Abstract
Novel disease emergence is often associated with changes in pathogen traits that enable pathogen colonisation, persistence and transmission in the novel host environment. While understanding the mechanisms underlying disease emergence is likely to have critical implications for preventing infectious outbreaks, such knowledge is often based on studies of viral pathogens, despite the fact that bacterial pathogens may exhibit very different life histories. Here, we investigate the ability of epizootic outbreak strains of the bacterial pathogen, Mycoplasma gallisepticum, which jumped from poultry into North American house finches (Haemorhous mexicanus), to interact with model avian cells. We found that house finch epizootic outbreak strains of M. gallisepticum displayed a greater ability to adhere to, invade, persist within and exit from cultured chicken embryonic fibroblasts, than the reference virulent (R_low) and attenuated (R_high) poultry strains. Furthermore, unlike the poultry strains, the house finch epizootic outbreak strain HF_1994 displayed a striking lack of cytotoxicity, even exerting a cytoprotective effect on avian cells. Our results suggest that, at epizootic outbreak in house finches, M. gallisepticum was particularly adept at using the intra-cellular environment, which may have facilitated colonisation, dissemination and immune evasion within the novel finch host. Whether this high-invasion phenotype is similarly displayed in interactions with house finch cells, and whether it contributed to the success of the host shift, remains to be determined.
Highlights
Novel disease emergence is often associated with changes in pathogen traits that enable pathogen colonisation, persistence and transmission in the novel host environment
We used the qualitative differential immunofluorescence (DIF) assay, which allows the differential visualization of intra- and extra-cellular bacteria in infected avian cells
We used the quantitative gentamicin invasion assay, which is based on antibiotic treatment of infected avian cells to kill all the extra-cellular bacteria and thereby permits the detection of viable intra-cellular bacteria only[45,46]
Summary
Novel disease emergence is often associated with changes in pathogen traits that enable pathogen colonisation, persistence and transmission in the novel host environment. At epizootic outbreak in house finches, M. gallisepticum was adept at using the intra-cellular environment, which may have facilitated colonisation, dissemination and immune evasion within the novel finch host Whether this high-invasion phenotype is displayed in interactions with house finch cells, and whether it contributed to the success of the host shift, remains to be determined. While contact with the novel host is necessary for a jump to occur in the first place, the success of pathogen emergence relies on the pathogen’s ability to infect and transmit within the novel host species[3,4] For this reason, pathogen emergence is likely to be associated with changes at key cellular virulence mechanisms that facilitate tissue colonization and disease progression, including the adhesion, invasion of, replication within and exit from host cells and tissues[5,6]. Given that M. gallisepticum can invade a variety of avian and non-avian cells, such as chicken erythrocytes (both in vitro and in vivo)[23], erythroblasts[44], and embryonic fibroblasts[22], as well as human (HeLa)[22,44] and murine embryonic stem cells[44], its invasion mechanisms have a broad host range and our measures in DF-1 cells are likely to be indicative of ones occurring in avian cells more largely
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