Parasitic infection shapes host metabolism, thermal tolerance and microbial diversity

Abstract

Parasitic infections impose physiological costs on hosts. Infection can alter host thermal tolerance, metabolism and host-associated microbial communities. When combined with thermal stress, infection may interact neutrally, increase resistance to subsequent stress, or act synergistically to exacerbate physiological cost. However, the mechanism underlying how these stressors affect host physiology remains poorly understood. We integrated physiological measurements with bacterial community profiling and host and parasite transcriptomics to assess how infection with the trypanosomatid Crithidia mellificae alters heat tolerance in the insecthost, the solitary bee Osmia cornifrons. Infection significantly reduced the upper thermal limit for host locomotion by an average of 11 °C, while combined infection and heat exposure produced the highest metabolic rates. Infection and heat stress were also associated with differences in bacterial community composition and Shannon diversity. Host transcriptomes showed increased expression of genes associated with detoxification under heat stress and reduced expression of genes associated with ATP production and amino acid biosynthesis during infection. Heat-stressed parasites increased expression of genes associated with chaperone activity and metabolic regulation. These results suggest that infection and thermal stress converge on shared metabolic constraints that reduce physiological resilience and narrow thermal safety margins. Our findings suggest that rising temperatures may destabilize host-parasite interactions and increase host vulnerability.