Toxoplasmosis impact on prematurity and low birth weight.

BACKGROUND: Toxoplasma gondii, one of the most common parasites, causes toxoplasmosis, one of the most frequent zoonotic diseases worldwide. T. gondii infects about one-third of the world's population. T. gondii infection is generally considered a major risk for spontaneous abortion, prematurity and low birth weight in the animal sphere. Less commonly, a toxoplasma serological profile is correlated with the particular data of delivery. Acute T. gondii infection during pregnancy often leads to spontaneous abortion and/or a severe injury of the eyes, brain, and other structures of the foetus. Latent T. gondii infection of pregnant women could lead to less obvious but important changes during pregnancy, including the end product of pregnancy and the timing of labour. This study aimed to contribute to the current knowledge by comparing serological T. gondii profiles of pregnant women with prematurity and low birth weights of newborns. MATERIAL AND METHODS: A retrospective study design was adopted. The study participants included a cohort of 1733 pregnant women who consecutively gave birth to their children and underwent regular antenatal biochemical screening between the 14th and 16th weeks of pregnancy. Prematurity was defined as the liveborn preterm delivery in gestational age of pregnancy <37 weeks. Low birth weight was defined as weight at birth of ≤2499 grams. The complement-fixation test (CFT) provided serological profiles for toxoplasmosis that expresses the overall levels of toxoplasma immunoglobulins of all classes. Enzyme-linked immunosorbent assay (ELISA) tests for IgG and IgM were used simultaneously. IgM positivity helped to differentiate acute from the latent stage of toxoplasmosis. Birth data, especially the week of delivery and fetal weight, were evaluated accordingly. RESULTS: Of the 1733 pregnant women, 25% were diagnosed as latent toxoplasma positive, and 75% as toxoplasma negative. There were 87 premature deliveries versus 1646 timely births. We observed 88 low birth weights and 1645 normal fetal weights. We found a statistically significant association between latent toxoplasmosis and prematurity, χ2(1) = 5.471, p = .019 and between latent toxoplasmosis and low birth weight of newborns, χ2(1) = 7.663, p = .006. There was a 1.707 times higher risk of prematurity for toxoplasma-positive women, while the risk for low birth weight was 1.861 times higher. The strength of both tests of association was mild. We tested the correlation between the levels of CFT titres and week of delivery and weight of newborns. No association was found between the level of latent toxoplasmosis and the week of delivery and fetal weight. CONCLUSION: Latent toxoplasmosis was associated with premature birth rate and lower birth weight of newborns. The odds of premature delivery was 1.7 and low birth weight 1.9 times higher in women with latent toxoplasmosis compared to toxoplasma negative women. Even though the strength of the association in our large sample is relatively mild, the combination of latent toxoplasmosis with other adverse factors could cause serious harm. Whole CFT and specific IgG levels of latent toxoplasmosis are not linked to the severity of prematurity or low birth weight in newborns.

SEROPREVALENCE OF TOXOPLASMA GONDII INFECTION AND. ASSOCIATED RISK FACTORS AMONG ASYMPTOMATIC PREGNANT FEMALES IN EGYPT.

Protozoan parasite Toxoplasma gondii is considered as one of the most critical risk factor for recurrent abortion in pregnant females and resulted in multi congenital malformation in fetus world-wide. The present study was carried out on 693 pregnant females from Alexandria, Beheira, Gharbia, Menoufia, Qalyoubia and Fayoum provinces,"The study determined the prevalence of toxoplasmosis in pregnant females during pregnancy trimesters and shed the lights on the main risk factors and possible contamination routes. Detection for the presence of Toxoplasma IgG antibodies were done by enzyme linked fluorescence assay (ELFA). It was found that the overall seroprevalence of T. gondii was 30.16%.The seroprevalence increased with age. Significant relations were observed between Toxoplasma IgG antibodies and abortion history, maternity trimester and consumption of under-cooked meat. No significant differences were reported due to parity, occupation, abortion trimester, contact with cats and/or other animals and exposure to soil.

[Arguments for an infectious cause of IUGR]. / Quels arguments pour déterminer l'origine infectieuse d'un retard de croissance intra-utérin?

Intra-uterine growth retardation (IUGR) is a frequent cause of consultation in antenatal care unit. The prognosis relies on the etiology: vascular, chromosomic, genetic, or infectious. Because of chronic fetal distress, hypotrophy increase morbidity, mortality and neurosensorial long term effect. Usually, infection is involved in 5 to 15% of the IUGR, mainly by Cytomegalovirus (CMV), Varicella Zoster virus, rubella, toxoplasmosis, herpes and syphilis. Maternal sera and amniotic liquid analysis make the diagnosis possible but fetal ultrasound scan is used to find other features. Most of the abnormalities are unspecific but their combination can worsen fetal prognosis. Infection should always be ruled out in the assessment of IUGR.

Diagnosis of fetal infections.

PURPOSE OF REVIEW: The purpose of this review is to present recent developments in the prenatal diagnosis of the most clinically relevant congenital infections. RECENT FINDINGS: Immunoglobin G avidity testing can help to differentiate between recent or prior infection. A combination of tests, including serology, avidity and polymerase chain reaction, may be necessary to improve accuracy of diagnosis. The interval between exposure to an infectious agent and prenatal testing can be critical to the interpretation of the test result. SUMMARY: This review reinforces the need for accurate testing to guide appropriate counseling and individual fetal risk assessment. The findings of viral-specific antibodies or sonographic abnormalities do not accurately predict the severity or outcome of fetal infection. Further research is necessary to determine the pathogenesis of transplacental viral transmission and thereby allow us to target prevention strategies.

Secuelas oculares en recién nacidos son síndrome de TORCH / Ocular sequelae in newborns with TORCH syndrome

Se evaluó la incidencia de alteraciones oculares en infantes nacidos de madres con titulación positiva contra el complejo TORCH y la infección por sífilis. Incluimos a 33 pacientes, captados en el periodo de septiembre de 1997 a junio de 1998. Se valoró la presencia de alteraciones oculares congénitas en infantes con antecedentes de infección intrauterina por el síndrome de TORCH. Se incluyeron 8 mujeres (24.2 por ciento) y 25 hombres (75.7 por ciento). Las lesione que más se encontró fue: catarata en 6 pacientes (18.1 por ciento), coloboma en 2 pacientes (6.0 por ciento), microftalmía, entropión, queratoconjuntivitis, masa retrobulbar, desprendimiento de retina, coriorretinitis y atrofia óptica en los restantes pacientes (3.0 por ciento). Las infecciones intrauterinas influyen en el dessarrollo del ojo. Estos datos sugieren que el diagnóstico temprano de tales infecciones por el complejo TORCH permite realizar el tratamiento adecuado

Pathomechanism of cerebral hypoplasia in experimental toxoplasmosis in murine fetuses.

In order to elucidate the pathological mechanism of cerebral hypoplasia in congenital toxoplasmosis, fetal toxoplasmosis was induced by intraperitoneal injection of Toxoplasma gondii into five pregnant mice on embryonal Day 5 (E5). The maternal and fetal brains were examined histologically and immunohistochemically; six fetuses were examined on E16 and 21 on E18. T. gondii organisms were immunohistochemically detected in the maternal brains, placentas and the ventricular zone of the fetal cerebrum. In none of the fetal brains was any gross deformity observed, except for cerebral hypoplasia. On E16 and E18, the cerebral cortices were seen to consist of immature laminations, and the cells had less cytoplasm and rounder hyperchromatic nuclei than those in the control mice. The cerebral walls and the cortical layers, except in the ventricular zone, were thinner than in the controls (P < 0.01 in each case). On E18, the proliferating cell nuclear antigen immunolabeling index was higher, and the cytoplasm of more cells in the cortical plate was immunoreactive with anti-beta-tubulin antibody compared with control mice. Using an in situ end-labeling technique, apoptotic cells were not observed in the cortices in mice of both groups. It is suggested that the cerebral hypoplasia following Toxoplasma infection is related to delayed maturation.

Fetal thrombocytopenia: a retrospective survey of 5,194 fetal blood samplings.

Fetal platelet counts were retrospectively studied in a series of 5,194 consecutive fetal blood samplings (FBS). The mean value was 245 +/- 65 x 10(9)/L, without significant variation between 17 and 41 weeks' gestation. After exclusion of false thrombocytopenia due to contamination with amniotic fluid, 247 fetuses had platelet counts less than 150 x 10(9)/L. In 70 cases, thrombocytopenia was due to congenital infectious diseases (toxoplasmosis, rubella, and cytomegalovirus). It was related to immune causes in 45 cases: anti-HPA-1a (n = 23), anti-HPA-5b (n = 2) or possible anti-HLA (n = 2) alloimmunizations, and immune thrombocytopenic purpura (n = 18). Chromosomal abnormality was the etiology in 43 cases (trisomy 13, 18, and 21, Turner's syndrome, triploidy), and other disorders (multiple birth defects, intrauterine growth retardation, rhesus disease, and gestational thrombocytopenia) in 62 cases. No specific cause for the low platelet count could be established in 27 fetuses (range, 115 to 149 x 10(9)/L). Severe thrombocytopenia (< or = 50 x 10(9)/L) occurred mainly in immune cases (16%), congenital infectious diseases (7%), and chromosomal abnormalities (1%). Diagnosis, prognosis, and management of fetal thrombocytopenia are presented in the different clinical situations. In this series, FBS was never associated with serious bleeding, and no fetal exsanguination was observed.