Canine babesiosis continues to create challenges for practitioners
Researchers at Oklahoma State University experimentally infected dogs with blood from two naturally infected Pit Bulls from Oklahoma. One of the source dogs had been treated twice with imidocarb but still had detectable organisms in the blood. Parasitemia was detected in all dogs within one to five weeks after innoculation and peaked at four to six weeks before declining. The degree of parasitemia was 1.9-6 percent, except in the splenectomized dog which reached 16.4 percent before euthanasia. All dogs developed regenerative anemia and marked thrombocytopenia within one to three weeks post innoculation. Clinical signs included lethargy, fever and pallor, but were mild or inapparent in some dogs (Photo 4). Parasitemia persisted for three to four weeks and then became undetectable as the dogs apparently entered a carrier state.
Initial reports of the Babesia gibsoni organism isolated from dogs in the Midwest and Southeast United States seem to indicate that it is not as pathogenic as the California isolate. Although acute infection is associated with severe anemia and thrombocytopenia, many dogs survive the acute phase and become chronic carriers. A recent study reported that 55 percent of American Pit Bull dogs tested in Alabama were subclinically infected. Dogs with subclinical infections had lower hematocrits and platelet counts and increased mean platelet volume compared to dogs that were negative. The tendency to relapse or exhibit signs of vasculitis, protein-losing nephropathy or hepatic failure that is seen in dogs infected with the California isolate has not been reported in dogs chronically infected with the Southeast/Midwest United States isolate.
Pathogenesis Babesia spp. sporozoites are present in the salivary glands of the infected tick vector and are transmitted to the dog during feeding. This transmission requires two or three days. The sporozoites enter the red blood cells and multiply by binary fission. Although dogs usually mount a good humoral immune response to infection, they are unable to clear the parasitemia and become chronic carriers. The parasites induce fibrinogen like proteases (FLP) that cause the red blood cells to become sticky, resulting in capillary sludging. Parasitized cells are sequestered in the spleen, and extravascular and intravascular hemolysis occurs (Photo 5, p. 10). The incubation period following tick transmission is 10-21 days.
Infected dogs may exhibit either peracute, acute or subclinical signs of disease. Pathogenicity is increased in young dogs, immunosuppressed dogs, heavily parasitized dogs, and when there is exposure to a virulent strain or concurrent infection with other tick-borne pathogens (ehrlichiosis, hepatozoonosis, leishmaniasis).
Most dogs in the Uinted States that are seropositive for Babesia canis or B. gibsoni have subclinical infections. However, severe disease has been seen in puppies born to seropositive dams, and has been reported in a dog that received a blood transfusion from an asymptomatic dog with a positive babesia titer. Babesiosis has also been implicated as an underlying factor in cases of acute hemolytic anemia in dogs.
Transmission Babesia organisms are transmitted to dogs by ticks during feeding. Known vectors outside the United States include Haemophysalis bispinosa and H. longicornis. In the United States, Rhipicephalus sanguineus is the suspected vector for both species. The risk of infection can be reduced for dogs living in endemic areas by providing aggressive tick control with a topical acaricide and flea/tick collar as well as inspecting them daily for ticks. It is possible that biting flies or other blood-sucking insects may be capable of transmission as well.