Neospora spp are an ampicomplexan protozoan parasite of dogs with a seroprevalence of approximately 5% worlwide. Canine neosporosis is relatively rare, despite the relatively high prevalence of this parasite.
Species which are pathogenic to dogs include:
- Neospora caninum
Rural and wild dogs are the definitive hosts of Neospora spp and are capable of shedding oocysts in feces after eating tissues of infected animals. Oocysts are relatively hardy in the environment and can lay dormant for weeks, where they can be ingested by other dogs, pigs, horses, cats and humans.
Intermediate hosts such as cattle are thought to become infected by ingesting oocysts. Cattle do not produce oocysts and thus do not transmit infections horizontally to other cattle, but latent infection endures permanently in their tissues. It is thought that the cycle is completed with dogs eating material contaminated with oocysts. However, experimental reproduction of the entire cycle has been unrewarding and dog to dog transmission may thus perpetuate the life cycle in the absence of intermediate hosts.
Co-infections with Toxoplasma spp is common and it is possible a corelationship between the two and the onset of clinical signs may exist. Dogs in rural environments are more commonly infected, due to a greater risk of exposure to soil where the organism is normally found.
In young dogs, N. caninum are mainly responsible for diarrhea but can also contribute to neonatal mortality. Infections can cross the placental membranes and infected unborn puppies, which can be born dead or develop typical hindlimb paresis. In young dogs, acute deaths may occur due to translocation of the protozoa across the intestinal epithelium. Neurological disease such as progressive hindlimb paresis associated with acute protozoal polyradiculoneuritis, myositis, nodular dermatitis and muscle atrophy have been reported.
Adult dogs may develop disseminated neosporosis, characterized by nonsuppurative encephalomyelitis, necrotizing cerebellitis, cerebellar atrophy, neuritis of the cauda equina, focal cutaneous nodules or ulcers, pneumonia, peritonitis, myocarditis and . ELISA testing needs to rule out Toxoplasma spp and Sarcocystis spp in these cases.
As has been observed with canine herpesvirus in dogs, recrudescence of latent infection can be triggered with use of cyclosporin, prednisolone or cyclophosphamide, initiating tachyzoite migration through visceral and neural tissues.
Diagnosis is based on presenting clinical signs, fecal examination for oocysts (usually unreliable), ELISA detection of N. caninum antibodies in tissue samples, light microscopy identification of tachyzoites in CSF or other tissues and PCR assays for species identification.
A differential diagnosis in deaths associated with neonatal acute pup deaths would include canine herpesvirus and canine distemper virus. Other protozoan parasites and some bacteria can cause similar symptoms and must be excluded as a possible cause, including Leishmania spp, Giardia spp and Brucella spp.
The recommended drug of choice in treatment is clindamycin (10 - 50 mg/kg orally for 2 - 4 weeks), with aggressive supportive therapy in acutely ill pups.
Dogs of any age with neurological signs have a more guarded prognosis.
- University of Liverpool
- Norwegian School of Vet Science
- Sousa ME et al (2012) Seroprevalence of antibodies to Neospora caninum in dogs in the state of Alagoas, Brazil. Rev Bras Parasitol Vet 21(3):287-290
- Barber, JS & Trees, AJ (1998) Naturally occurring vertical transmission of Neospora caninum in dogs. Int J Parasitol 28:57-64
- Piagentini M et al (2012) Neospora caninum infection dynamics in dairy cattle. Parasitol Res 111(2):717-721
- Hill,m DE et al (2001) Specific detection of Neospora caninum oocysts in fecal samples from experimentally-infected dogs using the polymerase-chain reaction. J Parasitol 87:395
- King JS et al (2011) Implications of wild dog ecology on the sylvatic and domestic life cycle of Neospora caninum in Australia. Vet J 188(1):24-33
- Alves Neto AF et al (2011) Viability of sporulated oocysts of Neospora caninum after exposure to different physical and chemical treatments. J Parasitol 97(1):135-139
- Bandini LA et al (2011) Experimental infection of dogs (Canis familiaris) with sporulated oocysts of Neospora caninum. Vet Parasitol 176(2-3):151-156
- Langoni H et al (2012) Detection and molecular analysis of Toxoplasma gondii and Neospora caninum from dogs with neurological disorders. Rev Soc Bras Med Trop 45(3):365-368
- Sicupira PM et al (2012) Factors associated with infection by Neospora caninum in dogs in Brazil. Vet Parasitol 185(2-4):305-308
- Bowman, DD (2009) Georgis' Parasitology for veterinarians. 9th edn. Saunders Elsevier, Missouri. pp:102-103
- Holt N et al (2011) Seroprevalence of various infectious agents in dogs with suspected acute canine polyradiculoneuritis. J Vet Intern Med 25(2):261-266
- Garosi L et al (2010) Necrotizing cerebellitis and cerebellar atrophy caused by Neospora caninum infection: magnetic resonance imaging and clinicopathologic findings in seven dogs. J Vet Intern Med 24(3):571-578
- Saey V et al (2010) Neuritis of the cauda equina in a dog. J Small Anim Pract 51(10):549-552
- Galgut BI et al (2010) Detection of Neospora caninum tachyzoites in cerebrospinal fluid of a dog following prednisone and cyclosporine therapy. Vet Clin Pathol 39(3):386-390
- Hosseininejad M et al (2010) Development of an indirect ELISA test using an affinity purified surface antigen (P38) for serodiagnosis of canine Neospora caninum infection. Vet Parasitol 171(3-4):337-342
- Nghiem PP & Schatzberg SJ (2010) Conventional and molecular diagnostic testing for the acute neurologic patient. J Vet Emerg Crit Care (San Antonio) 20(1):46-61
- Valadas S et al (2010) Occurrence of antibodies anti-Neospora caninum, anti-Toxoplasma gondii, and anti-Leishmania chagasi in serum of dogs from Pará State, Amazon, Brazil. Parasitol Res 107(2):453-457