Pathophysiology of bacteremia.
Despite the frequency and importance of both nosocomial and "community-acquired" bacteremia, definitive information concerning crucial pathophysiologic events in human bacteremia remains sparse. An extensive variety of clinical manifestations, such as fever, rigors, shock, altered circulatory dynamics, cutaneous manifestations changes in the coagulation, complement, and other mediator systems, and effects on the lungs, heart, kidney, liver, and other end organs, have been described, but it is difficult to determine the relative frequency of these events in bacteremia caused by different species. The extensive number of bacterial species capable of producing bacteremia and variations in the type of presentation, such as acute, asymptomatic, and chronic, even when bacteremia is produced by the same species, undoubtedly contribute to this difficulty and suggest that a variety of pathophysiologic mechanisms occur in various bacteremias. In contrast, the relative frequency of various manifestations and some pathophysiologic mechanisms have been better delineated in Gram-negative bacteremia. The development of bacteremia enhances the lethality of most types of localized infection and several studies have demonstrated a relation between the magnitude of bacteremia and the outcome of the disease. Among various pathophysiologic alterations, mechanisms involved in the production of fever have been delineated most clearly. Fever appears to reflect a "common pathway" with almost all infectious agents and results from release of endogenous pyrogen from phagocytic cells. Endogenous pyrogen regulates the thermostatic setting of the body through its effect on the anterior hypothalamus. Endogenous pyrogen seems identical with Interleukin 1 and exerts a variety of other biologic activities. An extensive number of bacterial components have been proposed as "effectors" and an equally large number of endogenous substances proposed as "mediators" of the pathophysiologic events in bacteremia. The importance of many of these effectors and mediators has been postulated largely on the basis of in vitro and animal studies. The lack of critical clinical studies hampers extrapolation of these experimental studies to human bacteremia. The development of more effective therapy for the complications of bacteremia, such as shock, will continue to be hampered until the mechanisms involved in the production of those pathophysiologic events that are crucial determinants of outcome have been delineated more precisely in human disease.
D001427:Bacterial Toxins / Q000494:pharmacology; D001777:Blood Coagulation; D001778:Blood Coagulation Disorders / Q000209:etiology; D003167:Complement Activation; D004211:Disseminated Intravascular Coagulation / Q000209:etiology; D004723:Endorphins / Q000502:physiology; D004731:Endotoxins / Q000494:pharmacology; D005334:Fever / Q000209:etiology; D006331:Heart Diseases / Q000209:etiology; D006801:Humans; D007674:Kidney Diseases / Q000209:etiology; D008099:Liver / Q000503:physiopathology; D011453:Prostaglandins / Q000502:physiology; D011749:Pyrogens / Q000096:biosynthesis; D012128:Respiratory Distress Syndrome / Q000209:etiology; D018805:Sepsis / Q000503:physiopathology*; D012768:Shivering; D012772:Shock, Septic / Q000209:etiology; D012877:Skin Manifestations
D001427:Bacterial Toxins; D004723:Endorphins; D004731:Endotoxins; D011453:Prostaglandins; D011749:Pyrogens