Health occupations

In reply: I welcome the comments of Murphy and of Shaban and colleagues on my recent editorial,1 which explored, as Shaban et al say, the “displacement of doctors in modern health care by nurse practitioners and physician assistants”. The main focus of the editorial was on the current philosophical relativism muddying the definition of what a doctor is and the academic qualifications underpinning all professional training. It calls for equally rigorous criteria to be applied to non-doctor practitioners and their scope for independent practice. Undoubtedly, the potential utility of non-doctor practice is dependent on bilateral mutualism, with a clearly defined scope of practice. However, the push for independent practice remains problematic. Whether there is a genuine commitment for bilateral mutualism to occur, beyond the usual rhetoric, is of concern — witness the recent difficult negotiations on defining the framework for cooperative practice, and the reticent views of doctors on the suitability of nurse practitioners and their scope for independent practice, as reported in Australian Doctor.2-4 The fundamental question, which must be addressed, is whether the granting of Pharmaceutical Benefits Schedule and Medicare Benefits Schedule privileges to non-doctors is simply a political strategy to create a two-tiered health system under the illusion of cost containment.

Martin B Van Der Weyden

Objective: To quantify women’s uptake of Medicare Benefits Schedule mental health items, compare characteristics of women by mental health service use, and investigate the impact on Medicare costs.Design, setting and participants: Analysis of linked survey data and Medicare records (November 2006 – December 2007) of 14 911 consenting participants of the Australian Longitudinal Study on Women’s Health (ALSWH) across three birth cohorts (1921–1926 [“older cohort”], 1946–1951 [“mid-age cohort”], and 1973–1978 [“younger cohort”]).Main outcome measures: Uptake of mental health items; 36-Item Short Form Health Survey (SF-36) Mental Health Index scores from ALSWH surveys; and patient (out-of-pocket) and benefit (government) costs from Medicare data.Results: A large proportion of women who reported mental health problems made no mental health claims (on the most recent survey, 88%, 90% and 99% of the younger, mid-age and older cohorts, respectively). Socioeconomically disadvantaged women were less likely to use the services. SF-36 Mental Health Index scores among women in the younger and mid-age cohorts were lowest for women who had accessed mental health items or self-reported a recent mental health condition. Mental health items are associated with higher costs to women and government.Conclusion: Although there has been rapid uptake of mental health items, uptake by women with mental health needs is low and there is potential socioeconomic inequity.

Julie E Byles BMed, PhD · Xenia Dolja-Gore BMaths, GradDipMedStats, MPhilMedSci · Deborah J Loxton BPsych(Hons), PhD · Lynne Parkinson BSc(Hons), PhD · Jennifer A Stewart Williams BCom(Econ), MCom(Econ), PhD

To the Editor: We report a case of measles in a 24-year-old man who returned from the Fédération Internationale de Football Association (FIFA) World Cup in South Africa in July 2010. Despite Australian health alerts about measles in South Africa,1 the patient had received no pretravel medical advice or vaccinations. Six days after returning home to the Northern Territory, the patient developed fever, headache and myalgia. The following day he developed vomiting, diarrhoea, and productive cough, with a widespread rash appearing the subsequent day. He visited two general practitioners, was prescribed doxycycline and then admitted to hospital on Day 6 of his illness. On examination, his temperature was 38.9ºC; pulse, 112 beats per minute; blood pressure, 133/72 mmHg; and oxygen saturation, 96% on room air. He had conjunctivitis, a widespread blanching maculopapular rash involving his face, trunk, limbs, hands and feet (Box) and cervical lymphadenopathy. He had bilateral basal lung crackles and tender hepatomegaly. Investigations showed thrombocytopenia (platelet count, 148 × 109/L; reference range, 150–450 × 109/L); hyponatraemia (sodium concentration, 131 mmol/L; reference range, 132–142 mmol/L); and abnormal liver function test results (alanine transaminase concentration, 417 U/L [reference range, < 40 U/L]; alkaline phosphatase concentration, 236 U/L [reference range, 39–117 U/L]). His chest x-ray was normal. The following day, measles virus RNA was detected from a throat swab, and the patient was put into respiratory isolation and therapy with doxycycline ceased. He made a full recovery. The patient reported receiving childhood vaccinations, and while he thought he may have received one measles, mumps and rubella vaccination, he had not had two. Follow-up was required for 84 identified contacts, with no measles cases subsequently notified in the NT. The FIFA World Cup is the world’s largest single-sport event, with an attendance this year of over 3 million people. Mass gatherings may be associated with outbreaks of communicable diseases such as meningococcal disease, measles and pandemic (H1N1) 2009 influenza, in addition to an increased risk of sexually transmitted diseases.2 These risks should be considered when seeing patients who have travelled to such events, in addition to country-specific health risks. Recent data from the GeoSentinal surveillance network showed that a systemic febrile illness was the most common presenting syndrome among travellers returning from South Africa. Most of these cases of illness (54.5%) were due to spotted fever group rickettsiosis.3 The risk of acquiring rickettsiosis increases among travellers visiting game parks, with an incidence of African tick bite fever (Rickettsia africae) among short-term safari tourists of 4.0%–5.3%.4 Measles has rarely been reported in travellers returning from South Africa,2 but the country is in the midst of a measles epidemic, with 17 354 confirmed cases between January 2009 and 12 August 2010.5 Measles presents with fever, cough, rhinorrhoea and conjunctivitis, followed by a widespread rash. The incubation period is usually 7–10 days, but may be up to 18 days. The virus is highly infectious, from 5 days before to 4 days after the onset of rash. Young adults from non-endemic countries such as Australia are at particular risk, as they may only have had one childhood vaccination for measles, with consequent inadequate protection. Although measles has been eliminated in Australia,6 sporadic outbreaks continue to occur,7 and travellers returning from overseas create an ongoing potential for the re-establishment of endemic measles. Given the public health implications of a delayed diagnosis, doctors must be alert to possible cases of measles in travellers returning from endemic countries. The patient’s widespread maculopapular blanching rash

Bridget E Barber · Krispin M Hajkowicz · Vicki L Krause · Kevin G Freeman · Bart J Currie

Divisions of General Practice are a significant part of Australia’s health care sector. The Australian Government intends to establish “Medicare Locals” (MLs), which will assume many of the roles currently undertaken by Divisions. MLs will, on average, be larger than Divisions and are likely to have different ownership, governance and accountability arrangements. While some Divisions may find transformation into an ML an appealing and relatively straightforward option, others may wish to follow alternative paths that allow them to maintain many of their current characteristics. Evidence suggests that the move to MLs might jeopardise the level of clinical involvement attained by Divisions.

Philip K Davies MSc, GAICD

Delegation to practice nurses may be the main reason for an increase in Level A consultations In their analysis of Medicare claims data for general practice consultations published in this issue of the Journal, Taylor and colleagues report a recent decline in Level C and D (long) consultations and an increase in Level A (short) consultations — a pattern they consider to be “at odds with health policy objectives that rely on long consultations to provide preventive care and chronic disease management”.1 They hypothesise that the increased use of Level A consultations may reflect: the administrative burden created by the complexity of Medicare Benefits Schedule (MBS) special items; an increase in encounters for “vaccinations, prescriptions, medical certificates or test results”; or greater use of practice nurses.1 Data from the BEACH (Bettering the Evaluation and Care of Health) program2 suggest that the third option — greater use of practice nurses — explains most of the increase in claims for short (Level A) consultations. The introduction of MBS items for practice nurses in May 20043,4 had a significant impact on the use of Level A consultations. Trends in utilisation of short consultations can be followed in BEACH data, with the lowest proportional use occurring in April 2004 to March 2006, when 1.0% of all claimable consultations (Medicare or the Department of Veterans’ Affairs [DVA]) were short consultations. By 2008–09, short consultations accounted for 1.5% of all consultations.5 However, the mean duration of measured consultations (claimable from Medicare or the DVA) did not change over this period (average, 15 minutes; median, 13 minutes).5 This suggests that the increase in shorter-duration consultations has been offset by an increase in longer-duration consultations. Short consultations in 2008–09 included a large number of procedures, and practice nurses were involved in 24% of these consultations, a much greater proportion than the average for all consultations (6.4%).2 This led us to compare consultations for 2008–09 with those for 2003–04,6 just before the introduction of MBS items for practice nurses. In both years, short consultations were relatively straightforward, involving, on average, 1.2 patient reasons for the encounter (fewer than the average for all consultations of 1.5–1.6 reasons) and management of fewer problems (single-problem consultations represented 89% of consultations in 2003–04 and 87% in 2008–09). However, in 2003–04, 26% of the problems managed were chronic conditions, while in 2008–09 this proportion had increased to 36%. Prescriptions, referrals and counselling were provided at low levels in both 2003–04 and 2008–09. However, procedures increased 3.4-fold, from 112 per 1000 short consultations in 2003–04 to 385 per 1000 in 2008–09 when practice nurses undertook almost two-thirds of all recorded procedures. More specifically, there was a fourfold increase in the categories “dressings” (from 20 to 78 per 1000 short consultations) and “excisions” (commonly cauterisation) (7 to 26 per 1000 short consultations), and a threefold increase in “incisions” (venesection and ear syringing being the most common) (5 to 14 per 1000 short consultations). There was no point-of-care INR (international normalised ratio) testing in 2003–04 but, in 2008–09, 31 INR tests were conducted per 1000 short consultations. Further, the number of vaccinations administered doubled, from 105 to 214 per 1000 short consultations. As regards administrative activities, these almost doubled between 2003–04 and 2008–09, from 19 to 35 per 1000 short consultations; in both years, almost half were for sickness certificates. Other administrative procedures recorded, including those related to health care plans, increased from 10 to 17 per 1000 short consultations. These BEACH study results show an increase of about 45% in claims for short consultations between 2003–04 and 2008–09. Two-thirds of these claims are accounted for by increases in vaccinations (23% of the increase), dressings (25%), INR tests (10%), and excisions (8%). Practice nurse involvement in procedural care accounts for about three-quarters of the increase in short consultations. By contrast, the rise in administrative activities accounted for only 5%–6% of the total. Taylor and colleagues suggest that their findings of an observed rise in Level A consultations1 is directly contradicted by reports from the BEACH study of a decrease in the number of single-problem encounters.5 While this decrease is true for the average of all consultations, it does not apply to short consultations, which are, in the main, single-problem encounters. Finally, Taylor et al propose that the increase in Level A consultations1 means there is an increasing proportion of “obvious” and “straightforward” patient encounters, and this “may support targeted delegation of such consultations to nurse practitioners or physician assistants”.1 As we have shown, assistance from, and delegation to, practice nurses may already be the main reason for the recent increased use of Level A consultations, with administrative activities accounting for only a small proportion. The newly announced enhanced role for practice nurses in primary health care (the federal government’s 2010 Budget),7 planned to commence in 2012, may further influence GPs’ utilisation of short consultations.

Helena C Britt BA, PhD · Salma Fahridin BAppSc(HIM), MHSc · Graeme C Miller MB BS, PhD, FRACGP

To the Editor: Infections caused by multiresistant gram-negative organisms are difficult to treat. Carbapenems are often used as a last resort but even these are under threat with the emergence of acquired metallo-b-lactamases worldwide, including Australia,1,2 India, China and Europe. We report the first case of a Providencia rettgeri producing the blaNDM-1 (New Delhi metallo-b-lactamase) type of metallo-b-lactamase in Australia. A man from Canberra, aged in his mid 50s, had elective plastic surgery in India in September 2009. This was complicated by a hypoxic brain injury, after which the patient spent 4 weeks in an intensive care unit. He was subsequently transferred to Canberra for ongoing hospital care. A urinary catheter specimen collected on admission in November 2009 showed a heavy growth of multidrug-resistant P. rettgeri and Pseudomonas aeruginosa. The P. rettgeri was resistant to all b-lactam antibiotics, including meropenem, as well as to all aminoglycosides, ciprofloxacin, tigecycline and colistin. The P. aeruginosa was resistant to all antipseudomonal antibiotics except for colistin (tigecycline was not tested as it has low or no antipseudomonal action). The patient was not given antibiotic therapy but the indwelling urinary catheter was changed and contact precautions were put in place. Both organisms were sent for molecular testing, which showed that the P. rettgeri had 100% homology with blaNDM-1.3 The patient cleared the organisms after 2 months, and since then has received ongoing inpatient care in the rehabilitation unit. The first NDM-1 type of metallo-β-lactamase was found in Klebsiella pneumoniae isolated from a Swedish patient who had recent medical contact in India.3 Data from the United Kingdom’s Antibiotic Resistance Monitoring and Reference Laboratory suggest that isolates with the NDM-1 enzyme have recently been repeatedly imported to the UK from the Indian subcontinent. There may now be circulation of these resistant isolates in the UK because some infected patients have no identifiable overseas links. Hospitals have been urged to be vigilant for multiresistant gram-negative bacteria in patients with recent hospital contact in the Indian subcontinent as well as the Eastern Mediterranean.4 Identification of an Enterobacteriaceae organism carrying blaNDM-1 is very concerning. No antibiotic may be available to treat patients who develop serious infection with such organisms, and there is the added concern regarding cross-infection in health care facilities. The plasmid carrying blaNDM-1 also contains genes that confer resistance to several other antibiotics.3 It appears likely that, in the near future, the NDM-1 enzyme will become a very successful metallo-b-lactamase globally. Patients infected with multiresistant gram-negative bacteria have entered the “post-antibiotic era”.

Geethanie A T P Fernando · Peter J Collignon · Jan M Bell

Two Australian blood donors were diagnosed with relapsing Plasmodium vivax malaria 5 and 15 months, respectively, after their most recent travel to a malaria-endemic country. Common features included travel to Papua New Guinea (specifically, the Kokoda Trail); full compliance with recommended malaria chemoprophylaxis; and negative results on malaria antibody testing at the time of donation. Although all fresh blood components from the two donors issued on the basis of these negative results were recalled before transfusion, these cases underscore the increased potential for relapse of P. vivax in donors returning from malaria-endemic countries, as well as the inability to identify the potential for relapse using current malarial screening tests. Clinical recordPatient 1A 63-year-old man donated blood to the Australian Red Cross Blood Service (the Blood Service) 12s7 days after returning from an organised trek on the Kokoda Trail, Papua New Guinea (PNG). An enzyme immunoassay (EIA) for Plasmodium falciparum and Plasmodium vivax antibodies was non-reactive at donation. Twenty-six days later, the donor’s wife notified the Blood Service that her husband had been admitted to hospital with fever and rigors; he was subsequently diagnosed with P. vivax malaria based on visible P. vivax parasites in a blood film (13 800 parasites/μL), and a positive result on a (non-P. falciparum) malarial antigen test (Box). He was successfully treated with primaquine. After his discharge from hospital, he was interviewed by a Blood Service medical officer and reported that he had no history of malaria; complied fully with malarial prophylaxis (doxycycline 100 mg daily, starting 2 days before entering PNG and finishing 14 days after returning home); had 2 months of lethargy after his return and developed febrile symptoms 20 days after donation; and had not travelled outside Australia after his donation. He also reported that seven of his 15 trekking companions were diagnosed with malaria after the trek. Patient 2A 39-year-old man donated blood 13 months after returning from PNG. He had made three previous donations, the first 5 months after returning from PNG, all testing negative for malarial antibodies. During the trip, the donor walked the Kokoda Trail and complied fully with prophylaxis (atovaquone–proguanil, 250 mg/100 mg daily, starting 1 day before and finishing 7 days after travel). He did not recall any recognisable malarial symptoms during the trek, but noted that a trekking companion had malaria on return to Australia. Approximately 66 days after his latest donation, the donor notified the Blood Service that he had recently been admitted to hospital with a febrile illness subsequently diagnosed as non-P. falciparum malaria; P. vivax was later confirmed from the blood film (0.5% parasitaemia) (Box). He was treated with atovaquone–proguanil (250 mg/100 mg four times daily for 3 days), made a full recovery and was discharged from hospital. He later confirmed that he had not travelled outside Australia after his return from PNG. Results of diagnostic testing of the two donors are summarised in the Box. DiscussionMalaria is transmitted predominantly through the bite of an infected female Anopheles mosquito, but, because the parasite invades and multiplies in red blood cells (RBCs), it can also be transmitted by transfusion of any blood component containing RBCs.1 Although malaria is not endemic in Australia, between 500 and 900 cases are notified annually, constituting an ongoing risk of transfusion-transmitted malaria (TTM).2 However, this risk is well controlled — the most recent recorded case of TTM occurred in 1991, involving a donor infected with P. falciparum.3 Notably, the transfusion recipient died, an outcome observed in about 10% of TTM cases caused by P. falciparum.4 To minimise TTM risk in Australia, each potential donor is asked questions to elicit if he or she has spent time in malaria-endemic countries or is at risk of having had malaria. Those identified at risk of infection are tested with an EIA for P. falciparum and P. vivax antibodies (Malaria EIA, NewLabs, Newmarket, United Kingdom). When the EIA is negative, the RBC component of the donation is considered for transfusion if at least 4 months have elapsed since the donor’s risk exposure. The 4-month waiting period minimises the possibility of false-negative test results that arise from testing within the putative 7–14-day “window period” before a complete antibody response is detectable. The Blood Service implemented serological testing of donors for malaria in 2005, replacing the previous strategy of restricting manufacture of fresh blood components from at-risk donations (ie, donations from people who had visited malaria-endemic countries in the previous 12 months or from those who had resided in an endemic country for a cumulative total of 6 months or more in the previous 3 years).5 While effectively minimising the risk of TTM, the older strategy resulted in significant loss of transfusible components (estimated in 2001 at about 5% of the Blood Service’s annual RBC production). This loss was considered unacceptable in the face of mounting demands on supplies of blood and blood products. The feasibility of serologically testing at-risk donors to reduce the period of restriction and consequent component loss had been established in Europe, where serum tests had been implemented in France6 and the UK.7 Furthermore, the use of a validated antibody test to reinstate donors after a minimum of 4 months is permitted by the applicable regulatory standard used by Australia.8 The predominant TTM risk is associated with so-called “semi-immune” individuals born or resident for extended periods in malaria-endemic countries.9 In the semi-immune person, the infection may take the form of an “equilibrium” in which very low parasite loads (generally undetectable by microscopy, and even polymerase chain reaction [PCR] testing) coexist with malarial antibodies without producing overt symptoms. Most recently recorded cases of TTM have resulted from the failure to detect and exclude the RBC-containing components of donations from semi-immune donors infected with P. falciparum.4,6 When parasite loads are extremely low, even the best plasmodial PCR assay is unable to interdict all potentially infectious donations, given that a transfusion contaminated with as few as 10 parasites can transmit infection.1 This underpins the rationale for antibody-based testing as the optimum donor-screening test, underscored by the Australian regulatory standard’s explicit exclusion of the use of molecular tests to screen donors.8 Another potential TTM risk is that both P. vivax and Plasmodium ovale have a hypnozoite form that can persist in the liver and lead to relapses after successful treatment of the primary infection.10 The interval from primary infection to relapse ranges from 1 month to 4 years.11,12 Chemoprophylactic agents are prescribed based on their efficacy against blood-stage parasites, but they are, with the exception of terminal (ie, postexposure) primaquine prophylaxis, ineffective against hypnozoites.13 Thus, they cannot prevent relapse but may delay its onset.11 Our two cases were strikingly similar, and the evidence strongly implicates PNG (specifically, the Kokoda Trail) as the site of primary infection for both. This is consistent with published evidence showing that, among non-immune travellers and soldiers returning to Australia, those from PNG and neighbouring countries were more likely to have relapsing malaria.13-15 These two cases of apparent relapse associated with P. vivax malaria in non-immune donors are, to our knowledge, the first reported cases detected by antibody testing. Further, they were unexpected because the perceived TTM risk is predominantly associated with P. falciparum infected semi-immune individuals. This either indicates that malarial antibody titres in individuals harbouring hypnozoites decline to undetectable levels 4 months or more after infection or, alternatively, that levels of parasitaemia during a “suppressed” primary infection may be too low to stimulate a significant antibody response. Thus, the current testing strategy cannot be relied on to discriminate donors at risk of relapse. This should not be seen as a reason to reject antibody testing per se, as no other available laboratory test for parasitaemia can reliably identify these individuals. Notably, the strongly positive EIA results in samples taken from the two donors at the time of admission to hospital support a robust antibody response and are consistent with the high sensitivity of the Newmarket EIA observed in samples taken from patients with acute disease.1 The TTM risk posed by relapsing P. vivax infection occurs during the asymptomatic period because symptomatic individuals would be prevented from donating. Although not precisely known, this period is expected to be short, perhaps several days. The TTM risk posed by our two patients was contained. One RBC component had been issued (Patient 1), based on its non-reactive malarial antibody test result, 20 days before symptom onset. This was successfully recalled, avoiding any potential risk to recipients. Considering the 20-day period between donation and symptom onset, it is highly likely that the donation was made before the onset of parasitaemia and, therefore, the RBC component would not have been infectious. No fresh blood components from Patient 2 were issued. What do these two cases suggest about the safety of the current Blood Service testing strategy? They certainly raise concern given that their late detection could have resulted in transfusion of potentially infectious blood components. However, such cases appear to be exceedingly rare — these are the only two reported in Australia in more than 4 years of testing. Furthermore, the contribution of such cases to overall TTM risk appears to be minute, as no TTM cases have been reported since testing began We recently published a comprehensive review that supports the existing strategy — it concluded that the current TTM risk was less than 1 in 3.3 million and had not measurably increased after implementing the testing strategy.16 Importantly, the Blood Service achieved this level of safety while recovering over 70 000 fresh blood components that would otherwise have been unavailable annually. Nonetheless, recognising the limitations of the testing strategy and the imperative to reduce recipient risk where possible, the Blood Service is considering mitigation options. As these two cases suggest travel to PNG carries a disproportionately high risk, the Blood Service is considering the feasibility of excluding donors returning from PNG from the testing protocol, and restricting fresh component production from their donations for appropriate periods of time. Blood testing for relapsing Plasmodium vivax in the two patients Place Time Pf/Pv antibody EIA* Pf/Pv antigen ICT† PCR‡ Blood film Patient 1 Sample 1 Blood Service At donation (127 days after return from PNG) Non-reactive (S/Co 0.28) Not tested Not tested Sample 2 Blood Service At hospital admission (26 days after donation) Reactive (S/Co 4.2, 3.6§) Positive Pf band negative Pan malaria positive Plasmodial DNA detected (4415 parasites/μL) Pv parasites visible (13 800 parasites/μL) Sample 3 Blood Service In hospital after treatment (33 days after donation) Reactive (S/Co 4.8, 3.7§) Negative DNA not detected Patient 2 Sample 1 Blood Service At donation (13 months after return from PNG) Non-reactive (S/Co 0.27) Not tested Not tested Sample 2 Hospital At hospital admission (66 days after donation) Reactive (S/Co > 19, 18.8§) Positive Pf band negative Pan malaria positive Plasmodial DNA detected (1861 parasites/μL) Pv parasites visible (0.5% parasitaemia) Blood Service = Australian Red Cross Blood Service. EIA = enzyme immunoassay. ICT = immuno-chromatographic test. PCR = polymerase chain reaction. PNG = Papua New Guinea. Pf = Plasmodium falciparum. Pv = Plasmodium vivax. S/Co = sample-to-cut-off ratio (this test relates to the level of antibodies in each sample compared with a predetermined cut-off level). * Malaria EIA, NewLabs, Newmarket, United Kingdom. † Binax NOW Malaria assay, Inverness Medical, United States. ‡ artus malaria RG PCR, Qiagen, Hilden, Germany. § Two values were reported because repeat testing usually requires a double check to ensure accuracy.

Clive R Seed BSc · Jacqueline T Coughlin MB BS, FRACGP · Anne M Pickworth MB BS · Robert J Harley MB BS, BMus, FRACGP · Anthony J Keller FRACP, MRCPath, FRCP

A 19-year-old Sudanese woman, who had lived for about a decade in Ugandan refugee camps, was referred for investigation of a 12-month history of a generalised rash. Two months later, her condition had deteriorated to include cachexia and drowsiness. Despite initial negative findings on investigation, human African trypanosomiasis (HAT) was suspected, and parasites were found in a double-centrifuged sample of cerebrospinal fluid. Eflornithine, the appropriate drug for treatment of late-stage disease, was obtained through the World Health Organization. This case highlights the diagnostic and therapeutic difficulties in managing late-stage HAT in a non-endemic country. Clinical recordIn January 2008, a 19-year-old Sudanese woman was referred from the community to a tertiary hospital for investigation of a 12-month history of generalised pruritus. There were no obvious precipitants or triggers for the itch. She was born in southern Sudan, but had lived in refugee camps in north-western Uganda for about a decade before migrating to Australia in November 2006. Her past medical history was non-contributory. Initial examination showed generalised hyperpigmented papules and nodules with excoriations. Prurigo was diagnosed, and treatment with topical corticosteroids was trialled. By March 2008, her condition had deteriorated, and she experienced lethargy, apathy, fevers, night sweats, weight loss, reduced rousability, abulia (impairment or loss of willpower) and seizures. The pruritus was pervasive and the scratching automatic. A past family history of human African trypanosomiasis (HAT) in her mother, which was diagnosed and treated in Uganda, was elicited. On examination, she had cachexia, and was drowsy, but rousable, and oriented to person, but not place or time. She had generalised itch with hyperpigmented, lichenified papules and excoriated nodules (Figure 1). Neurological examination showed symmetrical brisk reflexes, bilateral upper-limb cogwheeling, and myoclonic jerks involving her limbs, mouth and periocular muscles. She had palpable posterior cervical lymph nodes of less than 1 cm in diameter. Late-stage HAT was suspected, and she was admitted to hospital for further investigation. Differential diagnoses included other infective encephalitides (tuberculous and viral), vascular events and malignancies (lymphoma). Investigations showed that the patient had microcytic anaemia (haemoglobin concentration, 96 g/L; reference range [RR], 115–145 g/L), which was attributed to a known α-thalassemia trait: her renal function and hepatic function were normal. Her erythrocyte sedimentation rate was 42 mm/h (RR, < 20 mm/h). Elevated concentrations of total serum protein (104 g/L; RR, 60–80 g/L), gammaglobulin (32 g/L; RR, 8–16 g/L), IgG (24.3 g/L; RR, 5.8–13.7 g/L) and IgM (7.8 g/L; RR, 0.3–1.7 g/L) were detected. A skin biopsy suggested lichen simplex chronicus. Initial peripheral blood smears, lymph node and bone marrow aspirates all tested negative for parasites. Examination of the cerebrospinal fluid (CSF) revealed a mononuclear pleocytosis of 100 × 106 cells/L (RR, < 5 × 106 cells/L), an elevated protein level (0.9 g/L; RR, 0.15–0.45 g/L), markedly elevated level of IgM (0.36 g/L; RR, undetectable) and a low level of glucose (2.1 mmol/L; RR, 2.4–4.6 mmol/L); micro-organisms were not seen on examination of the centrifuged deposit. Gadolinium-enhanced magnetic resonance imaging (MRI) showed bilateral, symmetrical, widespread high-signal white matter change on T2-weighted imaging (Figure 2). Simultaneous T2-weighted images demonstrated high signal changes in the splenium, the brainstem and the cerebellar white matter (images not shown), and post-gadolinium images showed minimal leptomeningeal enhancement (images not shown). An electroencephalogram (EEG) showed diffuse delta-wave slowing consistent with a metabolic encephalopathy, with no evidence of ictal activity. Despite initial negative results on CSF testing, HAT was suspected on clinical grounds. Thus, repeat large-volume CSF examination was performed. Direct examination of CSF was again negative, but double-centrifuged CSF microscopy showed trypanomastigotes (Figure 3), confirming the diagnosis of late-stage HAT. Both subspecies of Trypanosoma brucei can be acquired in Uganda.1 We considered Trypanosoma brucei gambiense infection to be more likely in this patient as it is hyper-endemic in north-western Uganda and because of the subacute clinical presentation. However, as Trypanosoma brucei rhodesiense infection remained plausible, given the patient’s past travel to southern Uganda, subspecies testing was indicated. Lacking an Australian medical reference laboratory for this, we referred specimens to the Institute of Tropical Medicine (Antwerp, Belgium) for serological testing, and to a local reference laboratory for nucleic acid amplification testing.2 While awaiting results, the patient became uncommunicative, bed-bound and increasingly cachectic, making empiric trypanocidal therapy imperative. Treatment for late stage T. b. gambiense infection was commenced 19 days after admission, with intravenous eflornithine (obtained through the World Health Organization [WHO]) at a dose of 100 mg/kg every 6 hours for 2 weeks. This was tolerated without significant toxicity. At discharge on Day 39, the patient was orientated, communicative and walking independently despite persistence of slight limb hypertonia. Subsequently, subspecies serology showed elevated titres to T. b. gambiense on a serum immunofluorescent antibody test (IFAT; titre, 1:1600; RR, negative) and a card agglutination antibody test (CAAT; titre, 1:32; RR, negative). The CSF IFAT titre to T. b. gambiense was 1: 8 (RR, negative). The local nucleic acid amplification test suggested T. b. rhodesiense (data not shown), but this was felt to be clinically discordant. Three months after discharge, the patient was lucid, conversant in both English and her native tongue, neurologically intact and free from itch. Examination of her CSF showed improving pleocytosis with normal biochemical findings. MRI verified improvement; the post-contrast enhancement had resolved, but mild, diffuse cerebral atrophy was evident. She has resumed her studies and normal social activities and was relapse free at 16-month follow-up. DiscussionHuman African trypanosomiasis or sleeping sickness is caused by two subspecies of the haemoflagellate parasite Trypanosoma brucei — T. b. rhodesiense (east-African HAT) and T. b. gambiense (west-African HAT).1,3 The parasite is transmitted by the bite of tsetse flies (Glossina spp.).1 HAT is endemic only in sub-Saharan Africa, where the WHO estimates that between 300 000–500 000 people are currently infected, with 100 000 deaths directly attributed to this disease annually.3 Uganda is currently the only country where infection with both subspecies occurs. While the two foci of trypanosomiasis within Uganda appear separate, as a result of civil unrest, population displacement and the northward spread of wild and domestic animals from central and south-east Uganda, it is likely that these foci will soon converge.4-6 HAT is rarely diagnosed outside Africa. When T. b. gambiense infection is diagnosed, it is usually in the late (secondary) stage.1,7 To our knowledge, this is the first case of T. b. gambiense infection diagnosed in Australia. HAT is a biphasic disease. Early-stage disease (Stage I) denotes the post-inoculation period followed by haemo-lymphatic spread.1 An inflammatory nodule or ulcer (chancriform) may be seen at the site of inoculation, more commonly with T. b. rhodesiense infection.1 Lymphatic spread results in lymphadenopathy, with posterior cervical lymphadenopathy (Winterbottom’s sign) typical in T. b. gambiense disease.1,3 Haematogenous spread produces fluctuating fevers, hepatosplenomegaly, serositis and myocarditis, which occur in both forms of the infection, but are more common in T. b. rhodesiense disease.1 In late-stage disease (Stage II), the parasite passes through the blood–brain barrier into the central nervous system, resulting in meningoencephalitis, which is invariably fatal if not treated.1,3 Headache, ataxia, itching, speech disturbance, behavioural change, extrapyramidal signs and mental state changes may manifest.1,3 Pineal and thalamic invasion leads to hypersomnolence and circadian rhythm disruption.3 The natural history of the diseases caused by the two subspecies varies significantly; T. b. gambiense infection is insidious (over months to years), whereas T. b. rhodesiense infection usually progresses over days to weeks.1 Dermatological manifestations of HAT are non-specific. Pruritus is a pervasive symptom, present in over 50% of cases, and is a feature of disease chronicity.8 Pruritus generally correlates with greater CSF pleocytosis.8 Parasternal and generalised pruritus are common, as is peripheral oedema. Transient urticarial and macular eruptions have also been described.1,9 In very chronic disease (of more than 24 months’ duration), pruritus may decrease, heralding a pre-terminal phase of illness.8 Definitive diagnosis of HAT requires direct visualisation of the parasites in blood, CSF or tissue. Detection of trypanosomes in the CSF confirms late-stage disease. False negative results are common because of the low number of parasites in T. b. gambiense infection.1 As in the case we present here, concentration techniques such as double-centrifugation of CSF increase the sensitivity of microscopy.10 Non-diagnostic CSF changes include: lymphocyte counts of > 5/μL, increased CSF protein and IgM concentrations, and morula (Mott) cells.9,11 Identifying the subspecies of trypanosomes is difficult because both subspecies are morphologically identical. The serological tests CAAT and IFAT are available for the detection of T. b. gambiense antibodies, and this is useful in screening high-prevalence populations.9 The use of nucleic acid tests for the subspeciation of T. b. rhodesiense and T. b. gambiense is an emerging technique, and has been used successfully in the research setting.5,6,9 However, these assays are not widely available.9 Obtaining a detailed travel history from patients and recording the timing of symptoms and signs over the course of the illness remain important for differentiating the two forms of the disease. Treatment of HAT depends on the subspecies of infecting trypanosome and disease stage. Patients with early-stage disease should have CSF examination to exclude subclinical neurological involvement.9 In Australia, treatment is challenging because we have limited access to targeted therapies for HAT. The necessary drugs are accessible through the WHO. Treatments for early-stage HAT infections are parenteral pentamidine for T. b. gambiense disease and suramin for T. b. rhodesiense disease.1,6 For late-stage HAT, melarsoprol was formerly the treatment of choice.1 However, 3%–10% of patients treated with melarsoprol develop encephalopathy, which is fatal in 10%–70% of cases. Survivors of encephalopathy frequently have residual brain damage.12,13 Eflornithine is equally efficacious and less toxic than melarsoprol12,13 for late-stage T. b. gambiense infection, with lower treatment-related mortality (about 0.8%).13 Adverse effects of eflornithine include seizures, gastrointestinal upset and neutropenia, but treatment interruption is generally not required.1 Recently, one week of combination therapy with nifurtimox and eflornithine was shown to be equally effective, less toxic and easier to administer than eflornithine monotherapy for late-stage T. b. gambiense infection,14 and is now considered the treatment of choice for this infection.15 Recommended follow-up after treatment for late-stage HAT includes 3–6-monthly CSF examinations for 2 years.4 This case highlights the diagnostic and therapeutic difficulties in managing late-stage HAT in a non-endemic country. Clinicians need to be aware of infections that are non-endemic to Australia that can occur in recently arrived travellers and migrants. Appropriate treatment of HAT is life-saving and associated with good clinical outcomes. Figure 1 The patient’s rash on presentation in March 2008, showing hyperpigmented, lichenified papules and nodules with excoriation involving the trunk. Figure 2 Axial T2-weighted magnetic resonance image showing high signal in both basal ganglia (white arrow) and symmetrical high signal in the white matter, including the internal and external capsules (black arrows). Figure 3 Double centrifuged sample of the patient’s cerebrospinal fluid shown on direct microscopy showing a trypanomastigote typical of Trypanosoma brucei, the pathogen of human African trypanosomiasis (Giemsa stain; original magnification, × 800).

Paul Cherian MB BS · Ralph K Junckerstorff MB BS · David Rosen MB BS, FRACP, PhD · Prasad Kumarasinghe MD, FACD · Alan Morling BSc · Philip Tuch MB ChB, FRACP · Sonja Raven MB ChB, FRANCR · Ronan J Murray MB BS, FRACP, FRCPA · Christopher H Heath MB BS, FRACP, FRCPA

To the Editor: The Royal Flying Doctor Service (RFDS) has provided aerial emergency services to patients in the remote Kimberley and Pilbara regions of Western Australia since 1935. Until the 1980s, most evacuations were regional, and only small numbers of patients were transferred to Perth. Demand for long-distance transfers from northern WA has increased as a result of economic growth, improved resuscitation of the seriously ill, advances in treatment only available in major cities, and community expectations of more equitable access to tertiary care. In the Kimberley, a handful of specialists service an area twice the size of Victoria, confronting substantial health problems in the predominantly Indigenous population. The Pilbara, an even larger region (two and a half times the size of Victoria) and the epicentre of massive economic development in mining and energy, is also covered by only limited numbers of specialists and a single regional hospital. During the 12 months to 30 June 2009, the RFDS transferred 1018 patients from the Kimberley and Pilbara regions to Perth, up to 2200 kilometres away, and a similar number were evacuated to facilities within the regions, or to Darwin, up to 1500 kilometres away (Box 1). These patients routinely endure some of the longest medical retrievals anywhere in Australia, if not the world. With turboprop aircraft, retrieval times can be up to 12 hours. Pilot flight-time limitations over such distances mean that 93% of Kimberley patients require multiple aircraft and crews to achieve transfer (Box 2). Patient handovers increase transport time and clinical risk, and require considerable coordination. In October 2009, the RFDS in WA launched a fast long-range medical retrieval jet, available to all of the community, irrespective of their capacity to pay. The aircraft, a Hawker 800XP medium-sized jet, has been funded by corporate sponsorship from the mining company Rio Tinto, as well as by public fundraising and cost recoveries. The aircraft has been exclusively outfitted for its aeromedical role. It has the capacity to retrieve two patients in need of critical care with two medical retrieval teams on board, non-stop from the most distant locations in WA, and can carry a third stretcher patient if necessary. Although they are more expensive to purchase and operate, the use of pure jet aircraft can substantially reduce transport times for patients with complex or time-critical conditions, and thus improve clinical outcomes. This is the first jet in the history of the RFDS, and represents a quantum step forward from the “DH50 machine” referred to in the Journal in 1927,1 or the pressurised turboprop aircraft adopted in the 1980s.2 Flying times for patients will be effectively halved. The aircraft, designated “Rio Tinto Life Flight”, will be integrated into the existing RFDS state-wide retrieval service in WA, which coordinates and operates 14 turboprop aircraft from five centres. This is a significant initiative to improve access and equity to tertiary care for Indigenous and non-Indigenous Western Australians in remote areas. To date, aeromedical jet aircraft have not been government-funded. We hope that by demonstrating the viability and benefits of the service, government support will become available in future years. 1 Trends in Royal Flying Doctor Service long-distance medical retrieval from and within the Kimberley and Pilbara regions of Western Australia Years are financial years to 30 June. 2 Patients requiring more than one aircraft to achieve transfer to Perth Years are financial years to 30 June.

Stephen A Langford

I have always dreaded that moment at funerals when you see the coffin for the first time. Perhaps it’s the finality of death or the sadness of the loss, but that moment seemed an inevitable consequence of the dying process, until I was faced with the impending death of my father. My father was 75 years old when he died of cholangiocarcinoma. He was a man with many friends. He was curious and loved to chat, he loved a beer, he made people laugh, he worked hard and was well loved. He was cared for at home, mostly by my mother. Friends and family came to pay their respects, and some came again for another “last time”. We sat with him, tended to his needs and contemplated life without him. The palliative care team visited often and waited for the cue to arrange hospice care because we could no longer cope; to us, this meant dad leaving and being cared for by someone else. The cue never came. The family rallied and dad stayed at home. This raised another issue I had with dying — the moment of separation when the body is taken away from the family. I had witnessed it often in my working life and wondered how families determined the right time to go and how they felt about leaving their loved one behind. Would they want to take the body with them? A few days before dad died, the funeral director came to the house. We leafed through folders of coffins and flowers, and discussed the service. She said to call them at any time when he died and they would come to the house (to take him away). I took a breath. “Can’t we keep him here?” My mother looked at me. “Are you sure you’re allowed to?” We hadn’t discussed this option so I had no idea what she thought about it. In fact, I didn’t think I would raise it. I hadn’t thought it through completely but felt intuitively it was the right thing to do, for me and possibly for her. Between us we had attended many funerals but had no knowledge of anyone who had kept the body at home. Ultimately, the decision would be hers; he was her husband, and she would continue to live in the house. Maybe it would be too much for her to bear, but she didn’t seem opposed to the idea, and it was possible. In the warmer months a cold table can be provided, but we were in the middle of winter and the garage under the house was particularly cold, so a body could rest down there. After some discussion, we decided that dad would go to the garage and not leave us until the last. That decision would have a profound effect on my view of death and grieving. Dad died early one Sunday morning at home, with my mother by his side. The rest of the family slowly arrived. Dad stayed in his bed, where we washed him and dressed him as if ready for golf. The children came in and out of the bedroom. They tied up his shoes and added things to his pockets. We ate lunch. The civil celebrant conducting the funeral came over and we talked about dad. Someone would disappear into the bedroom for a while and come out with red eyes. In the afternoon, the funeral directors arrived. We carried dad downstairs and placed him in the coffin, next to the caravan my parents used as their second home on travels. His golf clubs were beside him and his work bench just behind. Mum moved into the caravan for two nights. Dad was now in the garage. Mum’s sister arrived after a long journey. After cups of tea, they went downstairs to see dad. The garage became a sanctuary where people came and went and the children ran and danced around the coffin. Being close by allowed many quiet moments to sit next to the coffin, talking, weeping and taking time. Mum sat beside him in the early hours of the morning. On the day of the funeral, the family gathered for more food, more cups of tea and last-minute writing of speeches. We went down to the garage and lifted the lid of the coffin. Dad was still the same, looking pale and peaceful. We cried, laughed and added extra things that we thought he might want, or that we wanted him to have. The hearse arrived and we carried dad out and drove slowly to the church in this small country town. The family carried the coffin into the church that was filled with dad’s family and friends, and the friends of his children and friends of friends. Many burst into tears at the sight of us and the coffin. It was a good ceremony, and then we carried him out again. We arrived at the cemetery and carried the coffin to the graveside. The children wondered whether we would also have to dig the hole. The coffin was lowered and we all went for more cups of tea, and sherry and cake. The death of my father was an experience I had not expected. I imagined being inconsolable with grief and unable to make decisions. However, it was a gentle time that brought the family together and created a wonderful memory. He had a good death at home and a good after-death. Keeping his body at home was an unusual decision in the eyes of many. For the family, it represented an opportunity to do something special for someone we loved, but it also facilitated the grieving process. It seemed to slow down the period from the death to the funeral. There was no pressure to have the body removed or to pay visits to the funeral home for a “viewing”. He was in the garage and we could see him whenever we wanted; we grew accustomed to looking at the coffin and began to come to terms with his death. There was also comfort in continuing to offer care until the end, rather than his body being in the care of someone else. There are cultures where it is the norm to keep the body at home. I had witnessed it in Tonga on my student elective, where I equally appreciated the symbolism of coming together and sharing a meal (or cups of tea!) at these times. In contrast, the ritual of keeping the body at home is uncommon in Australian culture. It certainly seemed uncommon to the funeral director and others I have spoken to. Maybe people think about it but don’t ask. Perhaps we should ask for them.

Karen L Dunn MB BS, FRACP, PhD

To the Editor: A 40-year-old, first-time traveller from the northern hemisphere, on an expedition cruise to the Antarctic Peninsula, experienced thirst, polyuria, fatigue and worsening headaches for several days before embarking on a rough Drake Passage crossing in January 2009. Being well-to-do, fit, and taking no regular medication, he had decided on an adventurous holiday rather than his usual high-end European resort vacation. En route to the expedition vessel in Ushuaia, Argentina, the passenger hurriedly obtained a non-prescribed supply of “adventure travel” medication from a pharmacist acquaintance in the Middle East. To ensure its effectiveness, the passenger had complied with the pharmacist’s recommendation to begin taking the medication prophylactically several days before sailing. On the outbound crossing, the passenger consulted me, the ship’s physician, about the aforementioned unusual constellation of symptoms that he had been experiencing for several days, which were now compounded by severe motion sickness. On examination, he was not confused, had no meningeal irritation, loin percussion tenderness or fever, and was mildly dehydrated. It was soon revealed that he had been using acetazolamide for several days, as recommended. On reflection, I thought the container for acetazolamide that he showed me bore some resemblance to the containers used to store promethazine in the ship’s clinic (similarly sized bottles with similarly coloured lids and labels), with promethazine being well recognised as an effective treatment for motion and sea sickness.1 The symptoms that he had had for several days while taking the “adventure travel” medication before embarking on the expedition vessel are ascribable to acetazolamide.2 The passenger had been given medication on the now apparent misunderstanding that it was for ameliorating symptoms associated with a “high altitude” rather than “high latitude” destination (the bottle had been dispensed after a brief conversation in English — neither party’s first language). The pharmacist had misunderstood, believing that the passenger was travelling to a destination at a high altitude, for which acetazolamide chemoprophylaxis would have been appropriate to reduce risk of high-altitude sickness.3 Polar expedition cruising remains a relatively exclusive though environmentally sensitive pursuit. In the 2008 southern summer season, 34 000 passengers departed for an Antarctic destination by ship;4 most experienced some degree of motion sickness exacted by rough passages across the Drake Passage (the “Drake Shake” rather than the much prayed for and preferred smooth crossing across the “Drake Lake”) to the Antarctic Peninsula. Misunderstanding can occur when high latitude (the Antarctic and Arctic) is confused with high altitude, with the adventurer passenger at risk of being prescribed the wrong chemoprophylaxis. This risk may be accentuated in countries where travel medicine and pharmaceutical dispensing are not well regulated. On another note, in my opinion, it may be helpful to give medication containers and tablets a colour related to their purpose; perhaps bilious green for sea sickness and clear blue for altitude illness.

Joseph Y S Ting

To the Editor: Two 35 cm long blue-tongue lizards live in the rockery above my home swimming pool (water temperature, 19ºC). While cleaning the pool, I was shocked to see one of them floating motionless on the surface, but with its head held out of the water. Rescue with a net revealed a sluggish but healthy lizard, that slowly crept into the ground cover. Returning to my task, I was devastated to see the other lizard motionless on the bottom of the pool. After rescuing it, I thought it was dead, but a trace of slow muscular movement led me to action. With its head down, I rhythmically squeezed the upper body circumferentially with one hand, expelling an amazing amount of water and then saliva-like fluid. The abdomen, which had been distended to about 7 cm in diameter, reduced in size at least 1 cm. Gradually, there was more sluggish body and limb movement, but no discernible respiration and no opening of the mouth. After about 10 minutes, the eyes opened and I reduced my gentle efforts, but still fluid drained if the head was held down. Eventually, the lizard was placed on the rockery and observed. After a few minutes, it opened its mouth widely, revealing the oral cavity completely full of froth. More head-down draining and rest gradually improved the situation and, some time later, normal respiration seemed to have returned. Later in the day, it had moved about 30 cm and, before nightfall, it had gone. Next morning, both lizards were seen, appearing perfectly healthy and normal. I have no idea how long they were in the pool, or why, but presumably they had had a tussle, a game of chasey or a fight and lost their bearings. After 3 years of retirement from general practice, I felt considerable personal and professional delight! Comment: Lizards generally have simple lung structures compared with those of mammals. Their lungs are basically two membranous sacs, with no bronchial tree that leads to the alveolar sacs in mammals. This means their capacity for oxygen exchange is less than that of mammals. They have, however, many physiological adaptations to compensate for this limitation, including a capability for prolonged anaerobic metabolism and the ability to perform right-to-left cardiac shunting. Consequently, reptiles are much better able to cope with hypoxia than mammals. If hypoxia continues for more than an hour, heart rate may fall 50%, and a right-to-left shunting of up to 80% of cardiac output occurs. Several species of lizards use their capacity to cope with hypoxia to advantage and will submerge themselves for several hours to escape predators. Blue-tongue lizards are a terrestrial species and generally avoid contact with water. If necessary, however, they are very good swimmers. They tend to inflate their lungs, and use their tails to propel themselves across the surface of the water. The lizard described by Darvall probably drowned because of exhaustion and hypothermia. In reptile drowning, it is important to help remove water and respiratory secretions from the lungs using gravity and coupage, particularly as reptiles appear to lack a good mucociliary clearance system. The pool water, being chlorinated, would have had reduced microbial levels, making bacterial pneumonia, seen in accidental drowning in reptiles, less likely. Keeping the reptile warm is also important, to stimulate muscle activity and respiration. Had this lizard failed to respond to drainage and coupage, it may have needed supplementary oxygen, a measure that warrants caution. The respiratory centre of reptiles responds mostly to low partial pressure of oxygen, unlike the respiratory centre of mammals, which normally responds to increased partial pressure of carbon dioxide. Thus, supplying 100% oxygen to reptile patients requiring resuscitation inhibits return to normal respiration. Reptile resuscitation is best provided with normal air, at a rate of six breaths per minute.

William L Darvall · Shelton Smith

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

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

A compilation of effective non-drug treatments could help increase their uptake in clinical practice In 2004, the Journal published a randomised controlled trial of graded exercise for chronic fatigue syndrome (CFS).1 As with several similar trials, this trial found that graded exercise was an effective intervention. But what is graded exercise? In response to numerous emails from both doctors and CFS patients who wanted further details of the exercise program, the authors of the study published a second article that provided the additional “how to” details and addressed different scenarios.2 I now keep the pdf file of this second article on my general practice computer to give to, and discuss with, CFS patients. The difficulties in accessing information on this simple, non-drug intervention are in stark contrast to the helpful tools available for prescribing pharmaceuticals: formularies, prescription pads, and pharmacies. The problem is not unique to graded exercise. In a review of studies selected for the journal Evidence-Based Medicine, we found that the adequacy of treatment descriptions in trials and systematic reviews appeared to be worse for non-drug treatments than drug treatments,3 with only about 30% of non-drug treatments (compared with 66% of drug treatments) being directly replicable from the information given. Fortunately, obtaining additional information from references, searches and authors increased this figure to around 65%.3 The poor descriptions and lack of easy reference may help explain the slow uptake of some effective non-drug treatments. For example, while the Epley manoeuvre for benign positional vertigo has been known as a simple effective physical treatment for over a quarter of a century, a German survey suggested that it is used in only 8% of affected patients.4 Though many general practitioners seem have heard of it, informal surveys of GPs at large educational seminars have shown that few know how to do it and fewer actually use it. Title page of a 1669 edition of Pliny’s Naturalis historiae, volume 1 For medicinal treatments, the need for an encyclopaedic collection with clear descriptions of how to prepare them was recognised long ago. Pharmacopoeias date back to at least the first century AD, when Pliny catalogued the herbal medicines in use in ancient Rome (Box).5 In the United Kingdom, the first list of approved drugs with information on preparation methods was the London pharmacopoeia, published in 1618. In 1864, the British pharmacopoeia (http://www.pharmacopoeia.gov.uk) was published to try to harmonise pharmaceutical standards through the merger of the London, Edinburgh and Dublin pharmacopoeias. Today, we cannot imagine the practice of medicine without a pharmacopoeia and a formulary. Outside pharmaceuticals, there seems to have been much less compilation and standardisation. This is not for lack of effective non-drug treatments. For example, a survey of 1464 randomised controlled trials supported by non-commercial sources in the UK between 1980 and 20026 found that more than half were for non-drug treatments, such as education, surgery, diet, exercise, and physical and psychological therapies. Although some of these are picked up by the relevant professions, many seem to fall between professional boundaries. For example, “bibliotherapy” (providing patients with informative reading material on self-management of their condition) has been used successfully in treating depression7 and irritable bowel syndrome.8 What would a formulary of non-drug therapies look like? Although an extensive compendium of all non-drug treatments would be worthwhile, for clinicians a non-drug formulary should be restricted to interventions shown to be effective by randomised controlled trials or other definitive evidence.9 As with drug formularies such as the British national formulary (http://www.bnf.org/bnf) or the Australian medicines handbook (http://www.amh.net.au), a non-drug formulary should also contain information on indications, contraindications and precise details of treatment. To be sufficient for a practitioner to replicate the treatment delivered in the trials, the treatment details will commonly need to be longer than the dosage, duration, and titration information typically given for pharmaceuticals. However, with the move to online information access, there are now minimal restrictions on space. Many journals now allow supplements, including video material, to be included with online versions of research articles. For example, the Journal of Visualized Experiments (http://www.jove.com) was established to capture the intricacies of life science research by providing online videos of experimental procedures. For non-drug interventions, it is essential that details of procedures and treatments are not copyright to a specific journal but are made freely available. Although pharmaceuticals have been central to many breakthroughs in medicine, non-pharmaceutical advances — in areas such as behavioural therapy, exercise therapy and nutrition — also offer many benefits, but their uptake has been less. For GPs, but also for the many discipline specialists, a non-drug handbook would be an important tool to foster a more balanced use of evidence-based treatments. I would like one on my clinic desk tomorrow, please.

Paul P Glasziou MB BS, FRACGP, PhD

Successful transition of students to competent work-ready health professionals requires an ability to work in health care teams. Poor communication and teamwork practice has been implicated as a contributing source of error affecting patient safety. Traditional university curriculum structures severely limit the time that students from different professions can spend together, learning about and from each other (interprofessional education [IPE]). IPE initiatives need to focus on whole-of-system impacts and organisational sustainability. The Health Care Team Challenge (HCTC) is a high-profile leadership strategy that engages students, academic staff, practising professionals, policymakers and industry in a whole-of-system approach to IPE and interprofessional practice. Interprofessional student teams compete at a live public event for a cash prize for the best management plan centred on a complex clinical case study. National and international HCTCs are planned for future years.

Rosalie A Boyce BSc, MBus, PhD · Monica C Moran MPhil(OT), GCertED, DSocSc · Lisa M Nissen BPharm, PhD, FSHP · Helen J Chenery BSpTher, MSpTher, PhD · Peter M Brooks MD, FRACP

Travel medicine. 2nd ed. Jay S Keystone, Phyllis E Kozarsky, David O Freedman, et al, editors. Philadelphia: Mosby, 2008 (xiii + 611 pp). ISBN 978 0 323 03453 1. This is a great book and worth the $215 asking price. It is a comprehensive tome for clinicians new to travel medicine, as well as having much to offer those with more advanced knowledge. It would be a useful tool for those studying for the International Society of Travel Medicine Certificate of Knowledge Examination. The book is well written, with up-to-date and practical discussions. The list of authors is a “who’s who” of the luminaries of travel medicine, each writing about their area of expertise. It is well laid-out and easy to read, with good use of colour, flow charts, tables, figures and photos. Boxes highlighting key points at the start of each chapter are a useful aid for the time-poor. The book comes with a searchable CD-ROM, although the book’s index and table of contents are so good that the CD-ROM seems almost superfluous. The scope of the discipline is well covered — from different travellers (eg, expatriate workers, people with disabilities, older people, pregnant women, and children) to different diseases (including extensive discussion of traveller’s diarrhoea) and health precautions (eg, vaccines, malaria medication, water purification); from pretravel to post-travel, different types of trips (eg, cruises, international adoption, medical tourism), along with psychological and environmental aspects of travel health care. A small component of the information is only relevant to readers in the United States, such as details about insurance companies and paying for visits. American spelling is used. There are a few minor omissions (such as the option of Quantiferon screening for tuberculosis). This does not detract from the excellence of the book. At 640 pages, it takes a bit of reading but the reader is well rewarded.

Deborah J Mills

General practitioners are often the first point of contact for patients with oral white lesions, which represent a wide spectrum of diagnoses of varying seriousness. Some clinical features are classical and others overlap between different diagnoses; they should be correlated with patient history, and sometimes other investigations, for diagnosis. Leukoplakia is a clinical term, and is a diagnosis of exclusion with no histopathological connotation. It has been redefined to describe a predominantly white lesion with premalignant potential. Patients with lesions that are potentially malignant should be referred to an oral medicine specialist or oral maxillofacial surgeon for systematic management.

Kai H Lee MB BS, FRACDS, FRACD(OMS) · Ajith D Polonowita BDS, MDSc

Clinical record In November 2006, a 59-year-old man was admitted to hospital with a 5-week history of dyspnoea secondary to type I respiratory failure, generalised weakness, poor mobility, and bilateral shoulder and knee pain. He had been diagnosed with inclusion body myositis in 1998. Comorbidities included systemic lupus erythematosus, pulmonary hypertension, interstitial pulmonary fibrosis (Figure, A), type 2 diabetes, obstructive sleep apnoea and gout; and he had undergone a bilateral total hip replacement, which enabled him to walk a limited distance unaided. Six months earlier, his general practitioner had noted a functional decline caused by a combination of poor pulmonary function, myositis and inactivity, which resulted in the patient requiring a wheelchair for mobility and help from his son with some activities of daily living. Methotrexate and azathioprine, which had been prescribed for management of the underlying connective tissue disease, were thought to be contributing to the respiratory failure and were withdrawn. Prednisolone therapy (50 mg daily) was begun, and some improvement in respiratory function was noted after 2 weeks. However, the patient did not regain baseline function and remained bed-bound, requiring assistance with all activities of daily living. Admission to a high-level residential care facility was considered, but the patient wanted to return home with his son as carer. A rehabilitation physician was consulted 3 weeks after admission, with a view to improving the patient’s functional status so that he could return home. The patient was left-hand dominant with bilateral poor grip due to distal muscle weakness and metacarpophalangeal and interphalangeal joint contracture secondary to systemic lupus erythematosus. Muscle strength surrounding the shoulder girdles, hips and quadriceps declined from 4/5 to 2/5 bilaterally over a period of 6 months owing to myositis and inactivity. Advanced osteoarthritic changes were evident in the glenohumeral joints, resulting in pain (greater on the left side) and global restriction of shoulder movements. Moreover, an x-ray showed avascular necrosis of the head of the left humerus (Figure, B). X-rays of the knee joints and lower legs showed bilateral recurvatum deformity (hyperextension) and gross mediolateral instability, caused by quadriceps weakness. He could transfer from bed to chair and stand with the aid of a mechanical lifting device and moderate assistance from two people. Knee pain prevented him from standing unaided for more than 2 minutes. An inpatient rehabilitation program was implemented by a multidisciplinary team comprising a rehabilitation physician, physiotherapist, occupational therapist and rehabilitation nurses. The program included strengthening exercises for weaker muscle groups, as well as training focused on building endurance to improve transfers and activities such as grooming, bathing and toileting. The patient was prescribed continuous home oxygen therapy (4 L/min) because of poor spirometry results (forced expiratory volume in one second [FEV1], ratio of FEV1 to forced vital capacity, and carbon monoxide diffusion in the lung were 60%, 91% and 21% of predicted values, respectively, with no bronchodilator response) and abnormal blood gas concentrations (Po2, 60 mmHg; Pco2, 26 mmHg; pH, 7.52). The myositis was monitored weekly by measuring erythrocyte sedimentation rate and levels of C-reactive protein and creatine kinase. The patient underwent a left suprascapular nerve block to alleviate the left shoulder pain. The degrees of pain and disability were assessed before and after the procedure using the Shoulder Pain and Disability Index;1 the patient reported a 75% reduction of pain in the left shoulder and 25% improvement in shoulder disability. A carbon-fibre hinged orthosis was prescribed for each knee to correct the recurvatum deformity and improve gait (Figure, C). The orthoses controlled hyperextension during walking and corrected the instability of the knees. C-reactive protein and creatine kinase levels remained within the reference ranges over a period of 6 weeks. After 6 weeks of rehabilitation, the patient required less oxygen (2 L/min) and maintained an oxygen saturation greater than 90%, with quick recovery after activity, indicating improved cardiovascular endurance. Also, his maximum heart rate 5 minutes after exercise decreased from 130 beats/min to 84 beats/min. The reduction in pain and dyspnoea resulted in improved transfers and ability to perform activities of daily living. In December 2006, after the 6-week rehabilitation period, he was able to walk 30 m with the aid of the orthoses and a walking frame, and he was discharged. Home-based exercises were implemented by his son, the nerve block was repeated every 4 months, and he continued to live at home until June 2008. In July 2008, he died due to pneumonia and septic shock. A: High-resolution computed tomography scan showing pulmonary nodules and ground-glass appearance of interstitial pulmonary fibrosis. B: X-ray showing degenerative changes and flattening of the head of the left humerus, suggesting avascular necrosis. C: Control of knee deformity using custom-made orthotics. This case highlights the capacity of therapeutic exercise, pulmonary rehabilitation, pain management and use of orthoses to reduce the impact of disability, restore function and potentially allow patients to live at home with family and community support. Our patient had several comorbid conditions that required specific management, in addition to general deconditioning after his acute illness. Inclusion body myositis. This late-onset inflammatory muscle disease results in impaired muscle function, muscle atrophy and weakness, affecting both proximal and distal muscles. It accounts for 17%–30% of idiopathic inflammatory myopathies and can be associated with autoimmune diseases.2-4 In the past, patients with myositis were discouraged from exercising owing to a fear of increased muscle inflammation. However, studies in the 1990s reported that exercise might have a non-specific benefit.5 Patients with inflammatory muscle disease benefit from mild to moderate muscle training and endurance exercise, and muscle inflammation does not increase after exercise.6-8 A specifically tailored rehabilitation program improved our patient’s physical function without evidence of increased muscle damage. Interstitial pulmonary fibrosis. This group of lung diseases affects the interstitium of the lungs, eventually causing restrictive lung disease. Pulmonary rehabilitation — involving strength and endurance training for arm and leg muscles (eg, walking, cycling, lifting small weights), education on energy conservation and anxiety management, chest physiotherapy, and breathing techniques such as pursed lip and diaphragmatic breathing — has been shown to reduce dyspnoea, improve exercise capacity, enhance quality of life and reduce hospitalisation.9 Chronic shoulder pain from arthritis. This type of pain can be safely and effectively treated by suprascapular nerve block, which avoids the side effects of oral analgesics.10 In our patient, it was an essential component of the rehabilitation program because it enabled him to perform activities of daily living and use a walking frame. Intra-articular steroid injection was not used as it might have worsened the avascular necrosis of the head of the left humerus. Genu recurvatum. This is an angular deformity (hyperextension at the knee) in the sagittal plane caused by quadriceps weakness. Mediolateral (valgus and varus) instability occurs in the coronal plane. Both deformities require three-point stabilisation. In our patient, orthoses with a free-motion joint and a hyperextension block controlled both deformities and allowed knee movement during walking.11 Gait training with such orthoses includes static weight shift and dynamic balancing exercise in parallel bars, followed by progression to a normal gait pattern. Few residential care facilities in Australia specifically cater for disabled patients younger than 65 years. Our patient, who had an able and willing carer available, was highly motivated to return home. We believe that the option of active rehabilitation should always be explored, regardless of the apparent severity of underlying medical conditions. Lessons from practice Patients with inflammatory muscle disease benefit from mild to moderate muscle training and endurance exercise. Pain, deformity and deconditioning are major contributors to disability, and amplify the effects of underlying medical conditions. The goals of multidisciplinary rehabilitation are to restore function and to enhance quality of life. Active rehabilitation should always be considered, regardless of the apparent severity of underlying medical conditions.

Anupam Datta Gupta MD, FAFRM, DipMuscMed · Nigel Quadros BM BS, PhD, FAFRM

Chronic diseases with a lifestyle-based aetiology currently make up a significant proportion of primary care consultations, but management often falls between the demands of public and clinical health. A modified clinical approach, based around the concept of “lifestyle medicine”, helps fill the gap by adding behavioural, motivational and environmental skills to conventional medical practice. When used in a multidisciplinary setting, lifestyle medicine offers potential cost and effectiveness benefits, which are beginning to be realised.

Garry J Egger BA, MPH, PhD · Andrew F Binns AM, BSc, MB BS, DROCG · Stephan R Rossner MD, PhD

It is said the medical profession should learn from the aviation industry, which has a much better safety record. This is possibly because pilots get a mandatory 8 hours’ sleep. They also have to rest between shifts, for longer than the hours worked. Pilots do everything in duplicate to ensure accuracy. Most importantly, the pilots know that if their passengers are going to die, they are going to die too. So, I think it is high time that medicine looks into emulating the aviation industry. Next week, after rewriting my 11th revision for the MJA until 3 am, I am going to walk into my outpatient clinic at 12 pm (after my mandatory sleep-in) and tell my patients I was following safety regulations. Perhaps I should make an announcement on the hospital paging system: Ladies and gentlemen, this is the doctor speaking — we apologise for the short delay. We’re about 3 hours behind schedule but hope to make up some time through the day ... I like the idea of having equal, if not longer, hours of rest after every shift. It means that when I am on call on Saturday and Sunday, I can take the next 2 days off. (Golf or tennis? The more I think about it, the more exciting it is.) What about doing things in duplicate? Next time I check a pulse and find that it is 72 beats/min and regular, I will confirm it only after I have my registrar check it too. I can hear her saying, “right wrist flexed and pronated, radial pulse checked, 72 per minute” — and my reply, “Roger”. When we get into a plane, we are told where we are going, how long it will take, and exactly what time we will get off the plane. I think this is an excellent idea. Imagine telling a patient: Mr Nair, you are going to the preoperative ward now to prepare for your surgery. Afterwards, you will be in the intensive care unit for 24 hours, and then stepped down to postoperative care. You will be leaving us in 7 days at 12:30 pm. Your surgeon will be —, assisting him will be —, and the anaesthetist will be —. To look after your comforts in the ward, we have the lovely Nurse — ... Not everything is done better in aviation than in medicine though. For instance, all airline passengers (possibly except those in the front with the free French wine) are expected to exit the plane in the same condition as they entered. In medicine, we expect that they will leave in better condition. In this regard at least, the airlines should learn from us. Once on the plane, there is the flight safety routine before departure. Imagine, during your first day at the hospital, watching a nurse demonstrating how to use a defibrillator. Having watched her do this once, you are then supposed to do it yourself the next time there is a cardiac arrest! I am not sure whether, in the panic of a “water landing”, I can even put on the life vest the way they have shown me. Why can’t airlines certify passengers before we board as able to don the life vest, with recertification required every 6 months? The seatbelt demonstration is another aviation routine that we do not need to emulate. Who does not know how to do up a seatbelt? (After all, I managed to drive myself safely to the airport so I could park in the ridiculously expensive car park.) If you don’t know how to put on a seatbelt, should you really be travelling? In medicine, we believe in evidence and scrutinise everything carefully. We do not take anything for granted. In flying, when requesting an exit seat (to more comfortably accommodate your obesity, osteoarthritis and sciatica), you are asked, “In the event of an emergency, are you willing and able to assist other passengers?” You agree, and they give you the seat. This is like believing the man with cirrhosis and delirium who lies about his alcohol intake! I often wonder whether that fat man in the exit seat could even fit through the emergency exit, let alone help anyone else. Should we have a limit on the body mass index for exit seats? Should we have a stress test or fitness test before the seat allocation? Then there are the oxygen masks. We do not tell chronic bronchitis patients, “In the event of your oxygen levels dropping, a mask will drop down above you” — we just give it to them. What about this idea of fitting your own oxygen mask before helping others? Just imagine if all doctors treated themselves first and then looked after the young, old and disabled. We are far more altruistic in our profession! There is one final thing to consider in which flying is far superior to medicine: the airport lounge. If you are a frequent flyer with a gold or platinum card, you enjoy special privileges. If you are a frequent attender in the hospital, should you also have a special area for waiting, depending on your status? If you are a gold or platinum patient, unlike those with silver cards, you should not have to wait in the emergency department for 24 hours to get an inpatient bed. I think it is time to review the whole thing. Clearly, we in medicine are good at some things; others, they do better in aviation.

Balakrishnan R Nair FRACP, FRCP, GradDipClinEpi

To the Editor: We conducted a qualitative study to explore the perspectives of general practitioners and allied and other health professionals on their interactions in the care of patients with chronic disease, especially where Team Care Arrangements (TCAs) are involved. We interviewed 16 clinicians from urban and rural New South Wales who were involved in the care of patients with type 2 diabetes, ischaemic heart disease and hypertension — four GPs, two practice nurses, two medical specialists and eight allied health clinicians. Interviews took place from late 2006 to early 2007. While all those interviewed felt that a coordinated approach provided optimal management of chronic disease, this did not always seem to translate into smooth working relationships. Allied health clinicians and medical specialists described two types of attitudes of GPs to team care. They perceived some GPs as accepting of the involvement of others in patient care, leading to mutually respectful and highly satisfying working relationships. However, they felt other GPs did not value the opinions of allied health professionals and referred patients to them to fulfil a process (either for TCAs or at the patient’s request), or saw them as competitors. As one urban allied health clinician said, “I think they’ve got to realise that we’re not there to compete, we are there to assist”. TCAs provide financial incentives for GPs to coordinate care.1 We have previously reported that multidisciplinary care plans are associated with improved attendance at allied health services and improved metabolic control for patients with diabetes.2 However, in the present study some respondents felt that TCAs were little more than “paper shuffling” — predominantly a mechanism to attract reimbursement, rather than to facilitate two-way communication. Although TCAs provide an opportunity for communication between health care professionals, they have not overcome all the barriers to communication, especially in cases where an interprofessional relationship based on clear understanding of each other’s roles has not already been established. Our findings suggest that relationship-building and discussions about roles in shared care, including the power differentials between professionals, would improve the functioning of TCAs. Other recent studies have also reported on the lack of effective collaboration between GPs and other health professionals in managing chronic conditions.2,3 Respondents felt that it was uncommon for clinicians to discuss and agree on a plan of care. Optimal management of chronic disease requires a team approach and, consistent with other studies,4,5 we found that all the professional groups interviewed acknowledge the desirability of team care and its potential to improve patient outcomes. With increasing emphasis on team care, it is imperative that policies fund and facilitate a real team approach that is in the best interests of patients — one that places greater emphasis on two-way communication rather than paper shuffling or gatekeeping. This requires working with allied health professionals, medical specialists and GPs to improve communication and trust between clinicians. The Divisions of General Practice must surely be well placed to facilitate this process.

Sue E Kirby · Joyce L Chong · Maureen Frances · Gawaine Powell Davies · David A Perkins · Nicholas A Zwar · Mark F Harris

Objective: To examine whether there was a reduction in demand for psychological services provided through the Access to Allied Psychological Services (ATAPS) projects after the introduction of the Better Access to Psychiatrists, Psychologists and General Practitioners through the Medicare Benefits Schedule (Better Access) program, and whether any such reduction was greater in urban than rural areas.Design and setting: A Division-level correlation analysis examining the relationship between the monthly number of sessions provided by allied health professionals through the ATAPS projects run by Divisions of General Practice, and allied health professional services reimbursed by Medicare Australia under the Better Access program, between 1 November 2006 and 31 March 2007.Main outcome measures: Uptake of each program, assessed by the number of sessions provided.Results: Overall, despite dramatic uptake of the Better Access program in the first 5 months after its introduction, the demand for ATAPS services was not reduced. The correlations between the numbers of sessions provided by both programs overall (r = − 0.078; P = 0.074) and in rural Divisions (r = 0.024; P = 0.703) were not significant. However, there was a significant negative correlation between the numbers of sessions provided by both programs in urban Divisions (r = − 0.142; P = 0.019).Conclusions: For the first 5 months of the Better Access program, the two programs seemed to operate relatively independently of each other in terms of service provision, but in urban Divisions there was a move towards services provided through the Better Access program. Early indications are that the two programs are providing complementary services and are working together to address a previously unmet need for mental health care.

Justine R Fletcher BPsych, MPsych · Bridget Bassilios BSc, GradDipPsych, DPsych · Fay Kohn DEd, MA, GradDipTESOL · Lucio Naccarella BSc(Hons), GradDipMHS, PhD · Grant A Blashki MB BS, MD, FRACGP · Philip M Burgess MA, PhD, FAPS · Jane E Pirkis MPsych, MAppEpid, PhD

Successful, “innovative” primary health care (PHC) models exist that have adapted to the specific circumstances of their rural and remote context. A typology of discrete, integrated, comprehensive and outreach rural and remote services exists rather than a “one coat fits all” PHC health service model. Successful models are characterised by macro-scale environmental enablers (supportive health policy, federal–state relations, and community readiness) and five essential service requirements (workforce organisation and supply; funding; governance, management and leadership; linkages; and infrastructure). Service sustainability depends on ensuring that key systemic service requirements are met at the local level in ways that accord with, and are supported by, the broader macro-scale environmental enablers. Based on these principles, these model types are amenable to generalisation and evaluation in other regions.

John S Humphreys BA, PhD, DipEd · John Wakerman MB BS, MTropHlth · Robert Wells BA · Pim Kuipers BA(Hons), MHumServ, PhD · Judith A Jones BA(Hons), GradDipAppSci(Comp), MSPD · Phil Entwistle BSc, MTropHlth, PhD

Objective: To determine if low-ankle-pressure graduated-compression tights (GCTs) reduce flight-induced ankle oedema and subjectively rated travel symptoms of leg pain, discomfort and swelling, and improve energy levels, ability to concentrate, alertness, and post-flight sleep.Design, setting and participants: Open, randomised crossover trial comparing the effects of GCTs (5 mmHg at ankle, 17–20 mmHg at calf and falling to 10 mmHg above knee and 4 mmHg at buttocks) among 50 adults on flights of 5 hours’ or more duration between 1 May and 8 October 2006; 47 volunteers (pilots and passengers) completed the trial.Main outcome measures: Differences in right ankle circumference before and after flight with GCTs and without GCTs; travel symptoms rated on visual analogue scales.Results: Low-ankle-pressure GCTs decreased ankle swelling (mean difference, − 0.19 cm; 95% CI, − 0.33 to − 0.65 cm; P = 0.012). Participants reported their legs felt better (mean, 1.6; P < 0.001; 95% CI, 1.0 to 2.1), warmer (mean, − 1.1; P < 0.001; 95% CI, − 1.6 to − 0.6), and they had a better night’s sleep (mean, 1.2; P < 0.001; 95% CI, 0.8 to 1.7) after the flight when they wore GCTs. Shifts in rating-scale probability distributions showed improvements in the ratings of pain (60%; P < 0.001), leg discomfort (50%; P = 0.001), leg swelling (45%; P = 0.006), energy levels (18%; P = 0.016), alertness levels (13%; P = 0.031), and concentration (12%; P = 0.023) when wearing GCTs.Conclusions: Low-ankle-pressure GCTs reduce flight-induced ankle oedema and subjectively rated travel symptoms of leg pain, discomfort and swelling, and improve energy levels, ability to concentrate, alertness, and post-flight sleep.Trial registration: Australian New Zealand Clinical Trials Registry ACTRN12606000150549.

Melissa J Hagan BSc, MEdSt · Stephen M Lambert RN, MAppSc

Objective: To describe a midwifery-led model of care in Far North Queensland and the outcomes obtained in its first year of operation.Design, setting and participants: Prospective analysis of data for all women who were booked for antenatal care with the midwifery-led unit at Mareeba District Hospital (MDH) and who gave birth during its first year of operation, from 27 June 2005 to 30 June 2006.Main outcome measures: Number of women giving birth at MDH; antenatal, intrapartum and postpartum transfers to a higher-level referral centre (Cairns Base Hospital [CBH]); and labour and delivery outcomes.Results: Of the 203 women who were booked for antenatal care at MDH and gave birth in the 12-month period, 170 were categorised as low risk and suitable to give birth at MDH. Of these, 147 (86%) did give birth at MDH, while 17 women (10%) had their care transferred antenatally to CBH, and six (4%) were transferred intrapartum. Of the 33 women categorised as high risk, 22 (67%) gave birth at CBH as planned, seven (21%) had elective caesarean sections performed by a general practitioner at MDH, and four (12%) presented to MDH in labour and gave birth there with no complications. Of the 158 women who gave birth at MDH, 146 (92%) had a spontaneous vertex delivery.Conclusion: Outcomes for the first year of operation of the midwifery-led model of care are consistent with a viable maternity unit, with delivery outcomes and transfer rates that compare favourably with other similar units in Australia.

Samantha Scherman MB BS, FRANZCOG · Jan Smith RM · Megan Davidson RM