Toxoplasmosis congénita en el valle de México. Resultados de una serie de casos

Abstract

ANTECEDENTES: En México prevalecen cepas “virulentas” de Toxoplasma gondii, por lo que el cuadro clínico puede ser diferente a los reportados para regiones donde circulan cepas no virulentas, como Europa, Estados Unidos y Canadá.MÉTODOS: Se reporta una serie de casos con toxoplasmosis congénita reclutados a partir de 2005 por tamiz prenatal o postnatal, o porque llegaron como casos clínicos al INP, y que conforman parte de una serie de casos.RESULTADOS: Todos los pacientes presentaron manifestaciones clínicas, pero el grupo de tamiz prenatal presentó una infección más localizada y menos grave, principalmente con espasticidad y retraso psicomotor leve. El grupo de tamiz postnatal presentó características clínicas intermedias, con retraso psicomotor leve, moderado o grave, bajo peso al nacimiento, micro o hidrocefalia, ictericia, hepatomegalia, esplenomegalia, calcificaciones intracraneales y espasticidad. Los pacientes más afectados fueron aquellos que se presentaron como casos clínicos, con una amplia variedad de manifestaciones clínicas y el peor pronóstico, incluida la muerte. Seis pacientes presentaron comorbilidades. Veinte casos fueron positivos para dos o más pruebas de laboratorio; el resto sólo para una.CONCLUSIONES. Nuestros resultados apoyan que la toxoplasmosis congénita en México es más grave que en otros países, y que urge implementar tamiz prenatal efectivo, para prevención y profilaxis.PALABRAS CLAVE: complejidad diagnóstica; evaluación prenatal; heterogeneidad clínica; tamiz postnatal; tamiz prenatal; toxoplasmosis congénita; Toxoplasma gondii

A Proinflammatory Immune Response Might Determine Toxoplasma gondii Vertical Transmission and Severity of Clinical Features in Congenitally Infected Newborns

“…Confirmation of congenital infections was done through serological tests by the detection of specific IgM and IgG neoantibodies by enzyme-linked immunosorbent assay (ELISA) and Western blot and through B1 parasite gene detection by quantitative PCR on peripheral blood, according to previously reported methods and algorithms (9,(19)(20)(21)(22). After the infection was confirmed and before treatment onset, we determined the levels of specific anti-T. gondii IgG1, IgG2, IgG3, and IgG4 antibodies and proliferation in vitro of peripheral blood mononuclear-specific cells and their cytokine production (19).…”

“…After the infection was confirmed and before treatment onset, we determined the levels of specific anti-T. gondii IgG1, IgG2, IgG3, and IgG4 antibodies and proliferation in vitro of peripheral blood mononuclear-specific cells and their cytokine production (19). Congenitally infected newborns were evaluated at 1-year follow-up, and their clinical features classified according to the location (neurological or disseminated) and severity (mild or moderate/severe) (9). In brief, local infection refers to patients with neurological, ophthalmic, or both alterations, such as intracranial calcifications, hydrocephalus, microcephalus, retinochoroiditis, uveitis, and intraocular hemorrhage.…”

“…Humans can become infected per os through the ingestion of food or water contaminated with sporulated oocysts released in the feces of the definitive hosts (felines) or of undercooked meat products containing tissue cysts (3), as well as by vertical transmission from mother to fetus during pregnancy (4)(5)(6). Congenital toxoplasmosis can promote clinical manifestations in the newborn that involve the central nervous system, such as hydrocephalus and hearing loss, or the eye, such as retinochoroiditis (7)(8)(9). Given the high prevalence of this disease and the wide range of clinical manifestations, it is of great importance to study the factors involved in congenital transmission of T. gondii and the severity of congenital toxoplasmosis in the newborn, but these aspects have been poorly explored.…”

“…Both humoral and cell-mediated proinflammatory responses have consistently been reported as crucial for the containment of this parasite in acquired toxoplasmosis (10). Regarding fetal damage, it has been hypothesized that disease results from the poorly developed fetal immune response, which is thought to be unable to control parasite replication (11), allowing T. gondii to invade different tissues of the host and thus contributing to the high heterogeneity of the clinical manifestations associated with the infection (9). This has been reinforced by the known inverse relation between the gestation time at infection and the severity degree (4,12).…”

“…The red dashed lines show the cutoffs. Mild vs. moderate/severe clinical groups were classified according the criteria previously reported(9). Mann-Whitney U test, *p ≤ 0.05; Fisher exact test, + + ++p ≤ 0.0001, + + +p ≤ 0.001.…”