Canine babesiosis continues to create challenges for practitioners

Canine babesiosis continues to create challenges for practitioners

Photo 1: Babesia canis in the red blood cells of an infected dog. Note the paired piriform shaped organisms.
Parasites of the genus Babesia are hemoprotozoan organisms that can infect red blood cells of vertebrate hosts. Although more than 100 species of Babesia have been identified, only two have been reported to infect dogs: Babesia canis and Babesia gibsoni. These organisms have traditionally been differentiated based on their appearance in stained blood smears. Babesia canis organisms are larger, and appear as bilobed piriform organisms that often occur in pairs and are about 4-5 um in length (Photo 1). Babesia gibsoni organisms are smaller (1-2.5 ┬Ám in diameter) and appear as round to oval or ring-shaped organisms, usually single, in red blood cells (Photo 2). Babesia canis is endemic in Europe, Southern Africa, Asia and the Americas. Babesia gibsoni is found in Southern Asia, the Middle East and Northern Africa. Recent reports indicate that Babesia gibsoni is an emerging vector-borne disease among dogs in the United States, as well.

Babesia canis - "large" babesia There are three subtypes of Babesia canis: B. canis canis, B. canis vogeli and B. canis rossi. These strains differ in virulence, geographic location and tick vector, but are identical in appearance. In the United States, the most common strain is B. canis vogeli, which is the least pathogenic form. Although severe hemolytic anemia, thrombocytopenia and life-threatening disease have been reported in young dogs, heavily parasitized dogs and dogs transfused with infected blood; most dogs infected with B. canis vogeli in the United States are subclinical carriers.

Photo 2: Babesia gibsoni organisms can easily be overlooked in a blood smear because they are small, usually single and pleomorphic. Most of the dogs in the United States reported to have Babesia gibsoni infection have been American Pit Bull terriers. Subclinical disease and a carrier state are common in this breed.
Although not highly pathogenic, the B. canis vogeli organism appears to be endemic in the Southeastern United States, particularly among Greyhounds. In 1992, Taboada found that 46 percent of Florida racing Greyhounds had positive titers for Babesia canis. In another study of dogs in California animal shelters, 13 percent were positive for Babesia canis. In 1995 alone, 16,000 Greyhounds were adopted into households throughout the United States. These dogs, as well as stray animals, provide a potential reservoir for the disease. A recent study differentiating the three subspecies of Babesia canis by polymerase chain reaction and restriction enzyme analysis suggests that they may actually be closely related but distinct and separate species. The most pathogenic type, B canis rossi, is endemic in South Africa. Babesia canis canis is found in Europe and parts of Asia and is considered intermediate in pathogenicity. A fourth type of large canine piroplasm was recently identified in a dog from North Carolina undergoing chemotherapy for lymphosarcoma. Although the organism was morphologically identical to B. canis, PCR and antibody tests for known canine species were negative and gene sequencing showed marked differences from B. canis and B. gibsoni gene fragment analysis.

"Small" babesia-gibsoni and others Small babesia organisms infecting dogs were first identified as Babesia gibsoni in dogs and jackals from India in 1910. This parasite is now considered endemic among dogs in Northern Africa, the Middle East and Southern Asia. The first case of a small babesia organism in a dog in the United States was reported in 1968, but this dog was a Bull Terrier from Malaysia that had been infected prior to shipment to the United States. In 1991, Conrad reported 11 dogs from Southern California that were infected with a small babesia organism and developed severe hemolytic anemia and thrombocytopenia. Based on morphologic appearance, the California organism was initially identified as Babesia gibsoni. However, recent evidence, based on PCR assays and gene sequencing, has identified at least three different small babesia organisms that infect dogs.

The organism initially identified by Conrad et al as Babesia gibsoni has now been shown to be genetically distinct from small babesia isolates originating from Japan, Sri Lanka and Malaysia. The genetic sequence of the California isolate most closely resembles Thelieria spp, and will likely be renamed in the future.

Experimental inoculation of dogs with the California isolate causes acute parasitemia, lethargy, anemia, thrombo-cytopenia and hemoglobinuria. Histopathologic lesions include diffuse nonsuppurative periportal and centrilobular hepatitis, multifocal necrotizing arteritis, membranoproliferative glomerulonephritis, reactive lymphadenopathy, diffuse erythrophagocytosis and extramedullary hematopoesis. In naturally infected dogs, parasitemia has been reported to be 5-40 percent. Cases of naturally infected dogs in California were initially misdiagnosed as immune-mediated hemolytic anemia because the parasites were not recognized on the blood smears of infected dogs and the dogs had positive direct antiglobulin (Coomb's) tests (Photo 3). It has been suggested that Giemsa or Field staining of blood smears is superior to Wright's or Diff-quick stains, and may facilitate detection of parasites. Treatment of the California isolate has not been rewarding. Although anti-babesial drugs may reduce circulating parasitemia, no treatment has been found that will eliminate the carrier state. Relapses were seen in two out of five dogs treated by Conrad et al, and six out of 11 died or were euthanatized. The chronic antigenic stimulation associated with persistent infection can result in chronic glomerulonephritis, hepatic failure or vasculitis. Even if recovered dogs do not succumb to chronic disease, they serve as a potential reservoir for infection of other dogs.