[Spanish Society for Pediatric Infectious Diseases guidelines on tuberculosis in pregnant women and neonates (i): Epidemiology and diagnosis. Congenital tuberculosis]. / Guía de la Sociedad Española de Infectología Pediátrica sobre tuberculosis en la embarazada y el recién nacido (I): epidemiología y diagnóstico. Tuberculosis congénita.

Tuberculosis (TB) screening in pregnancy using tuberculin skin test (TST) is recommended in case of symptoms of TB disease, close contact with a patient with infectious TB, or high risk of developing active disease. The new interferon gamma release assay (IGRA) tests are recommended in BCG-vaccinated pregnant women with positive TST and no known risk factors for TB, and in those immunocompromised, with clinical suspicion of TB but negative TST. TB diagnosis is difficult due to the non-specific symptoms, the increased frequency of extrapulmonary disease, the delay in radiological examinations, and the high rate of tuberculin anergy. Neonatal TB can be acquired in utero (congenital TB), or through airborne transmission after delivery (postnatal TB). Congenital TB is extremely rare and does not cause fetal malformations. It may be evident at birth, although it usually presents after the second week of life. In newborns with no family history of TB, the disease should be considered in cases of miliary pneumonia, hepatosplenomegaly with focal lesions, or lymphocytic meningitis with hypoglycorrhachia, especially in those born to immigrants from high TB-burden countries. TST is usually negative, and IGRAs have lower sensitivity than in older children. However, the yield of acid-fast smear and culture is higher, mostly in congenital TB. Molecular diagnosis techniques enable early diagnosis and detection of drug resistance mutations. There is a substantial risk of disseminated disease and death.

[Spanish Society for Pediatric Infectious Diseases guidelines on tuberculosis in pregnant women and neonates (ii): Prophylaxis and treatment]. / Guía de la Sociedad Española de Infectología Pediátrica sobre tuberculosis en la embarazada y el recién nacido (ii): profilaxis y tratamiento.

In pregnant women who have been exposed to tuberculosis (TB), primary isoniazid prophylaxis is only recommended in cases of immunosuppression, chronic medical conditions or obstetric risk factors, and close and sustained contact with a patient with infectious TB. Isoniazid prophylaxis for latent tuberculosis infection (LTBI) is recommended in women who have close contact with an infectious TB patient or have risk factors for progression to active disease. Otherwise, it should be delayed until at least three weeks after delivery. Treatment of TB disease during pregnancy is the same as for the general adult population. Infants born to mothers with disseminated or extrapulmonary TB in pregnancy, with active TB at delivery, or with postnatal exposure to TB, should undergo a complete diagnostic evaluation. Primary isoniazid prophylaxis for at least 12 weeks is recommended for those with negative diagnostic tests and no evidence of disease. Repeated negative diagnostic tests are mandatory before interrupting prophylaxis. Isoniazid for 9 months is recommended in LTBI. Treatment of neonatal TB disease is similar to that of older children, but should be maintained for at least 9 months. Respiratory isolation is recommended in congenital TB, and in postnatal TB with positive gastric or bronchial aspirate acid-fast smears. Separation of mother and infant is only necessary when the mother has received treatment for less than 2 weeks, is sputum smear-positive, or has drug-resistant TB. Breastfeeding is not contraindicated, and in case of mother-infant separation expressed breast milk feeding is recommended.

[The Spanish Society of Pediatric Infectious Diseases Guidelines for the diagnosis and treatment of congenital toxoplasmosis]. / Guía de la Sociedad Española de Infectología Pediátrica para el diagnóstico y tratamiento de la toxoplasmosis congénita.

Congenital toxoplasmosis is the result of transplacental fetal infection by Toxoplasma gondii after the primary maternal infection. The severity of the disease depends on the gestational age at transmission. First trimester infections are more severe, but less frequent, than third trimester infections. Acute maternal infection is diagnosed by seroconversion or by the detection of IgM antibodies and a low IgG avidity test. In these cases, spiramycin should be initiated to prevent transmission to the fetus. For identification of fetal infection, polymerase chain reaction (PCR) testing of amniotic fluid after 18 weeks gestation should be performed. If fetal infection is confirmed, the mothers should be treated with pyrimethamine, sulfadiazine and folinic acid. Most infants infected in utero are born with no obvious signs of toxoplasmosis, but up to 80% developed learning and visual disabilities later in life. Neonatal diagnosis with IgM/IgA antibodies or blood/cerebrospinal fluid PCR may be difficult because false-negative results frequently occur. In these cases diagnosis is possible by demonstrating a rise in IgG titers during follow-up or by the detection of antibodies beyond one year of age. Early treatment with pyrimethamine and sulfadiazine may improve the ophthalmologic and neurological outcome. Congenital toxoplasmosis is a preventable disease. Pre-pregnancy screening and appropriate counseling regarding prevention measures in seronegative women may prevent fetal infection.

[Neonatal convulsions and subarachnoid hemorrhage after in utero exposure to paroxetine]. / Convulsiones y hemorragia subaracnoidea tras exposición a paroxetina in utero.

INTRODUCTION: Selective serotonin reuptake inhibitors (SSRIs) are often used as antidepressants in pregnant women. SSRIs do not appear to increase the teratogenic risk when used in their recommended doses. However, not enough information is available at this time about the risk of toxicity and complications in newborns, after mother treatment with SSRI during the third trimester of pregnancy. We are limited to the existing reports that describe newborns with symptoms due to hyperserotoninemia or withdrawal. CASE REPORT: One newborn whose mother had been treated with paroxetine 20 mg/day during pregnancy, presented convulsions and subarachnoid haemorrhage in the first six hours of life. The newborn did not present symptoms of hypoxic ischaemic encephalopathy, withdrawal syndrome, infection, metabolic alterations, cerebral malformations or coagulopaties. DISCUSSION: The most probable etiology is that the paroxetine could decrease the seizure threshold, taking place the first seizure during delivery. The difficult fetal extraction would have provoked the subarachnoid haemorrhage in a patient with an impaired haemostatic function due to a depletion of platelet serotonin and may also contribute the increased vascular fragility due to paroxetine and reported in adults or in animals. CONCLUSION: Neonatal convulsions and subarachnoid haemorrhage may occur after paroxetine treatment in the third trimester of pregnancy. An accurate follow up of these newborns in the firsts days of life is strongly recommended.

[Severe neonatal encephalopathy, secondary to a prolonged vasovagal episode in a woman 31 weeks pregnant]. / Encefalopatía neonatal grave, secundaria a episodio vasovagal prolongado en una gestante de 31 semanas.

INTRODUCTION: Vasovagal syncope is not frequent during the second half of pregnancy, although the supine hypotension syndrome is common during this period. During these episodes, the marked hypotension may impede uteroplacental blood flow. CASE REPORT: A woman who was 31.5 weeks pregnant lost consciousness for 15 minutes on standing up. 24 hours later, when it was observed that foetal movement had diminished, a cardiotocographic recording was done. This showed a pathological pattern and foetal biophysical profile on echography showed a marked foetal hypotonia and absence of movement. Emergency caesarean section was carried out and a male foetus delivered, weighing 1.810 g, with an Apgar score of 5/6 and requiring intubation and mechanical ventilation for respiratory difficulties and generalized hyptonia with absent reflexes. During the following days he developed generalized hypertonia and died aged 18 days. At necropsy there was severe brain damage, of ischaemic type. Complementary tests on the mother were normal. CONCLUSIONS: Severe prenatal encephalopathy secondary to maternal vasovagal syncope is uncommon, and we have found no report of it in the literature. The prolonged duration of the hypotensive episode, together with prematurity, which implies poor regulation of cerebral blood flow, may have contributed to the severe damage to the central nervous system