In the majority of our experimental infections, a subset of the hosts succumb to infection while the remaining proportion survives. The individuals that die from infection typically do so with infection burdens that reach 100 million bacteria per individual fly. One surprising observation, though, is that D. melanogaster which survive our experimental bacterial infections rarely clear their pathogens. Instead, the infections stabilize after approximately two days and become largely asymptomatic, in some cases despite the continued presence of more than 10,000 bacterial cells circulating in the fly. We initially observed this behavior with Providencia rettgeri infections and we have since confirmed it after infection by a broad range of unrelated bacterial species. These chronic infections are remarkably stable over the lifetime of the host and cause no substantial decrease in lifespan or fecundity under laboratory rearing conditions. The host immune system remains upregulated in response to the infection but is ineffective at eliminating it. Our team is currently trying to understand how these chronic infections become established, why the bacteria become impervious to host immunity, and why there is so little associated pathology. We are using genetic and transcriptomic approaches on both the fly and the microbe to try to determine what changes occur in the bacteria during the transition from acute to chronic infection, and whether the switch from a lethal to a chronic trajectory is driven by the bacteria, the host, or an interaction between the two.

Although we were initially surprised at the ubiquity of chronic infections, we subsequently realized that nearly all of the bacteria that we regularly work with were originally isolated as infections of field-captured D. melanogaster. That collection would almost certainly be enriched for bacteria that are capable of establishing persistent infections with minimal adverse effects. Nevertheless, the observation that so many diverse bacteria are capable of establishing qualitatively similar infections raises questions of how they do it, whether they all do it the same way, and whether they do it the same way in different hosts.