Study of Emetic Receptor Sites for Staphylococcal Enterotoxin in Monkeys

Sugiyama, Hiroki; Chow, K. W.; Dragstedt, Lester R.

doi:10.3181/00379727-108-26855

Cited by 20 publications

(6 citation statements)

References 3 publications

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“…These included the clinical syndrome which terminated in shock (5,7,11), multiple changes in clinical chemistries (4), a hypotension-associated fall in renal function (10), and terminal depression of electroencephalographic patterns (7). Other workers have reported on the pyrogenic and emetic effects (2,3,14).…”

mentioning

confidence: 96%

Pathogenesis of Lethal Shock After Intravenous Staphylococcal Enterotoxin B in Monkeys

Hodoval¹,

Morris²,

Crawley³

et al. 1968

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confidence: 96%

Pathogenesis of Lethal Shock After Intravenous Staphylococcal Enterotoxin B in Monkeys

Hodoval¹,

Morris²,

Crawley³

et al. 1968

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“…Vomit-ing and diarrhea are the most common manifestations of staphylococcal food poisoning in humans (2). The site of emetic action of the SEs lies within the gastrointestinal (GI) tract (10,33,34) and generates impulses that reach the subcortical vomiting center via vagal and sympathetic afferents (33,34). However, the specific cells and subcellular structures involved in the intestinal site of action of SEs are not known.…”

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confidence: 99%

Effects of staphylococcal enterotoxin A on the rat gastrointestinal tract

Beery¹,

Taylor²,

Schlunz³

et al. 1984

Infect Immun

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Staphylococcal enterotoxin A (SEA) was administered orally (15 jig) to two groups of rats. A marked immune reaction was evoked in the stomach and proximal small intestine of the first group. The second group of rats was used to study the absorptive fate and sites of action of orally administered SEA, utilizing immunoperoxidase staining. After oral dosing of the second group of rats, SEA-related immunoperoxidase staining was confined to: (i) neutrophils and macrophages, principally in the duodenum, and (ii) glomerular neutrophils and cells of the proximal convoluted tubules. Peroxidase staining of the kidney was noted within 15 min of exposure, indicating that SEA or some major postabsorption antigenic product can promptly pass through an intact gastrointestinal mucous membrane and become renally localized. Intestinal and renal detoxification and removal was indicated by an absence of detectable antigen in rats 180 min postexposure. Neuronal binding of SEA in the gastrointestinal tract was not demonstrable.

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“…Diseases, in press.) There is an apparent causal relationship between the central nervous system and the emetic response to oral toxin (1;Sugiyama,unpublished data;25).…”

Section: Resultsmentioning

confidence: 97%

Clinical Chemistry of Staphylococcal Enterotoxin Poisoning in Monkeys

Crawley¹,

Black²,

Gray³

et al. 1966

Applied Microbiology

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values were examined in 90 monkeys administered a purified preparation of staphylococcal enterotoxin, type B, intravenously. These studies showed an early release of epinephrine accompanied by a mild increase in blood glucose. This was followed by progressively developing prolonged hypoglycemia. An early increase in bloodurea nitrogen occurred, presumably as a result of both prerenal azotemia and functional renal failure seen in association with the observed hypotension. Serum protein, Ca, and Cl concentrations decreased with time. Pi levels increased, whereas Na and K concentrations in serum remained unchanged. Serum enzyme concentrations were unchanged, with the exception of serum glutamic oxaloacetic transaminase, which rose rapidly when compared with prechallenge control observations or with values from sham-challenged monkeys. These changes were statistically significant. These results suggested that enterotoxin administered intravenously produced early change in glucose metabolism, possibly related initially to catecholamine release and later to increased utilization of glucose and metabolic acidosis. Other findings were compatible with tissue breakdown at as yet undetermined locations and with loss of endothelial membrane integrity, as evidenced by loss of protein from the vascular space.

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Study of Emetic Receptor Sites for Staphylococcal Enterotoxin in Monkeys

Abstract: 100 99 99 9 9 Y Y 70 i f Y9 99 70 Y? 7)

Cited by 20 publications

References 3 publications

Pathogenesis of Lethal Shock After Intravenous Staphylococcal Enterotoxin B in Monkeys

Pathogenesis of Lethal Shock After Intravenous Staphylococcal Enterotoxin B in Monkeys

Effects of staphylococcal enterotoxin A on the rat gastrointestinal tract

Clinical Chemistry of Staphylococcal Enterotoxin Poisoning in Monkeys

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