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Review
. 2015 Mar;23(3):172-80.
doi: 10.1016/j.tim.2014.12.004. Epub 2015 Jan 5.

Bats as 'special' reservoirs for emerging zoonotic pathogens

Cara E Brook  1 , Andrew P Dobson  2
Affiliations
Review

Bats as 'special' reservoirs for emerging zoonotic pathogens

Cara E Brook et al. Trends Microbiol. 2015 Mar.

Abstract

The ongoing West African Ebola epidemic highlights a recurring trend in the zoonotic emergence of virulent pathogens likely to come from bat reservoirs that has caused epidemiologists to ask 'Are bats special reservoirs for emerging zoonotic pathogens?' We collate evidence from the past decade to delineate mitochondrial mechanisms of bat physiology that have evolved to mitigate oxidative stress incurred during metabolically costly activities such as flight. We further describe how such mechanisms might have generated pleiotropic effects responsible for tumor mitigation and pathogen control in bat hosts. These synergisms may enable 'special' tolerance of intracellular pathogens in bat hosts; paradoxically, this may leave them more susceptible to immunopathological morbidity when attempting to clear extracellular infections such as 'white-nose syndrome' (WNS).

Keywords: Chiroptera; emerging zoonotic pathogens; immunological tolerance; immunopathology; reactive oxygen species.

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Figures

Figure 1
Figure 1
The vertebrate immune system. Pathways to humoral immunity include the innate complement response and the adaptive antibody response, while cell-mediated pathways necessitate action from innate effecter cells [i.e., phagocytes and natural killer (NK) cells] or adaptive T cells. Red arrows indicate possible host immune responses to infection with an intracellular pathogen (i.e., viruses, protozoa, and intracellular bacteria); blue arrows signify immunological pathways to clearance of extracellular pathogens (i.e., extracellular bacteria, fungi, and helminths). It should be noted that extracellular bacteria can also be cleared by the complement cascade.
Figure I
Figure I
Reactive oxygen species (ROS) levels can control cell fate. When low levels of ROS are produced, autophagic and mitophagic processes remove damaged mitochondria and allow cell survival (top). As ROS levels increase and cell repair systems fail, apoptotic cell death occurs (bottom). Adapted, with permission, from .
See this image and copyright information in PMC

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