Recent Advances in Determining the Pathogenesis of Canine Monocytic Ehrlichiosis

Abstract

Canine monocytic ehrlichiosis (CME) is a potentially fatal tick-borne disease caused by the rickettsia Ehrlichia canis (16). The etiologic agent was first recognized in Algeria in 1935 (8). Since then, it has been reported worldwide, causing extensive morbidity and mortality among domestic dogs and other canids (11, 28, 51). The principal vector of CME is Rhipicephalus sanguineus (11). Recently, it has been shown experimentally that Dermacentor variabilis is also capable of transmitting E. canis (24). The pathogenesis of CME consists of an incubation period of 8 to 20 days, followed sequentially by acute, subclinical, and in some cases chronic phases. The disease may be manifested by a wide variety of clinical signs of which depression, lethargy, weight loss, anorexia, pyrexia, lymphadenomegaly, splenomegaly, and bleeding tendencies are the most common. Principal hematologic abnormalities include thrombocytopenia, mild anemia and mild leukopenia during the acute stage, mild thrombocytopenia in the subclinical stage, and pancytopenia in the severe chronic stage. The main biochemical abnormalities include hypoalbuminemia, hyperglobulinemia, and hypergammaglobulinemia (16). CME has been researched extensively in the last decade, and special efforts have been made to elucidate the pathogenesis of the disease. Better understanding of major mechanisms involved in the pathogenesis of the disease may assist clinicians in understanding the disease process and providing appropriate treatment, affording a better prognosis to their patients. In the light of the recent emergence of similar ehrlichial pathogens that infect human patients, the understanding of pathogenic processes in CME may contribute to the understanding of human monocytic ehrlichiosis and human granulocytic ehrlichiosis. This article reviews recent investigations in the pathogenesis of CME with special reference to platelet disorders and serum protein alterations, the principal hematological and biochemical abnormalities in CME, respectively. Host immune response in both acute and persistent E. canis infection is discussed and is proposed to be involved in the pathogenesis of disease manifestations.

Evaluation of variation in serum globulin concentrations in dairy cattle

“…Indeed, hypoalbuminemia or decreased plasma oncotic pressure stimulates the production or reduces the rate of catabolism of serum globulins. 28,29 The results of this study suggest that serum globulin concentrations remain relatively constant over a medium-range time period (15 weeks) within a given physiological stage as long as environment and nutrition are not altered. However, total globulin concentrations can vary significantly among individuals, depending on breed, age, and lactational stage.…”

An acute severe ehrlichiosis in a dog experimentally infected with a new virulent strain of Ehrlichia canis

“…The liver necrosis may decrease the plasma protein level and colloidal osmotic pressure, which may eventually be the reason for oedema in CME. Harrus et al [2] speculated that the mechanism of thrombocytopenia in CME might be platelet consumption, increased splenic sequestration, and decreased platelet lifespan. Possible depleted synthesis of coagulation proteins in the liver due to necrosis may cause increased platelet aggregation, which may contribute to thrombocytopenia.…”

Serum Cardiac Troponin I Concentration in Dogs with Ehrlichiosis

“…5 Microscopic findings include lymphoreticular and plasma cell infiltration of the nervous system, kidneys, lungs, liver, and lymphoid tissues; severe hepatic steatosis and sinusoid congestion; chronic glomerulonephritis and renal vasculitis; and multifocal follicular hemorrhage and congestion in the spleen. [6][7][8] Cardiac abnormalities have been detected in dogs exposed to or experimentally infected with E. canis. [9][10][11] Although E. canis is considered a potential cause of cardiomyopathy, 12 its association with myocardial injury in a population of naturally infected dogs has not been clearly established.…”