Staphylococcus aureus bacteremia: A critical review of its treatment and association with infective endocarditis

Summary Bacterial endocarditis remains a serious complication of Staphylococcus aureus (coagulase positive) bacteremia. However, it occurs significantly less frequently in those who become bacteremic in hospital, in comparison to those whose infection is community-acquired. This difference appears related to a longer bacteremic period, prior to therapy, in those with community-acquired disease. Since a significant percentage of strains of Staphylococcus aureus are still resistent to penicillin, initial treatment should include a penicillinase resistent penicillin or cephalosporin. Those patients without endocarditis appear optimally treated with two to three weeks of appropriate antibiotic therapy.

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Staphylokokkus-aureus-Bakteriämie: Eine kritische Übersicht ihrer Behandlung und Beziehung zur Endokarditis

Zusammenfassung Die bakterielle Endokarditis bleibt eine ernste Komplikation der Staphylokokkenbakteriämie. Sie tritt jedoch bedeutend weniger häufig im Hospital auf im Vergleich zu außerhalb. Dieser Unterschied scheint in Beziehung zu stehen zu einer längeren bakteriämischen Periode vor der Therapie bei den außerhalb des Krankenhauses erworbenen Erkrankungen. Da ein erheblicher Anteil von Staphylokokkenstämmen immer noch penicillinresistent sind, sollte die Initialbehandlung mit Hilfe eines penicillinasefesten Penicillins oder eines Cephalosporins erfolgen. Die Patienten ohne Endokarditis erscheinen innerhalb von zwei bis drei Wochen bei entsprechender Wahl des Antibiotikums optimal behandelt.

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Dr. Austin is the recipient of a grant from the Ontario Government, Dept. of Public Health.     

METABOLISM AND FUNCTION OF GAMMA GLOBULIN IN ALEUTIAN DISEASE OF MINK

Aleutian disease-affected mink, which are markedly hypergammaglobulinemic, show a decreased half-life of the serum gamma globulin indicating that the hyperglobulinemia is due to increased production. No evidence that the gamma globulin was antibody to the infectious agent, to autologous or isologous tissues, or to antigens the animal was responding to prior to development of the disease was obtained. The increased gamma globulin was found to be of the 6.4S variety, and gamma globulin containing protein-protein complexes of 9S to 17S and 22S to 25S classes were observed in serums of affected mink. The findings are most consistent with the Aleutian disease virus acting as a direct and somewhat selective stimulus to plasma cell proliferation. There is no evidence that the arterial and glomerular lesions of Aleutian disease have an immunologic pathogenesis. It seems possible that these vascular changes may be directly caused by the viral agent, or may be the result of the increased gamma globulin levels.