Focus on Disease: Canine Babesiois

Paolo Silvestrini DVM SPCAA MSc PhD Dipl ECVIM-CA MRCVS

Published October 2016 

Reviewed and updated October 2019


Canine babesiosis is a tick-borne and transmitted disease caused by apicomplexan haemoprotozoan parasites of the order Piroplasmida. They are structurally, functionally and phylogenetically related to Plasmodium species which cause malaria. Babesia species infect a variety of domestic and wild animals, and also humans. In dogs, the three large (2.5-5 μm) Babesia species, B. canis, B. vogeli and B. rossi, and the small (1-2.5 μm) B. gibsoni, B. conradae and B. vulpis have been described. Canine babesiosis has a world-wide distribution that is largely dependent on the presence of suitable habitats for relevant vector tick species. However there has been evidence of dog-to-dog transmission independent of tick infestation by Babesia gibsoni in fighting dogs. In non-endemic areas such as the UK, cases are usually restricted to animals that have travelled to areas where Babesia infection is endemic. However, autochthonous (locally acquired) cases of canine babesiosis are being increasingly reported in what have previously been considered non-endemic regions including Norway, the Netherlands and recently in Essex in the United Kingdom.


Pathogenesis and clinical signs

Pathogenesis and clinical signs of the disease are variable and are influenced by the immune status of the host as well as the species or subspecies of the infecting parasites. The spleen has an important function in controlling the infection and splenectomy is an important risk factor for the development of the disease in humans as well as in dogs. Natural infections of Babesia spp. are principally transmitted to the dog during feeding by vector ticks carrying the protozoan parasites. Animals are infected when Babesia sporozoites are injected with saliva into the host’s skin during the blood meal. However, as stated above, blood-toblood transfer (transfusion of infected blood, fight with an infected dog, or mechanical transmission) and vertical transmission from infected dam to offspring may occur. Once in the host, parasites attach to erythrocyte membranes and invade the cell cytoplasm where they form ring-shaped trophozoites. The parasite then replicates within the erythrocyte and forms merozoites observed as the pairs of attached pear-shaped parasites that can further divide forming eight or more parasites in the same red blood cell eventually causing red blood cell lysis and release into the blood.



Practitioners in the UK should consider Babesia part of their differential diagnosis where dogs have either recently travelled to endemic areas, or in the UK, animals living or travelling close to the Essex area. Babesia infections may be confirmed microscopically by the observation of intraerythrocytic piroplasms on Romanosky-type stained blood films; however, it is not very sensitive. In addition, identification of the parasite by microscopic examination is not reliable for species differentiation. Immunofluorescence antibody tests are available and additional species-specific tests are offered by several veterinary medical diagnostic laboratories. Serology can be negative in early acute infection. PCR is probably the most sensitive and specific method of confirming infection and determining the Babesia species involved.


Treatment and prevention

Different drugs, doses and treatment duration are used for the different species of Babesia. Large Babesia are commonly treated with imidocarb dipropionate (Imizol) with a good clinical response. Small Babesia appear to be more difficult to treat and resistant to the conventional drugs. Diminazene and the combination of Atovaquone and Azithromycin have been used with variable success. Prevention relies mostly on topical and environmental acaricidal treatments aimed at reducing the exposure to vector ticks. A variety of products including permethrin, amitraz, fipronil, imidocloprid and other chemicals are available on the marked in collars, spot on formulations and sprays. Vaccines against Babesia canis are available in some countries in Europe and the reported efficacy is between 70% and 100%. Vaccination does not prevent infection but blocks the evolution of the disease and reduces the severity of clinical signs. In the UK, it will be important to monitor the national distribution of Babesia in dogs to see if autochthonous cases are spreading out from what currently appears to be a localised Essex focus.



COOK, S., ENGLISH, K., HUMM, K. 2016. Autochthonous babesiosis in the United Kingdom. J Small Anim Practice

COOK, S., SWANN, J.W. 2016. Canine babesiosis: autochthonous today, endemic tomorrow? Vet Rec 178, 417-419.

EICHENBERGER, R.M., RIOND, B., WILLI, B. et al. 2016. Prognostic markers in acute Babesia canis infections. J Vet Intern Med 30, 174-182.

HOLMAN, P.J., SNOWDEN, K.F. 2009. Canine Hepatozoonosis and Babesiosis, and Feline Cytauxzoonosis. Vet Clin Small Anim 39, 1035-1053.

LAU, A.O. 2009. An overview of the Babesia, Plasmodium and Theileria genomes: a comparative perspective. Mol Biochem. Parasitol. 164, 1-8.

PHIPPS, L. P., DEL MAR FERNANDEZ DE MARCO, M., HERNANDEZTRIANA, L. M., JOHNSON, N., SWAINSBURY, C., MEDLOCK, J. M., HANSFORD, K. & MITCHELL, S. (2016) Babesia canis detected in dogs and associated ticks from Essex. Vet Rec 178, 243-244

SAKUMA, M., SETOGUCHI, A., ENDO, Y. 2009. Possible emergence of drug-resistant variants of Babesia gibsoni in clinical cases treated with Atovaquone and Azithromycin. J Vet Intern Med 23, 493-498.

SOLANO-GALLEGO, L., BANETH, G. 2011. Babesiosis in dogs and cats – Expanding parasitological and clinical spectra. Vet Paras 181, 48-60.

SWAINSBURY, C., BENGTSON, G. & HILL, P. (2016) Babesiosis in dogs. Vet Rec 178, 172