Behavior and neuropsychiatric changes in experimental chronic toxoplasmosis: Histopathological and immunohistochemical studies

Document Type : Original Article

Authors

1 Departments of Medical Parasitology ,Faculties of Medicine,Zagazig University

2 Departments of Medical Parasitology ,Faculties of Medicine,Zagazig Universi

3 Departments of Zoonoses , Faculties of Veterinary Medicine, Zagazig University,

4 Departments of Pathology , Faculty of Medicine, Al-Azhar University, Cairo, Egypt

5 Departments of Medical Parasitology , Faculties of Medicine , Zagazig University,

Abstract

Background: T. gondii is an intracellular protozoan parasite that can establish a latent infection in the
central nervous system that may develop into chronic inflammation resulting in neurobehavioral problems
in the host. The processes behind these alterations are still largely mysterious.
Objective: Detection of behavioral, histopathological and immunohistochemical changes in mice infected
by T. gondii Me49 strain.
Material and Methods: A total of 105 adult male Swiss albino mice were divided into 60 used for
experimental infection, and 45 as control. Assessment of physical appearance was monitored for
acute toxoplasmosis daily for three weeks post infection (PI). Correlation between behavior changes
and the degree of infection was conducted by measuring histopathological (H&E and silver stain) and
immunohistochemical (presence or absence of CD3, CD138 and caspase-3 immunoreactive cells)
parameters weekly starting from 7th week to the 12th week PI.
Results: Infected mice had neurobehavioral problems. Variable degrees of perivascular and interstitial
inflammatory infiltrates, astrocytosis, deteriorated neurons, and meningitis were demonstrated by
histopathology when compared to uninfected controls. Inflammatory cells (mainly lymphocytes) entered
the parenchyma at mild, moderate, and severe levels in the brains of infected mice. Immunohistochemical
assessment of CD3, CD138 and caspase-3 revealed a substantial increase in CD3 expression by clusters of
activated astrocytes in the cerebral parenchyma, suggesting an increase in astrocyte numbers and function
that was progressive over time. CD138 and caspase-3 immunoreactivity showed decreased expression by
the activated astrocytes.
Conclusion: Chronic toxoplasmosis causes deterioration in cognitive and emotional behavior of the
infected host, resulting in neuropsychiatric and behavioral disturbances.

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