Meeting Abstract
When an animal’s immune system detects infection, it can kill the invading pathogen (resistance) or minimize per-pathogen reductions to host fitness (tolerance). Such responses not only have serious repercussions on individual health, but also impact the spread of disease through a population. While much research has focused on resistance, we understand little about the physiological causes or consequences of tolerance in wild animals. Finch mycoplasmosis is an infectious disease of North American songbirds caused by the bacterial pathogen, Mycoplasma gallisepticum (MG). It results in severe eye pathology, most striking in the house finch (Haemorhous mexicanus), that satisfies the cardinal signs of inflammation: swelling (tumor), erythema (rubor), heat (calor), and pain (dolor). Given the importance of inflammation in this disease, finch mycoplasmosis provides an ideal system to explore links among inflammation, tolerance, and pathogen transmission. Here, we report on two captive trials using non-steroidal anti-inflammatory drugs (NSAIDs) to dampen pro-inflammatory responses to MG infection. In our first study, 28 wild-caught, experimentally infected house finches were separated into three NSAID treatment groups: (1) no treatment, (2) oral meloxicam, and (3) topical flurbiprofen. Though both NSAIDs significantly enhanced tolerance, measured as the slope between peak pathology and peak pathogen load, flurbiprofen also enhanced resistance (i.e., reduced pathogen load). To test how tolerance changes infectiousness, we performed a transmission experiment comparing disease spread through flocks exposed to meloxicam-treated vs. wild-type birds experimentally infected with MG. We will discuss how these results link the mechanisms and consequences of tolerance in an ecologically relevant disease system.
