Saigas on the brink: Multidisciplinary analysis of the factors influencing mass mortality events

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Science Advances  17 Jan 2018:
Vol. 4, no. 1, eaao2314
DOI: 10.1126/sciadv.aao2314

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  • Response to Viktor Müller comments – Researcher, Eötvös Loránd University, Budapest
    • Richard Anthony Kock, Professor Wildlife Health and Emerging Diseases, Royal Veterinary College London

    Response by Science Article authors Saiga on the Brink:

    Dear Victor and colleagues,

    Thank you for your keen interest in this subject.

    We agree with your suggestion that this is not a usual expression of opportunistic infection and we would propose that the event lies outside of biological norms, based on its synchronicity, rapid evolution in discrete populations, and occurring at a massive scale and wide spatial extent. The scenario is characterised by apparently independent events within and between herds, without a clear transmission between animals, suggesting a simple environment to host or environment to pathogen interaction, leading to rapid breach of the mucosal barrier by commensal organisms, alone. Followed by rapid bacteraemia and haemorrhagic septicaemia (HS) and death. There were no obvious signs of stress in the population in 2015, the saiga were mostly in good physical condition and showing no abnormal behaviours or stresses, up to the point of the organism invading. We have no evidence to support risk factors other than weather, such as, increased host susceptibilities or immune-suppression to explain this expression of HS, as suggested by the eletter authors and from literature on other species and domestic animals e.g. transit sickness. It is also worth mentioning that in many well-studied outbreaks and in reviews, the epidemiology of HS was reportedly unclear.

    The eletter authors suggests possible environmental contamination,...

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    Competing Interests: None declared.
  • RE: Saigas on the brink – a hypothetical mechanism
    • Viktor Müller, researcher, Eötvös Loránd University, Budapest
    • Other Contributors:
      • Lajos Rózsa, researcher, MTA-ELTE-MTM Ecology Research Group, Budapest
      • Péter Apari, PhD student, Eötvös Loránd University, Budapest

    The analysis of Kock and colleagues [1] strongly suggests that the observed mass mortality event (MME) occurred due to a combination of environmental stress and opportunistic (facultative) pathogens. While the exact mechanism of how these factors precipitated the MME is at present unknown, it is generally assumed that facultative pathogens like P. multocida are able to cause disease when the defense of the host is weakened (e.g., by environmental stress), i.e., the switch to pathogenicity is regulated by host factors only. We have formulated the alternative hypothesis of the ‘microbiome mutiny’, stating that the causative organisms might play a more active role than previously thought: some facultative pathogens might be able to detect the weakened status of the host, and actively switch to an exploitative high-virulence strategy when the host is about to die soon, anyway [2].

    We have recently argued that lethal sepsis caused by opportunistic pathogens might represent a special case of the ‘microbiome mutiny’: the systemic dissemination of the pathogen (which is the direct cause of sepsis and death) might seed the corpse with a high pathogen load and enable efficient cadaver-borne transmission [3]. Under this scenario, death by sepsis is not an ‘accidental’ by-product of the infection and a dead end for the pathogen; rather, it might be an efficient means of 'last-minute' transmission from an already ailing host (from which long-term low intensity transmi...

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    Competing Interests: None declared.

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