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next generation of more powerful and expensive antibiotics, and are setting the stage for a time when antibiotics might no longer be effective for many infections. Another major reason for antibiotic resistance is the use of antibiotics in animals (eg, tetracycline in chicken feed) in subtherapeutic doses to promote growth. This important point was also highlighted very clearly in the article.1 As mentioned, many high-income countries have enacted laws to curb the practice of adding antibiotics to animal feed, even as early as 1971, to avoid antibiotic resistance in people. It is therefore time for countries like India and Nepal, and other low-income countries, to use antibiotics in animals only for the treatment of infections. Indiscriminate, subtherapeutic use of antibiotics for animal growth promotion must be stopped by governments; by increasing awareness in the general population about drug resistance, and by enacting laws so that antibiotics for saving human lives will continue to be effective, and the likelihood of resistance will decrease. If India takes the lead in this venture, it will probably be easier for smaller countries in the vicinity like Nepal to follow suit, because its pharmaceutical commerce is closely linked with India. I declare no competing interests.

Buddha Basnyat [email protected] Oxford University Clinical Research Unit, Patan Academy of Health Science, 252 Kathmandu, Nepal 1

Laxminarayan R, Duse A, Chand W, et al. Antibiotic resistance—the need for global solutions. Lancet Infect Dis 2013; 13: 1057–98.

I read with interest Simon Howard and colleagues’ Comment 1 on the increasing threat of antibiotic resistance and the necessity for a strong global response. That antibiotic use results in selective pressure favouring resistant bacteria is beyond dispute, and this is certainly a large part of the story, but not the entire one. Antibiotic resistance is probably ancient. 2 Researchers analysing 550

sediment samples obtained from deep below the earth’s surface at two sites in the USA found a diverse array of bacteria with resistance to 13 different antibiotics, and 90% of samples were resistant to at least one antibiotic. Perhaps most surprising, some of the bacterial strains were thought to be completely isolated from past human exposure, which raises the likelihood that they developed novel antibiotic resistance.2 In another study,3 30 000-year-old ice cores from the Beringian permafrost in Canada were collected. DNA segments from flora and fauna characteristic of the Arctic Pleistocene epoch were extracted and analysed. Metagenomic analysis revealed a highly diverse array of genes encoding resistance to multiple antibiotics such as β-lactams, tetracyclines, and glycopeptide antibiotics, including the VanA gene that confers the highest resistance to vancomycin.3 That antibiotic resistance pre-dates the anthropogenic antibiotic era might seem surprising, but it should not be. Bacteria are estimated to have originated more than 3·8 billion years ago, and antibiotics might be at least hundreds of millions of years old.4 In an effort to survive in competitive environments, bacteria and other pathogens have developed mechanisms to compete with other species, which include the production of antibiotics. As Howard and colleagues note,1 in one of history’s most famous examples, the mould Penicillium chrysogenum produces a substance that inhibits the growth of Gram-positive bacteria, which led to the discovery of the antibiotic penicillin.5 The widespread use of antibiotics has certainly accelerated the pace of antibiotic resistance that occurs naturally. The degree of resistance that exists, and the extensive head start that bacteria already have, increases the threat of antibiotic resistance even more. The pace of new antibiotic discovery and licensing has certainly

slowed in recent years, which threatens our ability in the future to fight off lifethreatening infections. But somewhere out there is probably a gene yet to be expressed that encodes a resistance mechanism to an antibiotic yet to be invented. Perhaps somewhere in the Beringian permafrost or the bathroom sink of a hospital near you… I declare no competing interests.

Jeffrey Jenks [email protected] University of California, San Diego Division of Infectious Diseases, La Jolla, CA 92093-0711, USA 1

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Howard SJ, Catchpole M, Watson J, Davies SC. Antibiotic resistance: global response needed. Lancet Infect Dis 2013; 13: 1001–03. Brown MG, Balkwill DL. Antibiotic resistance in bacteria isolated from the deep terrestrial subsurface. Microb Ecol 2009; 57: 484–93. D’Costa VM, King CE, Kalan L, et al. Antibiotic resistance is ancient. Nature 2011; 477: 457–61. Wright DG, Poinar H. Antibiotic resistance is ancient: implications for drug discovery. Trends Microbiol 2012; 20: 157–59. Rifkind D, Freeman G. The Nobel prize winning discoveries in infectious diseases. London: Academic Press, 2005.

We agree with Ramanan Laxminarayan and colleagues1 that antimicrobial resistance (AMR) in bacteria that cause community and health-careassociated infections (HAI) in lowincome countries poses a serious threat to global health. In the first 60 years of antibiotic use, resistance predominantly emerged from hospitals in highincome countries; now, health-care environments in low-income countries have also become an important crucible for the evolution of resistance. The increased resistance is eroding the effectiveness of local management strategies for life-threatening diseases such as pneumonia and meningitis. Increased interconnectedness means that resistance genes emerging in one place rapidly become a global threat. AMR and HAI are tightly related issues that are both poorly described in low-income settings, and basic data on the burden of disease are extremely scarce.2 The Global Burden of Disease studies have never estimated the effect of either HAI or AMR, but this is hardly surprising, in view of the www.thelancet.com/infection Vol 14 July 2014

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scarcity of primary data from lowincome countries, especially subSaharan Africa. For funding bodies and policy makers who use these estimates to guide allocation of scarce health resources, HAI and AMR in lowincome countries are therefore not just neglected diseases, but invisible ones. A large study of paediatric admissions at one hospital in rural Kenya between 2002 and 2009 estimated nosocomial bacteraemia to occur in six of 1000 admissions, with a very high associated mortality (53%).3 Deaths in this study were attributable, at least partly, to antimicrobial resistance. Based on these data, we estimated the disease-specific burden in sub-Saharan African children in 2005 by applying the admission rates,4 risk per admission, case-fatality ratio, and impact per case3 determined at this site for regional child population estimates.5 On the basis of these assessments, nosocomial bacteraemia could have accounted for 25 000 deaths and 270 000 additional inpatient days in African children in 2005. This approach has limitations; essentially, we multiplied the disease rate at a single site by the African child population, nonetheless, HAI and AMR contribute substantially to the morbidity and mortality burden in African children. Furthermore, detectable nosocomial bloodstream infections are merely the tip of the iceberg; most episodes of HAI are not bacteraemic, and the sensitivity of paediatric blood cultures is inherently poor. Results from studies in high-income countries show that HAI are usually preventable, and interventions are usually cost effective to implement and sustain. Health-care facilities in low-income countries face different challenges to infection control to those in high-income settings2— in low-income facilities, the effect of introducing infection control interventions largely remains to be determined. However, in view of the large size of this problem, and the affordability of interventions such as improved hand hygiene and surgical www.thelancet.com/infection Vol 14 July 2014

checklists, the gains could be high and hugely cost effective. A reduction in the amount of infections caused by antibiotic-resistant bacteria at their source would undoubtedly have measurable local and global health benefits. We declare no competing interests.

*Alexander M Aiken, Benedetta Allegranzi, J Anthony Scott, Shaheen Mehtar, Didier Pittet, Hajo Grundmann [email protected] London School of Hygiene and Tropical Medicine, WC1E 7HT, London, UK (AMA, JAS); Service Delivery and Safety, WHO, Geneva, Switzerland (BA); KEMRIWellcome Trust Research Programme, Kilifi, Kenya (JAS); Unit for Infection Prevention and Control, Division of Community Health, Faculty of Health Sciences, Stellenbosch University, Cape Town, South Africa (SM); Infection Control Program and WHO Collaborating Centre on Patient Safety, University of Geneva Hospitals and Faculty of Medicine, Geneva, Switzerland (DP); and Department of Medical Microbiology, University of Groningen, University Medical Centre, Groningen, Netherlands (HG) 1

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Laxminarayan R, Duse A, Wattal C, et al. Antibiotic resistance—the need for global solutions. Lancet Infect Dis 2013; 13: 1057–98. Allegranzi B, Bagheri Nejad S, Combescure C, et al. Burden of endemic health-careassociated infection in developing countries: systematic review and meta-analysis. Lancet 2011; 377: 228–41. Aiken AM, Mturi N, Njuguna P, et al. Risk and causes of paediatric hospital-acquired bacteraemia in Kilifi District Hospital, Kenya: a prospective cohort study. Lancet 2011; 378: 2021–27. Moisi JC, Gatakaa H, Berkley JA, et al. Excess child mortality after discharge from hospital in Kilifi, Kenya: a retrospective cohort analysis. Bull World Health Organ 2011; 89: 725–32. United Nations, Department of Economic and Social Affairs, Population Division, Population Estimates and Projections Section. World population prospects: the 2012 revision. http://esa.un.org/unpd/wpp/unpp/panel_ indicators.htm (accessed Feb 26, 2014).

Assessing the pandemic potential of emerging influenza Accurate identification of patients’ demo graphic charac teristics and case counts are key factors in understanding the pandemic potential of emerging influenza viruses, and the implementation of effective medical

surveillance and public health response actions. A recent Editorial in The Lancet Infectious Diseases1 contained an error about the provenance of the first human being with H5N1 avian influenza reported in the western hemisphere, and omitted key data from recent cases of H10N8 avian influenza in human beings in China. The first confirmed case of H5N1 detected in a human being in the Americas was in a woman, not a man—a hospital health-care worker who died around 1 week after her return to Canada from Beijing, China. The woman, who was travelling with a family member, experienced the first onset of symptoms during her return flight from Beijing to Canada on Dec 27, 2013. She was admitted to hospital on Jan 1, 2014, and died 2 days later on Jan 3.2,3 Local media reported that the woman was in her 20s, the age group at highest risk of death from H5N1.4 The Editorial cited a fatal case of H10N8 in December, 2013, in a man aged 75 years from China’s Jiangxi Province. However, two more cases, including a fatality, were reported from China’s Jiangxi Province between Jan 29, and Feb 13, 2013. The first additional case that ended in a fatality was in a woman aged 73 years, and the second case was a 55-year-old woman.5,6 These cases were detected through intensive ongoing surveillance for H7N9 cases in China, which have been most common in elderly people.4 The emergence and spread of new viruses should be tracked, and their pandemic potential predicted and countered more readily by the early identification of key, at-risk populations. The high variability of age and sex differences in morbidity and mortality rates from emerging zoonotic viruses, such as new coronaviruses and influenza viruses, can provide important indices of populations at highest risk of infection and death, and insights into potential mechanisms for transmission of these viruses to human beings, and between people. This information, 551

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