Vital Signs: Update on Zika Virus-Associated Birth Defects and Evaluation of All U.S. Infants with Congenital Zika Virus Exposure - U.S. Zika Pregnancy Registry, 2016.

BACKGROUND: In collaboration with state, tribal, local, and territorial health departments, CDC established the U.S. Zika Pregnancy Registry (USZPR) in early 2016 to monitor pregnant women with laboratory evidence of possible recent Zika virus infection and their infants. METHODS: This report includes an analysis of completed pregnancies (which include live births and pregnancy losses, regardless of gestational age) in the 50 U.S. states and the District of Columbia (DC) with laboratory evidence of possible recent Zika virus infection reported to the USZPR from January 15 to December 27, 2016. Birth defects potentially associated with Zika virus infection during pregnancy include brain abnormalities and/or microcephaly, eye abnormalities, other consequences of central nervous system dysfunction, and neural tube defects and other early brain malformations. RESULTS: During the analysis period, 1,297 pregnant women in 44 states were reported to the USZPR. Zika virus-associated birth defects were reported for 51 (5%) of the 972 fetuses/infants from completed pregnancies with laboratory evidence of possible recent Zika virus infection (95% confidence interval [CI] = 4%-7%); the proportion was higher when restricted to pregnancies with laboratory-confirmed Zika virus infection (24/250 completed pregnancies [10%, 95% CI = 7%-14%]). Birth defects were reported in 15% (95% CI = 8%-26%) of fetuses/infants of completed pregnancies with confirmed Zika virus infection in the first trimester. Among 895 liveborn infants from pregnancies with possible recent Zika virus infection, postnatal neuroimaging was reported for 221 (25%), and Zika virus testing of at least one infant specimen was reported for 585 (65%). CONCLUSIONS AND IMPLICATIONS FOR PUBLIC HEALTH PRACTICE: These findings highlight why pregnant women should avoid Zika virus exposure. Because the full clinical spectrum of congenital Zika virus infection is not yet known, all infants born to women with laboratory evidence of possible recent Zika virus infection during pregnancy should receive postnatal neuroimaging and Zika virus testing in addition to a comprehensive newborn physical exam and hearing screen. Identification and follow-up care of infants born to women with laboratory evidence of possible recent Zika virus infection during pregnancy and infants with possible congenital Zika virus infection can ensure that appropriate clinical services are available.

Severe Neurologic Disorders in 2 Fetuses with Zika Virus Infection, Colombia.

We report the results of pathologic examinations of 2 fetuses from women in Colombia with Zika virus infection during pregnancy that revealed severe central nervous system defects and potential associated abnormalities of the eye, spleen, and placenta. Amniotic fluid and tissues from multiple fetal organs tested positive for Zika virus.

Birth Defects Among Fetuses and Infants of US Women With Evidence of Possible Zika Virus Infection During Pregnancy.

Importance: Understanding the risk of birth defects associated with Zika virus infection during pregnancy may help guide communication, prevention, and planning efforts. In the absence of Zika virus, microcephaly occurs in approximately 7 per 10 000 live births. Objective: To estimate the preliminary proportion of fetuses or infants with birth defects after maternal Zika virus infection by trimester of infection and maternal symptoms. Design, Setting, and Participants: Completed pregnancies with maternal, fetal, or infant laboratory evidence of possible recent Zika virus infection and outcomes reported in the continental United States and Hawaii from January 15 to September 22, 2016, in the US Zika Pregnancy Registry, a collaboration between the CDC and state and local health departments. Exposures: Laboratory evidence of possible recent Zika virus infection in a maternal, placental, fetal, or infant sample. Main Outcomes and Measures: Birth defects potentially Zika associated: brain abnormalities with or without microcephaly, neural tube defects and other early brain malformations, eye abnormalities, and other central nervous system consequences. Results: Among 442 completed pregnancies in women (median age, 28 years; range, 15-50 years) with laboratory evidence of possible recent Zika virus infection, birth defects potentially related to Zika virus were identified in 26 (6%; 95% CI, 4%-8%) fetuses or infants. There were 21 infants with birth defects among 395 live births and 5 fetuses with birth defects among 47 pregnancy losses. Birth defects were reported for 16 of 271 (6%; 95% CI, 4%-9%) pregnant asymptomatic women and 10 of 167 (6%; 95% CI, 3%-11%) symptomatic pregnant women. Of the 26 affected fetuses or infants, 4 had microcephaly and no reported neuroimaging, 14 had microcephaly and brain abnormalities, and 4 had brain abnormalities without microcephaly; reported brain abnormalities included intracranial calcifications, corpus callosum abnormalities, abnormal cortical formation, cerebral atrophy, ventriculomegaly, hydrocephaly, and cerebellar abnormalities. Infants with microcephaly (18/442) represent 4% of completed pregnancies. Birth defects were reported in 9 of 85 (11%; 95% CI, 6%-19%) completed pregnancies with maternal symptoms or exposure exclusively in the first trimester (or first trimester and periconceptional period), with no reports of birth defects among fetuses or infants with prenatal exposure to Zika virus infection only in the second or third trimesters. Conclusions and Relevance: Among pregnant women in the United States with completed pregnancies and laboratory evidence of possible recent Zika infection, 6% of fetuses or infants had evidence of Zika-associated birth defects, primarily brain abnormalities and microcephaly, whereas among women with first-trimester Zika infection, 11% of fetuses or infants had evidence of Zika-associated birth defects. These findings support the importance of screening pregnant women for Zika virus exposure.

Study of bone marrow abnormalities in patients with HIV disease.

AIM: Present work was carried out to study the bone marrow abnormalities in patients with HIV/AIDS and to find their association with peripheral hematological abnormalities. METHODS: Seventy four patients of HIV/AIDS were included in the study. The patients had anemia, leucopenia, thrombocytopenia or pyrexia of unknown origin (PUO) as indications for bone marrow examination. A complete blood count, relevant biochemical investigations, HIV RNA load and CD4 positive lymphocyte counts were done, besides a thorough history and clinical examination. HIV positive patients were classified as those having AIDS and those without AIDS according to NACO criteria. RESULTS: Majority of patients (72.9%) had AIDS. Bone marrow was normocellular in 78.95% of non-AIDS and 74.55% of AIDS, hypocellular in 5.26% of non-AIDS and 7.27% of AIDS, hypercellular in 15.79% of non-AIDS and 18.18 % of AIDS patients. Myelodysplasia was present in 21.05% of non AIDS and 36.46% of AIDS and the most common series affected was granulocytic (15.79% of total in non-AIDS and 30.9% in AIDS). Dysplasia was statistically significantly associated with lower CD4 count (p = 0.031) and anemia (p = 0.013). Myelodysplasia was apparent even before patients developed anemia (16.67%). Increased plasma cells in bone marrow were observed in 57.89% of non-AIDS and 65.45% of AIDS, whereas decreased lymphoid cells were seen in 36.84% of non AIDS and 60.00% of AIDS patients. CONCLUSIONS: Myelodysplasia is found in 32.43% of cases of HIV/AIDS and is more common in AIDS than in non AIDS patients. Granulocytic series is most commonly associated with evidence of dysplasia. Myelodysplasia is more common in patients with CD4 count < 200/microl and in patients with anemia. 54.05% of patients had decreased lymphoid cells in bone marrow and it was more commonly seen in AIDS than in non AIDS.

Persistence of parvovirus B19 IgM antibodies and DNA in pure red cell aplasia resulting in myelodysplasia--a case report.

Human erythrovirus B19 (B19), previously known as parvovirus B19, is a small spherical, non-enveloped single stranded DNA virus. It has been shown to cause a wide spectrum of clinical conditons including various hematological disorders. We report here for the first time from Inida a case of pure red cell aplasia in a 45-year-old female for last 7 years due to chronic persistent B19 infection leading to myelodysplasia after 4 years. Her sera were positive for two times 4 months apart for B19 IgM and B19 DNA at the initial stage. Presently the patient is on repeated blood transfusion on every 15-20 days.

Excess FoxG1 causes overgrowth of the neural tube.

The winged helix transcription factor FoxG1 (Bf-1, qin) plays multiple roles in the development of the telencephalon, with different parts of the protein affecting either proliferation or differentiation. We examined the consequences of over-expression, via retroviral expression, of FoxG1 on the growth of different regions of the chicken brain. Excess expression of FoxG1 caused a thickening of the neuroepithelium, and ultimately large outgrowths of the telencephalon and mesencephalon. In contrast, the myelencephalon appeared unaffected, exhibiting normal apoptosis and growth characteristics. A DNA binding defective form of FoxG1 did not exhibit these abnormalities, suggesting that these effects are due to FoxG1's function as a transcriptional repressor. To examine the means by which excess FoxG1 caused overgrowth of the brain, we examined alterations in cell proliferation and death. No increase in proliferation was noted in any portion of the neural tube, rather a significant decrease in neuroepithelial apoptosis was seen. These results demonstrate a previously unrecognized role for winged helix factors in the regulation of neural cell apoptosis.

Is adenovirus a fetal pathogen?

OBJECTIVES: The purpose of this study was to test the relationship between adenovirus genetic material in the amniotic fluid and adverse pregnancy outcome. STUDY DESIGN: This was a prospective, observational study of women who were referred in the second trimester of gestation for either genetic amniocentesis or evaluation of fetal malformation. A 2-mL aliquot of amniotic fluid was subjected to multiplex polymerase chain reaction for a panel of viruses that included adenovirus and human genome controls. Fetuses with an abnormal karyotype were excluded from analysis. RESULTS: The prevalence of adenovirus was similar in normal (39/652) and anomalous fetuses (23/364; chi(2) test, P=.376). There was significant seasonal variation in the prevalence in both normal and anomalous fetuses (chi(2) exact test, P<.001), but no significant difference between groups. The monthly proportion of patients who underwent amniocentesis remained constant throughout the year (mean, 8.3%; chi(2) test, P=.67). Central nervous system anomalies and echogenic liver foci were significantly more common among fetuses with positive amniotic fluid polymerase chain reaction results for adenovirus (P<.005, respectively). CONCLUSION: Adenovirus is found in a similar prevalence and seasonal variation in sonographically normal and abnormal pregnancies. Although a specific fetal presentation was not identified, echogenic liver lesions with or without hydrops and neural tube defects were significantly more common in the presence of adenovirus. The significance of these findings deserves further study.

[Detecting pathogens of fetal defects in paraffin embedded tissues by polymerase chain reaction].

OBJECTIVE: To examine 3 types of pathogens in dead fetus with congenital defects for exploring the pathogenesis. METHODS: The paraffin embeded brain and liver tissues from 39 fetal autopsies with congenital defects were examined for toxoplasma, cytomegalovirus, and herpes simplex II by polymerase chain reaction. Among them 16 placentae were examined as well. RESULTS: Pathogens were detected in 25 of 39 cases, a positive rate of 64%. Nine out of the 13 fetuses with urogenital defects were positive for the shove pathogens, while 8 from the 12 with neural tube defects were positive as well. CONCLUSION: Intrauterine infection was one of the important causes of birth defects. The characteristics of placenta morphologic changes were described, and the significance of placenta investigation in congenital malformation was emphasized.