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Thrombocytopenia and Symmetrical Peripheral Gangrene Associated with Staphylococcal and Streptococcal Bacteremia

JAMES J. RAHAL JR., M.D.; H. EDWARD MACMAHON, M.D.; and LOUIS WEINSTEIN, PH.D., M.D., F.A.C.P.
Ann Intern Med. 1968;69(1):35-43. doi:10.7326/0003-4819-69-1-35
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SUMMARY:

Three cases of acute bacteremia due to gram-positive cocci in which thrombocytopenia was accompanied by either symmetrical peripheral gangrene or diffuse purpura were studied. The causal agent was Staphylococcus aureus in two and Streptococcus pyogenes in one. Plasma fibrinogen levels were normal in two patients and depressed in the third. Postmortem examination of the gangrenous fingertips of the patient in the first case (staphylococcal endocarditis) revealed occlusion of arterioles with fibrin thrombi, a dense polymorphonuclear reaction, and no demonstrable bacteria. The second patient had both peripheral gangrene and renal failure associated with streptococcal bacteremia. The renal glomeruli contained isolated capillary fibrin thrombi and blood in the capsular space. The third person developed purpura and hypofibrinogenemia during the course of staphylococcal endocarditis. Evidence of thrombosis was not present during life, but autopsy revealed bleeding into pulmonary alveoli and massive fibrin deposition in diffuse areas of septic infarction.

Available experimental evidence indicates that the extracellular toxins of both the staphylococcus and the streptococcus as well as the endotoxin of gram-negative organisms causes platelet damage and aggregation. Staphylococcal alpha toxin also produces marked vasospasm, and staphylocoagulase catalyzes the formation of fibrin from fibrinogen in vitro. The possible relationship of these substances to the clinical phenomena described has been discussed. It is concluded that a continuum exists between thrombocytopenia in severe staphylococcal and streptococcal infection and variable degrees of disseminated intravascular coagulation.

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