Cholera, a severe form of gastroenteritis, is one of the most widespread diseases in developing countries. The mechanism of intestinal infection caused by V. cholerae O139 remains unclear. In order to explore some morphological aspects of its infection in the intestine including Peyer's patches, we investigated the V. cholerae O139 infection at intestinal site of the rabbit gut-loop model. The electron microscopic analysis revealed denuded mucosal surface with loss of microvilli and integrity of the surface epithelium. Infection of the intestine with V. cholerae O139 induces destruction of villi, microvilli and lining epithelium with exposure of crypts of Lieberkuhn.
A case is presented of a fatal environmental accidental injuries of lightning. A pedestrian was struck by lightning. The macroscopic and microscopic lightning injuries are reviewed.
Hand, foot and mouth disease is mainly caused by enterovirus A71 (EV-A71) and coxsackievirus A16 (CV-A16), but EV-A71 is also associated with severe neurological complications. Host factors may contribute to the different clinical outcomes of EV-A71 and CV-A16 infections. A neurovirulent EV-A71 strain (EV-A71/UH1) from a fatal case, a non-neurovirulent EV-A71 strain (EV-A71/Sha66) and a CV-A16 strain (CV-A16/22159) from cases of uncomplicated HFMD were used. Replication of the viruses in SK-N-MC (neuronal) and HT-29 (intestinal) cell lines correlated with the severity of clinical disease associated with each virus. EV-A71/UH1 showed the greatest replication in neuronal cells. In HT-29 cells, both EV-A71 strains replicated well, but CV-A16/22159 showed no effective replication. The proteomes of mock and infected SK-N-MC and HT-29 cell lines were compared by 2D-SDS-PAGE. The differentially expressed proteins were identified by MALDI-TOF/TOF analysis. There were 46 and 44 differentially expressed proteins identified from SK-N-MC and HT-29 cells, respectively, categorized under apoptosis, stress, cytoskeletal, energy metabolism proteins and others. Western blot validation showed that EV-A71/UH1 and CV-A16 also differentially induced proteins involved in viral RNA translation and host cell stress responses in neuronal and intestinal cell lines.