[Histopathology changes in mice infected with Toxoplasma gondii Prugniaud strain]

To observe the symptoms and dynamic changes of histopathology in the organs from ICR mice infected by Toxoplasma gondii Prugniaud strain.

Thirty ICR mice were infected intraperitoneally with cysts, 10 cysts per mouse. 16 mice were injected with PBS. Incidence of the mice was observed. Three mice from the infected group and two mice from the control group were sacrificed, and the liver, spleen, lung, brain, kidney and heart were collected for pathology and immunohistochemistry examinations on the day 5, 10, 15, 20, 25, 30, 60 and 90 post-infection.

The infected mice began to fall ill at 6 d post-infection, symptoms including decreased appetite, pilomotor fur, sloth, shakes and diarrhea, with a mortality rate of 20%. From 5 d to 20 d post-infection, microscopic examination for HE stain-slides showed the destroyed liver structure, cellular edema, ballooning change, focal necrosis, sinus hepatic expansion and hyperemia, and inflammatory infiltration. Splenic corpuscles demolished and disappeared, red pulp widened and white pulp atrophied, splenic sinusoid extended with hyperemia. Lungs showed destruction of the structure and pathological changes of interstitial pneumonia. The pathological changes began to alleviate until recovery after 20 d post-infection. In the brain, neuronal degeneration and necrosis were found at 10 d post-infection. Some neuroglial cell tubercle, blood vessel sleeve cuffing, inflammatory cell infiltration on cavitas subarachnoidealis and cysts were observed from 15 d to 90 d. Granulation tissue was seen at 90 d post-infection. By immunohistochemistry test, internal organs showed toxoplasma antigen at 5 d post-infection, and the positive reaction was remarkable at 10 d post-infection, then began to taper until negative. Toxoplasma antigen was revealed in the brain from 10 d to 90 d post-infection.

Non-specific clinical manifestation and the degeneration, necrosis and inflammatory cell infiltration in poly-organs appear in earlier period of toxoplasma tachyzoite infection in the ICR mice, followed by the co-existing phenomenon of non-specific infection with cysts in the brain.