1. Epidemiology and Global Health
  2. Microbiology and Infectious Disease
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Poultry farmer response to disease outbreaks in smallholder farming systems in southern Vietnam

  1. Alexis Delabouglise  Is a corresponding author
  2. Nguyen Thi Le Thanh
  3. Huynh Thi Ai Xuyen
  4. Benjamin Nguyen-Van-Yen
  5. Phung Ngoc Tuyet
  6. Ha Minh Lam
  7. Maciej F Boni
  1. CIRAD, France
  2. Wellcome Trust Major Overseas Programme, Oxford University Clinical Research Unit, Viet Nam
  3. Ca Mau sub-Department of Livestock Production and Animal Health, Viet Nam
  4. Ecole Normale Superieure, France
  5. Pennsylvania State University, United States
Research Article
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Cite this article as: eLife 2020;9:e59212 doi: 10.7554/eLife.59212

Abstract

Avian influenza outbreaks have been occurring on smallholder poultry farms in Asia for two decades. Farmer responses to these outbreaks can slow down or accelerate virus transmission. We used a longitudinal survey of 53 small-scale chicken farms in southern Vietnam to investigate the impact of outbreaks with disease-induced mortality on harvest rate, vaccination, and disinfection behaviors. We found that in small broiler flocks (≤16 birds/flock) the estimated probability of harvest was 56% higher when an outbreak occurred, and 214% higher if an outbreak with sudden deaths occurred in the same month. Vaccination and disinfection were strongly and positively correlated with the number of birds. Small-scale farmers – the overwhelming majority of poultry producers in low-income countries – tend to rely on rapid sale of birds to mitigate losses from diseases. As depopulated birds are sent to markets or trading networks, this reactive behavior has the potential to enhance onward transmission.

Data availability

The study dataset is available online at the Open Science Framework, https://osf.io/ws3vu/.

The following data sets were generated

Article and author information

Author details

  1. Alexis Delabouglise

    ASTRE, CIRAD, Montpellier, France
    For correspondence
    alexis.delabouglise@gmail.com
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-5837-7052
  2. Nguyen Thi Le Thanh

    Wellcome Trust Major Overseas Programme, Oxford University Clinical Research Unit, Ho Chi Minh City, Viet Nam
    Competing interests
    The authors declare that no competing interests exist.
  3. Huynh Thi Ai Xuyen

    Ca Mau sub-Department of Livestock Production and Animal Health, Ca Mau, Viet Nam
    Competing interests
    The authors declare that no competing interests exist.
  4. Benjamin Nguyen-Van-Yen

    CNRS UMR 8197, Ecole Normale Superieure, Paris, France
    Competing interests
    The authors declare that no competing interests exist.
  5. Phung Ngoc Tuyet

    Ca Mau sub-Department of Livestock Production and Animal Health, Ca Mau, Viet Nam
    Competing interests
    The authors declare that no competing interests exist.
  6. Ha Minh Lam

    Wellcome Trust Major Overseas Programme, Oxford University Clinical Research Unit, Ho Chi Minh City, Viet Nam
    Competing interests
    The authors declare that no competing interests exist.
  7. Maciej F Boni

    Center for Infectious Diseases Dynamics, Pennsylvania State University, University Park, United States
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-0830-9630

Funding

Wellcome (098511/Z/12/Z)

  • Maciej F Boni

Defense Threat Reduction Agency

  • Maciej F Boni

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Ethics

Human subjects: The research collaboration was approved by the Hospital for Tropical Diseases in Ho Chi Minh City, and the study design was approved by the Ca Mau sub-Department of Livestock Production and Animal Health. The Ca Mau sub-Department of Livestock Production and Animal Health (CM-LPAH) specifically approved this study and is equivalent to an Animal Care and Use Committee that approves studies like this in Vietnam. CM-LPAH approved the publication of these results. No consenting process was required as the study involved no human biological samples, no patients, and no personal or identifiable information. The IRB that made this determination was the Hospital for Tropical Diseases Scientific and Ethical Committee (Ho Chi Minh City).

Reviewing Editor

  1. Joshua T Schiffer, Fred Hutchinson Cancer Research Center, United States

Publication history

  1. Received: May 22, 2020
  2. Accepted: August 21, 2020
  3. Accepted Manuscript published: August 25, 2020 (version 1)
  4. Version of Record published: September 21, 2020 (version 2)

Copyright

© 2020, Delabouglise et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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Further reading

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    David R M Smith et al.
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    The human microbiome can protect against colonization with pathogenic antibiotic-resistant bacteria (ARB), but its impacts on the spread of antibiotic resistance are poorly understood. We propose a mathematical modelling framework for ARB epidemiology formalizing within-host ARB-microbiome competition, and impacts of antibiotic consumption on microbiome function. Applied to the healthcare setting, we demonstrate a trade-off whereby antibiotics simultaneously clear bacterial pathogens and increase host susceptibility to their colonization, and compare this framework with a traditional strain-based approach. At the population level, microbiome interactions drive ARB incidence, but not resistance rates, reflecting distinct epidemiological relevance of different forces of competition. Simulating a range of public health interventions (contact precautions, antibiotic stewardship, microbiome recovery therapy) and pathogens (Clostridioides difficile, methicillin-resistant Staphylococcus aureus, multidrug-resistant Enterobacteriaceae) highlights how species-specific within-host ecological interactions drive intervention efficacy. We find limited impact of contact precautions for Enterobacteriaceae prevention, and a promising role for microbiome-targeted interventions to limit ARB spread.

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    Jiahui Si et al.
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    Background: Identifying environmentally responsive genetic loci where DNA methylation is associated with coronary heart disease (CHD) may reveal novel pathways or therapeutic targets for CHD. We conducted the first prospective epigenome-wide analysis of DNA methylation in relation to incident CHD in the Asian population.

    Methods: We did a nested case-control study comprising incident CHD cases and 1:1 matched controls who were identified from the 10-year follow-up of the China Kadoorie Biobank. Methylation level of baseline blood leukocyte DNA was measured by Infinium Methylation EPIC BeadChip. We performed the single cytosine-phosphate-guanine (CpG) site association analysis and network approach to identify CHD-associated CpG sites and co-methylation gene module.

    Results: After quality control, 982 participants (mean age 50.1 years) were retained. Methylation level at 25 CpG sites across the genome was associated with incident CHD (genome-wide false discovery rate [FDR] < 0.05 or module-specific FDR <0.01). One SD increase in methylation level of identified CpGs was associated with differences in CHD risk, ranging from a 47% decrease to a 118% increase. Mediation analyses revealed 28.5% of the excessed CHD risk associated with smoking was mediated by methylation level at the promoter region of ANKS1A gene (P for mediation effect = 0.036). Methylation level at the promoter region of SNX30 was associated with blood pressure and subsequent risk of CHD, with the mediating proportion to be 7.7% (P = 0.003) via systolic blood pressure and 6.4% (P = 0.006) via diastolic blood pressure. Network analysis revealed a co-methylation module associated with CHD.

    Conclusions: We identified novel blood methylation alterations associated with incident CHD in the Asian population and provided evidence of the possible role of epigenetic regulations in the smoking- and BP-related pathways to CHD risk.

    Funding: This work was supported by National Natural Science Foundation of China (81390544 and 91846303). The CKB baseline survey and the first re-survey were supported by a grant from the Kadoorie Charitable Foundation in Hong Kong. The long-term follow-up is supported by grants from the UK Wellcome Trust (202922/Z/16/Z, 088158/Z/09/Z, 104085/Z/14/Z), grant (2016YFC0900500, 2016YFC0900501, 2016YFC0900504, 2016YFC1303904) from the National Key and Program of China, and Chinese Ministry of Science and Technology (2011BAI09B01).