Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acute toxicity of soluble cadmium salts has almost exclusively been studied experimentally after parenteral exposures, where acute mortality is caused by hepatic necrosis. This report describes an alternative experimental model using oral exposure. A single oral toxic dose of CdCl2 to mice induced toxic gastroenteritis; subsequent hepatic and renal lesions were also observed. Whole-body gamma-counting after a single oral toxic 109CdCl2 dose to mice showed a dose-dependent delay of the fecal excretion of non-absorbed cadmium. This delay was absent when a low, non-toxic dose was administered. This effect is most likely due to decreased peristalsis and, at higher doses, intestinal atony due to oral cadmium toxicity. After fecal elimination of non-absorbed cadmium, the residual body burden of cadmium expressed as percent of initial dose reflects the fractional intestinal cadmium absorption due to slow reexcretion of absorbed cadmium. The fractional absorption increased with increasing doses of cadmium. The relative cadmium deposition in brain, testes and intestines decreased with increasing dose, whereas the relative liver deposition increased with dose. The delayed fecal elimination and increased fractional absorption of cadmium may significantly contribute to the development of both local and systemic toxicity in oral cadmium intoxication.
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PMID:Oral cadmium chloride intoxication in mice: effects of dose on tissue damage, intestinal absorption and relative organ distribution. 334 22

For feeding purposes shellfish filter large amounts of water but also concentrate infectious agents and toxins that are present in the marine environment either naturally or because of pollution. Thus, the consumption of raw or undercooked shellfish is a substantial source of foodborne poisoning, mostly epidemic and sometimes sporadic. Most of shellfish-borne infectious diseases are linked to fecal contamination of the marine environment; they include: thyphoid fever, salmonellosis, shigellosis, campylobacteriosis, cholera, Norwalk or Norwalk-like gastroenteritis and hepatitis A. In warm climates, shellfish contains naturally occurring halopilic Vibrios and may cause severe sporadic infections (septicemias) among very susceptible consumers (immunocompromised). Shellfish also causes outbreaks of paralytic shellfish poisoning (PSP) and diarrheic shellfish poisoning (DSP) when they are contaminated by toxins produced when Dinophisis, a marine plancton, proliferates. Chemical compounds (heavy metals and organic toxins) that are dumped in the environment (soil, air, and water) also reach shellfish harvesting waters where they are cocentrated. Although acute or chronic effects of the chemical contamination of shellfish have not been clearly documented, the cadmium pollution of some shellfish harvesting waters raises a serious problem. Since it is impossible to prevent completely the contamination of coastal waters by any of the agents cited above, the prevention of shellfish-borne diseases requires monitoring of the marine environment and shellfish flesh (coliform count, Dinophysis toxins, heavy metals...). This surveillance allows the classification of growing areas as suitable or not for harvesting and distribution of shellfish. However, this surveillance is not always sensitive enough. Indicators of fecal pollution are particularly not reliable for shellfish viral contamination. A better knowledge of marine biology, the limitation of coastal waters pollution, improved surveillance, the development of more sensitive indicators, the responsabilisation of the industry and the information of the public on the health hazards associated with shellfish consumption are the key issues for the improvement of shellfish-borne disease prevention.
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PMID:[Epidemiology of toxic and infectious risk related to shellfish consumption]. 896 39

Listeria monocytogenes is an intracellular pathogen causing gastroenteritis, central nervous system infections and abortions. Chromosomal virulence determinants have been extensively investigated. However, the function of genes encoded by plasmids in L. monocytogenes has not been fully understood. In this study, we determined the prevalence and molecular profile of plasmids in food isolates of L. monocytogenes and examined the contribution of four plasmid-borne cadmium-resistant genes to the susceptibility of L. monocytogenes to bacteriophage infection. The results showed that plasmids were isolated from 55% (11/20) of the isolates and the plasmids exhibited 10 molecular types as determined by restriction enzyme digestion. Furthermore, 65% and 15% of the isolates were tolerant to cadmium and benzalkonium chloride (BC), respectively. All the BC-resistant isolates were resistant to cadmium. The prevalence of predicted cadmium resistance determinants (cadA1, cadA2, cadA3 and cadC) was determined and the results showed that cadA1 (35%) in isolates of serotypes 1/2a and 1/2b was much more prevalent than cadC (15%). As expected, both cadA and cadC mutants had reduced resistance to cadmium, while the resistance to BC was not significantly affected. Interestingly, both cadA and cadC mutants showed significantly higher susceptibility against L. monocytogenes phage LipG2-5 and FWLLm3 compared with the wide-type strain. Based on these results, we concluded that plasmids from L. monocytogenes encoded important functional determinants that are not only associated with cadmium resistance, but also phage susceptibility.
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PMID:Plasmid-borne cadmium resistant determinants are associated with the susceptibility of Listeria monocytogenes to bacteriophage. 2572 72