Comparison of sampling techniques for detection of Arcobacter butzleri from chickens.

Arcobacter butzleri is a causative agent of human enteritis that has been recently differentiated from the genus Campylobacter. Previous work suggests that its transmission to humans is likely through a foodborne route with a substantial tendency to be located on poultry carcasses. For reducing the incidence of this pathogen on commercial poultry, improved protocols are needed to sample and identify A. butzleri from infected birds prior to slaughter. The purpose of this study was to compare sampling methods for this emerging pathogen from chickens that were artificially inoculated per os with A. butzleri. We tested three sampling techniques commonly used to determine the microbiological quality of poultry: cloacal swabs, fecal samples, and environmental surface (drag) swabs collected when birds were 3, 5, or 7 wk old. These samples were cultured in Johnson-Murano enrichment broth and analyzed by PCR. Results indicate that environmental surface swabs yielded the highest recovery percentage. A detection rate of 75 to 100% was observed for each sampling period (age of chicken). Additionally, A. butzleri could not be isolated from the intestinal tract (jejunum, ileum, cecum, colorectum) of inoculated birds.

Correlation of temperature and toxicity in murine studies of staphylococcal enterotoxins and toxic shock syndrome toxin 1.

This study describes a quick (<12 h) assay for detecting temperature decreases in BALB/c and C57BL/6 mice injected intraperitoneally (i.p. ) with staphylococcal enterotoxin A (SEA), SEB, or SEC3 or toxic shock syndrome toxin 1 and a potentiating dose of lipopolysaccharide (LPS). Toxin-specific antisera effectively neutralized the temperature fluctuations in this model. Orally administered SEA or SEB (50 microg/animal), with or without LPS, did not have an effect on temperature or lethality. Versus wild-type mice, transgenic knockout mice lacking the p55 receptor for tumor necrosis factor (TNF) or gamma interferon were protected against an i.p. challenge of SEA plus LPS. The p75 receptor for TNF and intercellular adhesion molecule 1 have a negligible role in this toxic shock model.