Consequences of chronic bacterial infection in Drosophila melanogaster

Abstract

Even when successfully surviving an infection, a host often fails to eliminate a pathogen completely and may sustain substantial pathogen burden for the remainder of its life. Using systemic bacterial infection in Drosophila melanogaster, we characterize chronic infection by three bacterial species from different genera - Providencia rettgeri, Serratia marcescens, and Enterococcus faecalis–following inoculation with a range of doses. To assess the consequences of these chronic infections, we determined the expression of antimicrobial peptide genes, survival of secondary infection, and starvation resistance after one week of infection. While higher infectious doses unsurprisingly lead to higher risk of death, they also result in higher chronic bacterial loads among the survivors for all three infections. All three chronic infections caused significantly elevated expression of antimicrobial peptide genes at one week post-infection and provided generalized protection again secondary bacterial infection. Only P. rettgeri infection significantly influenced resistance to starvation, with persistently infected flies dying more quickly under starvation conditions relative to controls. These results suggest that there is potentially a generalized mechanism of protection against secondary infection, but that other impacts on host physiology may depend on the specific pathogen. We propose that chronic infections in D. melanogaster could be a valuable tool for studying tolerance of infection, including impacts on host physiology and behavior.

The Genetic Basis of Natural Variation in Drosophila melanogaster Immune Defense against Enterococcus faecalis

“…This could explain why one of the main classes of immune response genes in Drosophila, the antimicrobial peptides, are thought to have rather broad-spectrum activities [45,46] rather than targeting specific pathogens [22,47]. It has recently been shown that infection with E. faecalis elicits lower AMP induction than other pathogens in Drosophila when infected at low dose [31]. Beyond broad-spectrum protective immune genes however, it may be that other genes have evolved to respond to specific pathogen threats.…”

“…Vials were then stored in an incubator at 22 • C on a 12 h day/night cycle. The number of surviving individuals was recorded five days after treatment, which is a reasonable proxy of infection outcome because numerous Drosophila infection studies have shown that flies tend to either die of infection within 48 h or survive beyond seven days, e.g., [22,31,32]. We found that DGRP line DGRP_321 was an extreme outlier in that most individuals died shortly after infection.…”

Common structuring principles of the Drosophila melanogaster microbiome on a continental scale and between host and substrate

“…Furthermore, in a systemic infection, pathogens can reach high titers of millions of bacteria before the fly dies (Galac and Lazzaro, 2011;Duneau et al, 2017). Finally, flies that survive systemic infections often continue to carry chronic infections with pathogen loads that can be in the range of tens of thousands of live bacteria with little effect on their lifespan (Chambers et al, 2014(Chambers et al, , 2019Duneau et al, 2017).…”

Ecological Factors Mediate Immunity and Parasitic Co-Infection in Sea Fan Octocorals

“…We first illustrate that sea fans exhibit altered expression of immune genes during infection with both parasites in the lab. The pre-existing nature of copepod infections could account for the increased amoebocyte densities relative to Aspergillus treatments, as chronic infections can lead to immune suppression or induction ( 70 , 71 ). However, the field survey provides additional support for an asymmetric response because amoebocyte density was elevated in existing copepod infections and not in existing fungal infections.…”