Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five fatal cases of poisoning from ingestion of Amanita phalloides, a very common mushroom in central Italy, are reported. The fact that four of the cases occurred simultaneously enabled uniform collection of clinical, pathology and toxicology data, which is presented with particular emphasis on the histological aspects. The fifth case involved a six-year-old girl, and is discussed with reference to differential diagnosis with respect to Reye's syndrome, which was the initial diagnosis, demonstrated incorrect by the histology, pathology and toxicology findings. The typical liver and kidney alterations of Amanita phalloides poisoning, consisting of massive hepatic central lobular cell necrosis and acute tubular necrosis of the kidney are described. Outside the liver, there was often general hemorrhagic diathesis and severe brain edema. Although poisoning by Amanita phalloides is rare, these cases confirm the requirement for as complete a comparison as possible between circumstantial histopathological and toxicological data for the purposes of forensic diagnosis.
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PMID:Histological criteria for diagnosis of amanita phalloides poisoning. 865 82

Clostridium perfringens type D isolates cause enterotoxemia in sheep, goats, and probably cattle. While the major disease signs and lesions of type D animal disease are usually attributed to epsilon toxin, a class B select agent, these bacteria typically produce several lethal toxins. Understanding of disease pathogenesis and development of improved vaccines are hindered by the lack of a small-animal model mimicking natural disease caused by type D isolates. Addressing this need, we developed an oral challenge mouse model of C. perfringens type D enterotoxemia. When BALB/c mice with a sealed anus were inoculated by intragastric gavage with type D isolates, 7 of 10 type D isolates were lethal, as defined by spontaneous death or severe clinical signs necessitating euthanasia. The lethalities of the seven type D isolates varied between 14 and 100%. Clinical signs in the lethally challenged mice included seizures, convulsions, hyperexcitability, and/or depression. Mild intestinal gas distention and brain edema were observed at necropsy in a few mice, while histology showed multifocal acute tubular necrosis of the kidney and edema in the lungs of most challenged mice that developed a clinical response. When the lethality of type D isolates in this model was compared with in vitro toxin production, only a limited correlation was observed. However, mice could be protected against lethality by intravenous passive immunization with an epsilon toxin antibody prior to oral challenge. This study provides an economical new model for studying the pathogenesis of C. perfringens type D infections.
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PMID:Development and application of an oral challenge mouse model for studying Clostridium perfringens type D infection. 1756 65