All Posts Tagged With: "hypersplenism"

Mechanisms of Thrombocytopenia in Tick-Borne Diseases

Full article: http://www.ispub.com/ostia/index.php

Excerpt:

Thrombocytopenia is a common manifestation of all tick-borne diseases. Low platelet numbers contribute significantly towards the morbidity and mortality of infection. However, the pathogenesis of thrombocytopenia in many of the tick-borne diseases is poorly understood. Quantitative changes in platelet counts associated with infection may result from decreased marrow production, hypersplenism, consumption due to widespread endothelial damage or disseminated intravascular coagulation, as well as immune-mediated platelet destruction. Infection-induced thrombocytopenia may infrequently be associated with serious thrombosis. Direct infection of platelets by selected tick-borne pathogens also facilitates their dissemination within the host. This article reviews the mechanisms of thrombocytopenia associated with tick-borne infections, and discusses the therapeutic options available for managing this potentially fatal complication.

Conclusions

Thrombocytopenia due to tick-borne infection is likely to be of multifactorial etiology. In many of these infections, however, the actual mechanism of thrombocytopenia still remains unknown. Iatrogenic causes in some cases, such as drugs, should not be overlooked. Low platelet numbers in infected individuals may not only manifest with increased bleeding, but may herald more widespread life-threatening microthrombus formation. In addition to quantitative platelet disorders, qualitative defects may also be present. For example, inhibition of platelet migration has been induced by serum from E.canis-infected dogs, even before platelet numbers declined and before the appearance of specific humoral
antibodies (Kakoma et al 1978). The release of platelet factor 3, a phospholipid released from activated platelets that is necessary for the intrinsic conversion of prothrombin to thrombin, is also markedly decreased as a result of ehrlichial infection (Pierce et al 1977). Furthermore, platelet aggregation in ehrlichiosis can be prevented by autoantibodies directed against their surface glycoproteins (Lovering et al 1980; Harrus et al 1996).

Therapy for thrombocytopenia requires treatment or removal of the underlying infection, in addition to maintenance of platelet counts and hemostatic function. However, identification and correction of a specific tick-borne infection is only possible if the infection is considered in the differential diagnosis of thrombocytopenia. Rapid treatment of the underlying infection should result in normalization of platelet counts. Ehrlichia, bartonella and RMSF should also be excluded in cases presenting with a clinical picture resembling TTP, particularly in those patients that prove difficult to manage, and in regions where the incidence of tick-borne illness is high. The efficacy of platelet transfusions in many of the tick-borne diseases is unclear and anecdotal (Van Eeden et al 1985).