Cyst burden in the brains of Wistar rats fed Toxoplasma oocysts

Abstract

Six strains of Toxoplasma oocysts were used to infect groups of 4-24 Wistar rats, with each rat being fed 10 1 -10 4 oocysts from a single strain. After 2 months, the rats were killed, their brains screened for Toxoplasma cysts and then bioassayed in mice if negative. Toxoplasma was either observed in the form of brain cysts or was recovered using the bioassay, from 113 out of 138 (82%) rat brains. As few as ten oocysts were capable of initiating a brain infection that lasted for at least 2 months in eight of the nine rats inoculated. However, judging from bioassay 10 2 -10 4 oocysts did not give rise to progressively higher rates of infection. Brain cysts were seen in only 68 of 138 rats (49%). The number of Toxoplasma cysts formed in the brains of rats was generally in the order of tens to hundreds. The frequency of infection in the brains with Toxoplasma and the number of brain cysts formed appeared to be influenced by the individual resistance of the rats as well as by the doses of oocysts and the Toxoplasma strains used. The information gathered is considered to be a basis for a rat model of immunity against acquired toxoplasmosis.

Association between prenatal treatment and clinical manifestations of congenital toxoplasmosis in infancy: A cohort study in 13 European centres

“…One possible explanation for the similarity of effect of spiramycin and pyrimethamine-sulphonamide on intracranial lesions could be that they both reduce the infective parasite burden. This burden, along with individual host resistance, route of infection and parasite strain, has been related to brain and ocular lesions in experimental animal studies [30,31]. If reduction of parasite burden is the mechanism, the timing of treatment might be critical, as conversion from tachyzoite to bradyzoite cyst, which is impenetrable to antibiotics, has been found to take place between 4 and 14 d after infection in immunecompetent experimental animals [1].…”

“…If reduction of parasite burden is the mechanism, the timing of treatment might be critical, as conversion from tachyzoite to bradyzoite cyst, which is impenetrable to antibiotics, has been found to take place between 4 and 14 d after infection in immunecompetent experimental animals [1]. However, why treatment should have an effect on brain but not ocular lesions remains puzzling as experimental and human fetal studies of ocular toxoplasmosis have found that severe lesions are associated with a locally increased burden of free tachyzoite [31,32]. We were unable to explore the effect of prenatal treatment on long-term development of retinochoroiditis.…”

Association between prenatal treatment and clinical manifestations of congenital toxoplasmosis in infancy: A cohort study in 13 European centres

“…One possible explanation for the similarity of effect of spiramycin and pyrimethamine‐sulphonamide on intracranial lesions could be that they both reduce the infective parasite burden. This burden, along with individual host resistance, route of infection and parasite strain, has been related to brain and ocular lesions in experimental animal studies 30, 31. If reduction of parasite burden is the mechanism, the timing of treatment might be critical, as conversion from tachyzoite to bradyzoite cyst, which is impenetrable to antibiotics, has been found to take place between 4 and 14 d after infection in immune‐competent experimental animals 1.…”

“…If reduction of parasite burden is the mechanism, the timing of treatment might be critical, as conversion from tachyzoite to bradyzoite cyst, which is impenetrable to antibiotics, has been found to take place between 4 and 14 d after infection in immune‐competent experimental animals 1. However, why treatment should have an effect on brain but not ocular lesions remains puzzling as experimental and human fetal studies of ocular toxoplasmosis have found that severe lesions are associated with a locally increased burden of free tachyzoite 31, 32. We were unable to explore the effect of prenatal treatment on long‐term development of retinochoroiditis.…”

Gender dimorphism in parasitic behavioural manipulation hypothesis

“…In other words, even after parasite clearance, the loss of fear phenotype is still observed in rodents [168]. It is more likely that cysts will secrete a substance that affects the innate fear pathway in the brain [94,169]. More importantly this model is unable to explain why other amygdala and nucleus accumbens dependent behaviours like conditioned fear, neophobia to novel food and social status remain intact [94,149] The Toxoplasma parasite has two genes that are analogous to the human tyrosine hydroxylase gene [92,[170][171][172].…”