BackgroundToxoplasma gondii is a ubiquitous protozoan parasite that can infect humans and animals. The severity of toxoplasmosis varies according to the immune status of the individual, parasite strain, and host species. In mammalian species, it has been observed that severe lesions of acute toxoplasmosis form in visceral organs such as the liver, lung, and spleen. Some epidemiological studies have reported an association of T. gondii infection with liver cirrhosis.MethodsAcute infection was induced in fifteen 30-day-old normal Swiss albino mice. The mice were infected by intraperitoneal inoculation of 5000 T. gondii RH strain tachyzoites. The mice were sacrificed in groups of 5 at 2, 4, and 6 days after inoculation. Another group of 5 mice were used as the controls. Anti-glial fibrillary acidic protein (GFAP) and anti-T. gondii antibodies were used to compare GFAP-immunoreactive cells and anti-T. gondii–immunopositive areas in the liver between the T. gondii-infected groups and the healthy controls, respectively.ResultsThere was a significant correlation between the numbers of GFAP-positive hepatic stellate cells (HSCs) when they were compared with T. gondii antigen immunostaining (p < 0.05). The amount of T. gondii immunostaining increased significantly with the increase in the number of HSCs.ConclusionsThere is a significant relationship between the number of HSCs and T. gondii antigens, which may represent an active role of HSCs in liver pathology and the pathobiology of T. gondii-related hepatitis.
A 1.5-month-old Kangal breed puppy from a dairy cattle farm died after showing severe diarrhoea and incoordination. Necropsy examination revealed multifocal pulmonary consolidation and necrosis and fibrinohaemorrhagic enteritis. Microscopically, there was necrotic and purulent bronchopneumonia, myocarditis and non-purulent encephalitis. In the jejunum and ileum there was villous atrophy and crypt hyperplasia with oocyst-like and schizont-like structures in the epithelia. Immunohistochemically, Neospora caninum antigen was detected in association with the intestinal protozoal structures, degenerative neurons and areas of necrosis in the lungs and heart. Polymerase chain reaction confirmed that the organism was N. caninum and not Toxoplasma gondii. The seroprevalence for N. caninum was 74.2% (49/66 animals) for the cattle and 57.1% (4/7 animals) for dogs on this farm. This report documents fatal systemic neosporosis and enteroepithelial stages of N. caninum in a naturally infected puppy. To the authors' knowledge, this is the first definition of intestinal neosporosis in a naturally infected dog as well as the first evidence of fatal canine neosporosis in Turkey.
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