Health occupations

One aim of Medicare’s Enhanced Primary Care (EPC) initiative is to encourage multidisciplinary care of patients with chronic disease by funding five allied health treatment sessions per patient per year. In many cases, the number of funded treatments is far less than standard clinical practice indicates, particularly when the five visits are shared between service providers. We believe clinical outcomes may be compromised by adhering to the funded hours, and inequity of outcome may arise based on socioeconomic status and the ability of patients to pay. Research that determines how patients and allied health practitioners are responding to this initiative is required. Research is also required to evaluate whether EPC enhances clinical outcomes compared with no allied health intervention and standard allied health practice.

Michele M Foster PhD · Geoffrey Mitchell FRACGP, PhD · Terry Haines BPhysiother(Hons), GCertHealthEcon, PhD · Sean Tweedy BHMS, MHMS, PhD · Petrea Cornwell BSpPath, PhD · Jennifer Fleming BOccThy(Hons), PhD

Meningitis and mentors seeded a passion to remedy health inequalities in Africa We have the capacity to feed everybody on our planet. We have the capacity to ensure that everybody has clean water . . . [and] affordable health care. We can prevent many of the diseases to which our children in the poorer parts of the world succumb . . . A person is a person through other persons . . . You can’t be human in isolation; you are human only in relationships. — Archbishop Desmond Tutu I’ll never forget the pounding, throbbing headache that heralded meningococcal meningitis. I remember leaning against the wall in the bathroom of my local doctor’s waiting rooms, steaming with a temperature of 40°C, and thinking “This is it. I must be dying”. The pain was so intense I just couldn’t see how my body could survive. Every skerrick of light seeping through my shut eyelids felt like lasers beaming through to burn my brain. As I was a boarder in a rural school, I was alone — I was afraid — and I was 14. After losing consciousness and a helicopter flight to Sydney, I awoke after a week, in the intensive care unit of the Children’s Hospital at Westmead. One week later, when I could stomach food, I was moved into a ward. I was sharing with a 2-year-old boy who also had meningitis, but whose septicaemia had taken hold of his young body more aggressively than it had of mine. I remember watching him being wheeled out of the room one morning, only to return 6 hours later with no lower legs. The author, surrounded by orphans in Nairobi, Kenya. Days passed, and much to everyone’s shock, I continued to recover, with no residual disability. The months to full health were many, yet the realisation of surviving a fatal disease, completely unscathed, began to sink in. I was left with a sense of “survivor’s guilt” — an intense appreciation of life and how fortunate I was, a realisation of the gift that life is, and a yearning to make the most of every living, breathing moment that remained. My first decision was to study medicine, to fulfil a desire to give something back to the profession that had saved my life. A month in a children’s hospital is the best work experience one could have, and despite coming from a family with generations of strength in the arts, especially music, I decided to take up chemistry at school and begin to focus on the sciences. Unprepared, I sat the undergraduate medicine admission test in my final year of high school, and my marks were nowhere near those required for entrance. Undeterred, I headed off on a gap year abroad, working as a music and drama teacher in the United Kingdom before studying Italian in Florence. I returned in 2001 to the Australian National University (ANU) in Canberra to study for a Bachelor of Science (Psychology)/Bachelor of Arts, following my sister’s footsteps to John XXIII College. A year later, a summer internship on the trading floor at Macquarie Bank in Sydney saw me shift to a Bachelor of Commerce/Bachelor of Science, and I returned to Macquarie Bank for three more challenging summers in finance. Equity markets and medicine are deceptively similar: both are fast-paced, intellectually demanding, unpredictable and exciting work environments. Yet despite the “buzz” of my experience in the financial world, I couldn’t shake my medical aspirations. During lunch hours in Martin Place, I would sit and stare at the homeless people seeking shelter under the buildings in which others were making millions, and I knew that a profession in medicine would be the only way to satisfy my desire to help people while challenging me intellectually. Education session and distribution of subsidised insecticide-treated nets by Hands of Help volunteers and health workers in Uganda. After two more unsuccessful attempts at the undergraduate medical admissions test, I turned to the postgraduate admission procedure. In the penultimate year of my undergraduate course, I sat the Graduate Australian Medical Schools Admissions Test (GAMSAT) as mere practice for the following year, but fortunately, my marks were high enough to result in a placement at the University of Sydney. I was bursting with enthusiasm to begin the postgraduate medical course after 4 inspired years as an undergraduate. To pay the bills during my days in Canberra, I had worked as a therapist for children with autism, conducting applied behavioural analysis for children with profound disability at a special education school in Woden. What began as a job soon turned into a passion as I learned how to communicate with children who had no speech, honing my empathy skills as I tried to learn to read their expressions and mannerisms to understand how they were feeling and what they were trying to say. These children, with beautiful personalities frustratingly stuck in less useful bodies, absolutely grew on me. My appreciation of life continued to grow and, while I hope the hours of therapy I did with those children helped them become a little more capable, ultimately they taught me far more. In my last holidays before beginning medicine, I made a trip to Africa, a continent which had fascinated me since reading Bryce Courtenay’s The Power of One as an impressionable teenager. In my commerce degree, I had majored in development economics and was inspired by a senior lecturer at the university, Dr Alan Martina, who brought to light for me the inequalities existing in our world today. My passion for the subject saw me begin to devour novels on the area, and an inspirational meeting with Nobel Prize nominee Professor Jack Caldwell, who has devoted much of his life to demography in Africa, sealed my interest. Thanking the Bufuula community for their hospitality at the end of the volunteers’ 3-month stay to build a primary school in 2005. I spent a month in East Africa those holidays, and was changed forever by the experience. In Africa, the continent on which we all began as Homo sapiens, it is impossible not to feel alive. There is a magic about the place and its absolute determination to defeat the myriad obstacles that have been placed in its way — geographical disadvantage, slavery, colonialism, and continuing epidemics — and this fiery determination burns through to your heart, making it impossible to walk away unchanged. I remember my plane taking off from Nairobi and promising to myself that I would return, but next time with more money, more time, and more people to make a difference. I graduated from the ANU and started studying medicine 6 months later. I had already emailed all my family and friends to rally interest in working and raising funds for the continent, but as the work began, the interest dissipated. Not knowing a soul in my new medical course, I took the plunge to email my entire year group about my idealistic plan. The response was amazing. The following summer, in December 2005, 17 volunteers, including 12 medical students from the University of Sydney, headed to Uganda to live in a remote community for 3 months, with no water or electricity, as we built a primary school for 650 children. We paid our own way to get there, juggling part-time jobs on top of full-time medical degrees, and left with our backpacks and $100 000 in the Hands of Help bank account — the result of an exhausting year of fundraising and the generosity of those supporting our idea. On the back of such enthusiasm, I set in motion the wheels to register ourselves as a charity, and Hands of Help was born, with a grassroots commitment to ensuring all funds raised reached the areas of the world that needed them most. To date, over 98% of our hundreds of thousands of dollars has been spent “on the ground” in Africa or Indigenous Australia, something we are proud of, and a figure not often achieved in the world of charitable organisations. A young girl in Bufuula, proudly wearing a Hands of Help armband. Living in an African community, experiencing life the way Africans do, is a once-in-a-lifetime opportunity. We grew close to the children, their parents and the local community council, and developed an understanding of health care in the developing world through visits to local clinics and hospitals. I rustled together a survey, which we conducted with local interpreters, of every household in Bufuula — the tiny village we were living in, located 3 hours south-east of Kampala, the capital of Uganda. As we sat in each home, showered with papayas, fresh milk from their cows and raw peanuts or coffee beans, we listened intently to their stories. We swallowed hard past the lumps in our throats as we heard recollections of their many children lost to malaria, while smiling toddlers sat in the corner of the hut eating cardboard to ward off their grumbling tummies. We stood humbly at the grave sites of mothers lost to AIDS while holding the hands of their children left behind, and we listened to their desperate pleas for access to health care and education. The first Hands of Help group of volunteers. Inspired, we headed off to Kampala to meet with Dr Ian Clarke, of the International Hospital Kampala (IHK), who agreed to support us to begin a community health project in Bufuula, training and employing Ugandans selected by their own communities to become grassroots health workers in areas where hospitals are out of reach. The project began in Bufuula and surrounding villages, and this year will reach as far afield as the war-torn areas of northern Uganda. Over 50 Ugandans have been trained as health workers by a public health specialist. Subsidised mosquito nets have been distributed, water sanitation satchels have been added to jerry cans, and HIV testing has been made available, along with education sessions on all relevant diseases, by these health workers who are proud and honoured to be trained as such. They see their new knowledge as such a privilege that they feel a responsibility to spread it to as many towns as possible. That summer was the beginning of years of achievements for Hands of Help. Seventeen volunteers, to whom I — and Africa — are forever indebted for believing in me and my ideas, left that initial project enlightened and inspired to be part of improving the inexcusable health inequalities facing so many in our world today. On the way home, our chance trip to an orphanage with unparalleled atrocious living conditions resulted in a commitment to help 250 orphans in Nairobi, Kenya. These orphans are now being given a chance at life, receiving a secondary school education through our child sponsorship program. Yet, also conscious of the issues in our own backyard, we returned to Australia and established a project to allow medical students to work with local Aboriginal medical services in remote Indigenous communities. And so I approach the final year of medical school, with years of hard work, sleepless nights and exhaustion from overwork behind me — and that’s before internship has even begun! It would be unrealistic, and lying, to say it has been easy, and I often look longingly at those enjoying a weekend off or a holiday. Yet, thanks to the hard work of dedicated committee members, a balanced partnership with medical student and Vice-President Joe Dusseldorp, who believed in Hands of Help from its inception, an extremely supportive family and partner, and the generosity of the Australian public, the charity has achieved more than I could ever have hoped for in that moment my plane took off from Nairobi. Over 100 volunteers have now given up their summers to build three new primary schools in Uganda, 50 Ugandans have been trained as community health workers, 250 Kenyan orphans have been given another chance at life, and a further 25 medical students have spent their holidays experiencing health care for Indigenous Australians. Meanwhile, awareness of African issues, and a chance for Africans to speak with their own voice, is provided by our Sydney African Film Festival1 and photographic exhibitions every year by a professional photographer (my partner, Hamish Gregory, who travels the globe with me). This summer, a further 30 volunteers will travel to the war-ravaged areas of northern Uganda to build a fourth school, while the Community Health Project will expand to service the two million people displaced by years of civil war in Gulu. Conducting hut-to-hut health surveys with local interpreters in Uganda. As I approach the coming years of my junior medical and specialty training with trepidation and curiosity as to where the path of medicine will take me, I find solace and inspiration from the thought that dozens of medical students now have a passion for our world’s health inequalities. I am continuously supported and encouraged by my parents and motivated by the work of doctors such as Catherine Hamlin, whose work with women with obstetric fistulas in Ethiopia has turned around the lives of 32 000 women, and Rowan Gillies, the former President of Médecins Sans Frontières. I am encouraged by supportive lecturers and honours supervisors, and always astounded by the passion of selfless doctors who take the time to pass on the secrets of medicine by teaching and motivating young students every day. But without a doubt, the thoughts that stay closest to my heart are the memories of an African child’s piercing stare delving deep into my soul, and the throbbing pain of that meningitic headache — and I pinch myself and remember how lucky I am to be here, where I am today, and I think of how much there is to squeeze into these short years — and how wonderful it is to be alive.

Phoebe C M Williams BComm, BSc

To the Editor: Security requirements for air travel have recently become very strict and include limitations on the carriage of medication and medical equipment. International flights to and from Australia are often lengthy, and patients needing regular medication can suffer serious complications without it. Diabetic patients are particularly vulnerable, as illustrated by this case. A 54-year-old engineer was returning to Australia after a 4-month placement in Norway. He had a history of type 2 diabetes, which had become insulin dependent 5 years previously. His diabetes was well controlled with 40 units of insulin twice daily, and he had no other major medical problems. At a Norwegian airport, his insulin, needles and syringes were detected on security screening of his cabin baggage. Security staff told him that he was not permitted to carry his insulin or equipment in the cabin without a letter from his doctor and a current valid prescription. The man’s protests were to no avail, and he boarded without his insulin. During the 25-hour journey to Sydney, he developed vomiting, polyuria, sweating and dyspnoea. Despite making cabin staff aware of the underlying problem, he was offered no assistance apart from a steady supply of airsickness bags. On arrival in Sydney, he was very ill and was taken by ambulance to St George Hospital, where he required admission to the intensive care unit. His pulse rate was 130 beats/min and respiratory rate 30 breaths/min. His urine was strongly positive for ketones and his blood glucose level was 51 mmol/L. Arterial blood gas analysis showed very severe metabolic acidosis with a pH of 6.9, Pco2 18 mmHg, and Hco3 4 mmol/L. His diabetic ketoacidosis was treated conventionally, with aggressive extracellular volume and electrolyte replacement, and insulin by infusion. His condition improved rapidly, and he was discharged home the next day. Australian doctors and their diabetic patients should be reminded that airline security requirements are now very strict in most countries, and that life-threatening ketoacidosis can readily develop over the course of a flight between Australia and the northern hemisphere. Insulin-dependent patients must continue to take their insulin during these flights and should not board without their supplies. In Australia, the Department of Transport and Regional Services stipulates that people with medical requirements may carry “prohibited items” such as hypodermic needles, but must also carry a doctor’s letter, a medical certificate, or a current National Diabetes Services Scheme card.1 Supplies should be clearly labelled, carried in a clear plastic bag and declared to security staff before being screened. The United Kingdom Department of Transport2 and the United States Transportation Security Administration3 have broadly similar requirements.

George Skowronski

To the Editor: Human normal immunoglobulin (NIG) has historically been used to provide passive immunity against hepatitis A infection for susceptible travellers to areas where the virus is endemic.1 The introduction of effective hepatitis A vaccines in recent years (which result in active, long-term immunity to the virus) should have largely replaced the use of NIG for travel prophylaxis.2 However, the Australian Red Cross Blood Service still receives requests to supply NIG for travellers, even though the intended recipients have no contraindications to vaccination. Requests for use of NIG for this purpose appear in many cases to be a consequence of the “out-of-pocket” cost to the patient of the hepatitis A vaccine, which is about $70–$100 (depending on the formulation used and the private dispensing fee charged). In contrast, NIG is provided free of charge to the recipient, but the community still incurs substantial costs related to blood collection and fractionation of plasma products. There is also the concern of unnecessary exposure of a healthy traveller to a pooled plasma product, which, despite blood donor screening, dedicated viral inactivation steps, and an excellent safety record in Australia, may theoretically transmit infectious agents. In addition, even if a small amount of NIG is used for this purpose, the plasma source would be better used for production of greater amounts of other scarce plasma-derived products (such as intravenous immunoglobulin). While NIG can effectively prevent hepatitis A infection from developing in susceptible contacts, immunity is short-lived and likely to be inferior to the results of active vaccination.1-3 Accordingly, NIG is only indicated for at-risk people who have a contraindication to vaccination, or in whom there is insufficient time to mount an endogenous antibody response (active immunity develops within 7–10 days of vaccination,3 and vaccination may also prevent hepatitis A infection even when the vaccine has been administered up to a week after exposure4). Use of NIG is also appropriate where at-risk contacts may be unable to mount a protective antibody response because they have a congenital or acquired immune deficiency. Although the extent of NIG use for travellers appears to be limited, we wish to highlight that, in the absence of contraindications to vaccination, it can no longer be advocated as best practice, and it is certainly not an appropriate cost-saving measure.

Jake Shortt · Denis Spelman · Erica M Wood

The demand for diagnostic imaging services has grown faster than the supply of radiologists in Australia. Given the predicted ageing of the population and contraction of the health care workforce, the current workforce model is not sustainable. Extending the role of radiographers in a specific range of radiological reporting tasks may help meet demand, relieving some pressure on radiologists. Experience overseas suggests that radiographer reporting can reduce patient waiting times, release radiologists for other duties and improve the retention of radiographers. Evidence shows that, with appropriate education and training, the accuracy of radiographers in interpreting plain x-rays is comparable to that of radiologists. Australian universities are well placed to offer radiographers postgraduate education in image interpretation.

Tony N Smith PhD · Marilyn Baird PhD

Objective: To determine whether eating Lactobacillus rhamnosus GG (LGG) in the form of commercially available yoghurt improves clearance of vancomycin-resistant enterococci (VRE).Design: Double-blind, randomised, placebo-controlled trial.Setting: Renal ward of Austin Health, a tertiary hospital, Feb–Oct 2005.Participants: 27 VRE-positive patients, 14 receiving active treatment and 13 controls.Interventions: Subjects were randomly assigned to either a treatment group (receiving 100 g daily of yoghurt containing LGG for 4 weeks) or a control group (receiving standard pasteurised yoghurt). Faecal samples were obtained three times at about weekly intervals. Treated patients were tested for VRE again at 8 weeks. Patients in the control group who had failed to clear VRE after 4 weeks were then given LGG-containing yoghurt for 4 weeks, as an open continuation.Main outcome measure: Number of faecal specimens clear of VRE.Results: Of the 27 patients enrolled, 23 completed the study. Two patients were lost to follow-up, one died and one withdrew. All 11 patients in the treatment group who completed the study cleared VRE. Three subjects reverted to VRE positivity after using antibiotics to which LGG is sensitive, while all others remained negative for at least 4 weeks after trial completion. Twelve control subjects completed the study, of whom one cleared VRE and 11 remained VRE-positive. Eight of these 11 patients were subsequently crossed over to receive LGG yoghurt, and all cleared VRE within 4 weeks.Conclusion: To our knowledge, this is the first description of a probiotic therapy to successfully treat gastrointestinal carriage of VRE in renal patients. Further investigation of the use of LGG in VRE-positive patients is warranted.

Karen J Manley BSc, MHumNutr, GradDipDiet · Margaret B Fraenkel BM BS, PhD, FRACP · Barrie C Mayall MB BS, FRACP, FRCPA · David A Power BM BS, PhD, FRACP

Acutaneous dental sinus tract is a channel which leads from a dental focus of infection to drain onto the face or neck.1 These tracts tend to occur more frequently from infected mandibular teeth (80%) than maxillary teeth (20%).2 Hence, they are more common in the submandibular or submental regions of the face.3 Sinus tracts may result from localised infections, such as an infected tooth, periodontal disease, actinomycosis or osteomyelitis.4 There are numerous reports of cutaneous dental sinus tracts in the dental literature,1,4-10 but comparatively few reports in the medical literature.2,3 Patients with these lesions often present first to general practitioners rather than to dentists,1-7 possibly because they do not associate lesions of the face with teeth and often have no associated dental pain. Lessons from practice Dental infection can present with cutaneous lesions of the face and neck. Dental assessment is recommended for non-healing face and neck lesions, particularly in submandibular and submental regions. Biopsies or excisions are not necessary and can cause scarring. Management of the dental focus of infection through endodontic (root canal) treatment or tooth extraction will resolve the sinus tract. Clinically, a cutaneous dental sinus tract may resemble a pimple, ulcer, nodule, or indurated cystic area. Because these tracts have a similar clinical appearance to other facial lesions and are relatively uncommon, they may be misdiagnosed, leading to inappropriate antibiotic therapy, aspiration or surgery. Unless the dental focus of infection is treated, recurrence is likely.1-10 When surgical intervention is attempted, breakdown of the wound can leave scarring and wound contracture.2-8 In our three patients, the dental sinus tracts occurred because of delays in diagnosis or management. The differential diagnosis includes pyogenic granuloma, furuncle, foreign body reaction, and cysts, such as sebaceous, epidermoid and thyroglossal cysts.3 Neoplastic causes, such as basal and squamous cell carcinomas, should also be considered,1 as well as other infective causes, including osteomyelitis, actinomycosis and tertiary syphilis gumma.2 Intraoral radiographic examination is a crucial diagnostic tool. A carious tooth or periapical radiolucency on a dental radiograph suggests a possible dental focus of infection. Dental assessment will confirm diagnosis. Usually, dental sinus tracts drain within the mouth, commonly in the vestibule adjacent to the affected tooth. However, they may drain onto the face, depending on the relationship of the muscle attachments and tissue planes of the face to the focus of infection. In the maxilla, if the focus of infection is superior to the muscle attachment, or in the mandible, inferior to the muscle attachment, a sinus tract may form on the face. Pus travels via the route of least resistance along facial planes until exiting cutaneously. When cutaneous sinus tracts are involved, the infected tooth is often free of pain as the tract provides an outlet for inflammatory exudates, allowing decompression.6 The infected, non-vital (ie, necrotic) tooth may be slightly tender to percussion. Histologically, sinus tracts show inflammatory tissue, granulation tissue or abscess formation. The tract may have an epithelial lining.4 Elimination of the source of infection by endodontic treatment or tooth removal results in resolution of the sinus tract, typically within 2 weeks.4,7,8 In most cases, the result is cosmetically acceptable, as in our Patients 1 and 2, but wound contraction and scar tissue may necessitate surgical revision (as in Patient 3).3 Biopsy should be avoided as it may lead to exacerbation of infection or scarring. Antibiotic therapy is indicated when there are signs of systemic involvement (eg, pyrexia or lymphadenopathy). Clinical records Patient 1 A healthy 40-year-old man presented to his general practitioner complaining of a non-healing pustule, and a swelling on his chin with an associated purulent discharge. The patient was referred by his GP to a hospital for excision of the lesion under the care of a surgeon. The surgeon believed the lesion to be a sebaceous cyst and attempted to remove it. Following the procedure, the patient developed fever, malaise, and marked swelling of the mental region. He was admitted to hospital for 2 days for intravenous antibiotic therapy. A dental origin for the lesion was then considered, and the patient was referred to a dental specialist (an endodontist) for assessment. The patient had a history of a car accident which caused trauma to the teeth 15 years previously. He did not receive dental treatment at the time. Clinical examination revealed an erythematous lesion on the chin measuring 0.5 cm in diameter, from which pus drained freely (Figure 1A). Routine clinical dental tests were conducted, including tooth percussion and CO2 dental pulp testing. Radiographic examination revealed a broad radiolucency associated with three of the lower incisor teeth (Figure 1B). These findings led to a diagnosis of chronic apical periodontitis caused by pulpal necrosis and infection of two lower incisor teeth (teeth 31 and 32). Tooth 41 was vital. The patient underwent endodontic (root canal) therapy to the lower incisor teeth (31 and 32) and reported that the discharge ceased a week later. Photographs taken at 3-month follow-up showed resolution of the tract (Figure 1C and 1D). Patient 2 A healthy 41-year-old woman presented to her GP with a non-healing pimple on her right nasolabial fold (Figure 2A). The GP referred the patient to a surgeon who attempted to excise the lesion. Reportedly, the lesion resolved, only to recur 3 months later. By this time, the surgeon suspected a dental aetiology, and referred the patient to an endodontist. Radiographic examination suggested that the lesion was related to an infected upper canine. A radiolucent area around the root of the tooth was characteristic of a periapical abscess (Figure 2B). The tooth was treated endodontically (Figure 2C), and the skin tract resolved. Patient 3 A 7-year-old girl presented to a dentist with toothache and a developing skin lesion under her chin. She had a history of trauma to her lower lip and teeth at 3 years of age. The lower right lateral incisor tooth was slightly tender to percussion, and radiographic examination revealed a radiolucency associated with the root of the tooth. The dentist referred her to an endodontist, who confirmed the diagnosis of chronic apical periodontitis with facial sinus tract. Endodontic treatment was begun, but, because of a dental phobia, the girl delayed completion of this treatment. She presented again 6 months later because the skin lesion had worsened, becoming raised, firm and erythematous (Figure 3A). Endodontic treatment was completed (Figure 3B), and the skin lesion began to heal. At 6-month follow-up, wound contracture had caused dimpling of the skin in the affected area (Figure 3C). This may require surgical revision.

Roland A Barrowman BDS · Mehdi Rahimi BSc, BDS · Mark D Evans MDSc, GradDipClinDent · Arun Chandu MDSc, MB BS, FRACDS(OMS) · Peter Parashos MDSc, PhD

Why try a doctor when you need a dentist? Oral conditions have some of the highest prevalence and incidence rates of all health problems in Australia.1 They are frequently associated with pain, functional limitations and interference with usual activities. Most people experiencing oral symptoms will visit, or at least contemplate visiting, a dentist. But why are some patients with oral conditions presenting to general practitioners? While signs and symptoms associated with dental caries and periodontal diseases are usually understood to be problems for dentists, sequelae of these conditions, such as abscesses, facial swelling, altered taste and halitosis, may sometimes be considered more of a medical than an oral problem. Furthermore, differences in the way dental and medical services are organised and delivered may provide a greater incentive for patients to present to GPs rather than dentists. This applies not only to conditions for which an ill-defined boundary exists, but also for management of acute symptoms of common oral conditions. Mansour and Cox outline some of these common oral conditions in this issue of the Journal (page 64).2 One result of the evolution of the medical and dental professions over the past century is a “separateness” that has diminished both professions’ understanding of the other’s discipline. While it is highly desirable to reduce this knowledge gap, it seems unlikely to be readily closed, given the existing curriculum pressures created by scientific and technological advances. A logical response to the inappropriate presentation of patients with oral conditions to GPs would be to both remove the incentives for this type of presentation and to provide more certain pathways for dental referral when they do occur. Indeed, Mansour and Cox recommended dental referral for most of the cases described and for all possible outcomes of their decision-making algorithm. But while the need for referral to dentists is generally well recognised, the ability to refer may be limited. Both the initial presentation to a GP and the difficulties in referral to a dentist are shaped by problems in accessing dental care in Australia. There are only about 9000 practising dentists in Australia (approximately 50 per 100 000 population),3 the vast majority of whom work in either the central business districts or middle-class residential suburbs of the major population centres, leading to significant maldistribution. Equally important is the fact that 86% of dentists work in the private sector, where they alone determine location, hours worked and fees charged. Outside normal business hours, the number of available dentists is very limited, and access is frequently restricted to existing patients of a practice. In some instances, major public hospitals and the limited number of dental hospitals do provide after-hours access to on-call dentists, but this is the exception rather than the rule. Publicly-funded dental care is usually restricted to holders of concession cards, which reduces those eligible to about 34% of the adult population. Further rationing of dental treatment occurs because of the limited facilities and shortage of dentists in the public sector. Only 19% of eligible dentate adults (ie, those with natural teeth) receive any dental care from public dental services in any year.4 An overall shortage of dentists makes access to dental treatment even more difficult. Within 4 years, Australia is predicted to be short of some 1500 dental care providers, mostly dentists.5 This shortage creates a bottleneck in the supply of dental treatment. It is most harshly felt by people already having difficulty obtaining dental treatment — low income Australians and those living in rural areas. However, the bottleneck also extends to dentistry in the “main street”; that is, private general dentists in middle-class residential areas. Increasing the number of positions in our universities for dental students may eventually overcome this problem — assuming there are academics to teach them and funding to competitively employ some of them in the public sector at the completion of their education. However, the current national output of less than 250 graduates a year does not begin to address the shortfall. Increased education of auxiliary dental personnel (hygienists and therapists) should lead to increased prevention programs, but is unlikely to address the problem of adults presenting with acute conditions. Cost is another significant barrier to accessing dental care. An estimated 25% of dental patients delay seeking treatment because of the expense.6 Public funding for dental treatment is dramatically less than for medical treatment. At present, public funding from the federal government is directed at the 30% private health insurance rebate, while state and territory government public funding is directed at low income adults and schoolchildren. The outcome is an inequitable pattern of public assistance in accessing dental treatment. Ironically, the average taxpayer may well pay the most and receive the least in terms of support in accessing dental treatment. The majority of patients will face the full cost of any dental treatment. The current average hourly rate for dental practices is $350 (of which overheads represent 73%).7 Thus it is likely that any substantial care (be it diagnostic or therapeutic) will represent a significant financial burden to the patient. The incentive for patients with oral conditions to present to a GP is obvious. GPs are more available, obtainable out of hours, and can be seen without the need to pay substantial out-of-pocket costs. The corollaries of these same issues are often the substantial barriers to dental referral for patients presenting to GPs. Recently, the federal government recognised the need for dental care among patients with a GP Management Plan and Team Care Arrangements or an Enhanced Primary Care multidisciplinary care plan. Essentially, approved patients may be referred to a dentist for an assessment and two other services within a 12-month period. In 2005, there were only 2055 referrals for dental assessment (Item 10975),8 and these resulted in 2500 items of treatment or referral to a dental specialist (Items 10976, 10977). The total cost of dental diagnostic and treatment procedures was just over $500 000 (or $250 per 100 000 population). These data indicate a negligible level of referral under these plans. Specific issues within these plans act as further barriers to referral for dental care. For GPs, the cost and time involved with administrative requirements far exceed the value of the remuneration. Referral cannot proceed until the original care plan has been completed and paid for, which largely negates treatment of acute conditions. The relatively small number of appointments permitted, dentists’ unfamiliarity with the Medicare remuneration system, and the level of remuneration make dentist participation professionally and financially unrewarding. The result is that current referral plans available under Medicare are unlikely to provide a simple or effective pathway for dental referral and treatment. Currently, patients with acute oral conditions should hope that the problem occurs during normal hours in a major population centre, that the condition is not part of a larger problem, and that they are wealthy enough to have a regular dentist who has the time to see them. For patients who are not so fortunate, presentation to a GP is likely to remain an option. As outlined by Mansour and Cox, on most occasions, little, if any, effective help can be offered beyond referral to a dentist. The short-term results are frequently only palliative, at best, and without appropriate follow-up care — resulting in increased costs to the public purse and ongoing suffering to the patient.

Roderick I Marshall BDSc, MDSc, FRACDS(Perio) · A John Spencer MDSc, PhD, MPH

Dentofacial pain is a common presentation in general practice, and more than 50% of cases arise from dentally related pathology. In a carious tooth, pain that is site-specific, severe and spontaneous usually denotes extension of caries into the tooth pulp. Caries does not always appear as a cavity in the tooth, but may lie beneath intact enamel or on surfaces between teeth. Examination of tooth pain should include firm percussion (eg, with a tongue depressor). Tenderness on percussion denotes progression of infection into the subdental tissue. Pain occurring 24–48 hours after a tooth extraction is commonly caused by superficial osteitis in the exposed alveolar bone. Examination will reveal the absence of a blood clot in the extraction socket and severe tenderness on local palpation. Severe pain related to impacted wisdom teeth is frequently caused by pericoronitis, an infection in the gingival tissues surrounding the tooth. The surrounding gingiva is erythematous and tender to palpation. Localised facial swellings of dental origin require immediate referral to a dentist. Progressive facial swelling requires aggressive antibiotic therapy and referral to hospital for definitive management.

Mohammed H Mansour MSc, MD · Stephen C Cox OAM, MSc, FRACDS

Magnetic resonance imaging and arthroscopy of the hip have shown that labral injuries, chondral injuries, rim lesions, synovitis and tears of the ligament teres are common causes of hip, groin and low-back pain. Hip arthroscopy is used both as a diagnostic and therapeutic tool; it has been shown to be of benefit in recent traumatic labral injury, but disappointing in the management of chronic hip pain (which may be associated with degenerative change, and chondral lesions of the acetabulum). The McConnell multimodal physiotherapy regimen is effective in treating patellofemoral pain. Anterior cruciate ligament rupture is three to five times more common in women, but neuromuscular training appears to decrease its incidence. Patellar tendon and hamstring grafts appear to be equally effective in anterior cruciate ligament reconstruction. Articular cartilage defects remain a significant problem, and the efficacy of treatments such as autologous chondrocyte implantation is still unclear.

Peter D Brukner MB BS, FACSP · Kay M Crossley BAppSci(Physio), PhD · Hayden Morris MB BS, FRACS · Simon J Bartold BSc, FASMF, FAAPSM · Bruce Elliott PhD, FAAKPE, FISBS

Diving and subaquatic medicine. 4th ed. Carl W Edmonds, Christopher Lowry, John Pennefather, Robyn M Walker. London: Arnold, 2002 (viii + 719 pp). ISBN 0 340 80630 3. One of the first books I was given to study when starting my hyperbaric term was the third edition of Diving and subaquatic medicine. It is still one of the few textbooks that I have literally read from cover to cover. The fourth edition builds on the success of the previous three editions as four of the most respected diving specialists in Australia have collaborated to produce an immensely readable book of a technically difficult subject. The contents include both the physics and physiology of diving medicine along with interspersed clinical vignettes of actual cases that are used to illustrate particular points. The book itself is well diagrammed and has extremely good photos (several in colour), which only enhance the clinical and theoretical discussions of each topic. I find it hard to think of a subject in diving medicine that this book has not covered very well, and the main topics (such as injuries to the ear) are covered in appropriate depth. The book also helpfully includes several common treatment tables and diving schedules, and it is still one of the most utilised books (as well as the most often liberated book) in the hyperbaric medicine unit. Diving and subaquatic medicine keeps to the topic well and is a reasonable size to keep readily available. It is probably the best all-round diving medicine book available, and its Australian origins make it particularly relevant. Even non-diving issues such as marine envenomation, near-drowning and underwater explosions (!) are covered in this comprehensive textbook. It is quite rightly known as the Diving Medicine Bible in Australia, and anyone who works in diving medicine, medically certifies divers or even has a mild interest in diving will enjoy this easy-to-read book.

Glen Hawkins

During the Australasian Antarctic Expedition of 1911–1914, Douglas Mawson and two companions, Belgrave Ninnis and Xavier Mertz, undertook an ill-fated mapping journey. Ninnis died when he fell down a crevasse, together with the sledge carrying most of their food supplies, and later Mertz became ill and died. Only Mawson returned. In 1969, Cleland and Southcott proposed that Mertz died of vitamin A toxicity and Mawson suffered from the effects of hypervitaminosis A because, with little food left, they were forced to eat their surviving dogs, including the liver. This hypothesis was supported by Shearman in 1978. After re-evaluating this hypothesis, I propose that Mawson and Mertz suffered from the effects of severe food deprivation, not from hypervitaminosis A, and that Mertz died as he was unable to tolerate the change from his usual vegetarian diet to a diet of mainly dog meat. I also suggest that Mertz’s condition was aggravated by the psychological stress of being forced to eat the dogs he had cared for for 18 months.

Denise Carrington-Smith BA(Psych), MSocSc(Archaeology)

Benjamin C Cowie,* Alan Breschkin,† Heath Kelly‡ * Infectious Diseases Physician, † Senior Scientist, Infectious Disease Serology, ‡ Head of Epidemiology, Victorian Infectious Diseases Reference Laboratory, 10 Wreckyn Street, North Melbourne, VIC 3051. Benjamin. CowieATmh.org.au To the Editor: Hepatitis E virus (HEV) infection is uncommon in Australia. The HEV cases detected are almost always in patients who have recently arrived from HEV-endemic regions of the world.1 We previously reported a significant increase in highly reactive serology results for anti-HEV IgG antibodies measured by enzyme im-munoassay (EIA) at the Victorian Infectious Diseases Reference Laboratory (VIDRL) in the first 6 months of 2004.2 Nine of the 10 Victorian patients with highly reactive samples in the previous report had had a history of recent clinically compatible illness and travel in a disease-endemic region within the incubation period (2–9 weeks). This indicated a strong association between highly reactive anti-HEV IgG measured by EIA and acute HEV infection, as has been shown previously.3 At the time, we hypothesised an association with overseas HEV epidemics, particularly in India, as seven of the nine patients with acute HEV infection had travelled there. We have now reviewed HEV serology results at VIDRL for the subsequent 9 months and compared them with our ex-perience of the past 5 years (Box). In the first quarter of 2005, we recorded the highest quarterly number of highly reactive anti-HEV serology results since testing commenced at VIDRL. Also marked on the figure are the dates, over the same time period, when an outbreak of hepatitis in India (either suspected or confirmed to be caused by HEV) was reported on ProMED-mail, the global electronic reporting program for emerging diseases hosted by the International Society for Infectious Diseases (http://www.promedmail.org). It would appear that epidemic HEV activity in India is reflected in significant increases in the number of highly reactive anti-HEV serology results in our laboratory. In fact, as shown in the Box, increases in highly reactive anti-HEV serology at VIDRL have sometimes preceded an outbreak noti-fication on ProMED-mail, and may provide early warning of such an event. A similar association is not observed for epidemics in other countries. Travellers to developing countries must be advised of preventive measures against HEV and other enterically transmitted diseases, and a diagnosis of HEV infection should be considered in any febrile traveller recently arrived from an HEV-endemic area, particularly if jaundice or abnormal liver function tests are present. This is especially important in pregnant women because of the risk of fulminant hepatitis, with maternal mortality in excess of 20% in the third trimester.4 All cases should be notified to state health authorities. Highly reactive anti-HEV IgG EIA results at VIDRL per quarter, 1 Apr 2000 to 31 Mar 2005. Also marked are confirmed (in bold) or suspected epidemics of HEV in India listed on ProMED-mail* during the same period EIA = enzyme immunoassay. HEV = hepatitis E virus. VIDRL = Victorian Infectious Diseases Reference Laboratory. * Available at <http://www.promedmail.org>.

Benjamin C Cowie · Alan Breschkin · Heath Kelly

Peter C Arnold Former General Practitioner, PO Box 280, Edgecliff NSW 2027. peterATarnold.name To the Editor: Schofield and Beard,1 discussing demographic shifts among doctors, raise the spectre of “workforce shortages within the next 5 years”. For decades, Australian health authorities have used various proxy indicators, ranging from Medicare utilisation to World Health Organization and other comparative data, to deny the existence of shortages of doctors. Based on those faulty premises, government policies have aggravated these shortages. The Oxford English Dictionary defines a “shortage” as “a deficiency”. For many years, there have been deficiencies in services provided by Australia’s doctors, including, among others: General practitioners available for house calls and visits to nursing homes; working past 6:00 pm on weeknights or on Saturday mornings; available at nights and on weekends; offering prompt appointments; and being available in locum tenens. Specialist initial consultations within a week or two, especially dermatologists, oncologists, neurologists, and, more recently, neurosurgeons and obstetricians. And all this in our cities and large towns. The sho rtages of all medical personnel in rural and remote areas has long been obvious. Our current reliance on overseas-trained doctors is undeniable proof of the existence of those shortages. For more than three decades, the general practice “positions available” advertisements in the medical newspapers have far outnumbered advertisements from doctors seeking GP positions.2 None of the proxy indicators of workforce adequacy, so beloved of politicians and bureaucrats, can rival the plain truth that the supply of doctors, probably in every field of medicine and in every region of Australia, is plainly insufficient to meet reasonable demand, and has been so for at least 30 years.

Peter C Arnold

A program for routine health surveillance on international cruise ships visiting the Port of Sydney has been developed since 1998. Before introduction of this program, ships only reported quarantinable diseases and were not aware of the Australian requirement to report other infectious diseases. Voluntary routine reporting, developed in partnership with the cruise ship industry, provides timely information on all infectious diseases of public health interest during every cruise. During 1999–2003, the program resulted in detection of and response to 14 outbreaks of gastroenteritis or acute respiratory infection, affecting more than 1400 passengers and crew. The program has improved preventive action, and risk communication and management by cruise ship operators, and led to more timely investigation and support by public health authorities.

Mark J Ferson MD, FRACP, FAFPHM · Kelly-Anne Ressler BSc(Nutr), MPH

Clinical recordsIn 2003, five patients presented to the Oral and Maxillofacial Surgery Unit at Royal Adelaide Hospital, South Australia, with painful exposed bone in the maxilla, or both the maxilla and mandible (Box 1 and Box 2 ). All patients were receiving either pamidronate (Aredia [Novartis]) or alendronate (Fosamax [Merck Sharp & Dohme]). Pamidronate was being given intravenously monthly at a dose of 60mg (one patient) or 90 mg (three patients). The patient taking alendronate received a daily oral dose of 40mg. Duration of bisphosphonate therapy was 6 months to 6 years. Associated risk factors for the development of avascular necrosis included renal impairment in one patient and hypoproteinaemia in another. Initial management of these patients comprised surgical debridement of the exposed bone. Histopathological assessment of surgical specimens showed no histological evidence of myelomatous deposits or Paget's disease from the affected sites in the jaws in any of the patients. None had exposed bone elsewhere in the body. Here we present five cases of osteonecrosis of the jaw associated with bisphosphonate use. In North America, several preliminary reports have been published of unusual cases of avascular necrosis of the jaw in patients using second-and third-generation nitrogen-containing bisphosphonates.1-4 These included pamidronate, alendronate, risedronate and zoledronic acid.2,3 In Australia, bisphosphonates have been available for several years and are commonly prescribed for a range of conditions, including osteoporosis, Paget’s disease, multiple myeloma,5,6 hypercalcaemia of malignancy, and bone metastases of malignancies such as breast and prostate cancer. An estimated 200 000 patients in Australia receive these drugs. Commonly reported adverse reactions involve gastrointestinal symptoms. Bone-marrow depression and thrombocytopenia are also reported rarely. The second- and third-generation bisphosphonates are significantly more potent than their first-generation predecessors, (etidronate, clodronate and tiludronate). They inhibit bone resorption by osteoclastic inhibition, through selective concentration at the interface of the active osteoclast and the bone-resorption surface. The specific mechanism of this inhibition is unknown, but there is evidence for several actions, including inhibition of osteoclast development from precursor cells, increase in osteoclast apoptosis,7 stimulation of osteoclast inhibitory factor, reduction of osteoclast activity, and down-regulation of matrix metalloproteinases. The resulting reduction in osteoclastic activity reduces bone resorption, supporting the use of bisphosphonates for the above indications. However, osteoclastic function is part of the cycle of bone turnover; osteocytes have a life span of about 150 days, after which osteoclasts resorb the mineral matrix of bone and release bone morphogenetic protein and insulin-like growth factors, which in turn induce local stem cells to differentiate into osteoblasts and form new bone. This cycle is critical to maintaining bone stocks and bone viability. If osteoclastic function is too severely impaired, dead and dying osteocytes are not replaced, and the capillary network in the bone is not maintained, resulting in avascular bone necrosis. Dental disease and denture-wearing are ubiquitous. Studies involving larger patient numbers have shown that nearly 80% of cases were initiated by tooth removal.3 Patients who have been using potent bisphosphonates for more than 6 months appear to be at highest risk.2 Other apparent risk factors are residual multiple myeloma or other malignancy, hypoproteinaemia, renal impairment from disease or drugs, and chemotherapy. Although a definite cause-and-effect relationship is yet to be established, the association between bisphosphonate therapy and osteonecrosis of the jaw appears strong.2-4,8-10 The incidence of the potential complication appears low. In South Australia in 2003, about 14 000 patients received prescriptions for the potent second- and third-generation nitrogen-containing bisphosphonates, with about 10% having intravenous administration. Our five patients probably represented all cases of the complication, as our Department is the only oral and maxillofacial surgery service in SA and receives referrals from around the state.8,9 Checking with colleagues and related hospital services has not revealed further cases in SA, but we are aware of other cases in all states of Australia. Indeed, the Adverse Drug Reactions Advisory Committee recently reported another nine cases.10 At present, there is no effective treatment for the condition. Patients are usually referred to oral and maxillofacial surgeons, but surgical intervention is difficult as it often exposes further bone, and, as bisphosphonates affect the whole skeleton, locating viable bone margins may be impossible. Furthermore, removal of painful teeth, while initially alleviating pain, also further exposes bone, causing more pain. Covering exposed bone with tissue flaps has been found ineffective because of the development of fistulae around the flaps and possible complete dehiscence (Box 1). Compounding the problem, some patients must continue with bisphosphonate therapy and/or other chemotherapies to control hypercalcaemia. Hyperbaric oxygen therapy is not useful in bisphosphonate-induced necrosis, and antibiotics are indicated only to treat secondary infection. Because of the lack of effective treatment for the condition, second- and third-generation bisphosphonates should be used only when benefits clearly outweigh risks. When intravenous or high-dose oral bisphosphonates are considered appropriate, referral for full dental assessment and treatment before the start of therapy should be considered. Once bisphosphonate therapy has begun, there should be regular clinical monitoring of oral health. Avoiding tooth removal and dental implants, non-surgical control of periodontal disease, and use of soft liners on dentures also seem prudent. In addition, major debridement surgeries should be avoided if at all possible. In established cases, the primary goals are palliation and control of osteomyelitis. In most cases, progression has been controlled with long-term or intermittent courses of dicloxacillin or cephalexin (to treat any secondary infection), chlorhexidine mouthwash (Savacol), and periodic minor debridement of soft-textured sequestrating bone and wound irrigation. The rapid expansion of indications for bisphosphonates has resulted in their widespread use across many medical disciplines, including endocrinology, rheumatology, medical oncology, haematology and general practice. Most medical practitioners are unaware of this serious and potentially permanent complication. Before prescribing bisphosphonates, medical practitioners should analyse the risks versus benefits for the individual patient, consider alternative drugs, and obtain informed consent after discussing this potential adverse reaction. We also encourage vigilant surveillance of patients who are using a bisphosphonate. Summary Five patients presented to the Royal Adelaide Hospital, South Australia, in 2003 with painful exposed bone in the maxilla, or both the maxilla and mandible. All had been receiving potent second- or third-generation bisphosphonate therapy — monthly intravenous pamidronate in four cases and daily oral alendronate in the other. These cases are among the earliest reported occurrences of this condition in association with bisphosphonate therapy in Australia. The condition presented after tooth extraction in four cases and denture pressure in the other. Osteonecrosis continued for more than a year in three patients despite treatment. 1 Necrosis of the maxilla in a 57-year-old man receiving pamidronate for multiple myeloma The oral cavity showing exposed necrotic maxillary bone and a large oro-antral communication. Computed tomography showing significant bone destruction in the right maxilla (outlined). 2 Clinical details of five patients with avascular necrosis of the jaw in South Australia, 2003 Age, sex Presentation Precipitant Bisphosphonate [indication] Other medications Treatment Outcome 57, M Painful exposed bone in maxilla and mandible Tooth extraction Pamidronate (90 mg IV monthly for 6 years) [multiple myeloma] Dexamethasone, methotrexate, warfarin, folic acid, ranitidine, metformin, hydroxychloroquine, verapamil, sertraline, morphine Hyperbaric oxygen, Le Fort I level maxillectomy, bisphosphonate continued Persistent necrosis of midface and mandible 64, M Ulcer in right hard palate with bone sequestrum Tooth extraction Pamidronate (90 mg IV monthly for 2 years) [multiple myeloma] Prednisolone, cyclosporin, itraconazole, sulfamethoxazole–trimethoprim, ranitidine, penicillin Sequestrectomy, local debridement, bisphosphonate continued Resolution 73, M Pain, swelling of anterior maxillary alveolus Tooth extractions Alendronate (40 mg orally daily for 5 years) [Paget’s disease] Amlodipine, tramadol, perindopril Local debridement, sequestrectomies, primary flap closure, bisphosphonate ceased Resolution 78, F Painful exposed bone in maxilla Denture pressure Pamidronate (90 mg IV monthly for 18 months) [Paget’s disease] None Hyperbaric oxygen, local debridement, denture reline, bisphosphonate ceased Persistent areas of exposed bone 84, F Non-healing extraction site in left maxillary alveolus Tooth extraction Pamidronate (60 mg IV monthly for 6 months) [Paget’s disease] Diltiazem, simvastatin, ferrous sulfate, aspirin, bendrofluazide Wide intraoral resection with primary flap closure, bisphosphonate ceased Persistent fistula IV = intravenous.

Glen Carter BDS, MB BS, FRACDS(OMS) · Alastair N Goss DDSc, FRACDS(OMS) · Chris Doecke BPharm, PhD

Clinical records The Adverse Drug Reactions Advisory Committee (ADRAC) has recently received 13 reports of osteonecrosis of the jaw associated with bisphosphonate use — 12 after intravenous bisphosphonate use, and one after oral alendronate use (Box). Ten of the reports implicated zoledronic acid, one pamidronate, and the other implicated both drugs in circumstances where the patient had switched from pamidronate to zoledronic acid. In the nine cases with information on bisphosphonate dose, the monthly doses accorded with those recommended in the product information (90 mg of pamidronate, 4 mg of zoledronic acid). Time to onset varied from 1 month to more than 4 years, although most reports did not specify date of onset, possibly because onset was insidious. Presenting symptoms included localised pain, numbness and altered sensation, exposed bone in the oral cavity, soft tissue infection and, in one case, loosening of several teeth. One report described a dental abscess after radiotherapy. All the reports described the osteonecrosis as occurring in the jaw; four specified the mandible, and two the maxilla. With the exception of the report implicating oral alendronate for treatment of osteoporosis, the reports indicated that the bisphosphonate was being used in the context of malignancy. Four reports documented dental extraction during bisphosphonate therapy in the months before the onset. One patient had had several teeth extracted because they had become loose during bisphosphonate therapy. A further report stated that onset of osteonecrosis occurred before dental extraction. Many of the 13 reports were received soon after diagnosis, but, in at least four cases, the problem had persisted for 2 to 3 months after withdrawal of the bisphosphonate. None of the 13 patients had recovered at the time of reporting. Recently, the United States Food and Drug Administration drew attention to the problem of osteonecrosis (also described as avascular or aseptic necrosis) of the mandible and/or maxilla, occurring in association with intravenously administered bisphosphonates used to control hypercalcaemia in metastatic bone disease.1 In addition, two case series were published recently summarising 99 case reports of osteonecrosis of the jaw associated with bisphosphonates.2,3 Combined with smaller case series, they bring the total reported to 129 cases.4-8 Not all bisphosphonates have been implicated. Most commonly associated with the problem were zoledronic acid and pamidronate, possibly because these are the only intravenous bisphosphonates in widespread use, and because zoledronic acid has been approved for regular use in metastatic disease. However, seven reports implicated oral alendronate or risedronate used to treat osteoporosis.4,6 Osteonecrosis of the jaw closely resembles the occupational disorder “fossy jaw”, which occurred in workers in match factories using white phosphorus in manufacturing.9 The condition was distressingly painful, refractory to treatment and disfiguring to the extent that some sufferers committed suicide. Bisphosphonates are not metabolised and have a strong binding affinity with osteoclasts. They can persist in bone for months and sometimes years after the drug has been discontinued. Accordingly, withdrawal of bisphosphonate therapy does not appear to hasten recovery of the osteonecrosis. Other treatments, including mouth rinses, systemic antibiotics, hyperbaric oxygen and surgical debridement have been tried, but so far none has proven consistently effective. The mechanism underlying the reaction is unknown, but it has been postulated that bisphosphonates inhibit new vessel formation, thereby impairing healing. Although dental extractions and other oral surgery have been identified as precipitants in many cases, there is evidence suggesting that alveolar bone can be involved before, and independently of, such procedures. Indeed, the clinical presentation may closely simulate dental abscesses, “toothaches”, denture sore spots, and osteomyelitis. Documented risk factors include a diagnosis of cancer, concomitant therapies (eg, chemotherapy, radiotherapy and corticosteroids) and comorbid conditions (eg, anaemia, coagulopathies, infection, and pre-existing oral disease).10 Concomitant chemotherapy and corticosteroid treatment, in particular, may result in immunosuppression and thereby predispose to ongoing local sepsis after minor trauma. Because this condition and its complications result in significant chronic pain, dysfunction and disfigurement which are difficult to treat, the focus should be on prevention. It is important that all health professionals, especially dentists, oncologists and oral surgeons, be aware of the possibility that patients being considered for dental extractions or other oral surgery are undergoing intravenous bisphosphonate therapy. Also, it is important for patients to be informed of the risk of this complication of bisphosphonate therapy, so that they have the opportunity to assess the need for dental treatment before starting therapy.11 It is not known at this stage whether discontinuing bisphosphonates before major dental procedures can help prevent the problem, but, given the persistence of bisphosphonates in bone, it is unlikely. Prescribers should also be aware that osteonecrosis of the jaw can occur in association with oral bisphosphonate therapy for osteoporosis. Summary 13 cases of osteonecrosis of the jaw associated with bisphosphonate use have recently been reported to the Adverse Drug Reactions Advisory Committee. Most cases were associated with intravenous bisphosphonate therapy (11 cases with zoledronic acid and one with pamidronate), but one was associated with oral alendronate used to treat osteoporosis. The condition causes chronic pain, dysfunction and disfigurement; no treatment has proven consistently effective, and withdrawing the bisphosphonate does not seem to hasten recovery. The focus should be on prevention through attending to any necessary dental treatment before bisphosphonate therapy begins. Clinical characteristics of 13 patients reported to ADRAC with osteonecrosis associated with bisphosphonate use Age, sex Bisphosponate used, other therapy Indication for bisphosponate Time to onset Symptoms Outcome 42, F Zoledronic acid (4 mg IV every 3–4 weeks), capecitabine, celecoxib, ranitidine, radiotherapy Breast carcinoma 6 months Tooth abscess, osteoradionecrosis (site not specified) Unknown* 46, F Zoledronic acid (4 mg IV monthly), previously pamidronate (90 mg), dexamethasone Breast carcinoma 4–6 months Jaw necrosis (site not specified) Not recovered† 46, F Zoledronic acid (4 mg IV monthly) Breast carcinoma 5 months Maxillofacial pain, exposed bone in oral cavity, dental extractions, gingival swelling, impaired healing Unknown† 57, M Zoledronic acid (4 mg IV, frequency not stated), corticosteroids, chemotherapy Prostate carcinoma > 2 years Exposed, painful bone in mandible, numbness, soft tissue infection Not recovered‡ 67, F Alendronate (oral) prednisolone, leflunomide, celecoxib Osteoporosis ns Maxillary alveolar necrosis, spontaneous loss of teeth, osteomyelitis, oro-antral fistula, condition recurred after surgery Not recovered* 73, M Pamidronate (90 mg IV monthly), thalidomide, corticosteroids Multiple myeloma 1 year Mandibular pain, hypoaesthesia, loosening of teeth, dental extractions, impaired healing, exposed bone Slowly improving§ 75, M Zoledronic acid (4 mg IV, frequency not stated), corticosteroids, chemotherapy Prostate carcinoma > 2 years Exposed, painful bone in mandible, numbness, dysaesthesia Not recovered‡ 79, M Pamidronate (90 mg IV monthly), prednisolone, melphalan Multiple myeloma 1 month Mandibular pain, dysaesthesia, dental extraction, impaired healing, exposed bone, osteomyelitis, recurrent soft tissue infection Not recovered† 80, M Zoledronic acid (4 mg, reduced to 2 mg IV monthly) Prostate carcinoma 8 months Jaw necrosis (site not specified), recent dental surgery Not recovered† 83, M Zoledronic acid (4 mg IV monthly) Prostate carcinoma 4.5 years Jaw necrosis (site not specified) Unknown† ns, F Zoledronic acid (dosage ns) Breast carcinoma ns Jaw necrosis (site not specified) after two dental extractions Unknown* ns, F Zoledronic acid (dosage ns) Breast carcinoma ns Jaw necrosis (site not specified) Unknown* ns, M Zoledronic acid (dosage ns) Multiple myeloma ns Jaw necrosis (site not specified), exposed bone (spontaneous) Unknown* IV = intravenous. ns = not stated. * Not known whether patient continued bisphosphonate therapy after presentation. † Patient stopped bisphosphonate therapy after presentation. ‡Patient continued bisphosphonate therapy after presentation. §Pamidronate was replaced by zoledronic acid, which was ongoing.

Patrick M Purcell MB BS · Ian W Boyd PhD

Despite recent and largely undeserved adverse publicity, mefloquine remains a useful antimalarial Although malaria causes most suffering among children in the tropics, it should not be forgotten that it remains a major cause of military casualties. In September 2003, about 300 US Marines and support staff were deployed to Liberia, West Africa. Of those troops who spent at least one night ashore, 69 contracted falciparum malaria, an attack rate of 44%.1 Forty-four required evacuation for medical care to Europe or the United States. While none died, several developed cerebral malaria and required mechanical ventilation. Malaria was also common among Australian Defence Force (ADF) personnel deployed to East Timor between 1999 and 2000, with 385 cases reported, an attack rate of 5%.2 Eighty-four per cent of these cases were caused by Plasmodium vivax, which, while not life-threatening, causes significant morbidity. Relapse of P. vivax infection, caused by the re-emergence into the bloodstream of parasites lying dormant in the liver (so-called hypnozoites), was a major problem in this group, with 96 relapses reported despite 2 weeks of primaquine therapy.2 This pattern of infection is frequently observed in patients who contract malaria elsewhere in Asia and the Pacific, as reported by Charles and colleagues in this issue of the Journal.3 Nevertheless, effective chemoprophylaxis is readily available for Australian travellers. The challenge for medical practitioners is to select the most appropriate regimen and then to convince patients to use it. Malaria chemoprophylaxis for areas with chloroquine-resistant malaria* (including the Pacific Islands, South-East Asia, the Indian subcontinent, China, Africa and South America)4 Atovaquone + proguanil 250 mg + 100 mg (child > 40 kg and adult) 1 tablet orally, daily (starting 1 to 2 days before entering, and continuing until 7 days after leaving, malarious area) OR Doxycycline (child > 8 years: 2 mg/kg up to) 100 mg orally, daily (starting 2 days before entering, and continuing until 4 weeks after leaving, malarious area) OR Mefloquine (child 15 to 19 kg: tablet; 20 to 30 kg: tablet; 31 to 40 kg: tablet) 250 mg orally, weekly (starting 2 to 3 weeks before entering, and continuing until 4 weeks after leaving, malarious area). * Whatever chemoprophylaxis is prescribed, patients should be counselled that no prophylaxis is 100% effective, and the importance of mosquito avoidance should be emphasised. Mefloquine as chemoprophylaxisMuch has been written (and broadcast) about the neuropsychiatric side effects of mefloquine. While a number of class actions have been instituted, none has as yet reached resolution. Identifying malaria chemoprophylaxis with any confidence as the cause of major psychiatric illness or behavioural disturbance is problematic,5 even more so during or soon after exposure to an extremely stressful military environment. This issue is illustrated by allegations that mefloquine was responsible for fatal assaults committed by Canadian soldiers in Somalia and British soldiers in Sierra Leone, and that it contributed to the killings of spouses by US soldiers recently returned from Iraq. Similarly, it was alleged that psychiatric morbidity among ADF personnel who had been deployed to East Timor was attributable to mefloquine therapy. While it is reassuring that in this issue of the Journal, Kitchener and colleagues report no excess morbidity among ADF personnel taking mefloquine prophylaxis,6 the issue of tolerability of mefloquine is a real one. A double-blind, randomised controlled trial of malaria chemoprophylaxis comparing mefloquine and atovaquone–proguanil (Malarone [GlaxoSmithKline]) found that 139 of 483 (29%) participants taking mefloquine experienced an adverse neuro-psychiatric side effect, most commonly insomnia or strange or vivid dreams.7 Such side effects were reported in 69 of the 493 (14%) participants taking atovaquone–proguanil. The overall frequency of adverse events was similar in the two groups (71% and 67%, respectively), but the events were sufficiently severe to require discontinuation of the drug in 5% of those taking mefloquine versus 1.2% of those taking atovaquone–proguanil. Assessing tolerance to mefloquine before exposure (as undertaken by the ADF) might identify many of those intolerant of this drug, allowing an alternative agent to be selected. Alternative agents for chemoprophylaxisIn Australia, doxycycline is the most widely prescribed drug for malaria chemoprophylaxis. While its side effects are relatively benign (eg, thrush, photosensitivity and oesophagitis), the challenge is to ensure compliance. Numerous studies have demonstrated that adherence to a daily prophylactic regimen is unsatisfactory, especially among those requiring long-term protection.8 Atovaquone–proguanil is highly effective for chemoprophylaxis, but is costly and, like doxycycline, must be taken daily. There has been a resurgence of interest in primaquine as chemoprophylaxis, a drug generally used to prevent relapse of P. vivax. However, it too must be taken daily for prophylaxis and, like many other old “off-patent” orphan drugs, it is inordinately expensive. Tafenoquine, a much-anticipated drug related to primaquine, is now in phase III clinical trials. After three well-tolerated loading doses, a single monthly dose appears protective.9 However, like primaquine, it can cause severe haemolysis in patients with glucose-6-phosphate dehydrogenase deficiency. Thus, it is necessary to screen for this condition before beginning the drug. New agents for treating malariaAs Davis and colleagues discuss in this issue, artesunate is a highly effective and well tolerated antimalarial agent.10 It belongs to the artemesinin class of drugs derived from the Chinese wormwood plant qinghaosu, and is taken by many expatriates as “emergency standby treatment” at the first sign of fever (unpublished observation). While this practice is effective, particularly when combined with appropriate diagnostic tests, such as the rapid antigen test used in the case reported in this issue by Howden and colleagues,11 it is not without risk. The very short half-life of the active metabolite, dihydroartemesinin, means that any parasites remaining in the blood after a short course of therapy may not be cleared, leading to recurrent parasitaemia.10 Suitable drugs to combine with artesunate include mefloquine, doxycycline (if taken for one week), or, in the few regions where these drugs remain effective, combined pyrimethamine and sulfadoxine.10 Further risks of relying on emergency standby treatment alone include failing to recognise non-classical symptoms of malaria (such as diarrhoea), and exhausting drug supplies through premature self-medication for non-malarial illnesses. Of note, counterfeit artesunate is offered for sale in several Asian countries where pharmaceuticals are unregulated; the only artemisinin derivative available in Australia is artemether in combination with lumefantrine.10 A malaria vaccineAn effective malaria vaccine suitable for non-immune soldiers, travellers and the even larger population of residents of malaria-endemic countries remains a priority. The long-standing search for a vaccine has been invigorated by the creation of the Malaria Vaccine Initiative, a public–private partnership supported by the Bill and Melinda Gates Foundation. The recently published phase II malaria vaccine trial in Mozambique involving this initiative and GlaxoSmithKline Biologicals is an example of the productivity of this partnership.12 While the vaccine produced a statistically significant level of protection (29.9% to 57.7%), it is likely that, for now, doctors will continue to advise mosquito avoidance and to reach for the prescription pad rather than the vaccine refrigerator when preparing patients for trips to malarious areas.

James S McCarthy FRACP, MD

Snow-capped Mount Kilimanjaro, in Tanzania, stands 5895 m (19 335 ft) high and is the highest mountain in Africa. The hike up the mountain, although considered arduous, is attempted by dozens of people each day. About one in four actually succeed. A few years ago, we set out to climb it, planning to get to the summit and down again in six days. We had pre-arranged an experienced guide and, rather than carrying tents, chose to stay in huts provided on the mountain. We hired some down-filled clothing and sleeping bags with the help of our guide — but, when offered crampons and ice axes for hire, we both laughed at the idea. “This is just a walk”, we joked, “not a real climb”. View of Mount Kilimanjaro (5895 m, 19 335 ft), Tanzania, from the road leading to the park entrance. It is two vertical miles higher than Australia’s highest mountain, Mt Kosciuszko. For years no one believed the early reports that a mountain near the equator had snow on its summit. The first two days of climbing were moderately hard and it became progressively colder. At one point, our guide spent some time talking intently to a colleague who was on the way down. He then explained that a group of hikers, two days ahead of us, had been climbing through a thunderstorm when a young American woman was struck by a bolt of lightning and killed instantly. She had literally “blown up”, with lightning bolts arcing down her body and out through her torso and limbs to the ground, leaving huge flesh wounds. This macabre event caused us some anxiety. Our guide thought she had been struck because she was wearing a red parka, believing that red objects “attract” lightning. We pondered whether there was some scientific rationale for red gear being more likely than other colours to attract lightning. Trying to warm up in the sun outside one of the huts on our rest day. We eventually reached the first hut and stayed overnight. Next morning was initially cold but comfortable. But then we struck rain, a strong wind blew up, and the chill factor sent the thermometer plunging. It became so unbelievably cold that we had to put on every piece of cold weather gear we had. This was our first sense of just how cold it can be at high altitude. As we sat on a rock to rest, one of us noticed a scrappy piece of red plastic on a bush and began to deride those nuisance climbers who “show a complete lack of respect for the beautiful mountain surroundings by leaving behind plastic rubbish to contaminate the pristine environment”. We then saw another piece of red plastic, then another, and soon realised that there were dozens of such pieces in a circle of about 10 m diameter. We then noticed a carefully constructed mound of rocks adorned with fresh flowers. It suddenly dawned on us that this must have been the spot where the young American woman had been blown apart by lightning. The rough rock memorial must have been constructed by her fellow climbers. We were both awestruck by the frightening power of lightning. We continued climbing fairly easily, and had decided in advance to spend an extra day at Horombo hut (at about 4000 m) to help us acclimatise. It was hard to watch our fellow climbers leave without us — people we had met in the first few days and who would probably reach the summit before us. As events unfolded, our decision to spend that extra day at Horombo set us up for life-theatening situations near the summit. On our fourth day, we reached the highest hut, Kibo, at 4700 m. The views were quite beautiful, with a pink sunset on neighbouring Mount Mawenzi and absolutely pristine clear skies. We had a small meal — no one has much appetite at altitude — and turned in for a few hours’ sleep before the final hike to the summit, with the aim of being there at dawn. We set off for the summit at about 12.30 am. It was a moonless night, but at that altitude the sky was filled with millions of stars that appeared so close we felt we could pluck them from the sky. Amazingly, the starlight was sufficiently bright to illuminate Kilimanjaro and adjacent Mount Mawenzi. It was unforgettably spectacular. We were climbing with our guide and a trainee guide on his first ascent. We felt fairly confident that this last section of the climb would not defeat us. We had both tried to get fit enough by running up and down 50 flights of hospital stairs three times a week, and had taken precautions to avoid altitude sickness — climbing slowly, drinking plenty of water, taking prophylactic acetazolamide, and taking the extra day to acclimatise. As we began, I was surprised to find that I was extremely breathless despite walking slowly. The snow was hard and, as we had not brought headlamps, we stumbled in the frozen boot marks of previous climbers. Recovering from each stumble required much energy and produced marked breathlessness. We found the climb extremely arduous, and experienced effort-induced nausea plus the bitter, penetrating cold. I felt certain that I would not make the summit. In lucid moments I cursed my oxygen-dissociation curve for its failure to “shift to the right” and be more generous in donating oxygen. The physical and mental struggle to reach Hans Meyer cave, a third of the way up to the summit push, was monumental. I had seen published photos of Hans Meyer cave (named after the first man to climb Kilimanjaro) — which show it as virtually dry. But we found the cave totally ice encrusted, with large icicles hanging down from its roof. The temperature was −20°C to −30°C. We rested briefly at the cave, which allowed me to recover somewhat. As we pushed on laboriously, we noticed the bright stars disappear and within a few minutes we were enveloped by cloud, strong winds, and then driving, icy snow. The blizzard made climbing treacherous and reduced visibility to almost zero. To our surprise, and alarm, virtually all of the other climbing groups had turned back. The only person who didn’t was obviously an experienced mountaineer, who rapidly passed us wearing crampons and swinging his ice axe rhythmically to cut steps in the snow. To see the other groups stop and then turn back made us a little concerned that we were taking a considerable risk in pushing on. Nonetheless, we were both determined to continue up the mountain. At this point, Mark, a cardiothoracic surgeon whose hands generally prove fairly useful in his profession, hadn’t been able to move or feel his fingers for some time and was convinced he had significant frostbite. This did not change his determination to continue the climb. He thought that, as he already probably had some frostbite, going on to the summit was unlikely to make it worse. It is hard to describe how much emotional effort was required to keep climbing. Taking each step required every bit of mental endurance and concentration. It would not have been so bad if we had crampons, but we only had boots and so we slipped a lot. And every slip was exhausting. Everything in our lives — our families, our professions and all our previous life experiences — faded into a vague, dark background as our whole world was reduced to the small space between our ice-encrusted eyes and the snow slope in front of us. Dawn began to break and we were able to see a little more clearly in the faint light through the billowing ice and snow. It was around this time that we had two frightening experiences. First, I lost my footing and began to slip backwards down the mountain. It crossed my mind, with surprisingly lucid mathematical precision, that my slide down the mountain may increase in velocity and end by my crashing at near terminal velocity into Kibo hut 915 m (3000 ft) below. However, I managed to roll over and, aiming for a large rock, slid feet first into it. This life-threatening event produced marked and unrelenting breathlessness. I recovered slowly, and we continued to struggle on up the steep slope towards the summit, kicking our boots as deeply into the snow as best we could to gain precarious footholds. Then the second frightening event occurred. Mark slipped and began sliding down the mountain. He frantically grabbed at a rock protruding from the snow and this stopped his fall. He hugged the rock above his head with both hands, his body hanging down, and his feet flailing helplessly, unable to get any foothold. Every effort to kick a hole in the snow to try to gain a footing caused the snow to just fall away down the slope. I tried to help him, but couldn’t do much. The guide retreated down to our position, kicked a foot hole himself and then helped haul Mark above the rock. Mark lay prostrate in the snow, unable to catch his breath for 10 minutes or so. He later described this sensation as what it must feel like to die of respiratory failure! The guide encouraged us to keep going if we wished, although he later confessed that on a number of occasions he had decided that neither of us could possibly make it to the summit. Doggedly, we pushed on. We reached the top at about 8.00 am. It was an anticlimax — we were unable to see much. Although the blizzard had eased off slightly we were still besieged by falling snow and mist. The only reason we realised we were at the summit was that there was a small sign welcoming us to the top of the mountain. With blue fingers, I am attempting to video at – 30oC without gloves. The video camera, laboriously carried to the summit, only worked for a few seconds in the cold, but that visual record of our achievement is very precious to us. We shook hands and joked with our guide. However, he was more interested in leaving the summit as quickly as possible, warning us that “the weather is going to get bad”. Mark remembers thinking at the time that this was a somewhat superfluous statement. It didn’t seem conceivable that it could get any worse! We hiked, slid, crab walked, and glissaded down the steep slope through the whiteout. It didn’t look like the same route that we had come up on — it looked even steeper and we both felt that our guide was completely lost, and that at any moment we would glissade over the edge of one of the cliffs. We had read that 10 people die on Kilimanjaro each year, some by getting lost and falling over ice cliffs, and we thought that the same fate was destined to befall us. Eventually, we reached Hans Meyer cave and began to feel that we would safely descend the mountain. What should have been a physically demanding, but easily manageable, hike turned out to be an unexpectedly dangerous adventure for us both. The disappointment at not being able to see the famous dawn view from the Kilimanjaro summit was minor compared with the sheer adventure of the experience, the knowledge that very few hikers made it to the summit that day, and the experience of two close friends struggling together against exhaustion, cold, fear, danger and disappointment. We were inexperienced mountaineers. But we were both able to help each other when we each faced danger, and we felt a very strong bond with each other. We felt an incredible sense of achievement because we had overcome all of the difficulties. Snowbound descent — this spot was totally dry and barren on the ascent. And we learnt some lessons: Get very fit by walking and running up stairs (not just on the flat) before undertaking a climb up Mount Kilimanjaro. Get professional advice on cold weather gear, especially modern thermal underwear, wind-resistant but “breathable” jackets, and good-quality down-filled gear. It can make the difference between being miserable or comfortable. (Many times as we climbed I said to myself that I would pay $10 000 to anyone who could have given me any of that gear, right there and then.) Take anti-altitude sickness precautions. Hire a reputable, experienced guide — inferior guides may not be primarily interested in getting you to the top — the earlier you turn back, the less work and less risk it is for them. And we did meet someone who could have died for lack of a good guide. As we descended through the storm, we found her stumbling along, severely hypothermic, disoriented and unable to speak. Her guide had let her set off up the mountain without gloves and other warm gear, and had not followed her into the storm. Hire crampons and an ice axe. We scoffed when we were offered crampons, but if we were doing the climb again we would undoubtedly hire these climbing aids, even though it is rare for Kilimanjaro climbers to strike a blizzard. Take digital cameras, including a video camera, with you, even though they are heavy and inconvenient to lug at such an altitude, and the exhaustion produced by climbing reduces one’s motivation to take photos. The resulting pictures are irreplaceable and worth every effort. A useful website is www.climbingkilimanjaro.com But, in the end, the experiences and rewards we gained from our adventure were such that neither of us could possibly have anticipated how much it would enrich us as individuals and friends.

Bruce W S Robinson MD, FRACP, FRCP · Mark G Edwards MB BS, FRACS, FRCS

Although cutaneous leishmaniasis is occasionally seen in Australia in overseas travellers and migrants, visceral leishmaniasis has been reported rarely and only in people who were immunocompromised. We describe an 18-year-old immunocompetent man who presented with pancytopenia and a 2-week history of fever and lethargy a year after visiting the Greek Islands. Visceral leishmaniasis was diagnosed after a bone marrow biopsy showed protozoa, and the patient responded well to treatment with liposomal amphotericin. To our knowledge, this is the first case of visceral leishmaniasis in an immunocompetent patient in Australia. The leishmaniases are a group of infections caused by protozoa belonging to the genus Leishmania. We report an immunocompetent patient with visceral leishmaniasis, probably acquired in Greece. As far as we are aware, this is the first report of visceral leishmaniasis in an immunocompetent person in Australia. Clinical recordAn 18-year-old man of Greek parentage presented with a 2-week history of dry cough, diarrhoea, lethargy, anorexia and fever. He had a past history of cutaneous vasculitis of uncertain aetiology and acne vulgaris. He was not taking any regular medication. On examination, the patient’s temperature was 37.5°C, but no other abnormalities were evident. Investigations (Box 1) showed that he had pancytopenia, raised erythrocyte sedimentation rate and hypergammaglobulinaemia. The raised rheumatoid factor and anti-dsDNA levels were thought to be most likely related to inflammation. Treatment was begun with intravenous ceftazidime and gentamicin because of the febrile neutropenia. A bone marrow biopsy performed on Day 2 to investigate the cause of the pancytopenia showed cellular bone marrow with relative erythroid hyperplasia. Multiple blood cultures gave negative results. As the fever persisted, roxithromycin was added to the regimen on Day 4, and vancomycin on Day 8. Serological testing was negative for multiple infections, including HIV infection, but positive for parvovirus B19 IgM, although negative for IgG, on Days 1 and 9. The provisional diagnosis was parvovirus-related pancytopenia. The patient was discharged without antibiotic therapy 12 days after admission, as he felt well, although he still had a fever. A month after discharge, the pancytopenia persisted. Repeated parvovirus B19 serological testing was negative for both IgM and IgG. A second bone marrow biopsy at this time revealed occasional macrophages containing amastigotes (the resting intracellular stage of leishmaniae, formerly known as Leishman–Donovan bodies; Box 2). Review of the first bone marrow biopsy specimen failed to show any protozoa. Further questioning revealed that the patient had visited Greece for a 5-week holiday a year before presentation. A diagnosis was made of visceral leishmaniasis, probably acquired through sandfly bites. The patient was treated with liposomal amphotericin B, 250 mg daily for 4 consecutive days and then weekly for 2 weeks. The diagnosis was confirmed when promastigotes (the motile form of the organism) were successfully cultured. Leishmaniasis is not notifiable in Australia. The patient’s blood count returned to normal 2 months after starting treatment with amphotericin. He remained well 2 years after ceasing treatment. DiscussionThis case illustrates an unusual cause of pancytopenia in Australia. It is important to consider leishmaniasis as a differential diagnosis when the patient has a relevant travel history, as in this case. The diagnosis was not made on the first bone marrow biopsy, as smears from bone marrow usually contain few organisms, and have a sensitivity of 80%–85%.1 The major clinical syndromes caused by the genus Leishmania are cutaneous, mucosal and visceral leishmaniasis. Leishmaniasis is transmitted by Phlebotomus or Lutzomyia sandflies and infects dogs and foxes as well as humans. Numerous cases of cutaneous leishmaniasis have been reported in Australia,2,3 but to our knowledge only three cases of visceral leishmaniasis — one in a renal transplant patient4 and two in patients with HIV infection.5 Visceral leishmaniasis occurs in the Mediterranean region, northern Africa, the Middle East and central Asia, China and parts of South America.6 The differentiation of species causing leishmaniasis is complex and is performed only in reference laboratories. Visceral leishmaniasis is caused by Leishmania donovani, L. infantum or L. chagasi. L. infantum is the common species in the Mediterranean littoral and probably the cause of our patient’s infection. The incubation period of visceral leishmaniasis is usually 2–8 months. Many infections are subclinical, but the classic presentation is with fever, weight loss, hepatosplenomegaly, pancytopenia and hypergammaglobulinaemia. The definitive diagnosis depends on demonstrating either amastigotes in tissue or promastigotes in culture. Splenic puncture is the most sensitive means of obtaining a diagnosis, but biopsy of the bone marrow and liver is almost as good. In immunosuppressed individuals, promastigotes can sometimes be cultured from the buffy layer of centrifuged blood, and amastigotes can be seen in macrophages in biopsy specimens from various tissues. Testing for antileishmanial antibodies is not generally available and may be difficult to interpret. Pentavalent antimony compounds have been used to treat leishmaniasis for decades, but often have severe side effects, and resistance is developing.7 The aminoglycoside aminosidine (also known as paromomycin) is also effective when used either alone or in combination with an antimonial compound.7 Amphotericin can achieve 98% long-term cure in both antimonial-unresponsive and previously untreated patients.7 Lipid formulations of amphotericin are the most active antileishmanial agents.8 Although leishmaniasis is rare in Australia, it needs to be considered as a possible differential diagnosis of pancytopenia, remembering that the disease can present up to several years after return from an affected area. If untreated, visceral leishmaniasis is potentially fatal. 1 Investigations in a patient with visceral leishmaniasis Investigation Result Reference range Haemoglobin level (g/L) 82 135–175 Total white cell count (cells/L) 2.2 × 109 4–11 × 109 Neutrophil count (cells/L) 0.8 × 109 2.0–7.5 × 109 Platelet count (cells/L) 106 × 109 150–400 × 109 Erythrocyte sedimentation rate (mm/h) 120 0–15 Antinuclear antibody titre 1/160 < 1/160 Anti-dsDNA level (IU/mL) 10 < 8 Rheumatoid factor level (kIU/L) 240 < 20 IgG level (g/L) 19.1 6.5–16.0 IgA level (g/L) 4.3 0.6–4.0 2 Bone marrow biopsy in visceral leishmaniasis Light micrograph of bone marrow, showing macrophages containing amastigotes characteristic of Leishmania spp. Amastigotes are the non-flagellated intracellular stage of the protozoan, formerly known as Leishman–Donovan bodies. They appear as spherical or oval organisms 2–6 μm in length that contain two darker-staining organelles — a nucleus and a kinetoplast (arrow). The latter is a distinct region of the mitochondria containing mitochondrial DNA. (Giemsa stain; scale bar = 10 μm.) Transmission electron micrograph of bone marrow, showing an amastigote with a kinetoplast characteristic of Leishmania spp. (arrow). (Scale bar = 1 μm.)

Oui Ju MB BS · David I Grove MD, FRACP, FRCPA · Wilfrid J Jaksic FRACP · Geoffrey W Dart FRACP, FRCPA

Joshua P Hanson,* Carmel T Taylor,† Ann R Richards,‡ Ina L Smith,§ Craig S Boutlis¶ *Registrar, ¶ Physician, Cairns Base Hospital, PO Box 902, Cairns, QLD 4870; † Scientist, § Research and Development Coordinator, Public Health Virology, Queensland Health Scientific Services; ‡ Public Health Nurse, Tropical Public Health Unit, Cairns, QLD. joshua_hansonAThealth.qld.gov.au To the Editor: The Japanese encephalitis flavivirus is the most common cause of encephalitis in Asia. Death occurs in 25% of clinical cases, and permanent neurological deficits occur in up to 50% of survivors.1 Infection is transmitted from amplifying hosts (primarily waterbirds and pigs) by Culex mosquitoes. Although the virus has been isolated in the Western Province of Papua New Guinea,2 and clinical cases have been described in the Western Province and suspected in the Milne Bay region,3 to our knowledge cases have not been reported from around Port Moresby. In January 2004, a 66-year-old man of European background was evacuated to our hospital with a 7-day history of fever and confusion. On examination, he had generalised upper motor neurone signs and a Glasgow coma score fluctuating between 6 and 10. Computed tomography and magnetic resonance imaging showed multiple non-specific white-matter lesions bilaterally. An electroencephalogram (EEG) demonstrated diffuse slowing in the delta to theta range in both hemispheres, with preserved response to painful stimulation. Lumbar puncture showed clear cerebrospinal fluid (CSF), with a leukocyte count of 65 × 106 cells/L (81% mononuclear) (reference range [RR], < 5 × 106 cells/L), normal erythrocyte count, raised protein level of 0.79 g/L (RR, 150–500 mg/L); glucose level of 4.3 mmol/L (RR, 2.8–4.0 mmol/L) and negative bacterial and fungal cultures. The CSF was also negative for cryptococcal antigen and by polymerase chain reaction (PCR) testing for enterovirus and herpes simplex, Japanese encephalitis, Murray Valley encephalitis and Kunjin viruses. Serological tests were negative for syphilis and human immunodeficiency virus infection. Paired sera from Days 2 and 19 of admission were tested in parallel against a panel of flaviviruses using a haemagglutination inhibition assay.4 This showed fourfold rises in antibody titre against dengue virus serotypes 1, 3 and 4, and Japanese encephalitis, Murray Valley encephalitis, Kunjin, Alfuy and Kokobera viruses, and twofold rises in titre against dengue virus serotype 2 and Stratford virus. Overall, these results were diagnostic of recent flavivirus infection but were non-specific. IgM antibody responses to the same flaviviruses were measured in sera and CSF using an in-house enzyme-linked immunosorbent assay (ELISA), with strongest reactivity demonstrated to Japanese encephalitis virus (Box). The patient had lived in Papua New Guinea since 1970, predominantly on a church-run farm at Bootless Bay, about 20 km from Port Moresby. He had not travelled outside this region in the month before his illness, and had no history of Japanese encephalitis vaccination or of dengue fever. The farm was situated about 150 metres from a piggery. The patient had no direct contact with this piggery. His accommodation was poorly screened against mosquitoes. After 3 weeks of primarily supportive intensive care, the patient was discharged to a general ward. His neurological recovery was slow. After 5 months, he was able to walk with assistance and required a tracheostomy to protect his airway. He was judged likely to experience permanent neurological deficits. The clinical, epidemiological, radiological, EEG and serological features of this case strongly support a diagnosis of Japanese encephalitis. Japanese encephalitis virus is difficult to detect in CSF by isolation or PCR because of neutralising antibodies and the limited duration of viraemia, which may have accounted for the negative PCR result in this case, despite the use of a highly sensitive method.5 This case highlights the desirability of further defining the epidemiology of Japanese encephalitis in the Port Moresby region, as well as reconsidering the current recommendation to vaccinate Australians only if they intend travelling to the Western Province of Papua New Guinea.1 IgM antibody levels, measured against a panel of flaviviruses by enzyme-linked immunosorbent assay (ELISA) JE = Japanese encephalitis. MVE = Murray Valley encephalitis. * IgM levels were measured as the P/N (positive/negative) ratio (ratio of the absorbance of the test sample to the absorbance of a negative control sample tested against the same antigen).

Joshua P Hanson · Carmel T Taylor · Ann R Richards · Ina L Smith · Craig S Boutlis

To the Editor: The Australian Technical Advisory Group on Immunisation (ATAGI) is responsible for maintaining and updating the Australian immunisation handbook, on behalf of the National Health and Medical Research Council (NHMRC).1 At its 25th meeting, in April 2004, ATAGI discussed data (then unpublished) presented by Hanson and colleagues on evidence for the spread of Japanese encephalitis virus beyond the Western Province of Papua New Guinea to the Port Moresby region.2 ATAGI believes it is probable the virus has spread to other parts of Papua New Guinea. The current (8th) edition of The Australian immunisation handbook states on page 179: “Current understanding of the ecology of the JE [Japanese encephalitis] virus elsewhere in Papua New Guinea is fragmentary and unsubstantiated. Therefore no definitive recommendations about JE vaccination for travellers to other parts of Papua New Guinea can be made at the current time.” ATAGI agreed that the evidence provided by Hanson and colleagues was compelling, and sufficient to warrant expanding the current recommendation for Japanese encephalitis vaccination. ATAGI is proposing the recommendation be changed to include travellers staying more than one month in all parts of Papua New Guinea, not just those planning to stay in the Western Province. A public consultation process to change this recommendation is being conducted as part of the requirements of the NHMRC Act 1992. A public consultation paper is available from the Immunise Australia Program website (www.immunise.health.gov.au). Submissions close on 17 September and can be directed to Ms Letitia Toms, Assistant Director, Immunisation Section, Department of Health and Ageing, MDP 14, GPO Box 9848, Canberra, ACT 2601 (letitia.tomsAThealth.gov.au).

on behalf of the Australian Technical Advisory Group on Immunisation (ATAGI)

Clinical record A 32-year-old woman presented to the Royal Brisbane Hospital immediately on disembarking from a flight from Bangkok. She had a 5-day history of gastrointestinal symptoms, fever and altered mental state. She was a university graduate and had travelled for 2 months across south-east Asia before becoming unwell in Phnom Penh, Cambodia. Her illness began with mood elevation, hallucinations, muscle spasms and paraesthesiae, shortly after ingestion of a “herbal pizza”. Within 24 hours, nausea, vomiting and profuse watery diarrhoea ensued. Despite empirical treatment for bacterial gastroenteritis, symptoms progressed to lethargy with altered mental state. The patient had been taking doxycycline for malaria prophylaxis, and had been vaccinated against viral hepatitis, tetanus, poliomyelitis and typhoid. She was aware of the availability of a Japanese encephalitis vaccine, but had been advised that it was not essential. On presentation, the patient was drowsy and dehydrated, with a temperature of 38°C and tachycardia. There was peripheral leukocytosis (white cell count, 17.9 x 109 cells/L; reference range [RR], 4.0–11.0 x 109 cells/L) with dominant neutrophilia, as well as hyponatraemia, but renal function was preserved. Fever and lethargy persisted over 48 hours despite rehydration and regular paracetamol. Increasing obtundation and a fine tremor were observed. The patient complained of persistent headache, mild photophobia and neck discomfort. Her partner commented on her slow mentation, reduced concentration and personality change. Investigations for malaria, typhoid, rickettsial disease and infectious diarrhoea were all negative. Magnetic resonance imaging of the brain detected no abnormalities. Cerebrospinal fluid (CSF) showed mononuclear pleocytosis (white cell count, 12 x 106 cells/L; 92% mononuclear cells [RR, < 5 x 106 mononuclears/L]), with mild elevation of protein level (0.62 g/L [RR, <0.45 g/L]), but was negative for herpes simplex virus by polymerase chain reaction. Flavivirus-specific IgM was detected in CSF and subsequently blood. The diagnosis of Japanese encephalitis was confirmed by a rise in titre of specific IgG in blood, from 80 (8 days after onset of illness) to 1280 (4 weeks after onset). The fever resolved spontaneously by Day 4 after presentation, and the patient was discharged after 10 days. At the time of discharge, her level of alertness had improved, but global impairment of higher cognitive functioning and tremor persisted. After a period of convalescence of approximately 5 months, during which she was cared for by her partner, the patient was able to return to work. Japanese encephalitis is the leading cause of viral encephalitis in Asia, with recent epidemics in India, Malaysia and Nepal.1 An outbreak of Japanese encephalitis in the Torres Strait Islands and the northern extremity of Cape York in March 19952 raised concern that this arbovirus may become established in feral pigs in northern Australia. Although the overwhelming majority of infections are asymptomatic, the case-fatality rate of symptomatic infection is 25%–30%, with neuropsychiatric sequelae seen in 30%–50% of survivors.3 The incubation period ranges from 4 to 21 days. The earliest symptoms are lethargy, high fever, headache and gastrointestinal symptoms.4 Japanese encephalitis should therefore be considered among unwell travellers returning from endemic areas, including those with undifferentiated fever.4 Blood and CSF are positive for flavivirus antibodies by 10 days after symptom onset. Specific IgM antibody may appear earlier in the CSF. Treatment is symptomatic. A vaccine is available for Japanese encephalitis and is administered as three doses over 30 days, at a material cost of over $300. Vaccination is recommended for: Travellers spending at least one month in rural areas of Asia or the Western Province of Papua New Guinea, particularly during the wet season, or if there is considerable outdoor activity, or suboptimal accommodation. It is possible that this recommendation will be expanded to include all areas of Papua New Guinea.5,6 Travellers spending a year or longer in Asia (except Singapore), even if lifestyle is predominantly urban.7 All permanent residents of the outer Torres Strait Islands over the age of 1 year and all non-residents who will be living in the region for 30 or more days during the wet season (December–May). Vaccine uptake among travellers in whom it should be considered has been hindered by the cost of the vaccine, and by occasional reports of delayed and (rarely) life-threatening adverse reactions.8 Overall, local injection-site reactions occur in about 20% of recipients. Systemic reactions, such as fever, rash, myalgia and gastrointestinal symptoms, are seen in about half that number.9 A new live, attenuated vaccine that allows a simpler administration regimen and is likely to produce fewer of these adverse reactions than the current vaccine is undergoing Phase II testing.10 Statistics on vaccine use include military personnel and residents of northern Cape York and the Torres Strait Islands, who receive free vaccinations under the Queensland Government Vaccination Programme. Separate statistics on vaccine use by travellers are unavailable. Adventure travel is popular among Australians. Uncertainty about disease risks and the financial burden of vaccination and antimalarial prophylaxis combine to make pre-travel counselling a challenge. This case of a rare vaccine-preventable infection with a potentially devastating outcome exemplifies these issues. As an efficacious vaccine for Japanese encephalitis is available, it should be considered for all at-risk travellers. This case also highlights the need to emphasise mosquito avoidance in pre-travel counselling, and to consider a broad differential diagnosis in unwell returning travellers. Lessons from practice Japanese encephalitis is a potentially devastating illness; it can be fatal and can have permanent neurological effects in survivors. Vaccination is indicated for many Australians who seek pre-travel counselling; they should be counselled about their risk of contracting Japanese encephalitis and the benefits of the vaccine. Mosquito avoidance is a key message in pre-travel counselling. Japanese encephalitis may present as an undifferentiated fever; gastrointestinal symptoms may be prominent.

Catherine M Geraghty MB BS · James S McCarthy FRACP, MD

Peter A Leggat,* Robin Griffiths† * Associate Professor, School of Public Health and Tropical Medicine, James Cook University, Townsville, QLD 4811; † Senior Lecturer in Occupational and Aviation Medicine, Wellington School of Medicine, University of Otago, Wellington, New Zealand. Peter. LeggatATjcu.edu.au To the Editor: Grace and Penny present some fascinating “travellers tales” concerning travel insurance and medical evacuation.1 Although I recognise that there may have been difficulties with individual cases, the article probably paints an unnecessarily bleak picture of travel insurance and medical assistance companies. About a fifth of travel insurance claims involve the successful use of the emergency assistance service, which mostly does not involve aeromedical evacuation.2 Evacuation by a dedicated air ambulance is uncommon among travellers.2 Almost all travellers in need of medical and dental treatment source treatment locally, for which they are generally reimbursed. Aeromedical evacuation, where needed, is more likely by scheduled airlines with or without an escort. The article may raise unrealistic expectations among travellers for aeromedical evacuation. Air ambulances do not operate and respond in the same way as ground ambulances. Time is required to assess and prioritise cases, select suitable aircraft, obtain flight plan clearance, check and equip aircraft, brief retrieval and receiving hospital personnel, and develop contingency plans. Aircraft may be required to refuel en route, as air ambulances tend to be based where they can be maintained and staffed adequately and safely — this may be far from the retrieval site. It is useful to raise travellers’ awareness of the possible difficulties in accessing adequate medical facilities in many developing countries, especially where tourism is promoted, and create a sense of travellers’ responsibility for their own health, safety and welfare. The International Society of Travel Medicine has articulated this in a recently released policy statement.3 Readers should be wary of generalising from a small number of case studies from a “popular tropical island holiday destination”.1 It would be useful to collect data on medical retrievals and emergency assistance provided from various sources and consult all interested parties before attempting to establish guidelines for medical evacuation. Grace and Penny do raise the important issue of the need for appropriate travel insurance for all travellers. This message needs to be conveyed by the travel industry and by travel health advisers. The article referred to a study of the travel health advice provided by general practitioners in New Zealand, but did not mention that only about half the GPs in that study routinely discussed travel insurance.4 A similar study in Australia indicated that less than 40% of GPs routinely give advice on travel insurance.5

Peter A Leggat · Robin Griffiths

Fred Gilligan,* Peter Sharley,† Andrew Berry‡ * Emeritus Director of Retrieval and Resuscitation, † Director, Retrieval Services, RAH Mediflight, Royal Adelaide Hospital, North Terrace, Adelaide SA 5000; ‡ Director, NSW Newborn & Paediatric Emergency Transport Services, Sydney NSW. To the Editor: As consultants in intensive care, experienced in transporting critically ill patients within Australia and internationally, we have also received complaints from clients about some travel insurance organisations.1 Poor service appears due partly to economic restrictions and partly to the paucity of experienced staff and specialised aircraft available. Assistance companies implement travel insurance policies for underwriters, quoting 24-hour emergency call centres. Some companies economise by subcontracting (eg, episodic diversion of calls to another organisation). This can result in coordinators lacking an understanding of regional geography, population and medical services and omission of the early, vital input of senior medical advisers. Information relayed between several people can be lost or distorted. Failure to ask key questions can result in inappropriate clinical planning. Furthermore, time zone differences can result in calls being received late at night, further reducing availability of immediate expert opinion. Only a well-organised (and thus expensive) control centre with a critical care focus can manage all these variables. Furthermore, it is difficult for a company to permanently employ current, high-grade healthcare staff in adequate numbers. Current critical care retrieval staff in Australia are confined to a few stand-alone aeromedical organisations or public hospitals which run aeromedical services for state governments and other organisations, using their regular anaesthesia, intensive care or emergency medicine staff. Reliable assistance companies tend to contract with these retrieval organisations or their off-duty staff. In Australia, ambulance aircraft able to travel offshore, with adequate oxygen systems, stretcher attachments, electrical power, and so on, are uncommon and expensive to equip. Portable equipment to care for a critically ill patient represents a capital investment of over $100 000, and some services try to achieve results with inadequate tools or by borrowing. ISAS (the International Society of Aeromedical Services, Australasian Chapter) promotes standards on staffing and equipment,2 including the Australian and New Zealand College of Anaesthetists/Australian College for Emergency Medicine standard for transporting the critically ill.3 Based on critical care practice, the standards are not legally binding, but one suspects they would be quoted in any litigation. It behoves all travellers to scrutinise their travel insurance policies closely — many think of them only in terms of lost or stolen baggage. Following serious injury or illness, the policy may dictate what kind of care is offered.

Fred Gilligan · Peter Sharley · Andrew Berry