R-044. Experimental Adaptation of Burkholderia Cnocepacia to a Novel Host Reduces Host Range
It is unclear whether pathogenic adaptation to a new host typically broadens or compromises host range, yet the answer bears on the fate of emergent pathogens. We are investigating this dynamic using a soil isolate of Burkholderia cenocepacia, a species that normally inhabits the rhizosphere, is related to the onion pathogen B. cepacia, and can infect the lungs of cystic fibrosis patients. We hypothesized that adaptation of B. cenocepacia to a novel host would compromise fitness and virulence in alternative hosts. We modeled adaptation to a specific host by experimentally evolving twelve populations of B. cenocepacia in liquid media composed of macerated onion tissue. Using genetically marked B. cenocepacia, we allowed populations to adapt to onion media by serially passaging populations for 1000 generations. We quantified fitness of evolved populations by head-to-head competitions with the ancestral clone and observed dramatic adaptation in all lines. Growth curves demonstrated that growth rate had doubled in many populations though relative fitness was more heterogeneous, suggesting multiple adaptive solutions to the new environment. We tracked adaptation at more frequent intervals in one population and observed rapid increases in fitness followed by periods of stasis, which suggests punctuated evolution owing to isolated selective sweeps of favorable mutations. Next, we evaluated effects of this adaptation on host range by conducting virulence assays of the evolved populations in a liquid C. elegans model, in which bacteria and worms serve as each other’s primary resource. Beginning with the ancestral strain, a highly potent nematode killer, we observed that adaptation to the onion environment was associated with a loss of ability to initiate infection and kill worms; this deficiency arose by 500 generations and populations became completely avirulent by 1,000 generations. In conclusion, we observed a narrowing of host range as a consequence of prolonged adaptation to a specific host, and suggest that emergent pathogens may face similar consequences if they become host-restricted.