Toxoplasmosis congenital

Infants (younger than 2 months of age) - Contraindicated, except as adjunctive therapy with pyrimethamine in the treatment of congenital toxoplasmosis. 

Hypersensitivity to sulfonamides or chemically related drugs (eg, sulfonylureas, thiazide and loop diuretics, carbonic anhydrase inhibitors, sunscreens with PABA, local anesthetics) pregnancy at term lactation infants less than 2 months of age (except in congenital toxoplasmosis as adjunct with pyrimethamine) porphyria salicylate hypersensitivity. 

Pyrimethamine, in combination with sulfadiazine, is first-line therapy in the treatment of toxoplasmosis, including acute infection, congenital infection, and disease in immunocompromised patients. For immunocompromised patients, high-dose therapy is required followed by chronic suppressive therapy. Folinic acid is included to limit myelosuppression. Toxicity from the combination is usually due primarily to sulfadiazine. The replacement of sulfadiazine with clindamycin provides an effective alternative regimen. 

Antibiotics also are active against other protozoans. Tetracycline and erythromycin are alternative therapies for the treatment of intestinal amebiasis. Clindamycin, in combination with other agents, is effective therapy for toxoplasmosis, pneumocystosis, and babesiosis. Spiramycin is a macrolide antibiotic that is used to treat primary toxoplasmosis acquired during pregnancy. Treatment lowers the risk of the development of congenital toxoplasmosis. 

Toxoplasmosis is a recurrent, potentially blinding, disease caused by the obligate intracellular parasite Toxoplasma gondii. Toxoplasmosis affects millions of people worldwide. Cats are the definitive host for the parasite but not the primary source of human infection. Environmental contamination of the soil, water, fruits and vegetables, and infection in other animals cause most human infections. Human infection may be either congenital or acquired, and acquired disease appears to be the most prevalent. 

Toxoplasmosis occurs frequently in immunosup-pressed patients. Retinal toxoplasmosis was seen commonly at the height of the AIDS epidemic, but was less frequent than CMV retinitis it occurred more often as a newly acquired infection rather than as reactivation of a congenital infection. 

R4. Remington, J. S., Miller, M. J., and Brownlee, I., IgM antibodies in acute toxoplasmosis 1. Diagnostic significance in congenital cases and a method for their rapid demonstration. Pediatrics 41, 1082-1091 (1968). 

Toxoplasmosis produces a wide-spectrum of pathological and clinical manifestations. The disease appears in two forms congenital and acquired. Congenital toxoplasmosis is usually fatal. The infection in newborns is marked by the presence of hydorcephalus, encephalitis, bilateral retinochoroiditis, hepatosplenomegaly and jaundice. In some cases the disease may be inactive at birth, but may develop as the child grows older. Such children may show esotropia, strabismus, microphthalmia, and cataract. 

Untreated acute toxoplasmosis among pregnant women can lead to infection of the fetus via transplacental transmission (Varella et ah, 2009.). At first examination, newborns affected by congenital infection may seem normal however, serious sequelae, such as neurological impairment and blindness, can develop witiiin a few years lafer (Dunn et ah, 1999 Remington et ah, 2006 Safadi et ah, 2003.). 

While prenatal diagnosis is based on the detection of T. gondii in the amniotic fluid, neonatal screening is based on the detection of parasites in the placenta and on the detection of IgM and IgA antibodies in newborns. PCR for the detection of parasite DNA in amniotic fluid has improved the sensitivity of prenatal diagnosis (Bessieres et ah, 2009). The accurate diagnosis of congenital toxoplasmosis is essential, since if the mother is treated it would reduce the probability of fetal infection by 50% (Desmonts and Couvreur, 1974). 

Bessieres, M. H., Berrebi, A., Cassaing, S., Fillaux, J., Cambus, J. P., Berry, A., Assouline, C., Ayoubi, J. M., and Magnaval, J. F. (2009). Diagnosis of congenital toxoplasmosis prenatal and neonatal evaluation of methods used in Toulouse University Hospital and incidence of congenital toxoplasmosis. Mem. Inst. Oswaldo Cruz 389-392. 

Gilbert, R., Dunn, D., Wallon, M., Hayde, M., Prusa, A., Lebech, M., Kortbeer, T., Peyron, F., Poliak, A., and Petersen, E. (2001). Ecological comparison of the risks of mother-to-child transmission and clinical manifestations of congenital toxoplasmosis according to prenatal treatment protocol. Epidemiol. Infect. 127,113-120. 

Mozzato, L. and Procianoy, R. S. (2003). Incidence of congenital toxoplasmosis in Southern Brazil A prospective study. Rev. Inst. Med. Trop. 45,147-151. 

Toxoplasmosis Disease caused by the protozoan Toxoplasma gondii that can cause congenital defects in newborns. 

Macrolides. Clinical papers report the use of spiramycin in the effective prevention of post-operative staphylococcal infections in the elderly, and possibly of congenital toxoplasmosis in pregnancy. Enhancement of erythromycin activity against gram-negative bacteria has been noted upon alkalinization of the assay medium or the urine. 

A. Kaye, Toxoplasmosis diagnosis, treatment, and prevention in congenitally exposed infants, J. Paediatr. Health Care, 2011,25, 355-364. 

---