A case of congenital Echovirus 11 infection acquired early in pregnancy.

Enterovirus (EV) maternal infection during pregnancy and its relation to fetal developmental pathology are seldomly described. When reported, the main manifestations of EV congenital infections are myocarditis or intra-uterine fetal demise (IUFD). No information on intrauterine Echovirus 11 infection or the effect of transplacental Echovirus 11 infection on development of the fetus has been described in literature up to date (excluding late-pregnancy infections). We report here a case of an extreme form of pulmonary hypoplasia in a neonate, characterized by total failure of development of terminal respiratory units. This pregnancy was marked by spontaneous demise of a co-twin at 14 weeks of gestation (WG), as well as by positive PCR for EV (Echovirus 11 serotype) in the amniotic fluid, performed for moderate pericardial effusion at 22WG. No signs of cardiac disease were further observed, but at 32WG a bilateral abnormal lung development was noticed After spontaneous delivery at 38WG, the child could not be resuscitated, and died at one hour after birth. Pulmonary hypoplasia is usually described following decrease intrapulmonary pressure due to oligohydramnios or compression due to intrathoracic mass of variable cause. However, rare cases of primary pulmonary hypoplasia are also described and usually of unknown etiology. The coexistence in our case of a congenital EV infection and a severe primary pulmonary hypoplasia with congenital acinar aplasia, challenges our understanding of the pathogenesis of this severe pulmonary growth arrest.

Congenital echovirus 21 infection causing fulminant hepatitis in a neonate.

Enteroviral infection in pregnancy is common and there is growing evidence relating it to congenital anomalies and neonatal mortality. Neonatal disease may range from unapparent infection to overwhelming systemic illness. Passively acquired maternal serotype specific antibodies determine the severity of the disease in the newborn. A fatal case of congenital echovirus 21 infection, confirmed by PCR in the patient's blood and positive culture of the mother's stools, is reported. A sibling had symptoms of respiratory tract infection and their mother had fever, which prompted iatrogenic delivery that same day. The newborn presented with bradycardia and hypotonia in the first minutes of life and later developed respiratory distress, disseminated intravascular coagulopathy, fulminant hepatitis, acute renal failure and necrotising enterocolitis. Death occurred on the 8 day of life. This case highlights the potential severity of Enteroviral infection in the newborn. Since only supportive treatment is available, prevention is paramount.

Neonatal sepsis due to echovirus 18 infection.

Clinical manifestations of neonatal echovirus type 18 infections include a nonspecific febrile illness, diarrhea, and meningitis with or without exanthem. We report a successful outcome in a case of neonatal sepsis with shock caused by echovirus type 18, a complication not previously associated with this serotype.

Congenital echo virus infection--morphological and virological study of fetal and placental tissue.

A prospective study of 78 pregnant women was undertaken to detect maternal enterovirus infection. Maternal faecal specimens and blood samples, placental and fetal tissue were taken for viral study, electron microscopy, histochemistry, and morphological examination. We present the post-mortem findings in three fetuses whose maternal infection was detected before delivery by isolation of ECHO virus type 33 and type 27 from faecal specimens and/or placental and fetal tissues. The morphological aspects were similar in all cases and included an acute infection of the placenta and hypoxic/hypotensive injury to fetal organs. In one case, viral particles were detected by electron microscopy of the fetal liver. This series of cases of intrauterine ECHO virus infection confirms the potential gravity of such infection during pregnancy and the need to prevent enteroviral disease.

Dissimilar manifestations of intrauterine infection with echovirus 11 in premature twins.

Echoviruses cause neonatal disease following intrauterine and intrapartum acquisition of the organism or by nosocomial infection. Dizygous twins apparently became infected following transplacental transmission of echovirus 11. At 5 days of age, both twins experienced poor feeding, lethargy and hypothermia, and evidence of coagulopathy and hepatitis. During the sixth week of illness, the convalescence of twin A was complicated by peritonitis and sepsis, and the infant died. Pathologic findings included scattered foci of dystrophic myocardial calcification, distortion of hepatic architecture with fibrous connective tissue surrounding regenerative nodules and large foci of dystrophic calcification, and adrenal hemorrhagic necrosis and calcification. Twin B recovered without sequelae. The disease in twin A was unusual because of the extensive myocardial involvement. Also of interest was the variability of disease in twins who presumably had received a similar inoculum of organism by the same route.

Disseminated neonatal echovirus 11 disease following antenatal maternal infection with a virus-positive cervix and virus-negative gastrointestinal tract.

An infant girl was born apparently well one week after her mother had had a mild illness with chills, fever, and diarrhea. On the third day of life, the infant became ill and died four days later with necrotizing hepatitis. On the same day, echovirus type 11 was recovered from the throat, rectum, and buffy coat of the infant and from the cervix of the mother. At this time, the mother had an IgM neutralizing antibody titer to echovirus type 11 and 1:128, but no IgG antibodies. The infant had no echovirus type 11 antibodies. The virus was also isolated from the baby's liver and adrenal at autopsy. These findings raise the possibility of enterovirus infection at delivery from a contaminated cervix.

Fatal echovirus 11 disease in premature neonates.

Four cases of fatal echovirus 11 disease occurred in premature infants during a community outbreak of enteroviral disease in Massachusetts in 1979. Each infant developed nonspecific symptoms and jaundice at 4 to 6 days of age, and subsequent progressive hepatic failure and generalized bleeding. Only one infant survived longer than six days. Virus was recovered from multiple sites premortem, and from virtually all tissue cultured at autopsy. Myocarditis was not present clinically or pathologically. Clinical and laboratory evidence implicated perinatal transmission of virus from mother to infant. Three mothers experienced a febrile illness with abdominal pain within the last five days of pregnancy. In two, the illness led to a false diagnosis of abruptio placenta and interruption of pregnancy by cesarian section. Review of case reports of this syndrome caused by other echovirus serotypes revealed that many had similar perinatal events. Each mother ultimately developed neutralizing antibody to echovirus 11. However, all four infants were born without passively acquired antibody, probably because they were delivered prior to the appearance of specific maternal IgG. Although laboratory studies by others have shown other factors may be responsible for the ability of enterovirus to cause overwhelming disease in neonates, uncontrolled data from these four infants and their mothers suggest that timing of maternal illness in relation to delivery of the infant may also be important.