While the pathogenicity of B. gibsoni is uniformly high, pathogenicity varies among the large Babesia species: B. rossi causes severe clinical disease; B. canis is variously pathogenic, and B. vogeli infection causes relatively mild subclinical disease except in puppies. The severity of disease is also influenced by the age, breed and immune status of the dog, previous Babesia infections or coinfection.
The duration of incubation is highly variable, in general 1-3 weeks, depending on the species of pathogen, but can occasionally be much shorter. The disease starts with fever, followed by reduced food intake, weight loss, anemia, thrombocytopenia, splenomegaly, quite often icterus and the most suggestive coloration of urine that turns to brown in color due to hemoglobinuria. Further signs including vomiting, syncope (fainting), edema, ascites, bleeding in the skin and the mucosa and diverse other symptoms up to central nervous disorders (i.e. with B. rossi) can be observed.
Apart from the suggestive acute forms presented above, canine babesiosis quite often appears as chronic infection with moderate hyperthermia, weight loss, lethargy, pulmonary or renal disease. In enzootic areas where many dogs are reinfected, the disease may be discovered in dogs that only show reduction of activity and anorexia.
The pathogenesis of babesiosis, caused by the intraerythrocytic protozoan parasites B. canis and B. gibsoni, involves progressive hemolytic anemia. The more severe disease caused by B. rossi can involve hypoxic, hypotensive shock with disseminated intravascular coagulation (DIC), systemic inflammatory response syndrome and multiple organ dysfunction syndrome (MODS). Some infections are sub-clinical, especially in dogs that are chronically infected.
Erythrocyte-bound autoantibodies are involved in the hemolytic form of the disease. There can be erythrocyte auto-agglutination and many dogs with babesiosis give a positive Coombs' test. In B. gibsoni infections hemoglobinemia and hemoglobinuria occur secondary to oxidative damage in parasitized red blood cells. There is enhanced damage by anti-erythrocyte antibodies and erythrophagocytosis occurs predominantly in the spleen.
Animals that recover usually become chronic (months to possibly lifelong) carriers of Babesia sp., even after treatment. Although these animals appear healthy unless subjected to stress, they provide a reservoir of infection for susceptible animals and have suboptimal athletic performance. They pose a risk if used as blood donors.
The clinical presentation of babesiosis may be complicated by co-infection with other tick-borne pathogens. Most commonly, co-infection with Ehrlichia canis occurs, as both pathogens share Rhipicephalus sanguineus as a tick vector. Dogs co-infected with these two organisms may be more likely to have hemolytic anemia complicated by hemorrhage secondary to the thrombocytopenia that occurs with canine monocytic ehrlichiosis (CME). Co-infections with other arthropod-borne agents have been documented, e.g. with bacteria of the genus Bartonella and Rickettsia.
- Fisher M, McGarry J: Focus on Small Animal Parasitology. 2006, Kingfisher Press Limited, London
- Shaw SE, Day MJ, Birtles RJ, et al.: Tick-borne infectious diseases of dogs. Trends Parasitol. 2001, 17, 74-80