks, with decreasing frequency. “So, as mysteriously as it had come, the killer departed,” Starr wrote. A popular hypothesis was that deaths were due to complicating bacterial pneumonia. Starr speculated that there should be little or no mortality in a future epidemic of influenza if antibiotics could prevent or cure the bacterial pneumonia. The essay first appeared in the Annals of Internal Medicine in 1976. Ann Intern Med Online, 27 June 2006 Dr Ann Gregory, MJA

Ann Gregory