Environmental health

To the Editor:A recent article by O’Brien and colleagues1 highlights the worsening epidemic of Buruli ulcer in Australia. The steep rise in both the incidence and severity of the disease is associated with estimated health care costs of over $2.5 million per year in Victoria.1 The increase in Buruli ulcer cases in Australia parallels the increase in non-tuberculous mycobacterial (NTM) infections, especially lymphadenitis and Buruli ulcer, reported worldwide. Although this rise might be partly attributable to improved awareness and diagnostic methods, it might also be related to the discontinuation of universal bacillus Calmette–Guérin (BCG) vaccination in settings where the rate of tuberculosis has declined. Routine vaccination with BCG through the school program was discontinued in Victoria in the mid-1980s. The live-attenuated strain of Mycobacterium bovis contained in BCG vaccine shares epitopes with NTM, which makes cross-protection plausible. Our recently published meta-analysis indicates that BCG vaccination has a protective effect against NTM.2 In particular, two randomised controlled trials provide strong evidence for protection against Mycobacterium ulcerans.3,4 However, immunity might only be short lived, as the highest protection was observed in the first year after vaccination. Nevertheless, studies also report that compared with BCG-naive individuals, those who have received the BCG vaccine have smaller skin lesions,4 a shorter duration to healing5 and protection against severe forms of Buruli ulcer with multiple skin lesions.6 Buruli ulcer is a serious condition, which, despite prolonged antibiotic treatment and surgical intervention, can lead to complications such as osteomyelitis and other crippling sequelae. In light of the worsening epidemic, the protective effect of BCG vaccination should not be overlooked.

Petra Zimmermann · Adam Finn · Nigel Curtis

To the Editor:Salmonella infection manifests as enteritis and enteric fever, predominantly acquired overseas. When required, therapy with azithromycin, ciprofloxacin or ceftriaxone is recommended by the Therapeutic guidelines: antibiotic;1 however, reduced susceptibility to fluoroquinolones in Asia limits the use of ciprofloxacin unless susceptibility is confirmed.2 The Australian Bureau of Statistics recorded a 546% increase in short term departures to Indonesia over 10 years, with 1.2 million nationally in 2016.3 A 31-year-old man was taking long term azithromycin 250 mg daily to prevent bronchiolitis obliterans syndrome after a bilateral lung transplant several years earlier for cystic fibrosis. Three weeks after returning from Bali, he was admitted with fatigue, fever, diarrhoea and abdominal pain. He had acute kidney injury. His C-reactive protein level was 190 mg/L (reference interval [RI], < 5 mg/L) and procalcitonin concentration was 3.5 μg/L (RI, < 0.05 μg/L). A single set of blood cultures was negative. Stool culture isolated Salmonella enterica serovar Paratyphi B var Java, sensitive to ceftriaxone and ciprofloxacin, with a raised azithromycin minimum inhibitory concentration (MIC) of 64 mg/L by ETEST (bioMérieux); an MIC > 16 mg/L indicates non-wild-type4 and is associated with treatment failures. Owing to his immunocompromised state, the patient received a 14-day course of ciprofloxacin (MIC, 0.016 mg/L). Our review of 2015–2017 data from the Western Australian public pathology provider revealed that two of 31 typhoidal Salmonella isolates (Salmonella Paratyphi A and Salmonella Typhi bacteraemia, each acquired in India) and one of 15 non-typhoidal Salmonella isolates (S. typhimurium, no clinical details provided) had an azithromycin MIC > 16 mg/L. Ceftriaxone resistance was low at 0% (0/117) of typhoidal Salmonella and 0.4% (7/1648) of non-typhoidal Salmonella; ciprofloxacin resistance was higher at 48.0% (47/98) of typhoidal Salmonella and 6.8% (94/1384) of non-typhoidal Salmonella. By comparison, azithromycin MIC > 16 mg/L was found in 16.1% of typhoidal Salmonella from travellers returning to the Netherlands,5 and in 1.3% of non-typhoidal Salmonella in the United States.4 Azithromycin use while travelling probably selected for resistant Salmonella infection in this case. However, our data show that azithromycin susceptibility cannot be assumed in Salmonella infections; testing should therefore occur in serious cases, along with ongoing surveillance for evolving resistance.

Alan J Rogers · Gar-hing A Lee · Peter Boan

To the Editor:The Editorial by Harvey and Diug1 on the value of food fortification as a public health intervention was prompted by demonstration of the effectiveness of mandatory iodine fortification in reducing iodine deficiency.2 Mandatory fortification of wheat flour for bread making was introduced in Australia at the same time to prevent neural tube defects. Harvey and Diug state that the two are conceptually different, as the former addresses a population iodine deficiency, whereas folic acid fortification is to compensate a presumed genetic defect that cannot be individually recognised, thus raising ethical questions about exposing the many for the benefit of the few. However, this is the case in almost all public health interventions. Using an example of Harvey and Diug, we expose the whole population to the mandatory fortification of flour with thiamine to prevent Wernicke–Korsakoff syndrome, a condition largely confined to people with a chronic alcohol problem. The concern they raise about mandatory folic acid fortification1 is exposure to unmetabolised folic acid, proposed as possibly increasing adverse effects, but which have not been clearly or conclusively shown. They refer to an Irish study reporting that seven of the 68 children in the study had detectable levels of unmetabolised folic acid in their blood.3 Ireland does not have mandatory folic acid fortification; the main sources of folic acid were voluntarily fortified breakfast cereals and fortified milk — products that are fortified with relatively high levels of folic acid. In Australia, breakfast cereals and other food products are also permitted to be fortified voluntarily — breakfast cereals often contain around 200–300 μg of added folic acid per 100 g (or about 100 μg per serve). This compares with mandatory fortification of flour of 200–300 μg per 100 g flour, or about 40 μg folic acid per slice of bread. While either source could lead to circulating unmetabolised folic acid, the higher doses in voluntarily fortified products are more likely to do so. With the introduction of mandatory fortification, there was a reduction in neural tube defects.4 Importantly, there has been a 68% reduction in previously higher rates of neural tube defects in Indigenous people.5 Mandatory fortification provides a more equitable, consistent and cheaper source of folic acid to the population than voluntary fortification. Let’s leave mandatory folic acid fortification preventing neural tube defects in our population.

Carol Bower · Fiona J Stanley · Mike Daube

To the Editor:With the release of the 2017 Australia’s Health Tracker by Socio-economic Status1 comes the latest evidence of an unjust health divide in Australia. With few exceptions, people who are more socially disadvantaged have worse health than their advantaged counterparts — a paradigm known as the social gradient of health.1 Despite increased need, socially disadvantaged individuals are less likely to access health care compared with advantaged people.2 It was refreshing, therefore, to read that the federal Shadow Minister for Health and Medicare Catherine King has placed health inequities front and centre of the Australian Labor Party health strategy, highlighting the importance of equitable prevention and public health and pledging to reduce the inequities in access to health care.3 Only 1.3% of the total Australian health expenditure is dedicated to the prevention of non-communicable diseases, much of which is directed at behavioural factors, including physical inactivity, poor diet and smoking1 — all of which are known to influence non-communicable diseases, such as diabetes, cardiovascular disease and osteoporosis.4 However, focusing primarily on behaviour ignores the wider context of health problems: the social, economic and cultural factors influencing that behaviour.5 The mounting costs of living and insecure employment increase vulnerability to non-communicable diseases. Improving the availability of affordable housing, quality employment and educational opportunities may better serve individuals at the economic margins, thereby addressing the stark inequities observed between advantaged and disadvantaged people. Dealing with these inequities would achieve discrete sectoral and health goals, providing cost-effective intersectoral cobenefits. What then is the role, for example, of the employment or educational sectors in driving the policies that address the socio-economic conditions which ultimately contribute to a healthy Australia? What is role for the health sector? The Department of Health could play a stewardship role, supporting and enabling other government agencies to manage their own sectoral goals while positively influencing health outcomes. Dealing with health inequities requires an intersectoral approach, a long term view, courageous leadership at the highest executive level, and support by an empowered public sector based on principles of fairness. Australia must act on social determinants of health and address this major problem for the health of our society.

Sharon L Brennan-Olsen · Sharon Friel

To the Editor: I write to comment on the Perspective by Wolfenden and colleagues1 on e-cigarette use by young people. In the article, the authors make regulatory recommendations for e-cigarettes based on the assertion that vaping causes young people to take up smoking — the so-called gateway theory. However, while many studies have found that adolescents who try vaping are more likely to try smoking, there is no evidence of cause and effect. The longitudinal studies described only show an association and are unable to demonstrate causality.2 An alternative explanation is common liability; that is, that young people who are more attracted to experimentation are more likely to try both products. In fact, international reviews suggest that vaping is diverting adolescents away from smoking and reducing smoking rates.3 As vaping rates have been increasing in young people, smoking rates are rapidly declining — a finding inconsistent with a gateway effect. Real world studies show that most vaping by young people is experimental and short lived and only a minority use nicotine. Regular vaping among teens is almost exclusively confined to those who already smoke. A recent analysis of five national surveys in the United Kingdom of 60 000 adolescents found that regular vaping by never-smoking 11–16-year-olds was 0.1–0.5%.4 Perhaps most important of all, Wolfenden and colleagues1 dismiss the substantial public health benefit that could result from vaping. Population studies have indicated that millions of smokers have quit using e-cigarettes and modelling studies have found a substantial net public health benefit, even using pessimistic scenarios.5 Banning wider access to e-cigarettes on the basis of an unproven risk to adolescents would prevent access to a life-saving quitting aid for millions of smokers. A better solution is to employ strategies to minimise youth access and make vaping available for adult smokers who are otherwise unable to quit smoking with conventional therapies.

Colin P Mendelsohn

To the Editor: Wolfenden and colleagues1 fail to justify the ban on the sale of nicotine-containing e-cigarettes in Australia and do not address the supporting arguments for allowing smokers to access these products.2,3 The concern that e-cigarettes may recruit young smokers justifies a regulatory response but not a ban on sales of nicotine-containing e-cigarettes to adults,3 who are thereby prevented from using these products. The authors cite a meta-analysis of studies that showed an association between the past 30-day use of e-cigarettes and combustible cigarettes;4 however, they ignore the weaknesses in the studies. First, most studies defined an adolescent e-cigarette user or cigarette smoker as one who had used either product in the past 30 days. These studies do not show that adolescents who used e-cigarettes were more likely to become daily smokers than their peers who did not use them. Second, the studies had substantial subject attrition (more than 30% in four out of nine studies) and they often poorly controlled for a shared liability to use drugs. The association was weakest in the largest and best controlled study.5 In addition, Wolfenden and colleagues make no mention of the steep decline in youth smoking rates that has occurred in both the United Kingdom and the United Sates while vaping has increased among young people.5,6 Nor do they mention that the UK’s smoking prevalence is now the same as Australia’s, in the absence of plain packaging or high tobacco tax.6 The authors’ claim that a relaxation of the ban on e-cigarette sales in Australia “has the potential for unintended harm” ignores the direct harms caused by the current ban; for example, the unregulated use of e-cigarettes, a black market, and the criminalisation of e-cigarettes users.6 Finally, even if the evidence for a gateway effect were accepted, it would, at most, justify a tighter regulation of e-cigarettes; it does not justify a prohibition on adult e-cigarette use. If it did, we would be morally obliged to prohibit the sale of cigarettes to smokers because on their argument this would be the most effective way of preventing adolescents from smoking cigarettes.

Wayne D Hall

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Sze Lin Yoong · Emily Stockings · Luke Wolfenden