Elizabethkingia anophelis (Ea) is an emerging pathogen that causes sepsis, meningitis, and death in people with comorbidities. While usually innocuous, a recent community outbreak resulted in at least 20 deaths and 66 laboratory confirmed cases. The outbreak stemmed from the rapid formation of a novel and more virulent Ea sublineage created by a conjugative element that disrupted the muty DNA repair gene. The virulence associated factors, pathogenic mechanisms, and ecology of Ea are not known. C. elegans is a well-established model for the characterization of pathogen-host interactions. When we exposed mixed stage wild-type C. elegans to Ea (Ag1 strain), the animals exhibited decreased movement, slowed development, early larval death, and an overall decreased fecundity compared to animals exposed to E. coli OP50 (Ec). We also made the striking observation that worms exposed to Ea actively avoided Ea lawns. To understand the aversive response, we conducted two-choice assays between Ea and Ec in experiments using L1 and L4 animals. L1s not previously exposed to a food source initially chose Ea over Ec (-0.75 CI, Choice Index [CI] of -1.0 represents Ea selection) but actively selected Ec over time (+0.41 CI at 96hrs). L4 animals first reared on Ec chose Ec over Ea in two-choice assays (+0.49 CI). Importantly, we found that staged adults placed on Ea bacteria without another bacterial food source adopted a lawn avoidance phenotype, suggesting that they are repulsed from Ea even in the absence of Ec. These avoidance responses depend on an intact odorant detection system because
lim-4(
ky403) and
tax-2(
p671);
tax-4(
p678) mutant animals failed to avoid Ea lawns. We used solid-phase microextraction (SPME) gas chromatography mass spectrometry (GC-MS) to identify volatile odorant differences between Ea and Ec and observed a marked increase in the amount of indole in Ec compared to Ea. Indole is an attractive compound recently shown to modulate predator-prey interactions between C. elegans and bacteria. To examine the pathogenic mechanisms of Ea in C. elegans, we exposed N2,
sek-1 (
km4),
tol-1(
nr2033),
dbl-1(
nk3) and
daf-2(
e1370) animals to Ea and Ec. Wild-type animals displayed several pathological changes when grown on Ea and died faster than their Ec exposed counterparts. Decreased lifespan and increased pathologies were found in
sek-1 while
daf-2 animals appeared immune to Ea. The
tol-1 and
dbl-1 alleles did not influence Ea pathogenicity. To complement these immunity assays we also examined the antimicrobial activity of
dod-24,
irg-1 and T24B8.5 in C. elegans exposed to Ea using transcriptional reporter GFP strains. We observed decreases in the expression of T24B8.5 and increased but more variable changes in
irg-1. Taken together these experiments suggest that Ea is pathogenic to C. elegans, opening new opportunities to investigate pathogen and host factors influencing Ea related disease.