Microbiome and resistome profiles of Cryptosporidium parvum–shedding and non-shedding calves
Background Neonatal calf diarrhea is a major cause for morbidity and mortality in young calves. One of the most important pathogens associated with this condition is the protozoan Cryptosporidium (C.) parvum, yet control of cryptosporidiosis remains difficult due to limited therapeutic options. A deeper understanding of parasite-associated effects on the intestinal microbial community is essential as a basis for developing new intervention methods. As the calf microbiome is recognized as a reservoir of antimicrobial resistance genes (ARG), it is also important to investigate how infection- and diarrhea-associated microbial shifts influence the resistome. This study analyzed the microbiota and ARG of calves infected with C. parvum. Samples were collected from n=15 calves of a dairy farm. The presence of C. parvum antigen was determined with an on-farm test (Fassisi BoDia®). Calves were categorized in three groups consisting of five calves, respectively: diarrheic calves shedding C. parvum (C.p.+/D+), non-diarrheic calves shedding C. parvum (C.p.+/D-) and non-diarrheic calves without any detection of C. parvum (C.p.-/D-). Fecal samples were subjected to shotgun metagenomic sequencing.  Results While the microbiome alpha diversity did not differ among groups, the beta diversity was significantly different. A distinct increase in the abundance of Fusobacterium (F.) was observed in calves that tested positive for C. parvum on the farm, both in diarrheic and non-diarrheic animals. This increase was driven by the species F. mortiferum. Low levels of C. parvum reads were also identified in the calves tested negative on the farm. In the resistome, the dominant ARG were similar across the clinical groups, while age influenced the diversity indices and total ARG abundance.  Conclusion In summary, C. parvum infection altered the calf microbiome, with a specific increase of F. mortiferum, while only small changes were observed in the resistome.