Sudden infant death syndrome and enteric infection.
The association of Helicobacter pylori in the stomach, trachea and lungs with the incidence of SIDS, gastric ulcers and cancer may have a counterpart in animals. In field studies of white muscle disease (WMD) and hepatic necrosis in selenium-deficient pigs dying suddenly, veterinarians identified gastric ulcers in 40% of inspected piglets. The lesion was also commonly observed by researchers in experimentally produced vitamin E-selenium deficiency and other researchers suspected that gastric ulcers in swine may be associated with vitamin E-selenium deficiency. Mice preferentially concentrated (75)selenium in peritoneal exudative cells (PEC) when (75)selenium as selenium selenate was administered by stomach tube to selenium-deficient mice. Selenium concentrated in PECs as glutathione peroxidase (GSHP(x)). GSHP(x)-deficient leucocytes in peritoneal exudate failed to kill yeast cells. GSHP(x) deficiency has also been associated with decreased microbicidal activity of leucocytes in patients with chronic granulomatosis. The selenium-deficient swine were usually growing rapidly in crowded conditions, and, apart from WMD and hepatic necrosis, edema was prominent in the spiral colon, subcutaneous tissues, lungs and submucosa of the stomach. The elevated immunological response in the spleen and lungs of SIDS victims suggests an initial defective microbicidal propensity of the peritoneal exudative cells.
Reid
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GM
D000818:Animals; D004269:DNA, Bacterial / Q000032:analysis; D016481:Helicobacter Infections / Q000150:complications* / Q000382:microbiology; D016480:Helicobacter pylori / Q000235:genetics / Q000302:isolation & purification; D006801:Humans; D007223:Infant; D051379:Mice; D012643:Selenium / Q000172:deficiency; D013398:Sudden Infant Death / Q000209:etiology*
D004269:DNA, Bacterial; D012643:Selenium