Global health

A 10-year-old boy from Papua New Guinea with multidrug-resistant tuberculosis and multibacillary leprosy developed acute glomerulonephritis while being treated as an inpatient at Thursday Island Hospital in the Torres Strait, Queensland. This is the first such case to be reported in Australia, where these diseases are uncommon and the combination is extremely rare, and it outlines important learning points regarding the aetiology of renal disease among patients with tuberculosis and leprosy. (MJA 2011; 195: 150-152) Clinical recordA 10-year-old boy from a remote village in Western Province, Papua New Guinea (PNG), presented to Saibai Island Primary Health Centre in the northern Torres Strait, Queensland, with a 4-year history of intermittent malaise, fevers, night sweats, recurrent skin sores and a cough productive of green sputum. He had received treatment for leprosy for 1 month the previous year at Daru Hospital (Western Province, PNG). There was a strong family history of leprosy and tuberculosis among both first- and second-degree relatives. On initial examination, the patient appeared cachectic. There was evidence of recent impetigo on both lower limbs and depigmented areas on his upper and lower limbs. He had thickened ulnar and posterior tibial nerves bilaterally, with normal sensation and motor function on repeated clinical assessments. His lungfields were clear to auscultation, but he had an ejection systolic murmur; he was also found to have hepatomegaly and enlarged inguinal, anterior and posterior cervical lymph nodes. He was transferred to Thursday Island Hospital for inpatient management. Slit skin smears were performed; phenotypic analysis of the right earlobe smear was positive for Mycobacterium leprae, confirming the diagnosis of multibacillary leprosy.1 An initial chest x-ray showed left upper lobe changes consistent with pulmonary tuberculosis; subsequent sputum samples and an aspirate of an anterior cervical lymph node cultured Mycobacterium tuberculosis resistant to rifampicin, isoniazid, streptomycin and ethionamide, in keeping with a diagnosis of disseminated multidrug-resistant tuberculosis (MDR-TB).2 HIV and hepatitis serological tests were negative. On admission, his serum creatinine level was 30 μmol/L (reference range [RR], 46–81 μmol/L). The patient was given intravenous amikacin and oral moxifloxacin, isoniazid, pyrazinamide, ethambutol, pyridoxine and rifampicin; cycloserine, aminosalicylic acid (mesalazine), dapsone and clofazimine were later added. One week after admission, the patient developed acute glomerulonephritis, which manifested as fluid retention (pulmonary oedema, peripheral oedema and ascites), hypertension (maximum blood pressure, 160/112 mmHg), haematuria, proteinuria (up to 9700 mg/L [RR, < 100 mg/L]) and impaired kidney function (serum creatinine level peaked at 69 μmol/L). He was treated with frusemide, nifedipine and prednisolone. There was serological evidence of recent infection with Streptococcus pyogenes (elevated antistreptolysin O and anti-DNAse B titres) and hypocomplementaemia (decreased complement component 3 [C3] concentration with normal complement component 4 [C4] concentration). The nephritic illness resolved slowly over the next few weeks. During this period, the patient developed painful, erythematous nodules over his upper torso and limbs (Box 1). His mother reported that he had experienced several such episodes in the past. The lesions measured 5–10 mm in diameter and were tender to palpation; in association with the cardiac murmur and elevated streptococcal serology there was some initial concern about the possibility of acute rheumatic fever and the patient was commenced on penicillin prophylaxis. However, expert consensus was that the lesions more likely represented erythema nodosum leprosum (ENL) — an immune complex-mediated inflammatory reaction that can occur in both acute and chronic relapsing forms among leprosy patients with a high mycobacterial load. Treatment options for this condition have historically included simple analgesics, steroids, non-steroidal anti-inflammatory drugs, clofazimine and thalidomide. A recent Cochrane review found a paucity of evidence for most treatments of ENL, and only a modest benefit from clofazimine and thalidomide.3 As the patient was already taking clofazimine, thalidomide was not considered to be a practical or necessary option in his case (given its significant side effects, the need for monitoring and the patient’s planned return to PNG); his several subsequent bouts of ENL were treated successfully with oral prednisolone. His renal function remained stable throughout these episodes, and an inpatient echocardiogram was normal. After three negative sputum smears, the patient was removed from isolation and continued treatment with intravenous amikacin. He was discharged home on oral therapy for both MDR-TB and leprosy, with follow-up planned at Saibai Island Primary Health Centre. Unfortunately, at the time of writing, due to unknown patient factors and unforeseen circumstances (such as the closure of the border and cancellation of outreach clinics), the patient has not been seen, nor his medications collected, for almost 6 months. DiscussionThe area encompassed by the Torres Strait and Northern Peninsula Area Health Service District in Queensland includes some of the most remote and isolated communities in Australia, and incorporates the porous maritime border with PNG. Thursday Island Hospital is the main referral hospital for the region and many PNG patients are seen in outer island clinics and treated as inpatients at Thursday Island Hospital. These include a significant number of patients with tuberculosis. Although accurate figures on the epidemiology of infectious diseases in PNG are difficult to obtain, it is likely that the rates of mycobacterial infections such as tuberculosis and leprosy in PNG are both underreported and among the highest in the world. The World Health Organization recently reported an annual incidence of 6.5 per 100 000 for leprosy in PNG,4 with historical prevalence of up to 3% recorded in some remote villages.5 For tuberculosis, PNG has reported an incidence of 233 per 100 000, of which about 25% may be MDR-TB.6 A recent literature review described only isolated case reports and small case series studies of concomitant infection with leprosy and tuberculosis over the past few decades.7 Most of these reported cases were from India, with documented co-infection rates (ie, the proportion of leprosy patients found to also have tuberculosis) in the order of 2.5%–7.7% in India and up to 13.4% in South Africa.8,9 Despite the relative dearth of published accounts of co-infection, it seems plausible that simultaneous infection with M. tuberculosis and M. leprae occurs more frequently than is described in published reports in regions with relatively high rates of both diseases (including countries in sub-Saharan Africa, South America, the Indian Subcontinent, and South-East Asia). Some postulated reasons for why rates of co-infection may nevertheless be lower than expected in high prevalence regions include improvements in the detection rate and treatment for both infections; the WHO’s initiative of providing free leprosy treatment in an effort to eliminate the disease; the effects of BCG immunisation; and the complex, possibly antagonistic interaction between the two strains of mycobacteria.7 Our patient developed acute glomerulonephritis as an inpatient receiving treatment for MDR-TB and leprosy; hence, a number of possible causes of his renal dysfunction were considered. Renal abnormalities occur among most patients with leprosy, particularly those with multibacillary disease (“borderline” or “lepromatous” disease using the Ridley–Jopling Classification of Leprosy), and renal failure is a frequent cause of death in patients with leprosy.10,11 Glomerulonephritis, nephrosclerosis, tubulointerstitial nephritis, amyloidosis and granulomas are the most common renal pathologies found on biopsy or autopsy of leprosy patients.12 Of the glomerulonephropathies, the proliferative glomerulonephritides are the most frequently described lesion among patients with leprosy.11,12 Hypocomplementaemia is a recognised association of renal disease in this setting, particularly among patients with multibacillary leprosy and ENL.12 Typical serum protein profiles seen among patients with renal disease associated with some selected infections are presented in Box 2. The pattern of hypocomplementaemia varies somewhat between the different forms of glomerular disease; low C3 with normal C4 (as in our patient’s case) tends to suggest either poststreptococcal or membranoproliferative glomerulonephritis.13 Evidence of streptococcal infection was found on biopsy from five leprosy patients with renal disease in India; the same case series reported two patients with microfilariae in peripheral blood samples, indicating the possibility of a range of concomitant infections contributing to renal disease in patients with leprosy.14 With respect to drug-induced nephrotoxicity, rifampicin (a common component of the pharmacological regimen for treatment of both leprosy and tuberculosis) has been implicated in acute renal failure, often associated with thrombocytopenia, immune haemolytic anaemia and intravascular coagulation.15 In our patient, however, the combination of oedema, hypertension, haematuria, hypocomplementaemia (in the pattern described), elevated streptococcal serological results and a history suggestive of recent skin infections is strongly supportive of a diagnosis of poststreptococcal glomerulonephritis, which is an uncommon form of renal disease in patients with leprosy. The patient did not undergo kidney biopsy as his condition was clinically improving and it was felt that this highly invasive procedure would not have yielded sufficient additional diagnostic information to make it worthwhile. It is also a moot point whether, given his nationality, this procedure would have been available to him. In summary, our patient had the misfortune to suffer simultaneous infection with multibacillary leprosy and MDR-TB (and may be the first such reported case in Australia), which was complicated by ENL and an acute glomerulonephritis that was probably poststreptococcal glomerulonephritis — a rare form of renal disease in a subset of patients among whom renal impairment is commonly due to other causes. 1 Erythema nodosum leprosum reaction, indicated by red patches 2 Serum protein profiles seen in renal disease associated with specific infections* Serum protein profile Group A streptococcus infection Acute glomerulonephritis Classic diffuse proliferative Decreased C3 Focal proliferative (IgA disease) Increased IgA Mycobacterium leprae infection Acute glomerulonephritis Proliferative forms Decreased C3 Cryoglobulinaemia (ENL) Decreased C3 and C4 Nephrotic syndrome Amyloid Increased AA Mycobacterium tuberculosis infection Nephrotic syndrome Amyloid Increased AA AA = amyloid A. C3 = complement component 3. C4 = complement component 4. ENL = erythema nodosum leprosum. IgA = immunoglobulin A. * The serum concentrations of certain proteins are altered in these conditions.

Lachlan J McIver MB BS, MPHTM, FACRRM · Shaun T Parish MB BS, DTMH, FACRRM · Samuel P Jones MB ChB, DTMH, JCPTGP · Alexander N Kippin MB BS, MPHTM · Timothy J Furlong MB BS, PhD, FRACP

Objectives: To assess the prevalence of latent tuberculosis infection (LTBI) in recently arrived refugees in the Northern Territory and to obtain comprehensive data for rates of treatment acceptance and completion for this condition.Design, setting and participants: Prospective data collection and follow-up of all 471 newly arrived refugees seen at the Centre for Disease Control, NT refugee health clinic from February 2006 to January 2009.Main outcome measures: Rates of LTBI determined by tuberculin skin testing; subsequent assessment and treatment compared with local protocols.Results: 458 of 465 eligible refugees were adequately assessed for LTBI, of whom 146 (31.9%) were diagnosed with LTBI. Older age, male sex and World Health Organization Eastern Mediterranean region of birth were associated with increased prevalences of LTBI. Of the refugees diagnosed with LTBI, 10 failed to attend for follow-up and 15 were not offered treatment. Isoniazid therapy was accepted by 93 of 121 refugees (76.9%), and 41 of these (44.1%) completed treatment. The most common reasons for discontinuation of therapy were medication-related side effects (most often gastrointestinal) and loss to follow-up. Increasing age was associated with failure to complete treatment.Conclusion: Outcomes of assessment and treatment for LTBI in newly arrived refugees in the NT are comparable to those for other target groups screened in developed countries. Loss to follow-up caused significant attrition in numbers, but complete data were obtained for a large proportion of eligible refugees. Most refugees who are offered treatment for LTBI accept, but less than half complete treatment.

James M Trauer MB BS · Vicki L Krause FAFPHM

Objective: To assess the number and characteristics of potentially harmful incidents occurring during placement of medical students in remote Aboriginal communities in the Northern Territory.Design, participants and setting: A retrospective audit of medical students’ files from Northern Territory General Practice Education placements in Central Australia for the period from January 2006 to December 2007.Main outcome measures: Number and type of potentially harmful incidents.Results: A total of 163 placements were undertaken. Of these, 98 (60%) had adequate documentation to determine whether an incident had occurred. There were 28 cases (17%) where potentially harmful incidents were judged to have occurred. Most incidents fell under several descriptive categories, but clinical supervision, professional practice and administrative issues were most common.Conclusions: One in six students experienced a potentially harmful incident during remote area placement in 2006–2007. While acknowledging the exploratory nature of this investigation and the major educational benefits that clearly arise from these placements, our findings indicate problems with clinical supervision and administration.

Ameeta Patel MB BS(Hons), FRACGP, DRANZCOG · Peter Underwood MD, FRACGP, MRCP · Hung The Nguyen MB BS, FRACGP, MPH · Margaret Vigants RN, BNBAS

Screening plus equitable provision of vitamin D supplements could mitigate many adverse outcomes For nothing worthy proving can be proven, Nor yet disproven: wherefore thou be wise, Cleave ever to the sunnier side of doubt. Alfred, Lord Tennyson, The ancient sage Tennyson may not have been alluding to the need for high-level evidence from randomised controlled trials (RCTs) to alter clinical practice, but he would have been aware of children with rickets. Evidence has accumulated linking vitamin D deficiency to adverse outcomes in pregnancy, such as pre-eclampsia, hypertension, higher rates of caesarean section and preterm delivery. Lau and colleagues (→ Serum 25-hydroxyvitamin D and glycated haemoglobin levels in women with gestational diabetes mellitus) contribute to this evidence by demonstrating that, in women with gestational diabetes mellitus (GDM), a lower serum 25-hydroxyvitamin D (25[OH]D) concentration was independently associated with poorer glycaemic control.1 Of 147 women who were studied late in pregnancy (at a mean of 35 weeks’ gestation), about 40% had vitamin D insufficiency or deficiency (serum 25[OH]D concentrations ≤ 50 nmol/L). Most of the women in this study were not white, and ethnicity, occupational status and season, not surprisingly, all influenced 25(OH)D concentrations, while body mass index did not. Perhaps more surprisingly, however, 25(OH)D concentrations were inversely associated with fasting and 2-hour glucose levels measured during an oral glucose tolerance test and with the marker of glycaemic control, glycated haemoglobin. Most importantly, serum 25(OH)D was an independent predictor of glycaemic control. In adults, a number of large cross-sectional studies have shown a consistent, independent and positive relationship between serum 25(OH)D and insulin sensitivity, and an inverse relationship with risk of diabetes.2-5 Serum 25(OH)D levels have been shown to account for 42% of the variation in insulin sensitivity assessed by hyperglycaemic clamp.3 Consistent with Lau et al’s findings, fasting and 2-hour levels of glucose and insulin have been shown to be independently and inversely associated with serum 25(OH)D levels.3-5 In a United States study, the odds ratio for diabetes was 0.25 (95% CI, 0.11–0.60) for non-Hispanic white participants in the highest versus the lowest serum 25(OH)D quartile.2 The highest-level evidence to date comes from a large prospective study with a 17-year follow-up that showed people in the highest quartile of serum 25(OH)D had a 40% decreased risk of type 2 diabetes compared with those in the lowest quartile.6 Based on these data, RCTs of vitamin D supplementation in adults to improve insulin sensitivity and reduce diabetes risk are underway. GDM is becoming increasingly more common, affecting up to 10% of pregnancies. The presence of GDM is not trivial and has long-term implications for the health of mothers and their children. The former have an increased risk of developing type 2 diabetes, while their offspring have an increased risk of obesity and diabetes later in life. Vitamin D deficiency is also very common in pregnancy. The prevalence of inadequate levels of vitamin D in Lau et al’s study is comparable with rates of vitamin D insufficiency of 47.1% and 83.5% in white and black pregnant women, respectively, in the northern US (defined as 25[OH]D < 80 nmol/L)7 and 65.3% in pregnant women in rural Victoria (defined as 25[OH]D < 75 nmol/L).8 RCTs of vitamin D supplementation, initiated early in pregnancy, are now required to demonstrate whether vitamin D supplementation might reduce the incidence or severity of GDM. International debate is currently focused on the optimal level of serum 25(OH)D. Based on meta-analyses using musculoskeletal end points in older individuals, cut points of 60 nmol/L and 75 nmol/L seem appropriate to prevent falls and fractures, respectively.9 However, a recent Institute of Medicine report recommended at least 50 nmol/L,10 which appears overly conservative and does not take season into account. The public health implications of vitamin D deficiency in pregnancy are far broader than glycaemic control. In Australia, there has been a resurgence of rickets — partly owing to an increased refugee population comprising dark-skinned and veiled women with vitamin D deficiency, and also because of decreased exposure of babies to sunlight, lack of supplementation of infant feeds with vitamin D and weaning of infants onto non-milk liquids. Milder forms of bone disease may also occur with vitamin D deficiency. Recently, a study that used three-dimensional ultrasonography in pregnant women showed that vitamin D deficiency was associated with increased femur metaphyseal cross-sectional area and increased femur splaying (the ratio of femoral metaphyseal cross-sectional area to femoral length) at as early as 19 weeks’ gestation.11 In addition, it was previously shown that children born to mothers with vitamin D deficiency (< 50 nmol/L) during pregnancy exhibit deficits in total body bone mineral content as great as 11% at 9 years of age.12 This could lead to an increased risk of osteoporotic fracture later in adult life, but this is unlikely to be evaluated in long-term studies. In addition, maternal or early life vitamin D deficiency has been linked to an increased risk of several other disorders, including neonatal craniotabes, prematurity, type 1 diabetes mellitus, schizophrenia, and childhood respiratory infections and wheeze.13,14 Current evidence strongly supports routine screening for vitamin D deficiency early in pregnancy. Furthermore, vitamin D supplementation to correct deficiency should be initiated early in pregnancy as it might reduce the incidence or severity of GDM and because changes in skeletal morphology of the fetus associated with deficiency are seen as early as 19 weeks’ gestation. The most common recommended daily doses of cholecalciferol are 1000 IU–2000 IU, however, daily doses of up to 4000 IU have recently been shown to be safe in pregnancy (Bruce W Hollis, Professor, Department of Paediatrics, Medical University of South Carolina, USA, personal communication). What is problematic is the equitable provision of vitamin D supplements to pregnant Australian women with deficiency. Pregnant and breastfeeding women who are most at risk of vitamin D deficiency are often the least likely to be able to afford supplements. In the United Kingdom, vitamin D supplements are provided free of charge to such women through the Healthy Start program.15 There is evidence to support more widespread use of vitamin D supplements during pregnancy in Australia, although more research is required. One way to increase access might be to alter the scheduling of higher-dose, lower-cost vitamin D supplements.

Peter R Ebeling MB BS, MD, FRACP

Obesity, linked to chronic disease, and global warming, linked to climate change, may be indicators of serious problems with our consumption-based economic system About 15% of the world’s population are now overweight or obese, and this is considered to be a factor in the rising incidence of chronic diseases.1 Excessive carbon concentrations now also exist in the atmosphere (50% higher now than 50 years ago), with implications for the environment and climate disruption.2 Although it is not immediately obvious, there is a connection between these two phenomena, with energy being the common factor — excess energy intake over expenditure in the case of obesity, and excess carbon from energy sources over the capacity of environmental “sinks” (oceans, soil, plants) to absorb carbon in the case of the environment. This suggests there may be a common distal driver, in which case obesity and global warming could be symptoms of a broader environmental disorder — similar “canaries” in the same “mineshaft”. Body fat in humans is essential for survival. Too little causes health problems (insulin resistance, type 2 diabetes, etc), as does too much. Unknown factors (probably genetic) seem to define a point — which may vary widely between individuals — beyond which further expansion of fat cells is limited, leading to a “spillover” of excess fat into ectopic stores (muscle, blood, viscera, etc). Before this point is reached, fat stores seem to be benign, or even healthy,3 even in some obese individuals. Beyond this, fat appears to become toxic, and to become linked to chronic disease,4 possibly through the medium of a form of low-grade systemic inflammation, or “metaflammation”.5 Metaflammation was shown over a decade ago to be distinct from classical inflammation. It seems to be caused not just by “spillover” fat, but also by lifestyle and environmental factors, some of which can cause obesity (poor diet, inactivity, inadequate sleep, etc), but many of which may not.6 Non-alcoholic fatty liver disease (NAFLD), often a precursor to chronic disease in the presence of such lifestyle behaviours without obesity7 or visceral fat,8 supports this idea, as does a reduction in NAFLD with exercise independent of weight loss.9 In this sense, obesity might be just a canary in a mineshaft, signalling bigger problems in the overall environment. But if obesity is the canary, what constitutes the mineshaft? A clue can be gained from looking at pro- and anti-metaflammatory stimuli. We have suggested elsewhere10 that pro-inflammatory “inducers”11 are new, arising as a result of the industrial revolution of the late 19th century, whereas those that are anti-inflammatory (or neutral versions of those causing inflammation) have been familiar to humans for thousands of years. The hypothesis proposed from this is that the human immune system reacts (albeit at a lower level than to injury or microbial invasion) to stimuli to which it has not had time to adapt.12 Metaflammation is thus to chronic disease what inflammation is to injury and acute disease. Inflammation normally relates to a physiological condition. However, it can apply, at least metaphorically, to the external (ecological), as well as the internal (biological) environment. The body is unable to “soak up” glucose as a result of insulin resistance, and this leads to metaflammation and biological abnormalities in the form of chronic diseases. In the broader ecological environment, the biosphere is unable to soak up or “sequester” carbon dioxide (and other greenhouse gases) because environmental sinks are overwhelmed by emissions from the oxidation of fossil fuels,2 resulting in a form of inflammation and “carbon resistance” in the ecosphere. This leads to potential ecological “abnormalities” that are metaphorically similar to the chronic diseases related to insulin resistance. Our metaphorical mineshaft can be identified by tracking back the causes of both forms of “inflammation” in a classical epidemiological fashion, as shown in the Box. From this, it is clear that the mineshaft is the modern postindustrial environment, in which a principal driver has been the system of exponential economic growth, particularly that driven by the use of fossil fuels. But how can something that has been so good for human health and wellbeing as economic growth be regarded as negative? The answer lies in the inherent dynamism of any growth system. There is little doubt that growth has been the biggest single contributor to human health in history.13 However, any form of exponential growth must eventually meet its limits. Leading up to this, one might expect to see diminishing returns on investment. In terms of health, this time may have arrived. Data from Sweden, the United Kingdom and other countries over the past 200 years show an initial close relationship between health and growth, but since the 1970s, a reversed relationship, in which further growth results in reduced progress in health.14 Increases in obesity, which follow from the consumption required to feed the growth system beyond the “epidemiological transition” (where the incidence of chronic diseases surpasses that of infectious diseases)15 in developing countries, is one consequence. Greenhouse gas emissions, which are related to the consumption driving obesity, also closely follow the business cycle at the micro level, as well as the growth in gross domestic product (GDP) at the macro level.16 A “sweet spot”17 in the material phase of growth therefore appears to have been reached and, in some aspects, overshot in developed countries, as reflected by the diminishing rate of return in health, as well as ecological wellbeing, from further growth. Obesity (and greenhouse gases), within this framework, represents a canary. In times past, canaries were taken into mineshafts to warn of problems with air quality, indicated by their sudden collapse. The mineshaft in our metaphor is the economic system — specifically monetary growth, as measured in terms of GDP and its consequent consumption — that drives the modern industrial environment. To attribute the epidemic in chronic disease to this is not fanciful. It is clear from the lessons of developing countries like India and China that chronic diseases are related to changes that occur with economic development past a certain point — the epidemiological transition. The fact that chronic diseases begin to increase rapidly around the same time as a society’s carbon footprint begins to grow is not coincidental. Unsequestered greenhouse gas emissions are the manifestation of a mineshaft of growth beyond a threshold of positive returns. Obesity — and climate change — are merely “collateral damage in the struggle for modernity”.17 The dramatic worldwide increase in obesity is the most visible biological warning that our consumer-driven, macroeconomic environment (the mineshaft) is in need of an overhaul. While it is imperative for us to keep trying, attempts to reduce obesity at the population level, and to control climate change at the world level, without dealing with these broader economic and environmental issues, is like trying to resuscitate an asphyxiated canary while leaving untouched the mineshaft that caused the asphyxiation. Epidemiological course of biological and ecological “inflammatory” processes

Garry J Egger MPH, PhD · John B Dixon MB BS, PhD, FRACGP

“Child deaths are falling, but not quickly enough to reach the target.” “Most maternal deaths could be avoided.” The Millennium Development Goals Report, 20101 “Where we are now in terms of health service delivery should be measured against where we have come from and not where we ideally should be. A lot of progress has been made.” Mary L Nannono, Permanent Secretary at Uganda’s Ministry of Health, 20082 The Millennium Development Goals (MDGs) report published in June 20101 shows that the targets to reduce maternal and child deaths will not be met, particularly in sub-Saharan Africa. Uganda is an east African country committed to achieving MDG 4 (the goal to improve child survival) and MDG 5 (the goal to improve maternal health). In recent years, there has been much work to improve Ugandan antenatal and neonatal care, scaling up emergency obstetric care services and child health policies. However, progress remains slow and, at current standards, Uganda is unlikely to attain the MDG 4 and 5 objectives (Box).3 Why has there been insufficient progress? What happens when mothers and children come to hospital? I am an Australian doctor training in paediatrics under the Royal Australasian College of Physicians. I also intend to train in anaesthesia. I decided to take a year-long break from the training scheme to do humanitarian aid work in a developing country, and I am now coming to the end of a 6-month sabbatical in Uganda. This personal perspective on paediatric and obstetric care provision in Uganda aims to illustrate some of the stumbling blocks in practice that are limiting progress towards the MDGs in maternal and child health. My time in Uganda was divided between the obstetric operating theatre of the National Referral Hospital in Kampala, and responsibility for a paediatric ward in rural Uganda at a not-for-profit mission hospital, run jointly by the local Catholic diocese and an international non-government organisation. Every morning on arrival at the obstetric theatre I was greeted by women waiting, lining up in the entrance hall or lying on plastic sheets on the floor of the ward, contracting in pain. All needed emergency caesarean sections. However, each woman waited in turn for her operation or spontaneous delivery, whichever came first. When her turn came, the patient would walk into theatre and struggle onto the operating table with minimal assistance, pausing only for a grunt or grimace during a contraction. My first day at the Kampala hospital theatre was particularly disappointing — six emergency caesarean sections resulted in two fresh stillbirths, one macerated stillbirth and two admissions to the special-care baby unit. We hand-ventilated one baby for an hour because there was no mechanical ventilator. Later that afternoon, the baby stabilised on continuous positive airway pressure, but died overnight. My colleagues and I decided to undertake a 1-month audit to review maternal and neonatal outcomes: were there avoidable delays for emergency caesarean sections, and could anything be done about them? The maternal mortality rate in my sample of 435 was 1%, the stillbirth rate was close to 7% (equivalent to the hospital’s 1968 rates14) and mothers waited on average for 5 hours for the emergency procedure. Reasons for delays included staff unavailability, a lack of running water, a non-functional autoclave (and hence no sterile drapes and gowns), and no spinal needles or drugs for spinal anaesthesia. As a result of the audit, the hospital expedited the building of two new obstetric and gynaecological operating theatres and undertook to ensure that highly qualified and experienced staff ran them. Mothers are advised to bring a delivery pack when they come to hospital — not a dressing gown, slippers and baby clothes, but their own cannulae, sterile swabs, suture materials and 10 packets of sterile gloves, in case the hospital supply runs out. During my second week, a woman in her seventh pregnancy joined the section queue. Her indication for surgery was obstructed labour at 38 weeks gestation, with a “poor obstetric history” that translated as six previous stillbirths. She waited patiently in line but when it was her turn there were no gloves in stock and she had brought only one packet. She waited while women with gloves had their procedures. Her blank emotionless expression when the surgeons told her over the drapes that her baby was stillborn will remain with me forever. How can this hospital function as a comprehensive emergency obstetric care provider when caesarean section priority relates to the number of gloves the patient can supply rather than the underlying urgency of surgery? My responsibility for a 23-bed children’s ward (often with two to three patients per bed) in rural Uganda also brought me many challenges. At this hospital, one difficult day started with a mother in obstructed labour who delivered her baby with shoulder dystocia. During our attempt to resuscitate the baby, there was a power failure and, as there was no fuel for the back-up generator, the oxygen concentrator did not work. The oxygen cylinders were empty, so there was no oxygen in the hospital. Sadly, we were unable to save the baby. The same day, a 4-day-old twin died of jaundice because our phototherapy machine was broken and the parents could not afford to travel to another hospital. Then the mother decided to discharge herself from hospital with her surviving twin, also jaundiced and on intravenous antibiotics, and consult a traditional healer. I remember a 3-year-old patient referred from a larger regional centre to our rural hospital for a blood transfusion because there was “no blood available”. The child’s haemoglobin level was 2 g/dL and she was in severe respiratory distress. I was confused by the cross-match form and unit number noted in her case notes, yet the clearly documented reason for transfer was “no blood available”. The mother reported that, while she and her daughter were at the regional centre, another child, as sick as her own, had arrived whose need for the blood, already crossed-matched for our patient, was decided to be the more urgent because his or her mother could contribute money. As health care practitioners, we make decisions that are generally evidence based and (hopefully) in the patient’s best interests. A premature neonate, with a gestational age of 27 weeks, had been labelled a “fighter” after surviving 3 days on only a whiff of oxygen. This was going to be a success story for Africa — the survival of a premature baby. One night, a 6-month-old boy presented in severe respiratory distress when the oxygen concentrator was away being repaired and the only oxygen cylinder that wasn’t empty (it was one-quarter full) was with the fighter, who hadn’t tolerated a trial on room air. Reluctant to take oxygen away from her, I told the mother of the boy that I had done all I could. He died 3 hours later and I could hear the mother wailing from my room. The next day, the condition of the fighter on oxygen therapy suddenly deteriorated and I was unable to revive her. Had I made the wrong decision? Hindsight is a torment for one’s conscience. However, the oxygen dilemma prompted us to adapt the oxygen tubing so that two children could receive low-flow oxygen at the same time. When I received my first Ugandan arrest call, I ran to the bedside. Almost 5 minutes after I arrived, the suction and some monitoring equipment appeared. Oxygen was not available until later and we also had to wait for resuscitation drugs. The outcome was poor, both for the patient and my confidence. After my third resuscitation call, I didn’t run any more. I walked “mpola mpola” (slowly, slowly) with the rest of the team — arrests are difficult to manage without basic equipment, and usually fatal because of delayed treatment. So far I have painted a somewhat bleak picture, but there were good days and successes. A 6-week-old girl was brought in severely malnourished, weighing 2 kg with sepsis and malaria. The good Samaritan who had picked her up as a newborn from the roadside after the mother abandoned her was feeding her cow’s milk. After antibiotics, antimalarials and commencing our formula feeding program, the child gained weight and even started to smile. Also heartening, and something that has constantly amazed me, is the resilience and good humour of the staff, who do their best with what is available. However, when I read in the local newspaper that the World Health Organization’s Making Pregnancy Safer program is to be extended, and more mothers will be encouraged to give birth in hospital, I remember all the critical events that I have witnessed. Surely this advice will not lead to improved outcomes while there is such a disparity between demand and supply, between concept and reality. Reliable running water and electricity; hospital supplies like basic disposables, oxygen, and blood for transfusion; and adequate staffing and staff training are essential requirements for emergency obstetric and paediatric care. My story highlights that if basic hospital facilities were improved and some systemic delivery deficiencies overcome, more progress towards the MDGs 4 and 5 in Uganda and all of sub-Saharan Africa would be made. Ensuring that 90 per cent of African mothers and newborns have access to the essential interventions already written into policy would cost a very affordable US$1.39 per capita.15 What are the Millennium Development Goals for maternal and child health and where does Uganda stand in achieving them? Millennium Development Goal (MDG) 4 aspires to a global target of a two-third reduction by 2015 in the mortality rate of children aged under 5 years. For Uganda, this means a decrease to below 56 deaths per 1000 live births; however, the rate only declined from 186 to 135 deaths per 1000 live births during the period 1990 to 2008.4 Globally, neonatal mortality accounts for 38 per cent of deaths in children aged under 5 years; hence, a substantial reduction in neonatal deaths is necessary if this goal is to be attained.5 A 2006 Ugandan survey reported a perinatal mortality rate (comprising the stillbirth rate and early neonatal mortality rate) of 36.3 per 1000 pregnancies.6 This amounts to 44 500 newborns dying and 45 100 stillborn babies each year.7 Childbirth is the time of greatest lifetime risk of mortality for a mother and her baby. Intrapartum complications account for an estimated 42% of the world’s 358 000 annual maternal mortality rate (MMR). Sub-Saharan Africa contributes 57% to the world’s annual MMR.8 The first target of MDG 5 is to reduce the MMR by three-quarters before 2015, equivalent to a reduction to 131 deaths per 100 000 live births in Uganda — the estimated MMR is currently 435 deaths per 100 000 live births.9 A 2005 study estimated the MMR at 645 deaths per 100 000 live births at the National Referral Hospital, my workplace.10 Many obstetric and newborn complications can be prevented or successfully managed with prompt interventions. The Lancet Newborn Survival Series demonstrated that skilled clinical care could effect a reduction in neonatal mortality rates of up to 72 per cent.11 Timely identification and management of childbirth complications is paramount, and while more mothers and newborns die during this period than at any other, coverage and quality of care often remains inadequate in resource-limited settings.12 It is also important to note that with gross under-reporting (deaths at home or en route to hospital are often not recorded), the true figures are undoubtedly substantially higher. However, Uganda’s slow progress towards MDGs 4 and 5 has put the spotlight firmly on maternal and child health delivery. The government has responded by developing a national roadmap to accelerate the reduction of maternal and child mortality and morbidity. It has been placed high on the political agenda and, with the country’s upcoming elections in February 2011, all major political parties in the country are promising to make maternal and child health a priority. In addition, the World Bank in May 2010 released a new 5-year action plan to help poor countries reduce their maternal and child deaths. Uganda is one of the sub-Saharan African countries targeted. There is hope that, with time, Uganda will achieve the aim of the United Nations 2009 global consensus on maternal, newborn and child health: to have “every pregnancy wanted, every birth safe and every newborn and child healthy”.13 “All needed an emergency caesarean section. However, each woman waited in turn for her operation or spontaneous delivery, whichever came first.” “My responsibility for a 23-bed children’s ward (often with two to three patients per bed) in rural Uganda also brought me many challenges.” Communication, Ugandan style!

Katie M Moynihan MB BS, DCH

Riwayat. Sanjay Patole, Ajay Rane, producers. Horizon Films, 2010. http://www.riwayatmovie.com. It’s not often that the Journal publishes film reviews. It’s not often, however, that two busy Australian clinicians get together to produce a full-length Bollywood extravaganza, complete with swooning love scenes and beautifully crafted song sequences. While the essential ingredients of love, death, family feuding and a happy ending are all present, Riwayat is no ordinary Bollywood set piece. Instead, Indian-born Townsville urogynaecologist Ajay Rane and Perth neonatologist Sanjay Patole have taken on the serious medical and social topic of “the missing millions” of Indian women — those female infants who, over the past few decades, were conceived and sometimes born but either aborted or killed at birth simply because they were female. “Riwayat” means “tradition” in Hindi — and, traditionally, many female infants in India have been killed at birth, mainly in poor communities. More recently, ultrasound has been misused, by those who can afford it, to detect female fetuses for the purpose of abortion. The film is in Hindi, with English subtitles, and will be screened in India as well as overseas. Riwayat is the story of three generations of the upper-class Desai family, whose two sons and their wives are expected to follow the dictates of its autocratic patriarch. This has already led to two abortions and the consequent psychological distress of the elder son’s wife. (Conveniently, the Desais include a private hospital and ultrasound facility in their substantial property portfolio.) The wife of the younger son, who had a love match rather than the traditional arranged marriage, is made of sterner stuff. Having also conceived a female child, she leaves the family home when ordered to abort and returns to the village where she has been working for a non-government organisation (NGO) — an opportunity for the filmmakers to display the beautiful Indian countryside, take a few digs at the doubtful benefits of NGOs to poverty-stricken Indian citizens, and demonstrate the weight of traditional customs at village level. Her Portia-like intervention in the court case of a villager who kills his daughter at birth is designed to show Hindi-speaking viewers the urgent need to cast off this dreadful aspect of their “tradition”, disastrous for those girls and women denied life, but also for society as a whole. Riwayat is both an enjoyable romp and an important piece of social commentary. Hopefully, it will be widely shown in Australia.

Caroline M De Costa

Mental health across cultures. A practical guide for health professionals. Jill Benson, Jill Thistlethwaite. Oxford: Radcliffe Medical Press, 2008 (xiii + 208 pp). ISBN 9781846192197. In an increasingly multicultural Australia, a medical practitioner is called upon, on a daily basis, to treat patients from diverse cultural backgrounds: migrants, refugees, students from other cultures and Indigenous people. This cultural diversity extends to differences in social status, age, religion, sexual orientation and many other sociodemographic aspects. A medical consultation across the cultural divide is fraught with the risk of miscommunication. Jill Benson and Jill Thistlethwaite, in this small information-packed volume, provide an antidote to such a predicament. Both authors are doctors who have worked in diverse settings in Australia and overseas, have treated patients from many different cultural backgrounds, are knowledgeable about diverse cultures and sensitive to differences, recognise the importance of mental health consultations in general practice, and take a keen interest in their patients’ stories. The first call they make in the book is for physicians to become aware of cultural differences. They then present a model for working across the cultural divide, beginning with self-reflection, developing an understanding of another culture through networking and mentoring and, most importantly, listening to the patient’s story. The primary care physician is first and foremost a healer, and this book presents a succinct view of the issues that come up when psychotherapy, behaviour therapy or narrative therapy must bridge a cultural divide. Even pharmacotherapy is not immune to transcultural challenges as miscommunication can affect adherence and appropriate use of drugs, and ethnic or racial differences can influence drug kinetics and dynamics. The strength of this book lies in the distilled wisdom of two practitioners who teach through real-life examples and present practical solutions. It can therefore be recommended to all physicians and medical students. If you are an international medical graduate practising in Australia or an Australian graduate wishing to work overseas, you will find the case studies particularly appealing. The book fills a gap in the cross-cultural health literature.

Perminder S Sachdev

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: As health professionals, we urge Australian politicians (and the public) to recognise the overlap in the underlying cause of two great health threats that our population now faces: the rise of obesity and its life-threatening disease consequences, and the great threats to health from global climate change.1-3 Big health gains have been made since the onset of industrialisation. However, we are now seeing the emergence of health risks caused by excesses in market-driven consumerism (including the consumption of energy-dense processed foods), energy-subsidised exertion-free living, an over-arching preoccupation with gross domestic product and (particularly relevant to climate change) population growth.4,5 In light of our profession’s long experience with the smoking–disease debate, we recognise the serious threat posed to population health by the well financed, doubt-fostering opposition of vested interests. In the case of smoking, it took 50 years and several million deaths to progress from acknowledgement of the health hazard to application of effective interventions. With climate change, we lack the luxury of time — and the stakes are much higher.6 Hence, a prudent, precautionary strategy to tackle the big issues is essential. We propose two initiatives: Convene a high-level, ongoing forum to discuss post-growth alternatives to unsustainable, consumption-based growth as the economic norm. This should involve health and social scientists, among others, and economists prepared to objectively take into account the real environmental costs of our actions; and Convene a multidisciplinary taskforce to develop an Australian population policy. Population is a key driver of energy use, greenhouse pollution and resultant ill-health.7 Despite the apparently widespread bias against public discussion of population issues, the topic is now attracting renewed attention and the debate should be facilitated. The irony of adopting a “no change” approach to these two issues is that, if this happens, involuntary change to everyone’s lifestyle will become unavoidable. We must seek a sustainable economic system and stable population size that ensures prosperity without endangering both health and environmental quality.8 For the moment, our actions are seriously damaging our planet and our children’s health. One in three children born today will become obese and/or diabetic in their lifetime, and the population at large will face increasing health risks from climate change.

Garry J Egger · Boyd Swinburn · Fiona Stanley · Kerryn Phelps

Objective: To determine why more than 2000 doctors have migrated from South Africa to Australia since 1948.Design, setting and participants: South African-trained doctors living in Australia and the spouses or adult children of deceased practitioners who had emigrated from South Africa were contacted by email between August 2008 and February 2009. The sample of doctors was gathered and expanded by an email “snowball” technique and through advertising in alumni and professional journals and newsletters. A questionnaire was emailed to 653 contacts.Main outcome measure: Primary reason given for migration.Results: Responses were received from 469 of the 653 email contacts (72%), from a population of about 2200 South African doctors in Australia. Of the 469 respondents, 434 (93%) had been motivated to emigrate by a wish to leave South Africa, rather than by Australian inducements. The primary reason for emigration before 1990 was opposition to apartheid (142/205 [69%]); the primary reason for emigration after 1990 was the level of violent crime (including “safety” issues) (116/264 [44%]).Conclusion: Most South African doctors who migrated to Australia were impelled to emigrate by South African issues, rather than attracted by Australia.

Peter C Arnold BSc, MB BCh BA · David E Lewinsohn DipAppChem, GDipDP, PGDipPDM

Two phenomena are shaping physician assistants and their futures: change in human societies and change in health care delivery The physician assistant (PA) is a global phenomenon: a product of medicine that enjoys unparalleled success within the health profession in many societies. Born in the 1960s, nurtured in the 1970s, and grown in the 1980s, the PA proved to be a capable player in American health policy in the 1990s. By 2000, the PA had emerged in a handful of countries, and by 2015, PAs will surpass 100 000 worldwide.1 Various explanations regarding why this profession is growing have been advanced. Clearly, PAs fit well in the entrepreneurial American health care system; economic advantages, clinical flexibility and dependence on doctors are factors that contribute to their success. But it is other countries that are building on the original model. With a worldwide shortage of 4.5 million doctors and an inadequate number of medical schools, the sheer weight of population growth demands more medical personnel and resources.2 In addition, improvements in childhood survival and the control of archaic diseases (eg, malaria, tuberculosis, dengue fever, smallpox, polio) have resulted in people living longer and more comfortably than their parents. Technological advancements are limited only by the logistics of delivery to populations, both urban and remote.3 The increasing years of productivity of individuals indicates the need for an unprecedented cadre of health workers. Without more doctors and nurses, the next group of providers to look to is PAs. Canada, the United Kingdom, South Africa and the Netherlands are examining not only their present workforces, but also what will be needed in decades to come. The alternative to not growing their own workforces is recruiting overseas-trained doctors — a strategy with its own ethical considerations.4,5 A sociological explanation for the emergence of PAs is an evolution in the division of medical labour, not a loss of autonomy for doctors. Medicine has become infinitely more complex over the past several decades and the information base required to practise medicine is enormous, leading to greater levels of team-based care. Health care knowledge was once a vaunted supremacy of doctors, but now diagnostic and therapeutic tasks are shared with other health care professionals (in part because modern-day doctors cannot know and do everything in so vast a field). Throughout the 20th century, analytical technologies and therapeutic approaches produced new specialties, and today we have genetics, interventional radiology, robotic surgery and the resurgence of midwifery. Further expansion of medical activities and capabilities will necessitate the inclusion of additional trained personnel who share the domains of doctors but remain dependent on doctors for directing care. Other social forces have had a major influence on the PA movement. Changing lifestyles — doctors’ preferences for greater work–life balance grew during the 1970s. Today, most are eager to work (though not as hard as their predecessors) and desire help. Gender shifting — women have entered the workforce in a major way. They have tried out careers that are traditionally dominated by men, and have found them to their liking. For PAs, the education path is shorter than for medicine but has similar rewards. The opportunity to be engaged in a well respected career and successfully raise a family ranks high with many female applicants. Doctor dependency — the unwavering commitment of the PA profession to remain dependent on doctors bolsters widespread acceptance of PAs by medical professional bodies. National competency — the establishment of program accreditation and an independent national board overseeing the specific skills and competencies of PAs allows states to focus on licensure, roles and supervision. Primary care — for PAs, the emphasis on training in general medical care and obtaining core competencies creates a known entity. Such a model permits more role flexibility and mobility (beneficial characteristics in a changing health care environment) than exists for doctors and nurse practitioners. The PA succeeds, in part, because of the attributes of individuals. Early entrants saw themselves as change agents who wanted to prove that allied health individuals trained in this PA model could benefit society safely and effectively. The PA profession continues to attract those who feel dead-ended in their current health care roles but do not want the burden of a protracted medical school experience or investment. For example, an experienced military medic may seek to use his or her skills in civilian life or an indigenous health care worker who is isolated without options for career progression may wish to upgrade his or her role to enable a return to cultural roots. Looking forward, key questions emerge. What does the future hold for the PA profession? How will the changing faces of various health care systems affect the PA profession? Will a PA trained and certified in Utrecht, the Netherlands, be able to work in Mt Isa, Australia, and be effective? Two phenomena are shaping PAs and their futures: change in human societies and change in health care delivery. These are on convergent paths that predict the growth of PAs for many years to come — at least in many countries. How Australia will fit this new provider into its health care system is contentious for some. For those who want to expand the capacity of its highly skilled workforce, the pace of change leaves few options.6

Roderick S Hooker PhD, PA

The relationship between drug dose and clinical outcome has not been established for many medications used to treat chronic disease. Evidence is emerging that chronic diseases can be treated effectively with low doses. Adverse drug reactions account for significant morbidity and mortality and are generally dose related. Optimal drug dose — the best balance of benefit and risk — varies between individuals and may change over time. When treating chronic disease it is important to establish and maintain the optimal dose for each patient by close clinical monitoring.

Simon B Dimmitt MB BS, BMedSc(Hons), FRACP · Hans G Stampfer MB BS, FRANZCP

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

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

To the Editor: A 27-year-old man who had recently emigrated from Sudan was admitted to our department with a 7-hour history of constant peri-umbilical pain. Physical examination revealed inconstant voluntary guarding of the lower abdomen. Full blood and electrolyte examinations were unremarkable. Urinalysis showed protein and traces of blood. A condition requiring surgery was considered unlikely and further investigations were undertaken. Significant bladder calcification was noted from an abdominal x-ray. A computed tomography scan confirmed this finding (Box), and also revealed circumferential distal ureteric calcification, appendiceal thickening with appendicolith, and adjacent fat stranding. Repeat abdominal examination demonstrated right iliac fossa tenderness with a positive Rovsing sign. Acute appendicitis was diagnosed and an inflamed, thickened, retrocaecal appendix was removed laparoscopically. The patient was discharged 2 days later, but did not attend his post-operative review. Histological examination of the appendix demonstrated transmural neutrophil infiltration, without eosinophils. Within the lumen there were numerous oval-shaped helminth ova, some with terminal spines, consistent with acute appendicitis caused by schistosomiasis. The patient did not have a general practitioner, therefore a referral to an infectious diseases clinic was made. He was thereafter lost to follow-up. Infection by schistosomes leads to chronic granulomatous inflammation in many body systems, including the gastrointestinal tract. Adult worms are not usually harmful to the host — eggs provoke a Th2-mediated immune response.1 Three major species of Schistosoma cause schistosomiasis in humans, of which two are endemic in sub-Saharan Africa — Schistosoma mansoni and Schistosoma haematobium. S. haematobium migrates against portal venous flow to the vesical venous plexus, causing urinary tract calcification through chronic inflammation and fibrosis. This species has also been described as a cause of appendicitis.2 Examinations of appendices removed from patients with acute appendicitis in endemic areas have demonstrated schistosomiasis in 2.3%–4.2% of samples, with 2.7% having histological evidence of acute schistosomal appendicitis in one study.3,4 Schistosomiasis can be diagnosed by histological analysis, or urine and stool microscopy. Serological testing cannot be used to differentiate past and present infection, however positive serological results are the basis for treatment of patients in endemic areas. After diagnosis, praziquantel should be prescribed. It is assumed that our patient did not receive praziquantel. He thus risks significant morbidity and mortality from possible gastrointestinal, hepatic, urinary, pulmonary and neurological complications related to chronic schistosomal infection. Surgeons and pathologists should be aware of the atypical pathology of acute schistosomal appendicitis. The number of immigrants arriving in Australia from endemic areas has increased markedly in recent years and further presentations may occur. Non-contrast computed tomography scan of a 27-year-old man with schistosomal appendicitis Calcification of the bladder (black arrow) and distal ureters (white arrows) is evident.

Jordan K Webb · Graeme Thompson

To the Editor: Climate change has an adverse impact on health.1 Procurement, waste production, transport, and energy and water consumption (ie, the ecological “footprint”) all contribute to climate change. If the principle underpinning the work of all health professionals is “do no harm”, addressing the harmful effects of the health care industry on the natural environment must become a priority. We argue that one way to rapidly achieve this would be to mandate more sustainable practices as part of hospital accreditation. The United Kingdom has specifically targeted its health system to reduce its large ecological footprint,2 but in Australia, progress towards environmental sustainability within health care is uncertain and unmonitored. The contribution by health care to Australia’s national carbon emissions is unclear, but we do know that, for example, Victoria’s public hospitals consume 60% of the total energy used by the state’s government departments,3 so we have the opportunity to make a major impact. There are excellent examples of hospital energy- and water-saving projects with financial recovery within 10 years.2,4 The Environment Protection Authorities of several Australian states are now mandating that heavy users of energy and water (including larger hospitals) have Environment and Resource Efficiency Plans to reduce their footprints,5 but action from hospitals has been unclear. Progress has typically been made on an ad-hoc basis by hospitals acting in isolation, although the Institute of Hospital Engineering, Australia is facilitating a more systematic approach.4 The Australian Council on Healthcare Standards (ACHS), through its Evaluation and Quality Improvement Program (EQuIP)6 accredits Australian hospitals against mandatory and preferred criteria. However, EQuIP does not currently include mandatory criteria that address issues such as energy, water and waste auditing, energy efficiency and the presence of a hospital environmental committee. The accreditation process offers an opportunity to encourage hospitals to prioritise these issues. The ACHS has awarded hospitals in the past for “environmental excellence”, but without a solid framework from the ACHS, the goal of all of our hospitals pursuing sustainability seems unlikely. In 2009, it is out of step with Australia’s shift to a low-carbon future that there are no requirements that hospitals achieve more sustainable use of energy, water and transport, and improve procurement and waste reduction. The introduction of broad environmental standards as part of the accreditation process could be a vehicle for achieving rapid improvements in sustainability across the hospital sector and shift our health system to one that “does no harm”.

Forbes McGain · Grant A Blashki · Kevin P Moon · Fiona M Armstrong

The current crisis in health and health care in South Africa results from a combination of factors: the legacy of apartheid; issues of poverty, income inequality and AIDS; and the more recent influence of neoliberal economic policies and globalisation. The legacy of apartheid has meant that both health and health care are skewed along racial lines, and 60% of health care expenditure goes largely to the 14% of the population who have private health insurance. A more equitable distribution of health care resources will result from the promised National Health Insurance, the details of which are still being debated. The AIDS epidemic in South Africa was exacerbated by the government not introducing antiretroviral treatment (ART) until the early 2000s. In 2005, it was estimated that more than 5.5 million South Africans were infected with HIV. Now all those with a CD4 count below 200 are eligible for ART. A better health service will not be enough to improve the health of South Africans. A whole-of-government approach is needed to address the persistent problems of poverty and inequality.

Gavin H Mooney MA · Diane E McIntyre BCom, MA, PhD

Saibai Island is the closest part of Australia to another country. Lying in the Torres Strait, off the tip of Cape York Peninsula, Queensland, the mangrove-rimmed mudflat is only 4 km from Papua New Guinea (PNG) — a mere 20 minutes in an outboard dinghy, but a journey from poverty to plenty in terms of health care for residents of the palm-thatched village of Mabaduwan, PNG, north of Saibai. Mothers bring their sick children to the primary health care centre in Saibai, and who can blame them? Once a dinghy beaches, a Rolls-Royce service is triggered. One mother recently brought her 1-month-old daughter to Saibai because she was sleepy and not feeding well. The carer in Saibai noted a full fontanelle and telephoned the administrative centre in Thursday Island, about 120 km away, at the tip of the Cape. A helicopter was sent to retrieve the mother and infant to Thursday Island, where hydrocephalus was suspected and advice was sought from the regional centre for neonatal care in north Queensland, in Townsville, about 1500 km south. The centre dispatched a retrieval team of doctor, nurse, incubator, ventilator and backpack of medicines to Thursday Island in a twin-engine King Air of the Royal Flying Doctor Service (RFDS). Thursday Island, however, is too small for a landing strip, so fixed-wing planes must land on nearby Horn Island, where passengers catch a bus to a jetty and then a barge across a fast-flowing strip of water to Thursday Island. Medical evacuations are facilitated by a small helicopter, which is based on Horn Island and hops back and forth. The retrieval team left Townsville as night fell, were helicoptered back and forth from Horn Island in the middle of the night and returned to Townsville just before dawn. They had confirmed the large fontanelle, floppiness, an unreactive left pupil, and a sluggish right pupil, and initiated ventilation for respiratory failure. In Townsville, ultrasonography revealed a massive lesion in the left cerebral hemisphere, which was confirmed by magnetic resonance imaging to be a tumour. Meanwhile, the mother, who spoke very little English and whose life to that day had been spent in rural simplicity, was plunged into the luxuries of our modern Parents’ Unit next to our busy intensive care ward: lamp-lit hut with split bamboo floor was exchanged for electric lights and carpet; wood cooking fire for microwave; sleeping mat for huge, sprung, blanketed mattress; tropical heat for refrigerated “comfort”; nocturnal silence for the cut, thrust and whistles of intensive care battle; and family and friends for armies of strangers contending at all hours. Worse, the trees near the beach had been replaced by a strange contraption, more like a well, and there was no sea water with which to clean herself. We wondered why she had chosen to sleep with the lights on until we realised she did not know how to turn them off. Why did she sleep on top of the bed, or was she sleeping on the carpet? We soon learned that she had no idea how to use the microwave and stove and, in any case, had no coins to turn them on so we, of course, provided food. Why did she devour the fruit and leave everything else? We learned she was ravenous for sweet potato and cassava and perhaps a piece of fish. We thought she might like to go outside, but she was terrified to leave the ward. The acres of parked cars and the traffic on roads running in all directions contrasted with the carless, unpaved pathways between huts in Mabaduwan. Not surprisingly, her mental health began to disintegrate, and she became so fearful she would not even go to the toilet unless accompanied by a nurse. We needed to talk to her — to explain things and get permission for the surgery —but were confounded by her dialect. Late on the Friday afternoon of her admission, we rang our translating service, the health clinic at Mabaduwan, the Saibai clinic, people who allegedly knew her husband on Saibai, her embassy, and various consulates to no avail, but as luck would have it, someone discovered a distant “cousin” who had a boy in our paediatric ward who had worked his way to Townsville from Mabaduwan in a similar manner. The cousin spoke English. Conversation about the apparent diagnosis, the remote chance for surgery, the risks of anaesthesia, and so on, was tricky and took quite a while, supplemented as it was with such basic information as how to use the bathroom, and reassurances that we were bringing a change of clothing. In the end, we convinced ourselves that the mother understood matters and agreed to surgery. Surgery revealed a fleshy mass infiltrating the brain, with necrosis and haemorrhage. Frozen section showed malignant glioblastoma. As much tumour las possible was removed, the wound closed and the baby returned to the ward, still ventilated. After the surgery was completed, conversation became even trickier as we tried to discuss the contending kindnesses of continuation or withdrawal of high-tech support. There was no doubt about mother’s continued retreat into herself. Ultimately, it was widely agreed to withdraw high-tech support and “let nature take its course” and, while the cousin was rallying a few friends to support the mother, we began to explore the ways of transporting mother and the baby’s corpse back to her village. She was adamant that she did not want to be separated from her daughter’s body, and we were keen to preserve what remained of her stability. It was clear that mother and daughter should travel together — one should not go with the luggage. Problems accumulated with each phone call. No commercial airline would even think of transporting a mother with a corpse in her arms. Discreetly wrapped? No way! How about in a small crib? Not on your life, mate. I tell you, we can’t sell a ticket to a corpse. Well then, how about doing us a favour and transporting the corpse free of charge in the luggage if we really have to do it that way? No chance — it is all tied up with regulations and corpses can only travel with the assistance of a qualified undertaker and in a proper casket. A funeral director was asked how much it would cost to transfer one small corpse to Saibai. At least $3000, was the reply which, we figured, was probably about 3000 times the mother’s accumulated wealth. Was there any chance the RFDS would take mother and corpse on a back load to Thursday Island? Its King Air is the only plane based in Townsville, and constant demands from the living relegate those of the dead to the bottom of the list. Moreover, there were certain rules about transporting corpses. What if we kept the baby alive, to be extubated on Thursday Island? Would the commercial airlines consider carrying a baby being discretely hand-ventilated by a nurse? It was not as if we were asking for room for our whole transport team and equipment. After all, that equipment is all we have and it, too, needed to be on call in Townsville for the needs of the living. At least the airlines considered this question, but later phoned to express regrets that other passengers in the small regional plane might be challenged by the phenomenon. Sensing it might be easier to transport the living than the dead, we postponed the extubation, which took a bit of explaining. Mother seemed to follow the logic, and phone calls to Saibai and Mabaduwan began to prepare for the possibility but, as night fell on the second day of fruitless organisation, there was no apparent answer to the problem. We hoped something would “turn up” in the morning. It did. The RFDS plane had been dispatched to pick up two adult patients in Cairns and bring them back to Townsville. Cairns is about halfway between Townsville and Thursday Island, and there was time to put in a “mercy” diversion to Thursday Island. The old problem of transporting corpses remained and it was very good the baby was still alive. We still did not want to be separated from our transport incubator for the journey, which was likely to take about 10 hours, and sent one of our experienced nurses to ventilate the baby by hand. It was not clear how we would get the baby from Thursday Island to Saibai but wondered if she could go with one of the regular field trips to those islands. On the other hand, perhaps the baby could be extubated on Thursday Island and mother and corpse could return to Saibai in some kind of unofficial way, for which the Torres Strait is renowned. As our time was limited, medical staff on Thursday Island agreed to meet our team on Horn Island from where the baby would be helicoptered to the hospital for extubation. This would be very helpful, but would involve four hops of the helicopter: to pick up a doctor or nurse from Thursday to meet the patient on Horn, to take her to the hospital and then return to base. Off flew our little group — up the coast over the Great Barrier Reef, then over the flat scrub of the Cape with its single four-wheel-drive track, determinedly heading for the tip where it would join the shore of the Gulf of Carpentaria, which had been receding from the west. Almost 3 hours after take-off, mother, baby and ventilating nurse alighted on red-soiled, sparsely treed Horn Island in the azure flows of the Torres Strait, to breathe the heavy, hot, watery air of the tropics. Mother was instantly at home. Nurse began instantly to perspire. Oddly, mother sighed “trees”. Did you not see any in Townsville, the nurse asked? Not one, said the mother, though the hospital is surrounded by them. Meanwhile, concerns had risen in the staff at Thursday Island when it was learned the child was returning for extubation at that hospital while her father and other family members were gathering on Saibai to see her before she died and to be with her when she did. It seemed heartless to pass a corpse on to the family and budget constraints joined the meltdown. A helicopter would be employed to return the baby and her mother from Horn to Saibai, and a nurse and experienced paramedic would go with her to continue hand ventilation. That helicopter was waiting on the airfield when our team arrived and in the hot haze of Horn, the child was passed from nurse to nurse and continued the journey home. Our team returned to Cairns. At about 4 pm, father was reunited with daughter but, taking her up, would not pass her on to anyone. He appeared to have been consumed by an isolating grief that excluded and even blamed his wife. Everyone was alarmed and no one really knew what to do, but time was passing and the helicopter needed to return before dark. With the sun low, the family gathered around the child and the tube was removed in expectant hush . . . but death did not follow. Stillness was punctuated by weak gasps that strengthened, quickened, and went on and on, all night, and into the morning when the family wondered if it would be all right to head off for Mabaduwan so the girl could see her grandparents. Something did expire that night — the bitterness of the father. In a transformation judged by the night nurse to be the most moving she had ever witnessed, father, mother and family were reunited. It was “the proudest moment” of the nurse’s career. At about 10 am, the dinghies were fired up and the family returned home, but I knew nothing of these latter events when, 2 days later, I took a call from the primary health care worker in the village in PNG. In broken English he explained the baby was now crying loudly, waving its arms and demanding food, and wondered if I had further advice? My English broke in reply. In retrospect, this medical venture had involved multiple sea trips, six helicopter flights, two ambulances, two long-haul plane retrievals with special staff on overtime, several days of life-supporting intensive care, neurosurgery, anaesthesia, medicines, laboratory investigations, social-work support, interminable phone calls, accommodation, meals, and changes of clothing . . . all for free. In return, a small girl lived for 6 months.

John S Whitehall FRACP, MRCP(UK), DCH

Volunteers and the Internet can provide education in public health where it is most needed The multiple health problems faced by low-income countries require urgent solutions. One solution, as articulated in the United Nations Millennium Development Goals, is to increase the health workforce.1 An editorial (and accompanying articles) in the Lancet highlighted the need for global health capacity building,2 and the first Global Forum on Human Resources for Health (in March 2008) produced the Kampala Declaration, which urged “. . . immediate action to resolve the accelerating crisis in the global health workforce . . .”.3 Part of this solution will involve boosting in-country public health capacity,4 and an educational initiative to do this was launched recently — the People’s Open Access Education Initiative, better known as the Peoples-uni (http://peoples-uni.org).5 The “open-source” movement describes collaborative software development, where products are shared and improved upon among developers and made freely available to others. It has transformed computer software. The movement to make open-source educational materials freely available on the Internet6 promises a mechanism to provide public health education at low cost. An ever-expanding range of high-quality open educational resources is freely available on the Internet, and a number of universities are providing open access to online educational material, but do not offer tuition or accreditation. The Peoples-uni aims to provide an educational context around these materials, using a competence-based approach and volunteers to develop and deliver an educational program. Through the Internet, health professionals can learn while they work, and local workforce is not depleted. Previous experience shows that distance and online learning in public health is feasible.7 The open-source approach is a new way for individuals and organisations to collaboratively develop and share the products of their work. The Peoples-uni offers involvement in the exciting and evolving field of the application of the open-source philosophy to education. A number of national and international partners have agreed to be part of the Peoples-uni, and momentum is building. A pilot of a course module on maternal mortality, run between October and December 2007, attracted a large interest and was well received. The draft of this module is available at <http://moodle.cawd.net/course/view.php?id=2>, and student evaluation is available on the Peoples-uni website. This draft is now being modified as part of the process of developing a set of new course modules covering some of the foundation sciences of public health and some major health problems facing low- to middle-income populations. The United Kingdom Royal Society for Public Health has agreed to oversee the assessment process and offer awards at certificate and diploma levels, and teams are currently being established for course development and online facilitation. Access to educational resources and teachers of high international quality will provide highly credible education at low cost. While Australia is committed to its responsibilities towards overseas development through its official development assistance, only 12% of this budget goes to health, and even this is not focused on the areas of greatest global health need.8 Australian universities, including their medical schools,9 contribute to global educational activities, but are constrained by the need to charge fees, which cannot be met by most people who would benefit from university education. In 2005, full-fee-paying students provided 15% of income within the higher-education sector, and education services were the third highest export-earnings generator for Australia.10 For these reasons, which are not confined to Australia, the Peoples-uni has been established outside the more traditional educational sector and will rely on volunteers to meet its goals. Is the volunteer approach sustainable? Will busy health professionals be willing to add to their activities, and in a way that may not help meet the goals of their employing institutions? To date, more than 80 people have agreed to take part in the development of course modules, and are working in 12 teams. Volunteers come from 24 different countries and range from established academics in senior positions to trainees and students. Some students from the pilot have joined the teams. The difficulties of maintaining a large volunteer workforce should not be underestimated, and it is a priority to develop a system that provides rewards, such as the opportunity to work with a diverse and interesting group of colleagues, and to keep up to date with advances in international public health issues and developments in information and educational technology, in addition to appealing to the altruism of those involved. Although the workload will vary according to the level of commitment of the volunteers, we have divided it into feasible amounts for busy people, such that even a small and short-term commitment of 2–3 hours a week for a 3-week period can be a valuable contribution. A similar approach to level of commitment has also been taken by the Clinical Toxicology Teaching Resource Project (http://wikitox.org), with which the Peoples-uni shares a number of philosophical ideals. The Peoples-uni provides a novel opportunity to contribute to-wards meeting global health workforce and public health needs. Australian health care professionals and academics have made, and continue to make, major contributions to international health. I hope that the Australian health professional community will be involved in contributing to and helping shape this initiative.

Richard F Heller FRCP, FRACP, FAFPHM

To the Editor: In his article “Teaching Tamil Tigers”,1 Whitehall gives the grossly false impression that the Sinhalese majority and Tamil minority are fighting with each other in Sri Lanka. It is not a conflict between Tamil and Sinhalese communities, but a terrorist issue. The terrorist organisation that calls itself the Liberation Tigers of Tamil Eelam (LTTE) is fighting the elected government of Sri Lanka in an attempt to carve out a separate monoethnic state in areas in the north and east of Sri Lanka. The LTTE’s terrorist approach is denounced by most of the democracies of the world. The LTTE claim that the Tamils in Sri Lanka are discriminated against by the majority Sinhalese. This claim is contradicted by the fact that the 54% of Tamils who live in the southern part of Sri Lanka live in harmony with the Sinhala and Muslim communities. In the south, Tamil businessmen perform better than their Sinhala counterparts in Colombo; Tamil students continue their university studies undisturbed; and the Tamil language is treated as one of the official languages, on a par with the Sinhalese language. These are facts publicly available for all. Whitehall claimed that “the conduct and cost of the conflict is obscured by suppression of the press on the government side and lack of access of the press to the other” — an unfounded statement that is deliberately crafted to tarnish the image of the Sri Lankan Government. Perhaps Whitehall is unaware of the numerous newspapers and other publications available in Sri Lanka that openly criticise the government and its conduct, and of the many international journalists and press organisations that report on the current situation in Sri Lanka on a daily basis to the rest of the world without any hindrance. Whitehall referred to Kilinochchi as the administrative centre of the “Tamil” land. He appears ignorant of the fact that there are no separate lands for Sinhalese, Tamil and Muslim communities on the island. There is only one territory in Sri Lanka, and that territory belongs to all its people. Whitehall describes the poor conditions at Kilinochchi Hospital. Kilinochchi was predominantly controlled by the LTTE terrorists, against whom the government forces are fighting to liberate the civilians. The LTTE requisitions whatever provisions are sent to the region by the government and utilises them for their cadres. Unfortunately, the outside world seems unaware of this situation. Perhaps Whitehall’s opinion would be different if he was aware that the LTTE has been proscribed in the United States, the United Kingdom, Canada, the European Union and India because of its atrocities against innocent civilians, politicians and moderate Tamils who disagree with the LTTE philosophy, and because of the assassinations of the former Indian Prime Minister Rajiv Gandhi and the former Sri Lankan President Ranasinghe Premadasa. The former Foreign Minister of Sri Lanka, Lakshman Kadirgamar, an ethnic Tamil, was also assassinated by the LTTE. Terrorism should be condemned wherever and whenever it manifests. The Sri Lankan Government is democratically elected and reserves the right to protect its citizens and the sovereignty and integrity of the state against a terrorist organisation. While using military forces to eliminate terrorism on its soil, the government of Sri Lanka is continuing its efforts to find a lasting solution to the conflict.

Asoka Girihagama

To the Editor: The Sri Lanka College of Paediatricians views with great concern the publication of Whitehall’s article “Teaching Tamil Tigers”1 in the Journal. Whitehall’s article ignores the ground situation and the actual realities in the Northern Province of Sri Lanka. Furthermore, it represents a biased and misleading point of view. It focuses on creating sympathy for the Liberation Tigers of Tamil Eelam (LTTE), without giving any credit whatsoever to the good work done by the Sri Lankan Government in protecting civilians, preserving democracy and maintaining health services and civil administration in the north in the face of enormous obstacles placed by the LTTE, a terrorist organisation. Whitehall was not registered with the Sri Lanka Medical Council during his stay in the country, and thus the alleged “services” he claims to have provided constitute an illegal act under the laws of the Democratic Socialist Republic of Sri Lanka. In view of this, his purported honest and sincere intention of being of service as a doctor in the Northern Province is of dubious value. Another cause for concern is the fact that Whitehall provided training to members of the medical wing of the LTTE. The government provides training to medical students at the University of Jaffna in the Northern Province according to the established norms and procedures for undergraduate medical education, as stipulated by the University Grants Commission and Sri Lanka’s Postgraduate Institute of Medicine. Thus, there was no necessity for Whitehall to teach medicine to LTTE cadres, who would, in any case, be inadequately educated and patently incompetent at performing responsible medical duties. There are fully trained doctors currently serving in the Northern Province, including those from the Sinhalese and Muslim ethnic groups. The Sri Lankan Government provides free medical services (including all infrastructure facilities, personnel, drugs and vaccines) to all citizens of Sri Lanka, including those in the Northern Province, irrespective of race, caste or religion. Thus, there is no truth in Whitehall’s claim that the government does nothing for the Northern Province. In spite of severe problems, mainly caused by the LTTE, it makes every effort to ensure that essential medical supplies reach the LTTE-controlled northern part of Sri Lanka, which includes the hospitals at Kilinochchi and Mullaitivu. The costs of medicines, consumables, meals, capital expenditure, maintenance, and salaries of all hospital staff are borne by the government of Sri Lanka. Free immunisation programs are also provided by the government. All these facts show that the government is genuinely concerned about people in the Northern Province and does its utmost to help them. It is pertinent to ask whether any country in the enlightened world, including Australia, would allow a foreigner who blatantly abuses the laws of the country to work and teach in that country. Would any civilised country allow people who are not properly registered with the relevant medical council to practise and to teach paediatrics to terrorists in that country? It is also disappointing that a medical journal of a country committed to eradicating terrorism from the world has deemed it fit to publish an article of this nature. Whitehall admits that he has written the said piece at the behest of the LTTE. This is obviously another publicity stunt by the LTTE to try to rebuild their deteriorating image internationally. In our opinion, by associating with a terrorist organisation that has been banned in many areas of the globe, Whitehall has blatantly violated the hallowed fundamentals of the Hippocratic Oath.

Sri Lanka College of Paediatricians

Comment: The article by Whitehall1 provoked a barrage of 15 emails to the Medical Journal of Australia that either criticised the Journal for publishing such an article or questioned Whitehall’s agenda and some details of the article. In short, it was suggested that the article was nothing but a propaganda tool for Tamil terrorists or a blatant attempt to romanticise “the terrorists”. Others were perturbed that the MJA saw fit to publish such a confronting article. However, these criticisms were balanced by another 40 emails congratulating the Journal for having the courage to expose what is occurring in Sri Lanka. The Journal strongly stands by its decision to publish Whitehall’s article, as it gives an Australian insight into the turmoil and suffering affecting people caught up in an internal conflict that is foreign to our stable and largely harmonious society.

Martin B Van Der Weyden

Global environmental change is threatening the health and survival of humankind — are we doing enough to ensure the environmental and social bases for health? Global warming and resultant climate change pose serious risks to human health.1-3 However, global warming is only one of a nested series of threats to the health — and even survival — of humankind. With this in mind, is our current approach to both clinical and public health sufficient? Parallel threats to the health and wellbeing of humanity arise from a myriad of anthropogenic problems (Box). All such problems, acting synergistically, stress the ecological and social foundations upon which humanity relies for air to breathe, water to drink, food to eat, and disposal of waste, and without which there can be no civilisation and no economy. Taken together, they comprise what has been described as global environmental change (GEC).4 There are many drivers of GEC. Our complex society is heavily dependent on oil to function, even though the supply of easily recoverable oil has peaked or is about to peak.5 However, the fossil fuel bonanza over the past century and a half has enabled a human population explosion that, in turn, has been driving GEC. As populations expand and encroach into new areas, destroying natural habitats and putting animals and humans into close proximity, humans are being increasingly exposed to novel animal diseases. HIV and emerging diseases such as Ebola virus, severe acute respiratory syndrome and H5N1 avian influenza may be manifestations of this.6 The rising population, ecological stress, and neoliberal-driven economic disparity all contribute to political unrest and human violence,7,8 which drive further GEC. Consequently, humanity is facing a series of serious, unprecedented ecological and social changes caused by ourselves. Of these, it is global warming that, if not the most dangerous threat, is the fulcrum about which to coordinate analysis and action. To express concern about the survival of humankind is not being alarmist. Our understanding of the threats facing humanity has moved to a point where the full range of possibilities confronting us can be appreciated. Where we end up consequent to GEC in the next two centuries will be somewhere on a continuum that extends from the extinction of Homo sapiens, through collapse or patchy disintegration of complex industrialised society, to a sustainable industrial civilisation. Exactly where we find ourselves on this continuum depends on how quickly and effectively we act environmentally, economically and socially. Our survival also depends on our ability to control weapons of mass destruction, which are more likely to be used as the consequences of GEC generate conflict over access to ever scarcer resources. As health carers, we are involved on several levels. Individually, we are both part of the cause of GEC and recipients of its effects. As health care professionals, we will need to modify both our health systems and the way we practise to meet the challenge of new health problems, and to adapt to old health problems in new guises. As health professionals, we also have a duty of care to our patients to strongly advocate for action. Serendipitously, GEC also presents unique opportunities. GEC and economic inequity have related causes. Thus, a strategic approach would enable humanity to derive a set of solutions that will make the world both environmentally sustainable and more economically just,7 with flow-on benefits for health. Indeed, Jonathan Patz proposed that “global climate change could be the greatest public health opportunity we’ve had in over a century”.9 Changes needed to mitigate and adapt to GEC present specific health opportunities; for instance, less car use means more exercise. Howard Frumkin has explained how redesigning cities and rearranging traditional work practices can enhance exercise, build social capital, and make a healthier society.10 While beneficial, such changes are not in themselves sufficient. GEC is adversely affecting our society and will continue to do so. The medical community can no longer limit its focus to hospital waiting times, fee levels, workforce shortages, obesity and diabetes. These issues all become starkly irrelevant if the ecological and social systems on which we depend for both our survival and our capacity to deliver services, save lives and care for people stop working. We need a profound shift in our paradigm. The health care sector is not only responsible for delivering health care, but must also ensure the environmental and social bases for health itself. To meet this responsibility, we can act personally — buy a hybrid car, for instance. Individually, we can join and financially support organisations that are working for change: Doctors for the Environment Australia, the Medical Association for Prevention of War, the Australian Conservation Foundation, and others. But collectively, our academic colleges and professional associations must advocate strongly and clearly to government about the gravity of our predicament and the need for urgent, wide-ranging action. Humanity needs a new vision for health for the year 2100: to make sure we have an economically equitable society on an ecologically healthy planet. The stakes are high — we must not fail. The challenge I put to all of us and to our health and political leaders is to work together to make this vision a reality. Serious current environmental problems* Destruction/loss of natural resources natural habitat (ecosystem services) wild food sources biological diversity soil (erosion, salinity, fertility) Ceilings on natural resources (soft ceiling, raising the ceiling costs) energy (fossil fuel and alternatives) fresh water photosynthetic capacity of plants Harmful things made or moved around toxic chemicals alien species atmospheric gases (greenhouse gases → climate change, ozone destruction) Increasing human population actual numbers impact per capita on the environment (resource use and waste) * Derived from Diamond J. Chapter 16. In: Collapse: how societies choose to fail or survive. London: Allen Lane, 2005.

Peter W Tait MB BS, FRACGP

The Alliance continues to tackle the problem of chronic disease by bringing the right people together With its self-described goal of “confronting the epidemic of chronic diseases”, the Oxford Health Alliance aims to fill the leadership void decried by Beaglehole and Yach,1 the Lancet2 and others. To this end, the Alliance enlists key thinkers and doers, to harness, shape and amplify the energy that is converging worldwide, to address socially and environmentally generated determinants of chronic diseases. It concentrates on high-level approaches, through government and industry, to tobacco control, physical inactivity and unhealthy diets. These, via chronic illness, are responsible for over 50% of the world’s mortality.3 Two years after the launch of the Oxford Health Alliance’s Asia Pacific Regional Centre,4 it is timely to review its progress. Locally, the Alliance is gradually reaching the consciousness of the public health, food and beverage, media and pharmaceutical industries, health departments, non-government organisations (NGOs), and urban designers and planners. Its progress will, no doubt, be accelerated by the global Oxford Health Alliance summit, scheduled for Sydney in February 2008, to debate issues concerning environmental determinants of chronic diseases and make recommendations about “building a healthy future”. Internationally, the Alliance has achieved surprising penetration, participating in World Health Organization, World Economic Forum, Youth Forum and similar high-level meetings and advising governments. It has a formidable network of academic institutions and public health luminaries (see http://www.oxha.org) and is currently conducting an innovative multicountry demonstration program, Community Interventions for Health, to illustrate models for successfully translating the evidence on chronic disease prevention into real life. The Oxford Health Alliance will shortly release the results of an international Delphi survey — spearheaded by the University of Toronto — of 200 international experts to identify “grand challenges” for chronic disease research. It has no qualms about drama, as exemplified by its full-page “global warning” against chronic diseases in The Times (London) last year (Box). Since the launch of its hub in Sydney, the Oxford Health Alliance board, headed by the Regius Professor of Medicine, John Bell from Oxford University, has focused the organisation on six work streams: mounting the economic case for action against chronic diseases; the physical environment (especially urban design) and health; health and wellness protection in the workplace and the role of industry and business in health promotion and prevention; youth — “20% of the present, 100% of the future” (an intention to engage young people, who can contribute to determining the kind of societies they will inherit as adults); the law and health policy; and community interventions for health, and barriers to chronic disease prevention in research. Interaction among these themes promotes rather different thinking about strategies for preventing chronic disease. To develop and promulgate this thinking, the Alliance brings together, through its annual summit meetings and to a lesser extent a series of smaller, local Oxford Dialogue meetings, players who are central to achieving change. Its primary method centres on: Finding the right people: looking outside health systems to other government administrations and the private sector; including people and organisations that influence health but do not often participate in the health debate; engaging those whose business activities are health determinants (eg, food and building design); choosing people who are at the cutting edge of their businesses and can influence colleagues, peers and decisionmakers; and finding and fostering champions of chronic disease prevention. Encouraging debate from a diversity of perspectives: respecting and taking account of differing views; being unafraid to mix youth with experience, left with right, establishment with alternative, and developed with developing world; and bringing to the planning table those who do not normally sit at the same table (eg, grouping food, building and other industries with organisations such as the WHO and the People’s Health Movement). Fostering a collaborative approach: avoiding “good guys versus bad guys” attitudes and approaches; and transforming combatants into collaborators. The Oxford Health Alliance is equally interested in the developed and the developing world and is currently working with Ovations (an arm of the largest private health insurer in the United States, United Healthcare) to establish three to five clusters of excellence to combat chronic diseases in developing countries. Yes, the Oxford Health Alliance works with industry and thereby incurs a risk, but firmly believes that the risk of not doing so is far greater. The Alliance is a United Kingdom-registered charity but, as the progeny of an academic–commercial collaboration between Oxford University and NovoNordisk A/S, Denmark, has sought to work with industry. It is under no illusions about the importance of the bottom line to business, and, like its own law work stream, does not consider that a legislative framework is irrelevant to confronting the problems of chronic disease. For example, the Alliance is a fierce defender of the WHO Framework Convention on Tobacco Control. However, it sees its role not as a legislator or enforcer, but as seeking commitment and involvement from the business sector, through discussion and debate and through recognising and working with companies that are prepared to embrace the necessary changes. The origins of the current chronic disease and environmental crises are located deep in society, suggesting that their resolution will require a complex and inclusive response from society, spanning business, government, academia, and civil society more generally. Hence, the 2008 Sydney summit will bring a diverse group of people together for 2 days to design and issue a formal challenge to government, business, industry, unions, universities, activists and bilateral and multilateral funders to progress the Alliance’s ambition of “healthy people and a healthy environment”. There are risks, but the potential gains are great, and as the Sydney summit will attest, the Oxford Health Alliance is ready to take the gamble.

Ruth Colagiuri BEd, GradCertHlthPolMgnt · Stig Pramming MD · Stephen R Leeder BSc(Med), MD, PhD