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Among all organ transplantations, those of heart or heart-lung carry the greatest risk of toxoplasmosis. The disease is observed mainly when the donor is seropositive and the recipient seronegative. In these mismatched couples the risk may be as high as 57 percent. Cardiac tissue transplants are responsible for most contaminations. A subclinical serological reactivation can be observed in seropositive recipients. Patent forms are associated with seroconversion in seronegative subjects. Toxoplasmosis is often severe with multivisceral foci; interstitial pneumonia is possible. The serological diagnosis is easy in cases with significant antibody movements, but it may be difficult if the titre is low or stable. The parasitological diagnosis rests on the isolation of toxoplasma in blood, cerebrospinal fluid, bronchoalveolar lavage fluid and cardiac or cerebral biopsy. Immune defence against toxoplasmosis is primarily cellular, with lymphocytosis and inversion of the CD4/CD8 ratio. Macrophages play a crucial role. Interferon-gamma is the major mediator of cellular resistance. In spite of its immunosuppressive action, cyclosporin clearly has an antiparasitic action in vitro and in vivo. A cytomegalovirus infection might facilitate toxoplasma reactivation. Prevention of toxoplasmosis in transplant recipients includes systematic serology of the recipient and, if possible, the donor, detection of mismatched couples and systematic treatment with pyrimethamine of recipients at risk (in seronegative recipients, this drug has reduced the risk from 57 to 14 percent). Cyclosporin should be used as immunosuppressant in preference to other drugs of this kind. Corticosteroids administered in rejections increase the risk of toxoplasmosis.

Eight-nine cases of fetal Toxoplasma infection are reported in women treated with spiramycin during pregnancy. Thirty-four pregnancy terminations were performed (2.7% of the total number of acquired Toxoplasma infections during pregnancy). Fifty-two pregnancies were allowed to proceed (43 being additionally treated with pyrimethamine and sulfonamides), leading to the birth of 54 live infants. After a mean follow-up period of 19 months, 41 infants had evidence of subclinical Toxoplasma infection, 12 had a benign form, and one had severe congenital toxoplasmosis (this infant did not receive the additional treatment during pregnancy). Efficacy of the additional treatment with pyrimethamine and sulfonamides was demonstrated by a significant reduction of severe congenital toxoplasmosis and the relative decrease of the ratio of benign to subclinical forms. We recommended that spiramycin treatment be started as soon as possible once the diagnosis of maternal Toxoplasma infection during pregnancy is proved or strongly suspected, because a prolonged time interval between onset of infection and start of treatment seems to be associated with the presence of severe fetal lesions at the time of prenatal diagnosis.