Co-circulation of genetically distinct highly pathogenic #avian #influenza A clade 2.3.4.4 (#H5N6) viruses in wild #waterfowl and #poultry in #Europe and East #Asia, 2017-18 (Virus Evol., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Virus Evol. 2019 Apr 22;5(1):vez004. doi: 10.1093/ve/vez004. eCollection 2019 Jan.

Co-circulation of genetically distinct highly pathogenic avian influenza A clade 2.3.4.4 (H5N6) viruses in wild waterfowl and poultry in Europe and East Asia, 2017-18.

Poen MJ1, Venkatesh D2, Bestebroer TM1, Vuong O1, Scheuer RD1, Oude Munnink BB1, de Meulder D1, Richard M1, Kuiken T1, Koopmans MPG1, Kelder L3, Kim YJ4, Lee YJ4, Steensels M5, Lambrecht B5, Dan A6, Pohlmann A7, Beer M7, Savic V8, Brown IH9, Fouchier RAM1, Lewis NS9,10.

Author information: 1 Department of Viroscience, Erasmus MC, Rotterdam, the Netherlands. 2 Department of Zoology, University of Cambridge, Cambridge CB2 3EJ, UK. 3 Staatsbosbeheer, Amersfoort, the Netherlands. 4 Avian Influenza Research and Diagnostic Division, Animal and Plant Quarantine Agency, Republic of Korea. 5 Avian Virology and Immunology, Sciensano, Brussels, Belgium. 6 Veterinary Diagnostics Directorate, Budapest, Hungary. 7 Institute of Diagnostic Virology, Friedrich-Loeffler-Institut, Insel Riems, Germany. 8 Croatian Veterinary Institute, Zagreb, Croatia. 9 OIE/FAO/EURL International Reference Laboratory for Avian Influenza, Swine Influenza and Newcastle Disease, Animal and Plant Health Agency (APHA)-Weybridge, Addlestone, Surrey, UK. 10 Department of Pathobiology and Population Sciences, Royal Veterinary College, Hawkshead Lane, North Mymms, Hatfield, Hertfordshire, AL9 7TA, UK.

 

Abstract

Highly pathogenic avian influenza (HPAI) H5 clade 2.3.4.4 viruses were first introduced into Europe in late 2014 and re-introduced in late 2016, following detections in Asia and Russia. In contrast to the 2014-15 H5N8 wave, there was substantial local virus amplification in wild birds in Europe in 2016-17 and associated wild bird mortality, with evidence for occasional gene exchange with low pathogenic avian influenza (LPAI) viruses. Since December 2017, several European countries have again reported events or outbreaks with HPAI H5N6 reassortant viruses in both wild birds and poultry, respectively. Previous phylogenetic studies have shown that the two earliest incursions of HPAI H5N8 viruses originated in Southeast Asia and subsequently spread to Europe. In contrast, this study indicates that recent HPAI H5N6 viruses evolved from the H5N8 2016-17 viruses during 2017 by reassortment of a European HPAI H5N8 virus and wild host reservoir LPAI viruses. The genetic and phenotypic differences between these outbreaks and the continuing detections of HPAI viruses in Europe are a cause of concern for both animal and human health. The current co-circulation of potentially zoonotic HPAI and LPAI virus strains in Asia warrants the determination of drivers responsible for the global spread of Asian lineage viruses and the potential threat they pose to public health.

KEYWORDS: H5N6; avian influenza; emerging diseases; highly pathogenic avian influenza; phylogeny; virology

PMID: 31024736 PMCID: PMC6476160 DOI: 10.1093/ve/vez004

Keywords: Avian Influenza; H5N6; H5N8; Reassortant Strain; Poultry; Wild Birds; European Region; Asia Region.

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#Equine #influenza virus in #Asia: phylogeographic pattern and molecular features revealed the circulation of an autochthonous lineage (J Virol., abstract)

[Source: Journal of Virology, full page: (LINK). Abstract, edited.]

Equine influenza virus in Asia: phylogeographic pattern and molecular features revealed the circulation of an autochthonous lineage

Samuel Miño, Laura Mojsiejczuk, Wei Guo, Haili Zhang, Ting Qi, Cheng Du, Xiang Zhang, Jingfei Wang, Rodolfo Campos, Xiaojun Wang

DOI: 10.1128/JVI.00116-19

 

ABSTRACT

Equine influenza virus (EIV) causes severe acute respiratory disease in horses. Currently, the strains belonging to the H3N8 genotype are divided into two clades, Florida clade 1 (FC1) and Florida clade 2 (FC2) which emerged in 2002. Both FC1and FC2 clades were reported in Asian and Middle East countries in the last decade. In this study, we described the evolution, epidemiology and molecular characteristic of the EIV lineages, with focus on those detected in Asia from 2007 to 2017. The full genome phylogeny showed that FC1 and FC2 constituted separated and divergent lineages, without evidence of reassortment between the clades. While FC1 evolved as a single lineage, the FC2 showed a divergent event around 2004 giving rise to two well supported and coexisting sub-lineages, European and Asian. Furthermore, two different spread patterns of EIV in Asian countries were identified. The FC1 outbreaks were caused by independent introductions of EIV from the Americas, being the Asian isolates genetically similar to the contemporary American lineages. On the other hand, the FC2 strains detected in Asian mainland countries conformed an autochthonous monophyletic group with a common ancestor dated in 2006 and showed evidence of an endemic circulation in local host. Characteristic aminoacidic signature patterns were detected in all viral proteins in both Asian-FC1 and FC2 populations. Several changes were located at the top of the HA1 protein, inside or near to antigenic sites. Further studies are needed to assess the potential impact of these antigenic changes in vaccination programs.

 

IMPORTANCE

The complex and continuous antigenic evolution of EIVs remains a major hurdle for vaccine development and the design of effective immunization programs. The present study provides a comprehensive analysis showing the EIV evolutionary dynamics, including the spread and circulation within the Asian continent and its relationship to global EIV populations over a 10-year period. Moreover, we provide a better understanding of EIV molecular evolution in Asian countries and its consequences on the antigenicity. The study underscores the association between the global horse movement and the circulation of EIV in this region. Understanding EIV evolution is imperative in order to mitigate the risk of outbreaks affecting horse industry and to help with the selection of the viral strains to be included in the formulation of future vaccines.

Copyright © 2019 American Society for Microbiology. All Rights Reserved.

Keywords: Equine Influenza; Horses; Asia Region.

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Acquisition and Loss of #CTX-M-Producing and Non-Producing #Escherichia coli in the Fecal #Microbiome of #Travelers to South #Asia (mBio, abstract)

[Source: mBio, full page: (LINK). Abstract, edited.]

Acquisition and Loss of CTX-M-Producing and Non-Producing Escherichia coli in the Fecal Microbiome of Travelers to South Asia

Edward R. Bevan, Alan McNally, Christopher M. Thomas, Laura J. V. Piddock, Peter M. Hawkey

George A. Jacoby, Editor

DOI: 10.1128/mBio.02408-18

 

ABSTRACT

Over 80% of travelers from the United Kingdom to the Indian subcontinent acquire CTX-M-producing Escherichia coli (CTX-M-EC), but the mechanism of CTX-M-EC acquisition is poorly understood. We aimed to investigate the dynamics of CTX-M-EC acquisition in healthy travelers and how this relates to populations of non-CTX-M-EC in the fecal microbiome. This is a prospective observational study of healthy volunteers traveling from the United Kingdom to South Asia. Fecal samples were collected pre- and post-travel at several time points up to 12 months post-travel. A toothpicking experiment was used to determine the proportion of cephalosporin-sensitive E. coli in fecal samples containing CTX-M-EC. MLST and SNP type of pre-travel and post-travel E. coli were deduced by WGS. CTX-M-EC was acquired by 89% (16/18) of volunteers. Polyclonal acquisition of CTX-M-EC was seen in 8/15 volunteers (all had >3 STs across post-travel samples), suggesting multiple acquisition events. Indistinguishable CTX-M-EC clones (zero SNPs apart) are detectable in serial fecal samples up to 7 months after travel, indicating stable maintenance in the fecal microbiome on return to the United Kingdom in the absence of selective pressure. CTX-M-EC-containing samples were often co-colonized with novel, non-CTX-M strains after travel, indicating that acquisition of non-CTX-M-EC occurs alongside CTX-M-EC. The same pre-travel non-CTX-M strains (<10 SNPs apart) were found in post-travel fecal samples after CTX-M-EC had been lost, suggesting return of the fecal microbiome to the pre-travel state and long-term persistence of minority strains in travelers who acquire CTX-M-EC.

 

IMPORTANCE

Escherichia coli strains which produce CTX-M extended-spectrum beta-lactamases are endemic as colonizers of humans and in the environment in South Asia. This study demonstrates that acquisition of CTX-M-producing E. coli (CTX-M-EC) in travelers from the United Kingdom to South Asia is polyclonal, which is likely due to multiple acquisition events from contaminated food and drinking water during travel. CTX-M-EC frequently persists in the fecal microbiome for at least 1 year after acquisition, often alongside newly acquired non-CTX-M E. coli strains. In travelers who acquire CTX-M-EC, pre-travel non-CTX-M E. coli remains as a minority population in the gut until the CTX-M-EC strains are lost. The non-CTX-M strains are then reestablished as the predominant E. coli population. This study has shed light on the dynamics of CTX-M-EC acquisition, colonization, and loss after travel. Future work involving manipulation of nonvirulent resident E. coli could be used to prevent colonization with antibiotic-resistant E. coli.

Keywords: Antibiotics; Drugs Resistance; Cephalosporins; E. Coli; UK; Asian region.

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#Prevalence of pretreatment #HIV #drug #resistance in West #African and Southeast #Asian countries (J Antimicrob Chemother., abstract)

[Source: Journal of Antimicrobial Chemotherapy, full page: (LINK). Abstract, edited.]

Prevalence of pretreatment HIV drug resistance in West African and Southeast Asian countries

Nicole Ngo-Giang-Huong Thu, H K Huynh, Anoumou Y Dagnra, Thomas-d’Aquin Toni, Almoustapha I Maiga, Dramane Kania, Sabrina Eymard-Duvernay, Martine Peeters, Cathia Soulie, Gilles Peytavin, Claire Rekacewicz, Marie-Laure Chaix, Avelin F Aghokeng, ANRS 12333 Study Group

Journal of Antimicrobial Chemotherapy, dky443, https://doi.org/10.1093/jac/dky443

Published: 12 November 2018

 

Abstract

Background

ART in the developing world has moved to a new era with the WHO recommendation to test and immediately treat HIV-positive individuals. A high frequency of pretreatment HIV drug resistance (PDR) can compromise ART efficacy. Our study presents updated estimates of PDR in seven countries from West Africa (Burkina Faso, Cameroon, Côte d’Ivoire, Mali and Togo) and Southeast Asia (Thailand and Vietnam).

Methods

Eligible study participants were adult ART initiators, recruited from December 2015 to November 2016 in major ART clinics in each country. HIV drug resistance (HIVDR) tests were performed for all specimens and interpretation was done using the Stanford algorithm.

Results

Overall, 1153 participants were recruited and 1020 nt sequences were generated. PDR frequency among all initiators was 15.9% (95% CI: 13.8%–18.3%) overall, ranging from 9.6% and 10.2% in Burkina Faso and Thailand, respectively, 14.7% in Vietnam, 15.4% in Mali, 16.5% in Côte d’Ivoire and 19.3% in Cameroon, to 24.6% in Togo. The prevalence of NNRTI resistance mutations was 12%; NRTI and PI PDR prevalences were 4% and 3%, respectively.

Conclusions

Our study shows that in most countries PDR exceeded 10%, warranting the conduct of nationally representative surveys to confirm this trend. In the meantime, actions to prevent drug resistance, including transition from NNRTIs to more robust drug classes should be urgently implemented.

Issue Section: ORIGINAL RESEARCH

Keywords: HIV/AIDS; Antivirals; Drugs Resistance; West Africa; Asian Region.

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#Threats of #Zika virus #transmission for #Asia and its Hindu-Kush #Himalayan region (Infect Dis Poverty., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Infect Dis Poverty. 2018 May 15;7(1):40. doi: 10.1186/s40249-018-0426-3.

Threats of Zika virus transmission for Asia and its Hindu-Kush Himalayan region.

Dhimal M1,2, Dahal S3, Dhimal ML4,5, Mishra SR6, Karki KB3, Aryal KK3, Haque U7, Kabir MI8, Guin P9,10, Butt AM11, Harapan H12, Liu QY13, Chu C14, Montag D15, Groneberg DA4, Pandey BD16, Kuch U4, Müller R4.

Author information: 1 Nepal Health Research Council (NHRC), Ramshah Path, Kathmandu, Nepal. meghdhimal@gmail.com. 2 Institute of Occupational Medicine, Social Medicine and Environmental Medicine, Goethe University, Frankfurt am Main, Germany. meghdhimal@gmail.com. 3 Nepal Health Research Council (NHRC), Ramshah Path, Kathmandu, Nepal. 4 Institute of Occupational Medicine, Social Medicine and Environmental Medicine, Goethe University, Frankfurt am Main, Germany. 5 Faculty of Social Sciences, Goethe University, Frankfurt am Main, Germany. 6 The University of Queensland, Brisbane, Australia. 7 Department of Public Health, Baldwin Wallace University, Berea, Ohio, USA. 8 Department of Epidemiology, National Institute of Preventive and Social Medicine, Ministry of Health and Family Welfare, Dhaka, Bangladesh. 9 Public Health Foundation of India, Gurgaon, Haryana, India. 10 Centre for Environmental Health, Gurgaon, Haryana, India. 11 Translational Genomics Laboratory, Department of Biosciences, COMSATS Institute of Information Technology (CIIT), Islamabad, 45550, Pakistan. 12 Medical Research Unit, School of Medicine, Syiah Kuala University, Banda Aceh, Indonesia. 13 WHO Collaborating Centre for Vector Surveillance and Management, SKLID, CCID, ICDC, China CDC, Beijing, China. 14 Centre for Environment and Population Health, Griffith University, Nathan, Queensland, Australia. 15 Barts and the London School of Medicine, Centre for Primary Care and Public Health, Queen Mary University of London, London, UK. 16 Department of Health Services, Ministry of Health, Government of Nepal, Kathmandu, Nepal.

 

Abstract

Asia and its Hindu Kush Himalayan (HKH) region is particularly vulnerable to environmental change, especially climate and land use changes further influenced by rapid population growth, high level of poverty and unsustainable development. Asia has been a hotspot of dengue fever and chikungunya mainly due to its dense human population, unplanned urbanization and poverty. In an urban cycle, dengue virus (DENV) and chikungunya virus (CHIKV) are transmitted by Aedes aegypti and Ae. albopictus mosquitoes which are also competent vectors of Zika virus (ZIKV). Over the last decade, DENV and CHIKV transmissions by Ae. aegypti have extended to the Himalayan countries of Bhutan and Nepal and ZIKV could follow in the footsteps of these viruses in the HKH region. The already established distribution of human-biting Aedes mosquito vectors and a naïve population with lack of immunity against ZIKV places the HKH region at a higher risk of ZIKV. Some of the countries in the HKH region have already reported ZIKV cases. We have documented an increasing threat of ZIKV in Asia and its HKH region because of the high abundance and wide distribution of human-biting mosquito vectors, climate change, poverty, report of indigenous cases in the region, increasing numbers of imported cases and a naïve population with lack of immunity against ZIKV. An outbreak anywhere is potentially a threat everywhere. Therefore, in order to ensure international health security, all efforts to prevent, detect, and respond to ZIKV ought to be intensified now in Asia and its HKH region. To prepare for possible ZIKV outbreaks, Asia and the HKH region can also learn from the success stories and strategies adopted by other regions and countries in preventing ZIKV and associated complications. The future control strategies for DENV, CHIKV and ZIKV should be considered in tandem with the threat to human well-being that is posed by other emerging and re-emerging vector-borne and zoonotic diseases, and by the continuing urgent need to strengthen public primary healthcare systems in the region.

KEYWORDS: Aedes aegypti; Aedes albopictus; Chikungunya virus; Dengue virus; Hindu Kush Himalayas; Mountain; Poverty, Zika virus

PMID: 29759076 DOI: 10.1186/s40249-018-0426-3

Keywords: Arbovirus; Dengue Fever; Chikungunya Fever; Zika Virus; Mosquitoes; Asia Region; Aedes spp.

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#Origins of the current #outbreak of #MDR #malaria in southeast #Asia: a retrospective genetic study (Lancet Infect Dis., abstract)

[Source: The Lancet Infectious Diseases, full page: (LINK). Abstract, edited.]

Origins of the current outbreak of multidrug-resistant malaria in southeast Asia: a retrospective genetic study

Roberto Amato, PhD, Richard D Pearson, PhD, Jacob Almagro-Garcia, PhD, Chanaki Amaratunga, PhD, Pharath Lim, MD, Seila Suon, MD, Sokunthea Sreng, Eleanor Drury, Sc, Jim Stalker, MA, Olivo Miotto, PhD, Rick M Fairhurst, MD, Prof Dominic P Kwiatkowski, FRCP

Published: 01 February 2018 / Open Access / DOI: https://doi.org/10.1016/S1473-3099(18)30068-9

© 2018 The Author(s). Published by Elsevier Ltd.

 

Summary

Background

Antimalarial resistance is rapidly spreading across parts of southeast Asia where dihydroartemisinin–piperaquine is used as first-line treatment for Plasmodium falciparum malaria. The first published reports about resistance to antimalarial drugs came from western Cambodia in 2013. Here, we analyse genetic changes in the P falciparum population of western Cambodia in the 6 years before those reports.

Methods

We analysed genome sequence data on 1492 P falciparum samples from 11 locations across southeast Asia, including 464 samples collected in western Cambodia between 2007 and 2013. Different epidemiological origins of resistance were identified by haplotypic analysis of the kelch13artemisinin resistance locus and the plasmepsin 2–3 piperaquine resistance locus.

Findings

We identified more than 30 independent origins of artemisinin resistance, of which the KEL1 lineage accounted for 140 (91%) of 154 parasites resistant to dihydroartemisinin–piperaquine. In 2008, KEL1 combined with PLA1, the major lineage associated with piperaquine resistance. By 2013, the KEL1/PLA1 co-lineage had reached a frequency of 63% (24/38) in western Cambodia and had spread to northern Cambodia.

Interpretation

The KEL1/PLA1 co-lineage emerged in the same year that dihydroartemisinin–piperaquine became the first-line antimalarial drug in western Cambodia and spread rapidly thereafter, displacing other artemisinin-resistant parasite lineages. These findings have important implications for management of the global health risk associated with the current outbreak of multidrug-resistant malaria in southeast Asia.

Funding

Wellcome Trust, Bill & Melinda Gates Foundation, Medical Research Council, UK Department for International Development, and the Intramural Research Program of the National Institute of Allergy and Infectious Diseases.

Keywords: Malaria; Asia Region; Antibiotics; Drugs Resistance; Artemisin; Piperaquine.

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#Azithromycin #resistance in #Shigella spp. in Southeast #Asia (Antimicrob Agents Chemother., abstract)

[Source: Antimicrobial Agents and Chemotherapy, full page: (LINK). Abstract, edited.]

Azithromycin resistance in Shigella spp. in Southeast Asia

Thomas C Darton1,2,  Ha Thanh Tuyen1,  Hao Chung The1,  Paul N Newton3,4, David A. B. Dance3,4,5,  Rattanaphone Phetsouvanh3,  Viengmon Davong3, James I Campbell1,  Nguyen Van Minh Hoang1,  Guy E Thwaites1,4, Christopher M Parry6,7,  Duy Pham Thanh1 and  Stephen Baker1,4,8*

Author Affiliations: 1 The Hospital for Tropical Diseases, Wellcome Trust Major Overseas Programme, Oxford University Clinical Research Unit, Ho Chi Minh City, Vietnam; 2 Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield Medical School, Sheffield, United Kingdom; 3 Lao-Oxford-Mahosot Hospital-Wellcome Trust Research Unit, Vientiane, Laos; 4 Centre for Tropical Medicine, Nuffield Department of Clinical Medicine, Oxford University, Oxford, United Kingdom; 5 Faculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom; 6 Clinical Sciences, Liverpool School of Tropical Medicine, Liverpool, United Kingdom; 7 School of Tropical Medicine and Global Health, Nagasaki University, Japan; 8 The Department of Medicine, The University of Cambridge, Cambridge, United Kingdom

 

ABSTRACT

Infection by Shigella spp. is a common cause of dysentery in Southeast Asia. Antimicrobials are thought to be beneficial for treatment, however antimicrobial resistance in Shigella spp. is becoming widespread. We aimed to assess the frequency and mechanisms associated with decreased susceptibility to azithromycin in Southeast Asian Shigella isolates and use these data to assess appropriate susceptibility breakpoints. Shigella isolated in Vietnam and Laos were screened for susceptibility against azithromycin (15μg) by disc diffusion and minimum inhibitory concentration (MIC). Phenotypic resistance was confirmed by PCR amplification of macrolide resistance loci. We compared the genetic relationships and plasmid contents of azithromycin resistant S. sonnei using whole genome sequences. From 475 available Shigella spp. isolated in Vietnam and Laos between 1994 and 2012, 6/181 S. flexneri (3.3%, MIC≥16g/L) and 16/294 S. sonnei (5.4%, MIC≥32g/L) were phenotypically resistant to azithromycin. PCR amplification confirmed a resistance mechanism in 22/475 (4.6%) isolates (19 mphA and 3 ermB). Susceptibility data demonstrated the acceptability of S. flexneri(MIC≥16g/L, zone≤15mm) and S. sonnei (MIC≥32g/L, zone≤11mm) breakpoints with <3% discrepancy. Phylogenetic analysis demonstrated that decreased susceptibility has arisen sporadically in Vietnamese S. sonnei on at least seven occasions between 2000 and 2009, but failed to become established. While the proposed susceptibility breakpoints may allow better recognition of resistant isolates, additional studies are required to assess the impact on clinical outcome. The potential emergence of azithromycin resistance highlights the need for alternative management options for Shigella infections in endemic countries.

 

FOOTNOTES

*Corresponding author: Professor Stephen Baker, the Hospital for Tropical Diseases, 764 Vo Van Kiet, Quan 5, Ho Chi Minh City, Vietnam. Tel: +84 89241761 Fax: +84 89238904 sbaker@oucru.org

Copyright © 2018 Darton et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.

Keywords: Antibiotics; Drugs Resistance; Shigella spp.; Azithromycin; Asian Region.

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