Letters

To the Editor: Buruli ulcer, caused by the bacterium Mycobacterium ulcerans, leads to the destruction of skin and sometimes bone. It has been reported in many tropical countries in Africa and in some temperate regions of Australia, Japan and China.1 In 2004, the World Health Organization recommended treatment with the combination of oral rifampicin and intramuscular streptomycin (or amikacin) for 8 weeks.2,3 In-vitro studies and new data from mouse models suggest that combinations of rifampicin with clarithromycin, rifampicin with moxifloxacin, or clarithromycin with moxifloxacin may be as effective as rifampicin and streptomycin.4,5 In June 2007, a woman who was 6-months pregnant with her first child and had a 7-month history of Buruli ulcer on her right upper limb (Box 1, A) was admitted to the Buruli ulcer treatment centre in Allada, Benin. She was otherwise in good health, and the fetal heart beat was normal. Routine laboratory examinations, including HIV serology tests, found no abnormalities. Swabs from the ulcer were positive for acid-fast bacilli by Ziehl–Neelsen stain, and for IS 2404 (DNA sequence specific for Mycobacterium ulcerans) by polymerase chain reaction testing, but no growth of M. ulcerans was obtained on culture. Histopathological analysis of punch biopsy specimens showed typical features of Buruli ulcer. As streptomycin is contraindicated in pregnancy, we treated the patient with a combination of oral rifampicin (600 mg daily) and oral clarithromycin (500 mg twice daily) for 56 days, beginning 2 weeks after presentation. The treatment was well tolerated. We monitored the clinical response through serial photographs (Box 1) and measurements of the circumference of the affected and unaffected limbs at defined points (Box 2). The patient gave birth to a healthy boy weighing 2.25 kg in September 2007, 2 weeks after completing antibiotic treatment. She underwent skin grafting a month later. The lesion healed without functional limitation (Box 1, D), and the patient was discharged in December 2007. At that time, the surface area affected by the lesion was reduced by 55%. To our knowledge, this is the first report of successful treatment of Buruli ulcer using fully oral treament with rifampicin and clarithromycin alone. We hope our experience will contribute to future discussion and studies to find an oral treatment for this devastating disease. 1 Serial views of Buruli ulcer in a woman treated with rifampicin and clarithromycin A: At presentation. B: After 4 weeks' antibiotic treatment. C: On completion of antibiotic treatment (8 weeks). D: At hospital discharge after skin grafting, showing full movement of the elbow joint (23 weeks). 2 Clinical response to treatment Week after treatment start 0 4 8 23 Limb circumference (cm) At wrist Affected limb 21 17.5 16.5 15 Unaffected limb 14 14 14 14 % difference 50% 25% 18% 7% At mid-arm Affected limb 36 33 30 25 Unaffected limb 22 22 22 22 % difference 64% 50% 36% 14% At elbow Affected limb 34 21 21 21 Unaffected limb 23 23 23 23 % difference 48% − 9% − 9% − 9% Lesion dimensions Diameter (cm)* 30.3 23.8 22.5 20.3 Area Estimate (cm2) 722 446 397 325 % reduction — 38% 45% 55% * Median diameter.

Ange D Dossou · Ghislain E Sopoh · Christian R Johnson · Yves T Barogui · Dissou Affolabi · Sévérin Y Anagonou · Théophile Zohoun · Françoise Portaels · Kingsley Asiedu

To the Editor: Kaposi’s varicelliform eruption (KVE) is a disseminated cutaneous infection caused by herpes simplex virus (HSV) in patients with predisposing factors such as atopic dermatitis, widespread skin injury and sun exposure.1-5 I report a patient with KVE but no apparent predisposing factors. A 54-year-old man presented with a 3-day history of a rapidly progressing vesiculopustular rash on his trunk, legs, arms and hands (Box). He reported a burning skin sensation and had a temperature of 38.2°C. He had no labial or oral erosions, and no history of skin disease, HSV infection or any systemic disease. He was not taking any medication and reported no excessive sun exposure before symptom onset. Haematological, biochemical and immunological parameters, including levels of C-reactive protein, immunoglobulins, complement components, lymphocyte blastogenesis and natural killer cell cytolytic activity were normal. An HIV test was negative. Skin swabs from the lesion were positive for HSV-1 by polymerase chain reaction (PCR) testing; HSV-1 was also isolated on culture. Cultures were negative for bacterial, fungal and mycobacterial pathogens. A diagnosis of KVE was thus established. Based on past experience treating KVE with a combination of oral valaciclovir and vidarabine ointment, which accelerated resolution of symptoms,6 I treated the patient with oral valaciclovir (1 g three times per day) and vidarabine ointment (three times per day). The lesions were completely healed after 7 days of treatment. HSV-1 antibody titres on Days 1 and 7, respectively, were: IgM, 3.1 and 5.2 (reference range, < 0.8); and IgG, < 2.0 and 4.7 (reference range, < 2.0). HSV-2 IgM and IgG antibody titres on Days 1 and 7 were within reference ranges (< 0.8 and < 2.0, respectively). This case is unusual as it occurred in an otherwise healthy patient. KVE is usually associated with healing second-degree burns, peribuccal dermabrasion and laser skin resurfacing,2-4 and sun exposure in patients with recurrent HSV infection.5 The origin of the patient’s HSV-1 infection was not identified: there was no outbreak of HSV infection in his city of residence; his wife and two children were healthy and had no systemic or skin diseases; PCR testing of their saliva for HSV-1 and HSV-2 DNA 3 days after the patient’s presentation gave negative results; and the patient had no apparent contact with HSV-infected patients before onset of symptoms. KVE has been successfully treated with intravenous aciclovir (three times per day) or oral aciclovir (five times per day).2,5 However, intravenous aciclovir requires hospital admission, and compliance with the dosage regimen of oral aciclovir is troublesome. In contrast, oral valaciclovir (three times per day) and vidarabine ointment do not require hospital admission and are easier for patients.1,3,6 Oral valaciclovir is also very effective for preventing herpes infection.7 This case highlights that KVE should be considered in otherwise healthy patients with a sudden, rapidly progressing vesiculopustular rash. Vesiculopustular lesions in a patient with Kaposi’s varicelliform eruption

Hajime Kimata

To the Editor: Serotonin toxicity is an under-recognised, potentially fatal syndrome that is becoming more common as the use of serotonergic drugs increases.1 We report a case of serotonin toxicity following the concomitant use of the antidepressant citalopram and methylene blue. A 44-year-old woman underwent elective partial parathyroidectomy for primary hyperparathyroidism. Three hours after surgery, the patient became agitated and restless while staring vaguely into space, making incomprehensible sounds (Glasgow Coma Scale: 11/15; motor response, 5; verbal response, 2; eye opening, 4). Her blood pressure (120/66 mmHg), pulse (100 beats/minute [sinus rhythm]), oxygen saturation (92% while breathing room air), and temperature (37.5°C) were not clinically significant. Neurological examination revealed bilateral pupillary dilatation with sluggish response to light, myoclonic movements of the lower limbs, brisk reflexes throughout and downgoing plantar responses. Clonus was absent and there was no focal neurological deficit. Blood tests showed a mild inflammatory response (white cell count, 12.7 × 109/L [reference range (RR), 4.0–11.0 × 109/L]; C-reactive protein, 23 mg/L [RR, < 10 mg/L]), normal serum levels of calcium (2.50 mmol/L [RR, 2.12–2.65 mmol/L]), and mildly elevated phosphate (1.5 mmol/L [RR, 0.8–1.4 mmol/L]). A computed tomography scan of the head showed no abnormalities. The patient’s medical history included ischaemic heart disease, hypertension, obesity and depression. Regular long-term medications included aspirin (75 mg daily), simvastatin (40 mg each night), atenolol (50 mg daily), isosorbide mononitrate (20 mg daily), bendroflumethiazide (a thiazide diuretic not available in Australia; 2.5 mg daily), felodipine (5 mg daily) and citalopram (20 mg daily). On the day of the operation, she received propofol, remifentanil, rocuronium, dexamethasone, morphine analgesia and a preoperative methylene blue infusion (560 mg in 500 mL of saline over 2 hours; used to stain the parathyroid glands). She had previously undergone general anaesthesia without complication. Serotonin toxicity was diagnosed, precipitated by the combination of methylene blue and citalopram. She was transferred to the intensive care unit, where she was sedated for 12 hours with propofol and alfentanil. Citalopram was withheld, and she received supportive treatment only. She was discharged to the ward 24 hours later and then home (3 days after discharge from the intensive care unit), with no long-term adverse effects. Three months after discharge, she continued to take citalopram, and serum calcium levels were in the normal range. Serotonin toxicity can be caused by a single drug or a combination of drugs with serotonergic activity. Methylene blue attenuates the metabolism of serotonin through inhibition of monoamine oxidase A.2 When used in combination with a selective serotonin reuptake inhibitor, such as citalopram, toxic accumulation of serotonin may result.3 Features include mental state changes, autonomic hyperactivity, and neuromuscular abnormalities. In mild cases, treatment is supportive, with withdrawal of serotonergic drugs and control of agitation. Moderate to severe cases require control of hyperthermia and autonomic instability, and administration of 5-HT2A (5-hydroxytryptamine2A) antagonists.1

Ali Khavandi · John Whitaker · Hanney Gonna

To the Editor: The 21 July 2008 “general practice” issue of the Journal raises a number of important issues about the future of generalist medical care, including the role of the general practitioner in the care of cancer patients. The editorial by Weller and Harris acknowledges the importance of multidisciplinary teams, including the full gamut of primary care practitioners, in meeting the diverse needs of people with cancer, from diagnosis to long-term “survivorship”.1 Jiwa et al propose a new model of an “integrated primary care hub” — with a “cancer care coordinator” — as a possible solution to the challenges of providing good team-based care.2 However, creating an entirely new disease-centred role would seem to ignore much of the debate in the rest of the general practice issue. Multiple morbidity is an emerging reality in Australia, and it is a fact that many survivors of cancer will die from other chronic conditions. Disease-specific care coordinators are currently being promoted as the new model for delivering chronic disease management to the community, but how many of these care coordinators will be needed for patients such as those described by Britt et al?3 And who will coordinate the coordinators? Gunn et al make a strong case for the generalist primary care medical practitioner as the overarching coordinator of care.4 We must stop seeing our patients through the eyes of our disease-centred hospital colleagues. Instead, we must create new mechanisms that will allow the experts in generalism — GPs — to move away from predominantly “reactive, consultation-based medicine”4 to high-quality integrated care planning in coordination with other members of the primary care team.

Jon D Emery

To the Editor: Venous thromboembolism (VTE) is frequently described among air travellers but data on VTE related to train travel are limited.1-3 We report a case of VTE in a patient after a prolonged train journey. A 35-year-old man presented with sudden onset of breathlessness, perspiration and syncope after a 14-hour train journey, during which he had limited mobility. He had no history of similar episodes, no significant comorbidities or previous periods of prolonged immobility and no family history of thromboembolic disorders, and he was vegetarian. Physical examination revealed tachycardia, tachypnoea, blood pressure of 90/60 mmHg, raised jugular venous pressure and a right ventricular third heart sound. Blood-gas analysis showed hypoxaemia with respiratory alkalosis: Pao2, 49 mmHg (reference range [RR], 95 ± 5 mmHg), pH 7.49 (RR, 7.40 ± 0.02), Paco2, 22 mmHg (RR, 40 ± 2 mmHg). A plasma D-dimer test result was positive. Electrocardiography revealed right axis deviation with an S1Q3T3 pattern. Echocardiography revealed right ventricular dilatation, a thrombus in the main pulmonary artery, and pulmonary arterial hypertension (pulmonary artery systolic pressure, 65 mmHg) (Box, A). Computed tomographic angiography of the pulmonary artery confirmed the presence of a large saddle embolus at the bifurcation of the main pulmonary artery (Box, B) and a wedge-shaped infarct in the middle lobe of the right lung. Venous Doppler imaging showed a thrombus in the left popliteal vein. The patient had fasting hyperhomocysteinaemia (plasma homocysteine level, 36.6 μmol/L; RR, 4.4–10.8 μmol/L] secondary to nutritional vitamin B12 deficiency (serum vitamin B12 level, 42 pmol/L; RR, 206–735 pmol/L]. Tests for antithrombin III, protein C, protein S, factor V Leiden mutation and antiphospholipid antibodies returned normal results. The patient was successfully treated with intravenous streptokinase followed by standard anticoagulation therapy and vitamin B12 supplementation. He was well on follow-up. The association between thrombosis and prolonged travel was first described in 1954.1 Symptoms usually develop within 1–8 weeks of travel. Any journey of more than 4 hours poses a risk of VTE. Factors involved are low humidity, hypoxia, immobilisation and cramped conditions.2,3 Individuals with underlying hypercoagulation states such as factor V Leiden mutation, prothrombin gene G20210A mutation, and protein C and protein S deficiency have increased risk of VTE.4 Recently, hyperhomocysteinaemia has also been identified as an important risk factor for VTE.5 Acquired risk factors include obesity, oral contraceptive use, pregnancy, recent trauma or surgery, malignancy and history of VTE. This case highlights the association between train travel and VTE, and the importance of considering all types of prolonged travel as potential risk factors for VTE. Echocardiogram and angiogram of a patient with venous thromboembolism after prolonged train travel A: Echocardiogram (parasternal long axis view) showing dilatation of the right ventricle (arrow) as a result of acute pulmonary arterial hypertension. B: Computed tomographic angiogram of pulmonary artery showing a saddle embolus (arrows) at the bifurcation of the main pulmonary artery (MPA).

Jeet Ram Kashyap · Sanjay D’Cruz · Sandeep Chauhan · Suman Kochhar

To the Editor: We report the case of a 41-year-old woman who sought medical opinion about an unpleasant body odour, first noticed when she was 7 years old. After experiencing ridicule, distress, shame, anxiety and low self-esteem during her school years, she first consulted a doctor about the problem at the age of 17 years, then again 2 years later, followed by a further four doctors over the next 20 years. All dismissed her concerns, and she was repeatedly told that she had a hygiene neurosis. Investigations and treatments during this time included being “sniffed”, vaginal swabs and vaginal cauterisation. Finally, a general practitioner referred her to a dermatologist, who consulted a microbiologist, and the diagnosis of trimethylaminuria (TMAU), or fish malodour syndrome, was confirmed by urinalysis. Now having a name for her condition, she found an Internet-based support foundation and referred herself for genetic counselling. TMAU is caused by an enzyme deficiency due to mutations in the flavin-containing mono-oxygenase 3 (FMO3) gene,1 resulting in excess excretion of trimethylamine in urine, sweat and breath. It is diagnosed by clinical symptoms and urine analysis.2 The characteristic body odour resembling rotting fish can be intermittent, variable and influenced by diet, hormones and medications. Restriction of choline- and carnitine-rich dietary precursors (eg, fish, eggs, soybeans, peas) is difficult to maintain and effective in only 25% of patients.2 Acid soaps and body lotions can often reduce the odour.3 The metabolic and clinical manifestations of TMAU are generally regarded as benign, as there is no associated organ dysfunction. This designation, and the fact that the condition is often unrecognised by doctors, can have important ramifications including missed or delayed diagnosis.4 Affected individuals experience shame and embarrassment, fail to maintain relationships, avoid contact with people who comment on their condition, and are obsessive about masking the odour with hygiene products and even smoking. The malodorous aspect can have serious and destructive effects on schooling, personal life, career and relationships, resulting in social isolation, low self-esteem, depression, paranoid behaviour, and suicide.4, Psychosocial problems resulting from delayed diagnosis, body odour and the lack of cure are considerable, making this a far from “benign” disorder. Recognition of TMAU as a significant clinical entity and increased understanding of the issues patients face are needed. Awareness of the typical patient history would facilitate prompt metabolic diagnosis and pre-empt some of the associated psychosocial sequelae. Referral of patients for genetic counselling enables short-term psychosocial support and family cascade genetic testing. Consultation with a metabolic clinic for dietary management may also be beneficial.

Helen Mountain · Joanna M Brisbane · Amanda J Hooper · John R Burnett · Jack Goldblatt

To the Editor: In their recent case series, Lintzeris and colleagues state that the symptoms leading to hospital presentation were “associated” with naltrexone implants.1 In half of the 12 cases, the symptoms were related to the induction of withdrawal rather than the presence of naltrexone — an important distinction that may not be apparent to all, but of which the authors would be aware. Three of the remaining cases reflect the complexities of pain management in patients being treated with naltrexone, which are not restricted to those with implants. This dilemma is also encountered in patients taking buprenorphine. Patient 8 had an anxiety disorder, and his symptoms probably related to an absence of opiate; and Patient 9 had symptoms that were probably due to cocaine use. Abstinence is a patient’s choice, and naltrexone can be effective in minimising the risks associated with the consequent lowered tolerance to opioids.2 I am concerned that undue emphasis appears to have been placed on the association of adverse outcomes with implants, with such statements as: “This case series identifies severe adverse events associated with the use of naltrexone implants”. In fact, the causal condition is usually the induction of opiate withdrawal rather than the presence of a naltrexone implant.3 The statement that “Most of these cases (8/12) can be attributed to the naltrexone implant or implantation procedure” is true, but it would be more appropriate to acknowledge that the procedure appeared to be the cause in most cases and that only in one case (Patient 7) could the implant be conclusively implicated. It is not appropriate to refer to difficulties in pain management as “severe adverse events”, as the blockade of the μ opioid receptor is the reason naltrexone is used. In addition, it is important to note that a trial of injectable naltrexone has shown promising results.4 While these facts are acknowledged by the authors, their emphasis on the association of adverse events with the presence of a naltrexone implant, rather than demonstrating causality, is concerning. Similarly, this approach appeared in Gibson and colleagues’ earlier commentary on overdose deaths in patients with naltrexone implants.5 Nonetheless, I commend the authors for raising the issues relating to the need to examine the role of naltrexone implants in treating opioid dependence and exploring alternatives to the use of rapid detoxification. I also endorse the need for thorough assessments, treatment planning and evaluation in patients undergoing such therapies.

D Martyn Lloyd-Jones

To the Editor: We read with interest the report of 12 hospital presentations related to the use of naltrexone implants.1 The accompanying editorial highlights how the rigorous scrutiny required to evaluate the efficacy and safety of this procedure is lacking.2 Regrettably, this study is likely to distort rather than inform the debate. Lintzeris and colleagues1 only identified patients with naltrexone implants who were referred to the Drug and Alcohol Consultation–Liaison services, not all patients presenting to the study hospitals. Additionally, the authors did not follow the methodology of chart reviews, as recommended by Gilbert and colleagues.3 Four of the 12 patients clearly had problems unrelated to their naltrexone implants. There was no attempt to identify the number of naltrexone implantations performed (ie, the denominator), nor was there any attempt to compare the naltrexone group with others being treated with agents such as methadone or buprenorphine. In 2003, we published our experience of naltrexone-accelerated detoxification in the emergency department (ED) of Sir Charles Gairdner Hospital.4 The hospital’s clinical toxicology service is based in the ED, and the hospital is located 2 km from the only private clinic in Perth that was using naltrexone during the study period in 2001. Working collaboratively with this clinic, patients developing complications from detoxification were referred to our service. In 6 months, 42 patients (7% of all those receiving naltrexone treatment) presented to the ED — 17 within 24 hours of treatment and 31 within 48 hours. Gastrointestinal symptoms of withdrawal were present in 18 patients, and central nervous system symptoms of withdrawal (predominantly agitation) in 14. Two patients required intubation for airway compromise secondary to a combination of agitation and chemical sedation. In 23 patients receiving naltrexone implants (rather than oral therapy), three developed infections and three complained of local pain. The mean length of stay for all patients was 18 hours (compared with 2.3 days in Lintzeris et al’s study), with the longest stay being 92 hours for one of the patients admitted to the intensive care unit. During the study period and the subsequent 6 months, four deaths of individuals who had undergone naltrexone-accelerated detoxification were reported to the Coroner, all being classified as probable drug overdose, probably opioid. None of these patients had presented to the hospital’s ED during the study period. It is important that good data are made available to inform the debate on naltrexone implants in the management of opioid dependence. Better communication and collaboration between clinics using naltrexone, EDs, and alcohol and drug services will improve the care of these patients.

Mark Little · Lindsay M Murray

To the Editor: The study by Lintzeris and colleagues1 and the associated editorial2 criticise naltrexone implants. However, the study is replete with errors regarding the 12 cases reported. A key to successful rapid opioid detoxification (ROD) is octreotide. An agonist of non-μ gut receptors, it prevents gastrointestinal symptoms of withdrawal.3,4 Earlier aggressive dosing is more effective. Only two of the six patients reported as having precipitate opiate withdrawal received octreotide, administered in both cases by their local doctor. Presumably this doctor performed the ROD. Why was the octreotide administration not repeated? Patient 7 was reported as having a localised abscess at the implant site. These may arise a variable period after implant insertion. Magnesium-monostearate, used as a binder in naltrexone and many other implants, may liquefy, resembling pus. Results of repeated microbiological examination are always negative. An actual infection at the implant site is rare. Patient 8 demonstrates that many patients use opiates and other drugs as self-medication for their psychiatric symptoms. It is regrettable that this patient’s psychiatrist was not involved in the decision making. Was the doctor doing the ROD aware that there was a psychiatrist involved? Transient psychosis may occur following ROD; use of antipsychotics is appropriate. Arrhythmias (as diagnosed in Patient 9) are a textbook in themselves. Pre-ROD preparation requires assessment for comorbidities including bacterial endocarditis and arrhythmia syndromes. Substance-misusing patients often use arrhythmogenic agents such as amphetamine. No mention was made of precipitate withdrawal symptoms in this patient, so an electrolyte abnormality is unlikely. Patients 10–12 had problems that were unrelated to the naltrexone implants and poorly managed by the receiving hospital. Naltrexone has 2 log the affinity for opiate receptors to that of morphine and most other opiates.5 This means that 1 mg of naltrexone will block 1 g of another opiate. Using opiates to treat patients in these circumstances therefore makes no sense. Ketamine, local anaesthetic blocks, paracetamol and non-steroidal anti-inflammatory drugs are alternative options for treatment. To compare naltrexone implants with thalidomide2 is emotive; all the components of the implants are approved agents. Similarly, to say they have not been fully tested is to condemn all products supplied by compounding pharmacists. Testing of serum naltrexone levels (to assess whether an implant is still working) is not rebatable under Medicare, so is expensive to perform. Research is a necessary component of naltrexone implants, and I would happily cooperate with any of the study authors in coordinating and performing such research.

Michael P W Kozminsky

To the Editor: A recent article by Lintzeris and colleagues,1 ostensibly about naltrexone implants, actually has little to do with implant treatment. Only one of the 12 reported cases involved problems linked specifically to naltrexone (antagonist) treatment being administered in implanted rather than oral form. This case involved infection at the implant site — undesirable, certainly, but about as noteworthy as the occasional infections that occur after abdominal surgery or breast implantation, despite antibiotic prophylaxis and careful technique. The remaining 11 admissions reflected not implant use but either the procedure of rapid antagonist induction (RAI) or the desired pharmacological effects for which naltrexone was prescribed in the first place (and one admission for unrelated pneumonia). RAI is needed because conventional antagonist induction requires complete opiate withdrawal before starting naltrexone. As true conventional withdrawal completion rates, even with inpatients, are typically below 30%,2 conventional techniques will typically achieve only derisory naltrexone induction rates. Various forms of RAI or accelerated induction, with induction rates typically around 100%, are more effective and more cost-effective.3,4 Similarly, complaining that pain management is difficult in naltrexone patients is like complaining that patients being treated with anticoagulants bleed or bruise more after surgery or injury. Fortunately, effective non-opiates (notably subanaesthetic ketamine) exist. The acute post-RAI problems seen in this case series would have been identical had every patient undergone RAI to oral rather than implanted naltrexone. Indeed, while 150 mg orally could block opiate analgesia for up to 72 hours, implants produce low but consistently effective naltrexone levels, disappearing within hours of implant removal, should that be unavoidable. I agree, however, that RAI clinics should optimise immediate post-RAI management. A recent conference featured the first presentations of the first four randomised controlled trials of implanted naltrexone. Three showed statistically and (more importantly) clinically significant advantages over “as usual” post-withdrawal treatment,5 or over oral naltrexone and placebo implants.6,7 The fourth,8 comparing implants with methadone maintenance in pre-release prisoners, had only modest statistical power (n = 21), but implant patients had less dropout and used about 50% less heroin. We already know that long-acting implants can largely prevent the opioid overdoses that are otherwise an intrinsic and sometimes lethal hazard of all abstinence-based programs;9 and that all implants prevent the otherwise high relapse rates typical of the first 4–6 weeks after detoxification.10 Surgeons, I am shocked to discover, have been using anaesthesia for 162 years without a comparable placebo-controlled evidence base.

Colin L Brewer

In reply: Our case series1 aimed to alert health practitioners to the types of hospital presentations associated with naltrexone implants and issues in managing such patients, particularly as these have not been well documented in the medical literature. These letters appear critical of any such communication. We maintain that our article1 identifies important clinical issues — such as the difficulties of providing analgesia in patients with implants of uncertain duration of effect (whereby the treating hospital staff have no way of knowing whether the implant is providing “active” plasma levels of naltrexone, given the lack of a licensed product). Ultimately, our study could not hope to provide the type of data that can only be accurately determined by independent clinical trials — such as the incidence rate of serious adverse events (as suggested by Little and Murray) or how these are most effectively managed (eg, the role of octreotide compared with ondansetron for managing protracted vomiting, as suggested by Kozminsky). A key complaint from the correspondents is whether the serious adverse events of opiate withdrawal and dehydration were caused by the naltrexone implant or by the rapid opioid detoxification process that accompanied the implant’s insertion. We acknowledged the difficulty of attributing causality in our article, but, unlike the correspondents, we cannot dismiss the possibility that the naltrexone implant may have contributed to the severity or duration of the opiate withdrawal syndrome. Clearly, there is a pharmacological basis as to how the presence of naltrexone from an implant may contribute to opiate withdrawal in a recently detoxified individual. Research comparing rapid opioid detoxification plus a naltrexone implant with conventional detoxification plus a naltrexone implant is required, to allow an assessment of whether naltrexone implants themselves contribute to the incidence, severity or duration of any opiate withdrawal. Until such data exist, it is appropriate to associate opiate withdrawal with naltrexone from the implants. We concur with several of the correspondents that further research is required to address many of the issues raised by our study, as well as better communication between service providers, better procedures for management of complications, and better assessment and patient selection. We maintain that naltrexone implants should not be routinely used until research has demonstrated their safety and efficacy, and, importantly, until there is a licensed naltrexone implant product with appropriate regulatory safeguards for patients and providers.

Nicholas Lintzeris

To the Editor: Two studies1,2 and an editorial3 on the vexed issue of medication errors in hospitals have recently appeared in the Journal. Yet none of them have mentioned patients, except as the passive victims of error, and all three have focused exclusively on public hospitals. This is unfortunate as, arguably, the public hospital system is evolving predominantly into a way station along the chronic illness journey within the wider health care system. To quote an 86-year-old patient of mine: “I’ve been taking the same tablets for 30 years, but as soon as I come to hospital they take them away and give me other ones, as if I’m incapable.” Indeed. Could patients continue taking their own regular medications (patients’ own drugs [PODs]) themselves? This would eliminate many errors of transcription and administration and eradicate in-hospital dispensing errors altogether. Although it might seem risky for patients to be given free rein with their medications, this is precisely what they are doing at home, and generally with no supervision whatsoever. Furthermore, if patients do make errors, they are more likely to omit some medications than to take toxic doses, and the consequences of such errors of omission are likely to be minor. If a self-administration system for PODs were to be implemented — including newly prescribed drugs that patients were expected to continue using on discharge, as well as medication strategies used in the home (eg, dosette boxes) — then any errors could be noted and corrected, just as a patient’s mobility is assessed before discharge. On the other hand, it is pertinent to note that many hospital admissions arise from medication errors, with one study demonstrating that up to 30% of admissions in patients aged 75 years and over are medication-related and up to 75% are preventable.4 Clearly, certain groups of patients and certain drugs should be excluded from a POD system. A sample protocol is available from the author on request. Would a POD self-administration system be cost-effective? Such a system has been used successfully in at least one Australian private hospital (in which I have worked) and in several hospitals in the United Kingdom.5 A systematic review has also been undertaken to examine the risks and benefits of the use of PODs, but it did not discuss the issue of self-administration.6 A MEDLINE search from 1996 onwards for patients’ own drugs/medications and self-administration yielded no results. As always, further research is required. What my patient’s comment highlights is that patients do have autonomy and some competence, and that these factors should be taken into account in any strategies aimed at reducing medication errors.

Frank T Formby

To the Editor: In May 2007, I began working in an Australian public hospital as a permanent consultant endocrinologist and physician. There are many differences between the health systems of Australia and Sweden, where I previously worked. In particular, there are striking differences in on-call work for the rostered consultant. In Sweden, the compensation (usually taken as leave) for every phone call, whether it was 1 minute or 30 minutes long, was half an hour during weekday hours of 4.30–9 pm and 7–8 am, and 1 hour during nights and weekends. Compensation also applied to ward rounds on weekends. I also received an on-call allowance of 6 minutes per hour during weekdays and 12 minutes per hour during weekends. During public holidays, rates were tripled. Every year, I earned 5–7 extra weeks on top of my normal 5 weeks of annual leave, some of which was used for well paid locum work, as private practice is almost non-existent in Sweden. Compensation could also be taken as payment; each department had its own agreement with staff on the preferred format, depending on staff levels and budget. The on-call frequency was usually 1 in 10, and the physician on call was responsible for all general internal medicine patients. For most of my career I worked in a large tertiary referral centre,1 but the rostering and compensation were similar in local general hospitals, with the only difference being fewer subspecialties with their own on-call roster. The surgical specialties had the same system. As in Australia, I was rarely called to attend the hospital, although contact during an on-call session was more frequent in Sweden (2–10 v 0–2 phone calls). Junior doctors in Sweden were more inclined to discuss patients and, in some wards, the nurses were instructed to call the physician on call first if the matter could be solved by phone. I was happy for every call, as I received extra compensation, but I never received any further phone calls once the on-call session finished. In Sweden, I did ward rounds on weekends, either of all medical wards in the local general hospitals or only the general medical wards in the tertiary centre when I was physician on call. Before seeing patients, I did a paper round with the nurses, when we decided which patients I needed to see. Patients were not admitted directly under me, but under the specialists responsible for the wards during office hours. However, I was temporarily responsible for all medical patients in the hospital. In Australia, at least in my current hospital, I have “my patients” in the wards (usually spread out over the entire hospital). If something suddenly happens to one of them, the intern, resident medical officer or medical registrar will phone me, even in the middle of the night or if I am away on leave. As the compensation is the same whether phone calls are received or not, and most medical patients are admitted under the physician on call, there is little incentive for the physician to volunteer for extra on-call sessions or to encourage junior doctors to phone.

Henrik Falhammar

To the Editor: Trachoma, caused by the bacterium Chlamydia trachomatis, is the leading cause of infectious blindness worldwide.1 In Australia, the burden of disease falls almost exclusively on the Aboriginal population.2 However, there has been little consistent data collection on the prevalence of trachoma in recent years in Australia.3,4 Furthermore, despite Australian Government recommendations for biennial screening of people aged 40–54 years and annual screening of people aged ≥ 55 years in areas where trachoma is or has been endemic,5 very little screening of older people for trachomatous trichiasis has been conducted.2,4 We report on the first large-scale population study in 30 years of the current prevalence of active and cicatricial trachoma in the Northern Territory Aboriginal population. We conducted a standardised clinical screening study of five Aboriginal communities in the Katherine Region of the NT over a 5-week period in 2007. A representative sampling frame of those believed to be currently living in each community was constructed using the medical clinic patient list, the council housing list and the local knowledge of Aboriginal Health Workers seconded from the clinics to assist with the project. All people in each community were invited to undergo a clinical eye examination for trachoma. The parameters of the World Health Organization simplified grading scheme6 were used to determine prevalence of the five signs of trachoma: tarsal conjunctival follicles, intense inflammation, tarsal scarring, trichiasis and corneal opacity. A total of 1316 people (85.2% of the total estimated population), including 415 children aged under 10 years, were screened for trachoma. Across the five communities, active trachoma (assessed as the presence of either follicles or inflammation in one or both eyes) was at an endemic level (> 10%). The prevalences of active trachoma, scarring and trichiasis in different age groups are summarised in the Box. The overall rate of active trachoma in children under 10 years of age was 19.8% (95% CI, 16.0%–23.9%) (n = 82), and two communities had hyperendemic prevalence of trachoma (> 20%) in this age group. The youngest child observed with active trachoma was just over 1 year old. The prevalence of scarring in people aged 20 years and over was 32% (95% CI, 28.3%–35.9%) (n = 193). The youngest person identified with scarring was 7 years old. Six people (2.3% of all people aged 40 years and over) were identified with trichiasis requiring urgent ophthalmological attention. Across the population, this placed the prevalence of unoperated trichiasis at more than four times the acceptable threshold set by the WHO. A seventh person had had trichiasis surgery. That trachoma is still hyperendemic in Aboriginal communities more than 30 years after the National Trachoma and Eye Health Program first identified the extent of trachoma is unconscionable. Urgent and sustained public health and clinical interventions are required, with greater commitment from politicians and health policymakers, if Australia is to join the ranks of other developed nations in eradicating endemic trachoma. The guidelines for trachoma control developed by the Communicable Diseases Network Australia5 need to be resourced appropriately and implemented. Prevalence of active trachoma, scarring and trichiasis in five Aboriginal communities in the Northern Territory in 2007, by age group* TFI = active trachoma (follicles [TF] and/or inflammation [TI]). TS = trachomatous scarring. TT = trachomatous trichiasis. * Vertical bars indicate 95% CIs.

Katrina Roper · Claude-Edouard C Michel · Paul M Kelly · Hugh R Taylor

To the Editor: The oculocardiac reflex is a potentially life-threatening phenomenon requiring prompt recognition and management. It is defined as a 20% or greater reduction in heart rate and/or the presence of arrhythmias during stimulation of the orbital contents.1 It is most commonly encountered in the context of paediatric squint surgery. We report its occurrence in a young healthy adult man after a traumatic facial injury. While being transported to hospital by ambulance, he had intermittent bradycardia, with a heart rate as low as 38 beats/min, and was administered a 1 g dose of intravenous atropine. His medical and ocular histories were unremarkable, and he had no history of unexplained syncope. In the emergency department, his heart rate remained low (40 beats/min) and his blood pressure was 122/52 mmHg. There was diffuse periorbital lid swelling and bony tenderness along the inferolateral orbital margin. He had restricted upgaze of his left eye; during this manoeuvre, his heart rate dropped to 20 beats/min and he developed hypotension, with a blood pressure of 92/48 mmHg. He was given three intravenous 500 μg boluses of atropine to improve his haemodynamic condition. An electrocardiogram showed sinus bradycardia, and subsequent recordings showed intermittent Mobitz II second-degree atrioventricular block. A computed tomography scan of the left orbit showed a moderately displaced fracture of the orbital floor involving the maxillary bone, with entrapment of orbital fat and the inferior rectus muscle (Box). Given the presence of the oculocardiac reflex with haemodynamic compromise, the fracture was immediately repaired surgically. Postoperatively, the patient’s blood pressure was 134/90 mmHg and his heart rate was 86 beats/min, with normal sinus rhythm. He recovered full eye movement, and no further oculocardiac reflex was recorded. He remained well 1 year after discharge. The oculocardiac reflex was first described by Aschner as a slowing of the radial pulse when pressure was applied to the eye.2 It is a rare but recognised occurrence among young healthy adults with orbital fractures. Clinical manifestations of the reflex may include bradycardia, hypotension, nausea, vomiting and syncope.3 The reflex is acknowledged as an important indication for immediate surgical repair of the orbit.4 In addition to reducing morbidity from the reflex, urgent repair is beneficial as it releases incarcerated soft tissue, leading to a more favourable outcome with less likelihood of squint.5 Cardiac decompensation due to traumatic facial injuries should alert clinicians to the possibility of the oculocardiac reflex and the need for urgent surgical intervention. Computed tomography scans of the patient’s left orbit Sagittal (A) and coronal (B) computed tomography scans showing left orbital floor fracture with entrapment of the inferior rectus muscle (arrows).

Vivek B Pandya · R Max Conway · Richard Conway

To the Editor: Microbial keratitis associated with soft contact lens wear is a well recognised, not uncommon, clinical entity and a preventable cause of ocular morbidity.1,2 A 31-year-old woman who occasionally wore soft contact lenses presented to a general practitioner with a 2-day history of bilateral red eye associated with ocular discomfort, photophobia and purulent discharge. She was diagnosed with bilateral conjunctivitis, commenced on chloramphenicol drops and told to return in 5 days. Her symptoms initially improved, but then worsened. Seven days after symptom onset, she presented to hospital for assessment. History revealed that she had worn soft monthly disposable contact lenses twice in the previous month to correct her mild myopia. On examination, the patient’s visual acuity was equivalent to being legally “blind”, being hand movement in the right eye and light perception in the left. On inspection, both eyes appeared grossly abnormal. The right eye had a large central corneal abscess and the left eye had a complete corneal abscess with 360° peripheral corneal thinning (Box, A) — a significant risk for globe perforation. The conjunctiva was markedly injected bilaterally. Corneal scrapes, the contact lenses and the case containing turbid solution were sent for urgent gram stains and microbiological culture. The patient was admitted to hospital and received intensive topical treatment with gentamicin 0.9%, cephalothin 5% and tobramycin ointment. The corneal scrapes revealed Pseudomonas aeruginosa as the causative organism. The patient showed slow improvement with antibiotic therapy. Although the infection cleared, the residual corneal scarring resulted in permanent loss of corneal clarity and hence vision. Four months after treatment was commenced, the patient’s visual acuity had improved to 6/24 in the right eye and 6/36 in the left (Box, B). An Australian review of outcomes after keratitis found that 52% of patients had a final visual acuity of worse than 6/12, the legal visual acuity for driving.3 In this patient, despite saving both eyes and the improvement in her vision, she still has significant functional impairment, being unable to work as a teacher or drive. Corneal transplantation is now her only option for potentially regaining the loss in her functional vision, with a minimum expected recovery time of 2 years. GPs have a difficult job distinguishing between red eye requiring immediate referral and red eye that is not vision-threatening. All contact lens wearers who present with red eye need to be examined for yellow/white corneal infiltrates and, if present, or if the patient cannot be assessed adequately, immediate referral is mandatory. P. aeruginosa is the most common pathogen and one of the most aggressive organisms isolated in contact lens-related microbial keratitis.4 As it is invariably resistant to the bacteriostatic chloramphenicol, the appropriate empirical treatment is either fluoroquinolones or cephalosporins, which ideally should be commenced after corneal scrapes have been performed.5 Left eye at presentation and after 4 months of treatment A: At presentation, there was marked conjunctival injection, 100% epithelial defect (stained with fluorescein [green]) and severe circumferential peripheral corneal thinning (arrow). B: Four months after presentation, there was dense central scarring and peripheral corneal neovascularisation (arrow). Vivek B Pandya, Ophthalmology Resident1Alessandra Martins, Ophthalmology Registrar1,2Shanel Sharma, Ophthalmologist1,21 Department of Ophthalmology, Sydney Eye Hospital, Sydney, NSW. 2 Department of Ophthalmology, Royal Prince Alfred Hospital, Sydney. shanelATunsw.edu.au Green M, Apel A, Stapleton F. A longitudinal study of trends in keratitis in Australia. Cornea 2008; 27: 33-39. <PubMed> Keay L, Edwards K, Naduvilath T, et al. Microbial keratitis predisposing factors and morbidity. Ophthalmology 2006; 113: 109-116. <PubMed> Green MD, Apel AJ, Naduvilath T, Stapleton FJ. Clinical outcomes of keratitis. Clin Experiment Ophthalmol 2007; 35: 421-426. <PubMed> Stapleton F, Keay L, Sanfilippo PG, et al. Relationship between climate, disease severity, and causative organism for contact lens-associated microbial keratitis in Australia. Am J Ophthalmol 2007; 144: 690-698. <PubMed> Constantinou M, Daniell M, Snibson GR, et al. Clinical efficacy of moxifloxacin in the treatment of bacterial keratitis: a randomized clinical trial. Ophthalmology 2007; 114: 1622-1629. <PubMed> (Received 17 Mar 2008, accepted 28 Jul 2008) ©The Medical Journal of Australia 2008 www.mja.com.au PRINT ISSN: 0025-729X ONLINE ISSN: 1326-5377

Vivek B Pandya · Alessandra Martins · Shanel Sharma

To the Editor: A 37-year-old man infected with HIV through exposure to men who have sex with men (MSM) presented with a 6-week history of intermittent fevers, patchy alopecia and a widespread brown/grey macular rash involving his face, trunk, abdomen and all limbs, with scaling of the face, palms and soles. He had no symptoms of meningism or visual disturbance, and had a chronic mild intermittent headache with no recent change in frequency or intensity. His most recent CD4 cell count was 70 cells/μL and his HIV viral load was > 100 000 copies/mL. On admission, a serological test for syphilis was reactive and showed a rapid plasma reagin (RPR) titre of 1 : 64 and a positive enzyme immunoassay for antibody (EIA-Ab), whereas at the onset of the rash 6 weeks previously, a serological test for syphilis was negative. A punch biopsy of the skin lesions showed a perivascular infiltrate with lichenoid inflammation consistent with secondary syphilis. An ophthalmological review showed a bilateral anterior uveitis. Examination of cerebrospinal fluid (CSF) showed a white cell count of 1 × 106/L (100% lymphocytes), a normal glucose level, a mildly elevated protein level of 0.45 g/L and a weakly positive result for a fluorescent treponemal antibody absorbed (FTA-ABS) test. CSF RPR, EIA-Ab and Treponema pallidum particle agglutination (TPPA) test results were all non-reactive. The patient was diagnosed with asymptomatic ocular and neurosyphilis, and treated with intravenous benzylpenicillin (1.8 g 4-hourly for 15 days) and prednisolone eye drops (four times daily for 14 days). The rash faded and the anterior uveitis subsided in the first week of treatment. There is currently a syphilis epidemic among MSM in Victoria, with the number of syphilis notifications increasing 25-fold between 2000 and 2006.1 A strong association between HIV infection and infectious syphilis has been demonstrated in recent years, including in Victoria.2 HIV-infected MSM with early syphilis have a 1.7% risk of having symptomatic early neurosyphilis3 and a 13% risk of having symptomatic ocular syphilis regardless of CD4 cell count.4 There is no pathognomonic finding in ocular syphilis, and the disease may manifest as uveitis, retinitis, optic neuritis, perineuritis, retinal detachment and papillitis. It is recommended that all patients with ocular syphilis undergo CSF examination and be managed as if they had neurosyphilis.5 Current guidelines also recommend CSF examination in HIV-infected patients who have late-latent syphilis, syphilis of unknown duration, any neurological signs or symptoms, or suspected treatment failure.6 The finding of asymptomatic ocular syphilis in our patient suggests there should be a low threshold for eye examination in HIV-infected people with early syphilis, even in the absence of any ocular symptoms, as the diagnosis of ocular syphilis dramatically alters the management of these patients.

Matthew T Kitson · Michelle K Yong · Jennifer F Hoy

To the Editor: Snowboarding is increasing in popularity, but Australian snowboarders have been shown to have 2.4 times as many fractures as skiers, with 35% of upper limb injuries being fractures.1 The most common site of injury is the wrist, accounting for 21.6% of all snowboarding injuries.2 It has been suggested that the use of wrist guards could reduce the risk of injury, particularly as snowboarding injuries tend to be impactive rather than torsional.3,4 However, concern has been raised that use of wrist guards will redistribute the impact of the force to more proximal areas of the arm, causing elbow injuries.5 We conducted a case–control study at the Mount Buller Medical Centre, Victoria, during the 2004 and 2005 ski seasons to assess: the association between wrist guard use and wrist fracture in snowboarders in Australia; and the association between wrist guard use and the severity of wrist and elbow injury. Cases were defined as any snowboarder seen at the clinic with a fractured wrist (n = 119). Controls (n = 375) were snowboarders — identified by their boots — who attended the clinic, either as companions to case participants or other patients, or as patients presenting for a reason other than wrist fracture. Study participants completed a questionnaire about wrist guard use and snow-sport behaviour. The site and severity of fractures were recorded by clinic staff. Logistic regression was used to determine adjusted odds ratios for risk factors against the main outcome measure of wrist fracture and injury in snowboarders with and without wrist guards. Characteristics strongly associated with wrist fracture were being of school age (odds ratio [OR], 2.37; P < 0.001) and being a novice at snowboarding (OR, 3.41; P < 0.001) (Box). After adjustment for all significant variables — sex, age, days of snowboarding and snowboarder ability — the odds of having worn wrist guards were lower in snowboarders with a wrist fracture (cases) than in those without such a fracture, but the difference did not reach significance (adjusted OR, 0.58; 95% CI, 0.32–1.04; P = 0.07). Full analysis of all factors considered is available from the authors. Among the sample of 494 snowboarders, 15 had elbow injuries, comprising: five with soft tissue injuries (4/86 wearing wrist guards v 1/391 not wearing wrist guards; adjusted OR, 17.6; 95% CI, 1.93–160.2; P = 0.01); and 10 with elbow fractures or dislocations (3/86 wearing wrist guards v 77/391 not wearing wrist guards; adjusted OR, 1.84; 95% CI, 0.46–7.30; P = 0.39). The association between wrist guard use and increased soft tissue elbow injuries, but not elbow fractures and dislocations, supports the value of wearing wrist guards to reduce overall injury severity. Despite a lack of overall statistical significance, the clinical context and consistency in direction of the findings suggest that snowboarders who wear wrist guards in Australian snow conditions could benefit from a reduction in wrist fracture injury of approximately 42%. This is consistent with reports from other countries that show a protective effect of wrist guards of 52% to 87%, with the greatest benefit in novice snowboarders.4 We suggest that wrist guard use should be strongly recommended for novices, and should be mandatory for school-aged snowboarders. Local schools in the Mansfield district, near Mt Buller, have adopted a policy of “no wrist guard = no snowboard”, and we hope that other schools visiting Mt Buller, and indeed other ski resorts in Australia, will follow this lead. Characteristics associated with wrist fracture among snowboarders Characteristic Cases (n = 119) Controls (n = 375) Odds ratio (95% CI) P for difference Wearing wrist guards today No 100 (84%) 299 (80%) 1.00* Yes 18 (15%) 75 (20%) 0.72 (0.41–1.26) 0.25 Missing data 1 (0.8%) 1 (0.3%) Age (years) 0–19 72 (61%) 149 (40%) 2.37 (1.55–3.63) < 0.001 > 19 46 (39%) 226 (60%) 1.00* Missing data 1 (0.8%) Ability of snowboarder Novice 60 (50%) 112 (30%) 3.41 (1.79–6.49) < 0.001 Intermediate 43 (36%) 173 (46%) 1.58 (0.82–3.04) 0.17 Advanced 14 (12%) 89 (24%) 1.00* Missing data 2 (2%) 1 (0.3%) * Reference category.

Graham M Slaney · Judith C Finn · Angus Cook · Philip Weinstein

To the Editor: Streptococcus suis is an emerging zoonosis in humans and a common pathogen in Australian pigs.1 However, only two cases of human infection have previously been reported in Australia.2,3 We recently treated two Australian piggery workers, from the same town in New South Wales, for S. suis endocarditis. The first patient, a previously healthy 46-year-old woman, presented in October 2006 with a 3-month history of fatigue, anorexia, night sweats and weight loss of 20 kg. Her job involved hands-on work at a piggery. She was afebrile, with blood pressure of 145/50 mmHg, bilateral clubbing, splenomegaly, and a long diastolic murmur without evidence of heart failure. Transthoracic echocardiography confirmed severe aortic regurgitation associated with a vegetation. Blood cultures grew S. suis. The patient was treated with benzylpenicillin (1.8 g, 4-hourly for 6 weeks) and gentamicin (60 mg, 8-hourly for 2 weeks). Severity of aortic regurgitation necessitated aortic valve replacement. The second patient, a 58-year-old man, presented in January 2008 with headache, fever (38.7°C), neck stiffness and confusion. He had been unwell for 1 month with fevers, sweating, fatigue and weight loss of 6 kg. His job involved transporting pigs from local piggeries, including the one at which the first patient worked, to an abattoir, and involved direct contact with pigs. On admission, he was treated with ceftriaxone (2 g) and benzylpenicillin (2.4 g). Cerebrospinal fluid (CSF) examination showed leukocytosis (10 300 × 106/L; reference range, < 5 × 106/L) with 95% polymorphs. Scanty gram-positive cocci were visible, but there was no growth on culture of the CSF. Blood cultures grew S. suis. Transthoracic echocardiography revealed an aortic valve vegetation with trivial regurgitation. The patient was then treated with benzylpenicillin (1.8 g, 4-hourly for 4 weeks) and gentamicin (80 mg, 8-hourly for 2 weeks), and made a full recovery. Both cases were investigated by the NSW Department of Health, including assessment of workplace practices, staff education and rates of porcine infection at the piggeries and abattoir at which the patients had worked, but no significant factors for infection were identified. Since the first reported human infection with S. suis in Denmark in 1968,4 more than 400 cases have been reported, including an outbreak in China in 2005 that affected 215 people.5 The most common manifestations are meningitis (affecting 72.5% of patients) and bacteraemia (24.2%); endocarditis is relatively uncommon (1.1%).5 In a series of 16 cases of S. suis endocarditis, the mean period between onset of symptoms and diagnosis was 23 days, and seven patients required valve replacement.6 Similarly, our patients had subacute presentations: severe aortic regurgitation and secondary meningitis. In Australia, it is likely that there have been other S. suis infections in humans that have gone unrecognised because of mild presentations, difficulties with laboratory diagnosis, and empirical treatment of unrecognised infection. While it is unlikely that S. suis is a common zoonosis in Australia, these cases show that it is an occupational hazard in Australian piggeries, with potential public health, animal health and medicolegal implications.

Karina J Kennedy · Assad A Jadeer · Chong W Ong · Sanjaya N Senanayake · Peter J Collignon

To the Editor: The study by Nichols and colleagues1 and the associated editorial by Hughes2 struck a chord of familiarity for me, as patient safety issues are currently high on the political agenda in the United Kingdom. An estimated 850 000 incidents of harm or near harm affect National Health Service (NHS) hospital patients in the UK each year.3 In April 2004, the Health Foundation (an independent charity that aims to improve the quality of UK health care), together with the Institute for Healthcare Improvement, launched the Safer Patients Initiative (SPI). The four hospitals initially chosen to participate conducted hospital-wide programs to radically improve patient safety, with the aim of reducing adverse events by 50% by October 2006. In November 2006, Phase 2 was launched, adding 20 more sites.3 These hospitals meet regularly to report on progress and exchange ideas. Discrete projects focus on medicines reconciliation, ward-based care, critical care, and perioperative care. The overall aim of the SPI is to improve the patient safety culture within each organisation. Specific targets for all participating hospitals include a 15% reduction in mortality of in-hospital patients; 300 days between central line bloodstream infections in critical care units; 80% of blood sugar levels in diabetic patients falling within their target treatment range; a 30% reduction in cardiac arrest calls; and 50% reductions in methicillin-resistant Staphylococcus aureus bloodstream infections, harm from anticoagulation, and surgical site infections. In my intensive care unit, hand hygiene compliance among medical staff has been regularly audited and has improved from a range of 20%–90% per day to 60%–100%. This compares favourably with a recent Australian hand hygiene initiative.4 When practice improvements are shown in one location, the project team takes on the responsibility of spreading these across the hospital. Initial scepticism from senior clinicians and nurses in my hospital has generally been replaced by cooperation and, in many cases, ideas for other ways to improve delivery of safer clinical care. Large multisite evidence-based trials in intensive care units in the United States showed that, with focused effort on sterile technique and catheter care and by rectifying lapses in standard procedures, a reduction of 66% in catheter-related bloodstream infections was possible.5 The SPI is trying to replicate results such as these within a relatively short period. My intensive care unit has now gone 190 days without a line-related bacteraemia; previously, we had infections almost every month. The SPI Phase 2 completion date is November 2008, with full national reporting due at that time. It is intended that practice improvements will then be spread across the NHS. The experience in my hospital has been that sharing experiences both within the hospital and externally has led to tangible progress in this area.

Peter J Shirley

To the Editor: The recent article on the review of the University of Sydney Medical Program (USydMP)1 by Goulston and Oates included a lengthy list of “changes made or planned in accordance with key recommendations”.2 Regrettably, and to the despair of many, the most needed change will not take place. It is reported in the review that the average age of future USydMP graduates will be 29–30 years, as it has been for the past decade.1 From 2008, those who aspire to be surgeons will competitively enter the new Surgical Education and Training (SET) program of the Royal Australasian College of Surgeons (RACS) after completing “at least their second postgraduate year”.3 The SET program is for 5–6 years, depending on the specialty. Most trainees subsequently take a subspecialty fellowship for 1–2 years, either in Australia or overseas, by which time our hapless graduates will be 40 years old. A woman may have to have leave of absence for a pregnancy. A postgraduate degree is now a prerequisite for an academic career and this involves an additional 2–3 years of full-time research. Finally, it takes in the order of 5 years to establish a referral specialist practice in most branches of medicine. In the review document, Goulston and Oates nihilistically state “There is no opportunity for streaming within the USydMP”.1 There is no mention of undergraduate education in Australia, let alone the streaming of such education, in the article from the RACS outlining the SET program.4 However, strangely enough, it is noted therein: “North American students must make their long-term career choice in the final year of their medical school and are streamed accordingly”. One wonders if there is any purposeful communication between the RACS and our universities. There certainly should be. It is imperative in this day and age that undergraduate and postgraduate medical education be considered as a continuum so that we can begin to rid ourselves of the absurdly long and manifestly inefficient process outlined above. The historian and journalist Paul Johnson put his astute finger on the problem in writing a column about universities generally: “. . . a visitor from another planet, unfamiliar with the history of the institution, would think it odd that our ablest boys and girls, at a time when their mental and physical powers are at their highest, are withdrawn from the service of society and kept in comparative idleness . . .”5 One can but conclude that, at least for future surgeons, the wrong people are at the helm at the RACS and at the University of Sydney’s Faculty of Medicine.

Thomas K F Taylor

In reply: Taylor raises several issues that the Royal Australasian College of Surgeons (RACS) has carefully considered. The new Surgical Education and Training (SET) program commenced this year.1 The acronym SET could equally mean Shorter Efficient Training. In the previous program, 2–5 years of basic surgical training was followed by 4–6 years of advanced training, resulting in surgeons entering specialist practice an average of 10 years after graduating with their medical degrees. We responded to societal and regulatory factors, including the older age of medical (compared with other) graduates, sex, work–life balance, safe-hours requirements, workforce pressures and competition from other specialties. Our new system aims to streamline training by early selection directly into one of nine surgical specialties and completion of training by Postgraduate Year 7 or 8 in most cases. It is not only shorter, but more comprehensive than previously. It is much more than an apprenticeship, where training occurs by random clinical exposure. We are covering defined curriculum objectives for every trainee by offering training in metropolitan and regional hospitals, synthetic laboratories and the private sector. We are moving away from reliance on the number of years of training and numbers of operations as measures of experience. We are focusing on the development of a range of surgical competencies encompassing professionalism, communication, collaboration, clinical decision making, scholarship, leadership and health advocacy, as well as essential medical and technical expertise. These competencies are regularly monitored by performance assessment throughout training. At the completion of training and the RACS fellowship examination, a surgeon is competent to commence practice as a specialist. Additional formal training experience is optional. Of course, the RACS promotes the concept of lifelong learning. The RACS and universities are communicating. Common concerns are the compromised state of basic science education and the limited exposure of medical students to a range of surgical specialties. The College has had discussions with many universities and health authorities about the possibility of “streaming” in the later years of medical school and in Postgraduate Years 1 and 2. It is worth noting that the University of Sydney has plans for the final 2 years of its course to be integrated, with increased emphasis on critical care and surgery.2

Ian R Gough

In reply: We are in sympathy with Taylor’s concerns about the length of medical training and point out that a more careful reading of our review of the University of Sydney Medical Program1 contained the following comments (on page 203): Discussion with the Royal Australasian College of Physicians canvassed the possibility that students might master some educational modules during their medical degree which would be credited by the College. This could well apply to other Colleges. Such a process would be more easily achieved if the Colleges moved to an overall “point system” i.e. students (especially in nonclinical areas such as Ethics, Quality and Safety etc) could study postgraduate modules pari passu with the USydMP, gaining some points towards their chosen college specialty qualification. This is followed by three recommendations on page 204: Students with an early interest in a specialty could gain some speciality experience or credit towards their specialty by either working towards an MPhil and by making use of the electives, options and Honours research project. The future situation with regard to medical training in some of the specialties is fluid eg, the Royal Australasian College of Surgeons is introducing a method of streaming for surgical training (SET) and IMET [Institute of Medical Education and Training] is looking at criteria for competency in the residency years. In view of this the Dean should explore further opportunities for streaming when the options for future specialty training become clearer. Early streaming should be re-examined by Faculty when the curriculum and educational changes being considered by some of the Colleges become clearer.

Kerry J Goulston · R Kim Oates

To the Editor: During the recent international cricket series between Australia and India, we were alarmed by the sight of our Australian cricketers prominently badged with the logo of the fast food giant KFC. Australia is experiencing an epidemic of overweight and obesity, a problem that is especially affecting children, adolescents and young adults.1 This epidemic is worsening as a direct result of unhealthy eating habits and low levels of physical activity. Obesity is associated with chronic and costly diseases that lead to premature death and ill health. These include diabetes, cardiovascular disease, respiratory problems, sleep apnoea, certain cancers, mental illness and osteoarthritis, which can begin in adolescence.1 Cricket in Australia enjoys considerable popularity and a strong national following. Our cricketers are national sporting heroes who enjoy widespread support and respect throughout the community, particularly among younger members of the community, who aspire to emulate them. Against this background, we are increasingly concerned and disappointed that Cricket Australia has a sponsorship agreement with, and consequently promotes, KFC — going as far as publicly declaring the company the “official fast food restaurant of Cricket Australia”.2 This advertising uses the standing of cricket and its players to endorse and promote unhealthy eating habits, one of the major root causes of obesity in Australia. KFC products have caloric and fat contents well above the national dietary guidelines, which recommend < 30% energy from total fat and < 10% energy from saturated fat.3 For example, a standard serve of original-recipe chicken contains about 58% total fat and 24% saturated fat.3 Furthermore, we have shown that even one common KFC meal per week can adversely affect recommended healthy diets.4 It is ironic and regrettable that Cricket Australia, while having done so much for the sport, encourages the promotion of unhealthy, high-fat, high-calorie KFC products that negate the benefit of increased physical activity associated with playing cricket. With the explosion of obesity-related illness, we need champions to encourage health-promoting behaviours, particularly healthy eating and increased physical activity. The enthusiastic encouragement of unhealthy and undesirable eating habits should have no place in sporting sponsorship. Not so long ago, similar sentiments were being expressed about tobacco sponsorship of sport, which fortunately has been eradicated. Cricket Australia should consider its responsibilities to Australia’s children and youth and review its sponsorship by KFC. This would benefit the health of the community and demonstrate leadership and social responsibility by Cricket Australia and Australia’s elite cricketers.

Stephen Colagiuri · Ian D Caterson

In reply: Cricket Australia (CA) actively supports physical activity, healthy eating and healthy lifestyles and continues to invest considerable effort in encouraging Australians to play cricket, in everything from formal, organised competitions to social games in the backyard, in parks and schoolyards and at the beach. In a time of declining community physical activity, we are heartened to see that active participation in cricket is growing strongly, and note that female cricket is the fastest growing female sport in Australia. As a community-based, not-for-profit organisation, we are heavily dependent on the support of all of our sponsors, including KFC, to be able to implement the activities we undertake. These range from community-based programs that get kids running around outside to programs in schools, clubs and Indigenous communities, and further activity needed to develop and put elite international cricketers onto the field. In relation to KFC, we believe in a little of everything and everything in moderation. Setting aside the truly elite athletes, the formula that is going to work best for most cricketers and cricket fans is reasonable, not extreme, training and physical activity, together with a balanced diet, not one that features total abstinence from high-energy foods. Our view on alcohol is the same. Our CA advertising featuring Merv Hughes encourages fans to enjoy a beer, but not at the rate of one per over. The overall issue is about balance. Consumer research — commercially confidential, so it can’t be referenced here — shows that KFC consumption in Australia is an occasional treat, not a dietary staple. More broadly, CA is comfortable that Australian cricket’s collective activity has a net positive impact in encouraging healthy and active lifestyles.

Peter Young