RESUMO
A geriatric captive bobcat (Lynx rufus) was euthanized due to progressive anorexia and lethargy. Meningoencephalitis with intralesional apicomplexan organisms was identified histologically. With immunohistochemistry, the organisms were immunolabeled by anti-Sarcocystis neurona antibodies. PCR targeting the ITS region of the parasite yielded an amplicon with >99.6% identity to several Sarcocystis dasypi, S. neurona, and S. speeri sequences. Amplification of the 18S region yielded a sequence that was 99.9% similar to sequences of both S. neurona (MN169125) and S. speeri (KX470746). Inflammatory disease of the CNS due to Sarcocystis sp. infection is uncommonly reported in felids and has not been reported previously in bobcats, to our knowledge. Here, we briefly review Sarcocystis-associated CNS disease in other felids, confirm that it can affect bobcats, and highlight the challenges of species-level identification of Sarcocystis sp. in routine diagnostic work.
RESUMO
The role of commensal microbiota in enteric viral infections has been explored extensively, but the interaction between human gut microbiota (HGM) and human norovirus (HuNoV) is poorly understood. In this study, we established an HGM-Transplanted gnotobiotic (Gn) pig model of HuNoV infection and disease, using an infant stool as HGM transplant and a HuNoV GII.4/2006b strain for virus inoculation. Compared to germ-free Gn pigs, HuNoV inoculation in HGMT Gn pigs resulted in increased HuNoV shedding, characterized by significantly higher shedding titres on post inoculation day (PID) 3, 4, 6, 8 and 9, and significantly longer mean duration of virus shedding. In addition, virus titres were significantly higher in duodenum and distal ileum of HGMT Gn pigs on PID10, while comparable and transient HuNoV viremia was detected in both groups. 16S rRNA gene sequencing demonstrated that HuNoV infection dramatically altered intestinal microbiota in HGMT Gn pigs at the phylum (Proteobacteria, Firmicutes and Bacteroidetes) and genus (Enterococcus, Bifidobacterium, Clostridium, Ruminococcus, Anaerococcus, Bacteroides and Lactobacillus) levels. In summary, enhanced GII.4 HuNoV infection was observed in the presence of HGM, and host microbiota was susceptible to disruption upon HuNoV infection.