Secondary prophylaxis of toxoplasmosis in pregnancy in an HIV-positive woman.

A 39-year-old HIV-positive black African woman with previously treated cerebral toxoplasmosis experienced a foetal intra-uterine death due to congenital toxoplasmosis. This case demonstrates the complexities of screening for maternal toxoplasmosis in the context of pregnancy and HIV infection-related cell-mediated immunosuppression. Additionally, the case highlights the challenges in providing effective preventative and therapeutic drug options for congenital toxoplasmosis.

Anomalias congênitas e suas principais causas evitáveis: uma revisão / Congenital anomalies and its main avoidable causes: a review

As anomalias congênitas (AC) podem ser definidas como todas as alterações funcionais ou estruturais do desenvolvimento fetal, cuja origem ocorre antes do nascimento. Elas possuem causas genéticas, ambientais ou desconhecidas. As principais causas das anomalias são os transtornos congênitos e perinatais, muitas vezes associados a agentes infecciosos deletérios à organogênese fetal, tais como os vírus da rubéola, da imunodeficiência humana (HIV), o vírus Zika, o citomegalovírus; o Treponema pallidum e o Toxoplasma gondii. O uso de drogas lícitas e ilícitas, de medicações teratogênicas, endocrinopatias maternas também podem ser citados como causa de AC. Estima-se que 15 a 25% ocorram devido às alterações genéticas, 8 a 12% são causadas por fatores ambientais e 20 a 25% podem ser causadas tanto por alterações genéticas quanto por fatores ambientais. Neste artigo, serão abordadas as principais causas das AC, com foco naquelas que podem ser evitadas. (AU)

Congenital anomalies (CA) can be defined as all functional or structural changes of fetal development that originate before birth. They have genetic, environmental or unknown causes. The main causes of anomalies are congenital and perinatal disorders, often associated with infectious agents deleterious to fetal organogenesis, such as rubella virus, human immunodeficiency virus (HIV), Zika virus, cytomegalovirus; the Treponema pallidum and the Toxoplasma gondii. The use of licit and illicit drugs, teratogenic medications, and maternal endocrinopathies can also be cited as causes of CA. It is estimated that 15 to 25% occur due to genetic alterations, 8 to 12% are caused by environmental factors and 20 to 25% can be caused by both genetic and environmental changes. In this article, the main causes of CA will be addressed, focusing on those that can be avoided. (AU)

High frequency detection of Toxoplasma gondii DNA in human neonatal tissue from Libya.

BACKGROUND: Toxoplasma gondii is a parasite that causes significant disease in humans. Toxoplasmosis is normally asymptomatic, unless associated with congenital transmission, or in immunocompromised people. Congenital transmission generally occurs at low frequencies. In this study, we use PCR to investigate possible congenital transmission of T. gondii during pregnancy in a cohort of mothers from Libya. METHODS: Two hundred and seventy two pregnant women (producing 276 neonates) were recruited to obtain umbilical cord tissue from their neonates at birth; DNA was extracted from that tissue and tested for T. gondii DNA using two specific PCR protocols based on the sag 1 and sag 3 genes. RESULTS: Toxoplasma gondii DNA was detected in the umbilical cord DNA from 27 of the 276 neonates giving a prevalence of 9.9% (95% CI 6.8-13.9%). Compared with more commonly reported rates of congenital transmission of 0.1% of live births, this is high. There was no association of infection with unsuccessful pregnancy. CONCLUSIONS: This study shows a high frequency presence of T. gondii DNA associated with neonatal tissue at birth in this cohort of 276 neonates from Libya. Although PCR cannot detect living parasites, there is the possibility that this indicates a higher than usual frequency of congenital transmission.

[Severe congenital toxoplasmosis secondary to toxoplasma reactivation in an HIV-infected mother]. / Toxoplasmose congénitale sévère secondaire à une réactivation toxoplasmique chez une mère infectée par le VIH.

Congenital toxoplasmosis is a potentially serious fetal infection associated with maternal seroconversion or a reactivation of toxoplasmosis during pregnancy. We report the case of congenital toxoplasmosis with severe neurological injury with normal prenatal obstetric ultrasounds in a mother infected with HIV at the AIDS stage and previously immunized against toxoplasmosis.

Functional echocardiography in the fetus with non-cardiac disease.

We describe the hemodynamic changes observed in fetuses with extra cardiac conditions such as intrauterine growth restriction, tumors, twin-twin transfusion syndrome, congenital infections, and in fetuses of mothers with diabetes. In most fetuses with mild extra cardiac disease, the alterations in fetal cardiac function remain subclinical. Cardiac function assessment has however helped us to achieve a better understanding of the pathophysiology of these diseases. In fetuses at the more severe end of the disease spectrum, functional echocardiography may help in guiding clinical decision-making regarding the need for either delivery or fetal therapy. The growth-restricted fetus represents a special indication for routine cardiac function assessment, as in utero hemodynamic changes may help optimize the timing of delivery. Moreover, in intrauterine growth restriction, the altered hemodynamics causes cardiovascular remodeling, which can result in an increased risk of postnatal cardiovascular disease.

Monitoring of plasma concentration of pyrimethamine (PYR) in infants with congenital Toxoplasma gondii infection--own observations.

The study objective was to determine plasma concentration of pyrimethamine in 24 infants aged 1-5 months, treated for congenital toxoplasmosis. Pyrimethamine was used in a single daily dose at an amount of 0.35-0.98 mg/kg daily, with sulfadiazine (50-100 mg/kg/day) in divided doses 2-3 times a day, and folinic acid given twice a week (7.5 mg). This regimen was continued for 2-6 months, then Fansidar was administered. Pyrimethamine concentration in plasma was measured using high-performance liquid chromatography method (HPLC). A total of 70 tests were performed. Concentration of pyrimethamine ranged from 0.01 to 1.2 microg/ml. In 14 children (58 tests) the concentration of pyrimethamine achieved therapeutic value. In 7 patients (8 tests) the concentration was below therapeutic level, and in 3 patients (4 tests) above therapeutic level. In 11/24 (46%) children transient moderate neutropenia was observed. Modification of therapy was necessary in 12 patients. Monitoring of pyrimethamine concentration in plasma improves safety and effectiveness of the therapy and is useful in obtaining correct individual dose of the drug. Neutropenia is the most common side-effect of pyrimethamine observed even when using the recommended dose.

Is routine TORCH screening and urine CMV culture warranted in small for gestational age neonates?

BACKGROUND: congenital infections are associated with a wide variety of clinical symptoms, including small for gestational age (SGA). AIMS: to determine the co-occurrence of SGA and congenital TORCH infections, as diagnosed by TORCH serologic tests and/or cytomegalovirus (CMV) urine culture. STUDY DESIGN: we performed a retrospective study of all neonates admitted to our neonatal intensive care unit from January 2004 to February 2010 in whom SGA was diagnosed and TORCH serologic tests and/or CMV urine cultures were performed. RESULTS: TORCH serologic tests (in neonatal or maternal serum) and/or a CMV urine culture were performed in 112 neonates with SGA. None of the neonates tested positive for Toxoplasma gondii, Rubella, and Herpes simplex virus. Positive CMV urine culture was detected in 2% (2/112) of neonates, but their CMV IgM titers were negative. CONCLUSIONS: the co-occurrence of TORCH congenital infection in infants with SGA is rare. Routine TORCH screening in neonates with isolated SGA does not seem warranted and should be limited to CMV urine cultures.