Canine babesiois
Paolo Silvestrini, examines the pathogenesis, diagnosis, treatment and prevention of canine babesiois, a tick-borne and transmitted disease caused by apicomplexan haemoprotozoan parasites of the order Piroplasmida.
These parasites are structurally, functionally and phylogenetically related to the Plasmodium species that cause malaria. Babesia species infect a variety of domestic and wild animals and also humans. In dogs, the three large (2.5-5μm) Babesia species, Babesia canis, Babesia vogeli and Babesia rossi, and the small (1-2.5μm) Babesia gibsoni, Babesia conradae and Babesia vulpis have been described.
Canine babesiosis has a worldwide 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. These include Norway, the Netherlands and 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 species 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-to-blood 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.
Clinical signs can vary, ranging from subclinical infections to multi-organ failure and risk of death. This, as reported above, is influenced by many factors including the host's age, immune competence, previous splenectomy, concomitant infection and/or disease. Differences in virulence have been also described among Babesia species. Babesia vogeli is considered the least pathogenic, while Babesia rossi is the most virulent one. In general, the pathogenicity of small-sized Babesia species, such as Babesia gibsoni and Babesia vulpis, is higher than large Babesia species.
Lethargy, weakness, anorexia and pale mucous membranes are the most common clinical signs reported in dogs with babesiosis. On physical examination, fever, enlarged lymph nodes and spleen, petechiae, ecchymosis and jaundice can often be present. Anaemia, thrombocytopenia, hyperbilirubinemia and pigmenturia are commonly detected on blood and urinalysis. Anaemia can be moderate to severe, regenerative or non-regenerative and generally caused by a combination of intra- and extravascular haemolysis due to parasite-caused injury and rupture of red blood cells, increased osmotic fragility and secondary immune-mediated haemolysis (IMHA). Immune-mediated neutropenia (IMN) and thrombocytopenia (IMTP) are also often detected.
Dogs infected with Babesia rossi can develop very severe clinical signs including acute glomerulonephritis, disseminated intravascular coagulopathy (DIC), acute liver failure, IMHA and IMTP, shock, gastro-intestinal diseases (vomiting and diarrhoea), pancreatitis, acute blindness, rhabdomyolysis and acute respiratory disease (pulmonary oedema, haemorrhage).
Diagnosis
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. Polymerase chain reaction (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. These are aimed at reducing the exposure to vector ticks. A variety of products including permethrin, amitraz, fipronil, imidacloprid and other chemicals are available on the market 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.
References
- Cook, S., English, K., Humm, K. 2016. Autochthonous babesiosis in the United Kingdom. Journal of Small Animal Practice
- Cook, S., Swann, J.W. 2016. Canine babesiosis: autochthonous today, endemic tomorrow? Veterinary Record 178, 417-419
- Eichenberger, R.M., Riond, B., Willi, B. et al. 2016. Prognostic markers in acute Babesia canis infections. Journal of Veterinary Internal Medicine 30, 174-182
- Holman, P.J., Snowden, K.F. 2009. Canine Hepatozoonosis and Babesiosis, and Feline Cytauxzoonosis. Veterinary Clinics of North America: Small Animal Practice 39, 1035-1053
- Lau, A.O. 2009. An overview of the Babesia, Plasmodium and Theileria genomes: a comparative perspective. Journal of Molecular Biochemistry. 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. Veterinary Record 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. Journal of Veterinary Internal Medicine 23, 493-498
- Solano-Gallego, L., Baneth, G. 2011. Babesiosis in dogs and cats – Expanding parasitological and clinical spectra. Veterinary Parasitology 181, 48-60
- Swainsbury, C., Bengtson, G. & Hill, P. (2016) Babesiosis in dogs. Veterinary Record 178, 172.