Annals of Internal Medicine · 1968 · 52 citations · 48 references
Life SciencesInfectious DiseasesPathologyBacteriologyHost-pathogen InteractionsMedical MicrobiologyBacterial InfectionsBacterial PathogenesisBacterial PathologyBloodstream InfectionsClinical BacteriologyMedical BacteriologyGangrenous InfectionGangrenous NecrosisGram-negative BacteremiaGram-negative Bacterial InfectionsGram-negative Bloodstream InfectionGram-positive Bacterial InfectionsGroup A Streptococcal InfectionStreptococcus Species
Article1 July 1968Thrombocytopenia and Symmetrical Peripheral Gangrene Associated with Staphylococcal and Streptococcal BacteremiaJAMES J. RAHAL JR., M.D., H. EDWARD MACMAHON, M.D., LOUIS WEINSTEIN, PH.D., M.D., F.A.C.P.JAMES J. RAHAL JR., M.D., H. EDWARD MACMAHON, M.D., LOUIS WEINSTEIN, PH.D., M.D., F.A.C.P.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-69-1-35 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThree 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....References1. MCKAY DG and MARGARETTEN W: Disseminated intravascular coagulation in virus diseases. Arch. Intern. Med. (Chicago) 120: 129, 1967. CrossrefMedlineGoogle Scholar2. SHAFFNER W, MCLEOD AC, and KOENIG MG: Thrombocytopenic Rocky Mountain spotted fever. Arch. Intern. Med. (Chicago) 116: 857, 1965. CrossrefMedlineGoogle Scholar3. CHERNOF D: Hypofibrinogenemia in scrub typhus. Report of a case. New Eng. J. Med. 276: 1195, 1967. CrossrefMedlineGoogle Scholar4. 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LEVIN J and CLUFF LE: Platelets and the Shwartzman phenomenon. J. Exp. Med. 121: 235, 1965. CrossrefMedlineGoogle Scholar62. RODRÍGUEZ-ERDMANN F: Pathogenesis of bilateral cortical necrosis of the kidneys. Hematological observations after the injection of staphylococcal toxin. Med. Pharmacol. Exp. (Basel) 15: 85, 1966. CrossrefMedlineGoogle Scholar63. RODRÍGUEZ-ERDMANN F: Bleeding due to increased intravascular blood coagulation. Hemorrhagic syndromes caused by consumption of blood-clotting factors (consumption-coagulopathies). New Eng. J. Med. 273: 1370, 1965. CrossrefMedlineGoogle Scholar64. MCKAY DG and MULLER-BERGHAUS G: Therapeutic implications of disseminated intravascular coagulation. Amer. J. Cardiol. 20: 392, 1967. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: JAMES J. RAHALJR., M.D.; H. EDWARD MACMAHON, M.D.; LOUIS WEINSTEIN, PH.D., M.D., F.A.C.P.Affiliations: Boston, MassachusettsFrom the Infectious Disease Service of the New England Medical Center Hospitals and the Departments of Medicine, Pediatrics, and Pathology, Tufts University School of Medicine, Boston, Mass.These studies were supported by training grant 5TIAI-276, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Md.Dr. Rahal was supported in this work by a research fellowship from the Medical Foundation, Inc., Boston, Mass.Requests for reprints should be addressed to James J. Rahal, Jr., M.D., New England Medical Center Hospitals, 171 Harrison Ave., Boston, Mass. 02111. 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HIRSCHMAN, M.D., F.A.C.P., WILLIAM SLOAN, M.D.DISSEMINATED INTRAVASCULAR COAGULATIONCase 48-1969 1 July 1968Volume 69, Issue 1Page: 35-43KeywordsAlveoliAutopsyBacteremiaEndocarditisFibrinFibrinogenInfectious diseasesStreptococcus pyogenesThrombosisToxins ePublished: 1 December 2008 Issue Published: 1 July 1968 PDF downloadLoading ...
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