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At least 937 records · Page 52Linked to original sources
PubMed2002

Congenital toxoplasmosis in a Indo-Pacific bottlenose dolphin (Tursiops aduncus).

Toxoplasma gondii was identified in tissues of a stillborn late-term fetus from an Indo-Pacific bottlenose dolphin (Tursiops aduncus). Myocardial necrosis and nonsuppurative inflammation in the heart and nonsuppurative necrotizing encephalitis were associated with tachyzoites and tissue cysts. The diagnosis was confirmed by immunohistochemical staining with anti-T. gondii-specific polyclonal rabbit serum.

Animals↗
PubMed1987

Placental transfer of specific antibodies during ovine congenital toxoplasmosis.

The passage of non-Toxoplasma antibodies from dam to fetus through damaged placenta was studied in sheep inoculated with Toxoplasma gondii. Six ewes were inoculated with chicken globulins and Leptospira bacterins 2 months before oral inoculation with Toxoplasma gondii oocysts. Ewes were euthanatized between 42 and 62 days after T gondii inoculation. Antibody titers against chicken globulins, Leptospira spp, Haemonchus contortus, Sarcocystis spp, and T gondii were measured in the maternal and fetal sera. All ewes became infected with T gondii and had grossly visible necrotic foci in the placentas, and T gondii antibodies were found in the fetuses and the ewes. Appreciable amounts of antibodies to Haemonchus contortus, Sarcocystis sp, Leptospira spp, and chicken globulins did not cross the placental barrier. Seemingly, serologic examination of the fetus was reliable for the diagnosis of ovine congential toxoplasmosis.

Animals↗
PubMedDate not supplied

[Exploration of immune response in a murine model of congenital toxoplasmosis].

We used a model of acquired toxoplasmosis to study the immune response in pregnant BALB/c mice (IL4+/+) and in pregnant transgenic IL4-deficient BALB/c mice (IL4-/-) during acute toxoplasmosis. Female BALB/c mice were infected orally by 20 tissue cysts of the avirulent PRU strain of Toxoplasma gondii on day 11 of pregnancy. After infection, cultured spleen cells from pregnant mice produced more IFN gamma (a type 1 cytokine) and more NO than non pregnant mice, and the type 2 response (IL4 and IL10) was weak. Although this kind of immune response may be required for mice to recover from toxoplasmosis, pregnant mice were more susceptible to infection than non pregnant mice, as illustrated by a larger parasite load in lungs and brain. Pregnant IL4-/- mice showed lower susceptibility to T. gondii infection and a lower materno-fetal transmission rate (24% versus 53% infected fetus) without increased production of type 1 cytokines (IFN gamma and NO). These data indicate that type 2 response plays an important role in increasing mouse susceptibility to T. gondii infection during pregnancy and that IL4 and pregnancy-associated substances increase the transplacental passage of T. gondii. This is the first time that biased towards type 2 immune response induced by pregnancy was shown to increase susceptibility to T. gondii.

Animals↗
PubMed1997

Immune response in a murine model of congenital toxoplasmosis: increased susceptibility of pregnant mice and transplacental passage of Toxoplasma gondii are type 2-dependent.

We used a model of acquired toxoplasmosis to study the immune response in pregnant BALB/c mice (IL-4+/+) and in pregnant transgenic IL-4-deficient BALB/c mice (IL-4-/-) during acute toxoplasmosis. Female BALB/c mice were infected orally by 20 tissue cysts of the avirulent PRU strain of Toxoplasma gondii on day 11 of pregnancy. Splenocyte cultures were used to explore proliferative responses and cytokine production in vitro. Parasite loads were determined in the lungs on day 7 post-infection and in the brain on day 30 post-infection. After infection, cultured spleen cells from pregnant mice produced more IFN-gamma (a Type I cytokine) and more NO than non pregnant mice, and the Type 2 response (IL-4 and IL-10) was weak. Although this kind of immune response may be required for mice to recover from toxoplasmosis, pregnant mice were more susceptible to infection than non pregnant mice, as illustrated by a larger parasite load in lungs and brain. Pregnant IL-4-/- mice showed lower susceptibility to T. gondii infection and a lower materno-fetal transmission rate (24% vs. 53% infected fetuses) without increased production of Type I cytokines (IFN-gamma and NO). These data indicate that Type 2 response plays an important role in increasing mouse susceptibility to T. gondii infection during pregnancy and that IL-4 and pregnancy-associated substances increase the transplacental passage of T. gondii.

Animals↗