Gut microbiome dysbiosis and functional alterations in Campylobacter-associated gastroenteritis using metagenomic approaches.

Campylobacter species are a major cause of bacterial gastroenteritis worldwide. Using shotgun metagenomic sequencing of stool samples from PCR-confirmed Campylobacter-positive patients and symptomatic PCR-negative controls, we reveal dysbiosis marked by reduced species richness (median Shannon diversity was significantly lower in the Campylobacter-positive group [3.24] vs. Campylobacter-negative group [3.63], P = 0.038), taxonomic shifts toward inflammation-associated taxa (Campylobacteriaceae, Enterobacteriaceae, Pasteurellaceae), and depletion of key commensals involved in short-chain fatty acid (SCFA) production (Ruminococcaceae, Bacteroidaceae, Eubacteriaceae). These changes define a distinct microbial signature of infection, suggestive of a perturbed gut environment with reduced colonization resistance and impaired barrier function. Despite these taxonomic and ecological disruptions, resistome profiling showed no increase in the burden or diversity of antimicrobial resistance genes (ARGs), suggesting that the observed microbiome disruption may not lead to broader expansion of ARGs in the gut microbiome. Whole-genome sequencing of cultured Campylobacter jejuni and C. coli isolates revealed common ARGs, including bla OXA-193, tet(O), and gyrA_T86I, some of which overlapped with metagenomic findings. Moreover, metagenomics identified low-abundance Campylobacter species in PCR-negative controls, underscoring the need for greater taxonomic resolution. These results delineate a Campylobacter-associated microbial and functional footprint in the human gut, with implications for diagnostics and antimicrobial stewardship.