SUMMARY Staphylococcal and coliform infections theoretically could lead to the circulation of potent toxins throughout the body. Moreover, staphylococcal enterotoxins are important causes of food poisoning. The present investigation was undertaken to examine the characteristics of purified staphylococcal enterotoxin B (seb) given to goats by iv (dose 0.02 to 2 μg/kg) and intramammary routes (1 mg). Rectal temperature, heart rate, rumen motility, plasma zinc and iron concentrations, and certain other blood biochemical and hematological values were studied and compared with the changes seen after Escherichia coli endotoxin is administered (dose: 0.1 μg/kg iv and 1 mg intramammarily). Similar changes such as fever, tachycardia, inhibition of rumen contractions, drop in plasma zinc and iron concentrations, lymphopenia, and neutropenia followed by neutrophilic leukocytosis and changes in serum enzymes activities were observed, although the patterns were different for the 2 toxins. In contrast to the effects of E coli lipopolysaccharide (lps), seb induced abdominal cramping pain, watery diarrhea with pseudomembranes, hemoconcentration, and increase in blood urea nitrogen. However, the latter effects were not present after intramammary seb administration. Fever, tachycardia, and decrease in plasma zinc and iron concentrations in the absence of a marked inhibitory effect upon rumen motility were seen after intramammary E coli lps infusion. The results obtained demonstrate that the goat is a susceptible species and a useful model to study the gastrointestinal effects caused by seb. Moreover, the results obtained after intramammary administration indicate that endogenous inflammatory substances may be released from the udder instead of E coli lps absorption. However, absorption of seb from the udder could not be excluded. The present finding that no clear relationship could be found between the temperature response, and the alterations in plasma zinc and iron plasma values support the theory that the febrile reactions and the changes in plasma trace metals are mediated by different proteins released by activated macrophages.
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Miert et al. (1983) studied this question.