Staphylococcal Enterotoxin B.

a. Clinical Syndrome.

(1) Characteristics. Staphylococcal Enterotoxin B (SEB) is one of several exotoxins produced by Staphylococcus aureus, causing food poisoning when ingested. A BW attack with aerosol delivery of SEB to the respiratory tract produces a distinct syndrome causing significant morbidity and potential mortality.

(2) Clinical Features. The disease begins 1-6 hours after exposure with the sudden onset of fever, chills, headache, myalgia, and nonproductive cough. In more severe cases, dyspnea and retrosternal chest pain may also be present. Fever, which may reach 103-106° F, has lasted 2-5 days, but cough may persist 1-4 weeks. In many patients nausea, vomiting, and diarrhea will also occur. Physical findings are often unremarkable. Conjunctival injection may be present, and in the most severe cases, signs of pulmonary edema would be expected. The chest x-ray is generally normal, but in severe cases, there will be increased interstitial markings, atelectasis, and possibly overt pulmonary edema. In moderately severe laboratory exposures, lost duty time has been <2 weeks, but, based upon animal data, it is anticipated that severe exposures will result in fatalities.

b. Diagnosis.

(1) Routine Laboratory Findings. Laboratory findings are noncontributory except for a neutrophilic leukocytosis and elevated erythrocyte sedimentation rate.

(2) Differential Diagnosis.

(a) In foodborne SEB intoxication, fever and respiratory involvement are not seen, and gastrointestinal symptoms are prominent. The nonspecific findings of fever, nonproductive cough, myalgia, and headache occurring in large numbers of patients in an epidemic setting would suggest any of several infectious respiratory pathogens, particularly influenza, adenovirus, or mycoplasma. In a BW attack with SEB, cases would likely have their onset within a single day, while naturally occurring outbreaks would present over a more prolonged interval. Naturally occurring outbreaks of Q fever and tularemia might cause confusion, but would involve much smaller numbers of individuals, and would more likely be accompanied by pulmonary infiltrates.

(b) The dyspnea of botulism is associated with obvious signs of muscular paralysis: its cholinergic blocking effects result in a dry respiratory tree, and patients are afebrile. Inhalation of nerve agent will lead to weakness, dyspnea, and copious secretions. The early clinical manifestations of inhalation anthrax, tularemia, or plague may be similar to those of SEB.However, rapid progression of respiratory signs and symptoms to a stable state distinguishes SEB intoxication. Mustard exposure would have marked vesication of the skin in addition to the pulmonary injury.

(3) Specific Laboratory Diagnosis. Toxin is cleared from the serum rapidly and is difficult to detect by the time of symptom onset. Nevertheless, specific laboratory tests are available to detect SEB, and serum should be collected as early as possible after exposure. In situations where many individuals are symptomatic, sera should be obtained from those not yet showing evidence of clinical disease. Most patients develop a significant antibody response, but this may require 2-4 weeks.c. Therapy. Treatment is limited to supportive care. No specific antitoxin for human use is available.

d. Prophylaxis. There currently is no prophylaxis for SEB intoxication. Experimental immunization has protected monkeys, but no vaccine is presently available for human use.

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