Abstract
Bacterial infections are one of the major sources threatening public health. Pathogen host shifts – where a pathogen jumps from one host species to another – are important sources of emerging infectious diseases. Although viral pathogens are a major source of emerging infectious diseases, there is a growing focus on the emergence of novel bacterial infections through host shifts. However, compared to viruses, we know relatively little about the factors that determine whether a bacteria can infect a novel host, such as how host phylogenetics constrains variation in pathogen-host range and the link between host phylogeny and the infectivity and virulence of a pathogen. Here, we experimentally examined susceptibility to bacterial infections using a panel of 36 Drosophilidae species and four pathogens (Providencia rettgeri, Pseudomonas entomophila, Enterococcus faecalis, Staphylococcus aureus). The outcomes of infection differed greatly among pathogens and across host species. The host phylogeny explains a considerable amount of variation in susceptibility, with the greatest phylogenetic signal for P. rettgeri infection, with 94% of the variation in mortality being explained by the host phylogeny. Positive correlations were observed between mortality and bacterial load for three out of the four pathogens. Correlations in susceptibility between the four pathogens were positive but largely non-significant, suggesting susceptibility is mostly pathogen-specific. These results suggest that susceptibility to bacterial pathogens may be predicted by the host phylogeny, but the effect may vary in magnitude between different bacteria.
Author Summary Bacterial host shifts, where bacterial pathogens jump into and establish infection in a new host species, are an important source of emerging infectious diseases. Here, we use four bacterial pathogens to infect a panel of 36 species of fruit flies that shared a common ancestor ∼50 million years ago. We found large amounts of variation in susceptibility across host species to these bacterial pathogens. This variation is explained by the host phylogeny to varying degrees, with hosts clustering into clades with distinct levels of susceptibility. However, the magnitude of the effect varies between the four bacterial pathogens. For three out of the four pathogens tested mortality was correlated with bacterial load, suggesting it is a result of bacterial proliferation in the host. This work has important implications for our understanding of the emergence of bacterial pathogens, and to date there are few large-scale experimental studies of bacterial host shifts.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
Author information: Hongbo Sun* hs766{at}exeter.ac.uk, Mark A. Hanson m.hanson{at}exeter.ac.uk, Sarah K. Walsh Sarah.Walsh.2{at}glasgow.ac.uk, Ryan M. Imrie Ryan.Imrie{at}glasgow.ac.uk, Ben Raymond b.raymond{at}exeter.ac.uk, Ben Longdon b.longdon2{at}exeter.ac.uk
Title revised, minor revision on introduction, results and discussion, online repository updated.
