Pathophysiology of staphylococcal enterotoxin, Type B, (SEB) toxemia after intravenous administration to monkeys

Beisel, William R.

doi:10.1016/0041-0101(72)90167-5

Cited by 46 publications

(35 citation statements)

References 16 publications

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“…The progressive hypotension which we observed after SEB was similar to results obtained by others, 3 ' 9 but appears to be at variance with observations reported by Liu et al 22 Liu's group found that MABP in monkeys was relatively constant for at least 6 hours after iv SEB and then decreased, but never to values less than 90 mm Hg until immediately before death. These different results probably are related to the fact that monkeys used by Liu's group had higher initial blood pressures (MABP = 135 ± 10 mm Hg) than did our monkeys (MABP = 112 ± 5 mm Hg) or those used by Elsberry et al 9 (MABP = 118 ± 4 mm Hg); others 23 ' 24 have reported that the MABP of a normal unstressed monkey is about 110 mm Hg.…”

Section: Discussioncontrasting

confidence: 54%

“…3 Also, since the cardiovascular responses of endotoxemic rhesus monkeys have been shown to be similar to the responses of humans to Gram-negative sepsis,' 18 we hypothesized that the response of the rhesus monkeys to SEB might be similar to that of man.…”

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confidence: 99%

“…2 Intravenous (iv) injection of enterotoxins in very small doses in rabbits and monkeys produces lethargy, fever, shock, and death. 3 There is evidence that during staphylococcal wound infections and purulent skin lesions, enough enterotoxin is released into the circulation of an infected patient to stimulate synthesis of antibody specific to the toxins produced. 4 Since circulating enterotoxins might contribute to the hypotension and shock often observed in these patients, we decided to study possible mechanisms by which enterotoxin causes circulatory shock.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Enterotoxic shock in rhesus monkeys. The role of selected bloodborne factors.

Pettit¹,

Yamada²,

Wing³

et al. 1978

Circulation Research

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SUMMARY Staphylococcal enterotoxin B, a protein exotoxin from Staphylococcus aureus, produced progressive hypotension and shock when injected (1 mg/kg, iv) into rhesus monkeys. Plasma levels of factors which have been implicated in the pathogenesis of other types of shock were measured. Endotoxin-like activity was measured by the Limulus lysate technique, fibrin degradation products (FDP) were quantified by electroimmunoassay, and activation of the complement system was assayed by measuring total hemolytic complement. Activation of the intrinsic coagulation cascade was assessed by measuring activated partial thromboplastin time (APTT). Activation of the kinin system was evaluated by measuring prekallikrein activity and kininogen. Myocardial depressant factor (MDF) was measured by paper chromatography. Endotoxin-like activity did not appear in plasma, and the complement system was not activated. The appearance of FDP and a significant trend for prolongation of APTT indicated activation of fibrinolysis and the intrinsic coagulation cascade, and suggested that disseminated intravascular coagulation was occurring. Activation of the kinin system was shown by a progressive and significant depletion of kininogen from 338 ± 37 to 226 ± 22 ng kallidin generated/ml, and a significant depletion of plasma prekallikrein activity from 169 ± 8 to 110 ± 15 tosyl arginine methyl ester (TAMe) esterase U/ml. Analysis of covariance indicated that activation of the kinin system was related to changes in blood pressure. MDF did not increase until immediately before death (increase from 1.08 ± 0.15 to 1.92 ± 0.11 paper chromatographic U//tl, n = 6). We conclude that kinins, MDF, and disseminated intravascular coagulation, but not complement or endotoxin, may contribute to the pathogenesis of enterotoxic shock in rhesus monkeys.ENTEROTOXINS isolated from cultures of Staphylococcus aureus are protein exotoxins (28,000-29,000 daltons, molecular weight) which are capable of producing acute food poisoning in humans 1 and other primates.2 Intravenous (iv) injection of enterotoxins in very small doses in rabbits and monkeys produces lethargy, fever, shock, and death.3 There is evidence that during staphylococcal wound infections and purulent skin lesions, enough enterotoxin is released into the circulation of an infected patient to stimulate synthesis of antibody specific to the toxins produced. 4 Since circulating enterotoxins might contribute to the hypotension and shock often observed in these patients, we decided to study possible mechanisms by which enterotoxin causes circulatory shock.When Josefczyk 4 measured anti-enterotoxin antibodies in normal patients and patients with staph- ylococcal infections, antibody to staphylococcal enterotoxin type B (SEB) was the most common type in each group. SEB has been isolated in purity greater than 99%, 5 and its amino acid sequence has been determined. 6 To help to elucidate the mechanisms by which enterotoxins produce shock, we injected SEB (1 mg/kg, iv) into rhesus monkeys and measured plasma l...

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Section: Discussioncontrasting

confidence: 54%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Enterotoxic shock in rhesus monkeys. The role of selected bloodborne factors.

Pettit¹,

Yamada²,

Wing³

et al. 1978

Circulation Research

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“…Among the shared properties of the PTSAgs is their capacity to induce lethal shock in susceptible animal hosts (8,11,24,75,154). For example, TSST-1 and SPE A each produce a lethal disease resembling TSS when administered as continuous infusions to rabbits over a 7-day period (94,125).…”

Section: Pathogenesismentioning

confidence: 99%

Exotoxins of Staphylococcus aureus

Dinges

Orwin

Schlievert

2000

Clinical Microbiology Reviews

1,091

619

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“…Clinical symptoms and pathological reactions in monkey and human SEB-induced shock cases are similar (3,4,29). However, monkeys are expensive, genetically diverse, and limited in number.…”

Section: Introductionmentioning

confidence: 91%

Murine Lethal Toxic Shock Caused by Intranasal Administration of Staphylococcal Enterotoxin B

Savransky

Rostapshov²,

Pinelis

et al. 2003

Toxicol Pathol

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Currently available murine staphylococcal enterotoxin B (SEB) shock models require pretreatment with various agents to increase mouse sensitivity to SEB. This study was performed to show that C3H/HeJ mice are highly susceptible to intranasal SEB inoculation, which caused toxic shock without using pretreatment agents. For this purpose, mice were injected intranasally with different doses of SEB and observed for up to 1 month. The median lethal dose of SEB was determined using the probit procedure. Tissue samples were taken at different time points for histopathological examination. The LD 50 was found at 1.6 µg/g (95% fiducial limit (f.l.) 0.7 to 2.2), the LD 80 at 2.7 µg/g (95% f.l. 1.9 to 4.0) and the LD 90 at 3.6 µg/g (95% f.l. 2.7 to 6.4). Histopathologic examination revealed pulmonary edema and bronchopneumonia. Mucosal-associated lymphoid tissue first became activated, followed by increasing lymphocyte apoptosis and depletion. In the liver there were intralobular and portal inflammatory foci with increasing lymphocyte apoptosis and degenerative necrosis. The splenic white pulp was characterized by early activation and subsequent depletion of lymphoid follicle germinal centers. The thymus initially was activated, followed by increasing apoptosis and migration of lymphoid cells from the cortex to the medulla. The pathological features detected in the mice were similar to those of rhesus monkeys treated with SEB aerosol challenge.

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Pathophysiology of staphylococcal enterotoxin, Type B, (SEB) toxemia after intravenous administration to monkeys

Cited by 46 publications

References 16 publications

Enterotoxic shock in rhesus monkeys. The role of selected bloodborne factors.

Enterotoxic shock in rhesus monkeys. The role of selected bloodborne factors.

Exotoxins of Staphylococcus aureus

Murine Lethal Toxic Shock Caused by Intranasal Administration of Staphylococcal Enterotoxin B

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