Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.4.3 (phospholipase C)
 18,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies have implicated various toxigenic bacteria and their toxins in the aetiology of sudden infant death syndrome (SIDS). Therefore the effect of six bacterial toxins on the cardiorespiratory system of the rabbit was studied as a model for SIDS. The toxins' effect on the heart rate, arterial blood pressure, and breathing of anaesthetized rabbits was determined and their action compared to that of endotoxin. Intravenous injection of Clostridium perfringens enterotoxin and alpha-toxin, Staphylococcus enterotoxin B, Escherichia coli heat-stable toxin (STa), Clostridium difficile toxin A and B reduced heart rate, blood pressure, respiration and increased, slowed and prolonged thorax expansion, and at higher concentrations caused sudden death without visible stress or trauma. A combination of a low concentration of enterotoxins caused a greater reduction of these activities and sudden death. These effects were generally similar to those produced by endotoxin. In non-anaesthetized rabbits, the toxins slowed metabolism until death occurred without agitation, spasms, visible distress or prolonged illness. Intestinal production of these toxins by toxigenic strains, when conditions are suitable, and their systemic absorption, could therefore cause SIDS by an endotoxin-like shock mechanism.
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PMID:Is cardiorespiratory failure induced by bacterial toxins the cause of sudden infant death syndrome? Studies with an animal model (the rabbit). 766 Mar 68

Faecal samples from 123 infants who died with sudden infant death syndrome (SIDS) and from a comparative group of 52 age-matched babies were analysed for toxigenic bacteria and their toxins. Serum samples from the SIDS infants were also analysed for these toxins. A significantly higher proportion of toxigenic bacteria and their toxins were found in faecal samples of SIDS babies than in samples from the comparative group. These toxins were also found in serum from the SIDS babies. Clostridium perfringens was found in 54 (45.4%) of 119 SIDS cases compared with 10 (19.6%) of 51 healthy babies (chi 2 = 10.1, p < 0.01); C. difficile in 33 (27.7%) of 119 SIDS cases compared with 8 (14.8%) of 54 healthy babies (chi 2 = 3.43ns, p < 0.1); Staphylococcus aureus in 12 (27.3%; 66.7% enterotoxigenic) of 44 SIDS cases compared with 12 (85.7%; non-enterotoxigenic) of 14 healthy babies (chi 2 = 14.9, p < 0.001); C. botulinum in 6 (5.0%) of 120 SIDS cases compared with 0 of 53 healthy babies (chi 2 = 2.74, p < 0.1). Campylobacter jejuni, Yersinia enterocolitica, Vibrio parahaemolyticus, salmonellae and Bacillus cereus were not detected. Heat-labile toxin, lethal to mice (HLML) was found in 32 (27.1%) of 118 SIDS faecal samples compared with 5 (10.6%) of 47 healthy babies (chi 2 = 5.24, p < 0.05); cytotoxins in 38 (30.9%) of 123 SIDS faecal samples compared with 0 of 21 of healthy babies (chi 2 = 8.8, p < 0.01) and 24 (27.6%) of 87 SIDS serum samples. C. perfringens enterotoxin was detected in 33 (34.4%) of 96 SIDS faecal extracts compared with 0 of 23 of healthy babies (chi 2 = 10.94, p < 0.001), and in 27 (24.5%) of 110 SIDS serum samples. C. perfringens alpha-toxin (presumptive) was detected in 14 (17.5%) of 80 SIDS faecal extracts compared with 0 of 17 from healthy babies (chi 2 = 3.5ns, p congruent to 0.05) and in 2 (2.3%) of 87 SIDS serum samples. C. difficile toxin was detected in four SIDS faecal samples and two serum samples. C. botulinum toxin was detected in only one of 120 SIDS faecal samples compared with none of 49 from healthy babies. Staphylococcal enterotoxins were detected in 8 (19.5%) of 41 SIDS faecal samples compared with 0 of 19 from healthy babies (chi 2 = 4.278, p < 0.05), and in 4 (10.8%) of 37 SIDS serum samples.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Enterotoxigenic bacteria in the sudden infant death syndrome. 834 6

The rabbit catecholamine responses to bacterial toxins commonly found in Sudden Infant Death Syndrome (SIDS) victims were studied as part of a proposed animal model for SIDS. Six bacterial toxins commonly isolated from SIDS baby feces and a comparison endotoxin were injected intravenously (i.v.) and intraluminarily (i.l.) to determine their effects on catecholamine levels. I.v. injected toxins clearly altered catecholamine levels causing sharp rises in adrenaline and noradrenaline levels and at critical toxin concentrations sudden death ensued. Clostridium perfringens enterotoxin and alpha-toxin, Clostridium difficile enterotoxin (A) and cytotoxin (B), Escherichia coli STa toxin and staphylococcal enterotoxin B caused rises in catecholamine levels similar to that caused by E. coli endotoxin. Control rabbits showed very little or no obvious change in catecholamine levels. Clostridium difficile enterotoxin (A) and cytotoxin (B) injected i.v. exhibited synergy. Toxins injected into the duodenum, jejunum, ileum, cecum and large intestine caused behavioural changes ranging from reduced appetite and diarrhea to, in rare cases, death. Changes in the catecholamine levels of these animals however were not significantly different from those of the control animals. The results are discussed in relation to the possible effect of certain conditions (physiological, viral infections and environmental) which increase toxin permeability and allow absorption of these toxins, possibly resulting in sudden infant death.
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PMID:The effect of enteric bacterial toxins on the catecholamine levels of the rabbit. 927 Oct 18

The aim of this project was to characterise the type of damage caused to the intestine of the infant rabbit by bacterial enterotoxins implicated in sudden infant death syndrome (SIDS). Samples of the duodenum, jejunum, ileum, caecum and large intestine exposed to the toxins for up to 6 hours were examined by scanning (SEM) and transmission electron microscopy (TEM). The damage was quantitatively assessed (% villi damaged) by SEM and qualitatively by SEM and TEM. Clostridium perfringens enterotoxin, staphylococcal enterotoxin B and Clostridium difficile toxin A + toxin B combined all caused severe damage to the villi in the small intestine (80-90% damage). Clostridium difficile toxin B caused only slight damage (17% to the jejunum, 26% to the caecum). Clostridium perfringens alpha-toxin caused moderate damage to the small intestine (duodenum 34%, caecum 35%), and Escherichia coli STa caused significant damage to the small (53-70%) and large intestine (51%). The level of toxin damage increased with time, the small intestine being more susceptible generally to damage than the large intestine. Each toxin differed in its ability to damage the villi, microvilli, enterocytes and lamina propria.
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PMID:The effect of bacterial enterotoxins implicated in SIDS on the rabbit intestine. 1135 52