This study examined whether the survival of Vibrio cholerae O1 on contaminated cooked rice was influenced by the type of rice. Vibrios survived unchanged on clumps of glutinous white rice (wet, grains adhered) held at room temperature for 24 h. On nonglutinous white rice (slightly moist, grains separate), 30% viable vibrios remained at 24 h. On nonglutinous brown rice (moist, separate, covered with a mucus-like substance), the number of vibrios increased 2.7-fold at 24 h. Survival rates of vibrios on the surfaces of a row of five cooked rice grains after 2 h of exposure at room temperature were 86, 29, 12, and 4% for glutinous rice, white rice, and the endosperm and pericarp of brown rice, respectively. (Each boiled brown rice grain surface was partly pericarp and partly endosperm, which became exposed by a rupture of the pericarp.) Covering each inoculated grain with a similar cooked rice grain surface increased the corresponding figures to 93, 99, 60, and 94%. Scanning electron microscopy revealed that each type of cooked grain surface possessed a distinct microtopography. For example, the surfaces of glutinous rice grains consisted of separated overlapping strips with many holes, while the pericarps of brown rice were flat interspersed with small pits. In conclusion, each type of boiled rice produced a distinct survival pattern of V. cholerae O1 caused by both the distinct gross features and the fine surface characteristics of the rice. The significance of this finding is that the type of rice consumed can be a factor in cholera transmission by contaminated rice.
Helicobacter pylori CagA modifies the signalling of host cells and causes gastric diseases. Although CagA is injected into gastric epithelial cells through the type IV secretion machinery, it remains unclear how CagA is transported towards the machinery in the bacterial cytoplasm. In this study, it was determined that the proton-dependent intracytoplasmic transport system correlates with the priming of CagA secretion from H. pylori. The cytotoxicity of neutral-pH- and acidic-pH-treated H. pylori was examined in the AGS cell line. The amount of phosphorylated CagA in AGS cells incubated with acidic-pH- and neutral-pH-treated H. pylori was determined by enzyme immunoassay and Western blot. The production of CagA and adherence of the treated bacteria were examined by enzyme immunoassay and light microscopy, respectively. To clarify how CagA is transported towards the inner membrane of the treated bacteria, the localization of CagA was analysed by immunoelectron microscopy. The proportion of hummingbird cells in the AGS cell line rapidly increased following the inoculation of acidic-pH-treated H. pylori but increased more slowly with neutral-pH-treated H. pylori, and the phenomenon correlated with the amount of phosphorylated CagA in AGS cells. CagA was densely localized near the inner membrane in the acidic-pH-treated bacterial cytoplasm, but this localization was not observed in the neutral-pH-treated bacterial cytoplasm, suggesting that CagA shifts from the centre to the peripheral portion of the cytoplasm as a result of an extracellular decrease in pH. This phenomenon depended on the presence of UreI, a proton-dependent urea channel, but not on the presence of urea. The pH treatments did not enhance CagA production or the adherence of the bacterium to AGS cells. The authors propose that H. pylori possesses a proton-dependent intracytoplasmic transport system that probably accelerates priming for CagA injection.