Neospora caninum

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Neosporosis, a disease with a global distribution and caused by the coccidian parasite Neospora caninum, is important in domestic animals and causes high abortion rates in cattle and fatal neuromuscular disease in dogs. The infection is present in several wildlife species and they are probably involved in the sylvatic cycle of the parasite [1] By and large, the occurrence and importance of neosporosis in wildlife remains unknown but there are currently no indications that this infection has an adverse effect on any of the wildlife populations in which it has been detected[2]. The parasite is not considered to be a zoonotic threat although serology has indicated its presence in immunocompromised humans[2].

[3] [4] [5] [6] [7] [8] [9] [10]

African wildlife

The infection has been detected serologically in a range of African wildlife species in a number of African countries[11][12][13]

Carnivora: African wild dog, spotted hyena, common genet, Egyptian mongoose, cheetah, lion[14], caracal, and serval[2][15].

Artiodactyla: African buffalo, Thompson's gazelle, lechwe, eland, and sitatunga[2].

Perissodactyla: Zebra, and white rhinoceros[2][16] [17][18].

Rodentia: Various, including the crested porcupine[19][2].

Lagomorphs: Various[2].

Insectivora: Various[2].

Proboscidea: Not reported in African elephants[2].

Cetacea: Bottle-nosed dolphins[2].

Pinnipedia: Various[2].

Marsupials: Rare[2].

Birds:: Various free-ranging birds[2].

Snakes: : Various[20]


The epidemiology of the disease in wildlife is unknown. The source of the infection in the white rhinos that succummed could not be traced [21]


Sporozoites transform into tachyzoites that have the ability to infect a wide range of host cells. They are transferred throughout the body after entering mononuclear blood cells. In host cells they develop within parasitophorous vacuoles. Progressive cycles and the release of tachyzoites cause the development of cell lysis and initiation of immonopathological mechanisms of tissue damage. Following about 20 replication cycles, the tachyzoites differentiate into bradyzoites within tissue cysts allowing them to escape the effects of the host's immune system allowing long-term parasitic persistence and a chronic asymptomatic infection. Recrudesence of this chronic infection may be caused by states of immunosuppression or immuno-incompetence with the development of clinical disease[2]

Clinical signs and pathology

With the exception of white rhinos, no other wildlife species have been diagnosed with clinical neosporosis and death due to the infection[16][17][18].

In white rhinos the following features were reported:

Aborted foetus[17]: The seven-month-old foetus was aborted spontaneously. The female was in good health althought she had a history of manifesting indistinct neurological signs since a previous and the placenta was also normal. At necropsy the liver was enlarged and histologically it contained multiple random foci of hepatocellular necrosis in association with small numbers of lymphocytes, plasma cells and neutrophils. Protozoal tachyzoites were present in clusters between the hepatocytes and within the necrotic debris. Similar parasites were also present in the cerebellum.

Neonatal death[18]: A sixteen-day-old white rhino calf died suddenly with lesions at necropsy indicating heart failure due to cardiac hypertrophy. Histologically there was a marked multifocal to diffuse myocarditis with disruption and disintegration of myofibres, and a marked round cell inflammatory reaction. The inflammatory cells comprised macrophages, plasma cells, lymphocytes and scattered neutrophils. Giemsa-stained sections revealed the presence of cysts and free organisms within the cells and within the interstitium interspersed with the inflammatory cells. With the exception of the liver in which there was mild centrilobular fibrosis and single cell necrosis of the perivenular hepatocytes (most likely as a consequence of congestive heart failure) no specific lesions or parasites were present in any of the other organs examined histologically[18]

Adult animal[16]: A 15-year-old zoo-kept rhino died after a short illness. At necropsy conspicuous lesions were present in the liver, lungs, spleen, and kidneys. Most of the lesions reflected the presence of necrosis in association with haemorrhage. The lesions in the liver were multifocal, firm and necrotic ranging in diameter from 1 − 13 cm. Gastric erosions and ulcers with accompanying bleeding were present. Numerous large haemorrhages occurred in the various organs, lymph nodes and adrenal. Histologically necrotic lesions were seen in the liver, kidney, adrenal cortex, spleen, lymph nodes, and in the small intestine. Numerous tachyzoites were present in the liver, spleen, adrenal cortex and in the kidneys. No protozoa were seen in the central nervous system of in the heart.


Neospora caninum is an obligate, intracellular, cyst-forming coccidian parasite. It is closely related to Toxoplasma gondii and very similar to it in terms of its biological features and its morphology [2]. N. caninum has a complex facultative heterogenous life cycle involving a definitive canine host and a number of intermdiate hosts. Sexual replication takes place in the canid host (domestic and feral dogs, gray wolves, coyotes and dingos), and the asexual stage in intermediate hosts such as cattle, and a number of wildlife[2].

The life cycle has three known stages: sporozoites in sporulated environmentally resistant oocysts, and tachy- and bradyzoites in tissue cysts. Oocysts undergo sporulation with the development of two sporocysts each containing four sporozoites. [2].

The presence of the parasite can be detected histologically in HE- and Giemsa-stained sections, and its genus confirmed by immunoperoxidase and PCR techniques[17][16].


Control measures for neosporosis in domesticated animals is complicated, given the likely role of wildlife in its life cycle.


  1. Gondim, L. F. (2006). Neospora caninum in wildlife. Trends in Parasitology, 22(6), 247-252.
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 Donahoe, S. L., Lindsay, S. A., Krockenberger, M., Phalen, D., & Šlapeta, J. (2015). A review of neosporosis and pathologic findings of Neospora caninum infection in wildlife. International Journal for Parasitology: Parasites and Wildlife, 4(2), 216-238.
  3. Šlapeta, J. R., Modrý, D., Votýpka, J., Jirků, M., Lukeš, J., & Koudela, B. (2003). Evolutionary relationships among cyst-forming coccidia Sarcocystis spp.(Alveolata: Apicomplexa: Coccidea) in endemic African tree vipers and perspective for evolution of heteroxenous life cycle. Molecular Phylogenetics and Evolution, 27(3), 464-475.
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  8. Haas, S. K., Hayssen, V., & Krausman, P. R. (2005). Panthera leo. Mammalian Species, 1-11.[0001:PL]2.0.CO;2
  9. Ayinmode, A. B., & Akanbi, I. M. (2013). First report of antibodies to Neospora caninum in Nigerian cattle. The Journal of Infection in Developing Countries, 7(07), 564-565.
  10. Beechler, B. R., Manore, C. A., Reininghaus, B., O'Neal, D., Gorsich, E. E., Ezenwa, V. O., & Jolles, A. E. (2015). Enemies and turncoats: bovine tuberculosis exposes pathogenic potential of Rift Valley fever virus in a common host, African buffalo (Syncerus caffer). Proceedings of the Royal Society of London B: Biological Sciences, 282(1805), 20142942.
  11. Ferroglio, E., Wambwa, E., Castiello, M., Trisciuoglio, A., Prouteau, A., Pradere, E., ... & De Meneghi, D. (2003). Antibodies to Neospora caninum in wild animals from Kenya, East Africa. Veterinary Parasitology, 118(1), 43-49.
  12. Millán, J., Chirife, A. D., Kalema-Zikusoka, G., Cabezón, O., Muro, J., Marco, I., ... & Mugisha, L. (2013). Serosurvey of dogs for human, livestock, and wildlife pathogens, Uganda. Emerging Infectious Diseases, 19(4), 680.
  13. Asmare, K., Regassa, F., Robertson, L. J., & Skjerve, E. (2013). Seroprevalence of Neospora caninum and associated risk factors in intensive or semi-intensively managed dairy and breeding cattle of Ethiopia. Veterinary Parasitology, 193(1), 85-94.
  14. Mukarati, N. L., Vassilev, G. D., Tagwireyi, W. M., & Tavengwa, M. (2013). Occurrence, prevalence and intensity of internal parasite infections in African lions (Panthera leo) in enclosures at a recreational park in Zimbabwe. Journal of Zoo and Wildlife Medicine, 44(3), 686-693.
  15. Cheadle, M. A., Spencer, J. A., & Blagburn, B. L. (1999). Seroprevalences of Neospora caninum and Toxoplasma gondii in nondomestic felids from southern Africa. Journal of Zoo and Wildlife Medicine, 248-251.
  16. 16.0 16.1 16.2 16.3 Sommanustweechai, A., Vongpakorn, M., Kasantikul, T., Taewnean, J., Siriaroonrat, B., Bush, M., & Pirarat, N. (2010). Systemic neosporosis in a white rhinoceros. Journal of Zoo and Wildlife Medicine, 41(1), 165-168.
  17. 17.0 17.1 17.2 17.3 Sangster, C., Bryant, B., Campbell-Ward, M., King, J. S., & Šlapeta, J. (2010). Neosporosis in an aborted southern white rhinoceros (Ceratotherium simum simum) fetus. Journal of Zoo and Wildlife Medicine, 41(4), 725-728.
  18. 18.0 18.1 18.2 18.3 Williams, J. H., Espie, I., Van Wilpe, E., & Matthee, A. (2002). Neosporosis in a white rhinoceros (Ceratotherium simum) calf: special report. Journal of the South African Veterinary Association, 73(1), p-38.
  19. Harrison, T. M., Moorman, J. B., Bolin, S. R., Grosjean, N. L., Lim, A., & Fitzgerald, S. D. (2007). Toxoplasma gondii in an African crested porcupine (Hystrix cristata). Journal of Veterinary Diagnostic Investigation, 19(2), 191-194.
  20. Šlapeta, J. R., Modrý, D., Votýpka, J., Jirků, M., Lukeš, J., & Koudela, B. (2003). Evolutionary relationships among cyst-forming coccidia Sarcocystis spp.(Alveolata: Apicomplexa: Coccidea) in endemic African tree vipers and perspective for evolution of heteroxenous life cycle. Molecular Phylogenetics and Evolution, 27(3), 464-475.
  21. Rosypal, A. C., & Lindsay, D. S. (2005). The sylvatic cycle of Neospora caninum: where do we go from here?. Trends in Parasitology, 21(10), 439-440.

External links

Wikipedia: Neospora caninum