ABSTRACT
The Florida Department of Health, Florida, United States, is investigating a Vibrio cholerae O75 outbreak. Ten cases with disease onsets from 23 March to 13 April 2011, presented with gastrointestinal symptoms of diarrhoea, nausea, vomiting, cramps, chills, and/or fever, after consuming raw or lightly cooked oysters harvested from Apalachicola Bay, Florida. Symptoms were milder than those during outbreaks of epidemic (serogroup O1 and O139) Vibrio cholerae; no case required rehydration treatment or hospitalisation.
Subject(s)
Cholera/epidemiology , Disease Outbreaks , Foodborne Diseases/epidemiology , Ostreidae/microbiology , Shellfish/microbiology , Vibrio cholerae/isolation & purification , Adult , Aged , Animals , Cholera/prevention & control , Female , Florida/epidemiology , Food Microbiology , Humans , Male , Middle AgedABSTRACT
We hypothesized that particular genetic backgrounds enhance rates of colonization, increase severity of enteritis, and allow for extraintestinal spread when inbred IL-10(-/-) mice are infected with pathogenic C. jejuni. Campylobacter jejuni stably colonized C57BL/6 and NOD mice, while congenic strains lacking IL-10 developed typhlocolitis following colonization that mimicked human campylobacteriosis. However, IL-10 deficiency alone was not necessary for the presence of C. jejuni in extraintestinal sites. C3H/HeJ tlr4(-/-) mice that specifically express the Cdcs1 allele showed colonization and limited extraintestinal spread without enteritis implicating this interval in the clinical presentation of C. jejuni infection. Furthermore, when the IL-10 gene is inactivated as in C3Bir tlr4(-/-) IL-10(-/-) mice, enteritis and intensive extraintestinal spread were observed, suggesting that clinical presentations of C. jejuni infection are controlled by a complex interplay of factors. These data demonstrate that lack of IL-10 had a greater effect on C. jejuni induced colitis than other immune elements such as TLR4 (C3H/HeJ, C3Bir IL-10(-/-)), MHC H-2g7, diabetogenic genes, and CTLA-4 (NOD) and that host genetic background is in part responsible for disease phenotype. C3Bir IL-10(-/-) mice where Cdcs1 impairs gut barrier function provide a new murine model of C. jejuni and can serve as surrogates for immunocompromised patients with extraintestinal spread.
