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TREATMENT, PREVENTION, AND CONTROLAs with the other mosquito-borne flaviviruses, treatment for uncomplicated Zika virus infection focuses on symptoms. No Zika virus vaccine exists; thus, prevention and control measures center on avoiding mosquito bites, reducing sexual transmission, and controlling the mosquito vector. Potentially effective methods of prevention that are focused on reducing infections among pregnant women include avoiding unnecessary travel to areas of ongoing Zika virus transmission, avoiding unprotected sexual contact with partners who are at risk for Zika virus infection,103 and using mosquito repellent, permethrin treatment for clothing,120 bed nets,121 window screens,122,123 and air conditioning.124,125 The most effective A. aegypti vector control relies on an integrated approach that involves elimination of A. aegypti mosquito breeding sites, application of larvicides, and application of insecticides to kill adult mosquitoes. However, each of these approaches has substantial limitations. Communities are often mobilized to reduce A. aegypti breeding sites, but this strategy often fails, in part because of inconsistent participation among households and the presence of cryptic breeding sites in modern urban settings.126,127 Dengue control programs make extensive use of peridomestic insecticide spraying during outbreaks, but little evidence supports its efficacy as a single control intervention.128 The application of larvicides129 and indoor residual spraying129,130 have been effective in some settings. Given these limitations, an integrated prevention and vector-control approach combined with timely detection of illness, communication of up-to-date and correct information, and development of a rapid response that involves the community are recommended.131

VIROLOGYDespite a limited number of available full-length Zika virus sequences, the molecular data are sufficient to reveal patterns of viral evolution and movement. The virus is likely to have originated in East Africa and subsequently spread to West Africa and then to Asia, resulting in distinct lineages (Nigerian Cluster, MR766 Cluster, and the Asian genotype).101,117 All strains currently associated with the outbreak in the Americas are of the Asian genotype and are most closely related to strains from Yap, Cambodia, Thailand, and French Polynesia.118 The strains from the Americas that have been examined to date are genetically very similar to each other, with approximately 99% nucleotide homology. Furthermore, there is strong conservation among all Zika virus strains overall, with less than 12% divergence at the nucleotide level.119 This is important for diagnostic assays, which rely on precise sequences and epitopes, as well as for the development of therapeutics and vaccines. The current similarity data suggest that any vaccine product developed against any strain of Zika virus should be protective against all strains. The very nature of the close relatedness among the flaviviruses is responsible for the challenges in developing diagnostic algorithms for distinguishing among these viruses.

DIAGNOSISThe mainstays of the routine diagnosis of Zika virus infection are the detection of viral nucleic acid by RT-PCR and the detection of IgM antibodies by IgM-capture enzyme-linked immunosorbent assay (MAC-ELISA). The detection of viral nucleic acid in serum provides a definitive diagnosis; however, in most instances viremia is transient, and diagnosis by RT-PCR has been most successful within 1 week after the onset of clinical illness.67,101 In contrast, viral RNA was detected in serum approximately 10 weeks after infection in a pregnant woman whose fetus had evidence of congenital infection.95 In addition, viremia is generally low level, which makes viral isolation from clinical samples difficult.101 Although the precise timing of the onset and the duration of the IgM antibody response to Zika virus that is detectable by MAC-ELISA have not yet been defined, extensive experience with other, related flaviviruses suggests that IgM will appear as viremia wanes within the first week after symptom onset and will persist for several months.102Thus, RT-PCR testing of serum samples obtained within the first week of clinical illness and MAC-ELISA testing of samples that are not tested by RT-PCR or that are found to be negative by RT-PCR are likely to have the highest diagnostic yield.103 The considerable cross-reactivity of flavivirus antibodies presents major challenges for the interpretation of serologic test results. For example, recent Zika virus infection may also evoke a positive MAC-ELISA result for dengue. The plaque reduction neutralization test (PRNT), the most specific test used to differentiate antibodies of closely related viruses, can be used to help verify MAC-ELISA results.104 However, this test is labor-intensive and costly, involves handling of live virus, takes up to a week to perform, requires standardized reagents that often are not available, and is not widely performed. In settings where PRNT is not available or the volume of testing makes PRNT impractical, specimens that are found positive by Zika virus MAC-ELISA and negative by dengue MAC-ELISA may be interpreted as a presumptive recent Zika virus infection. However, the diagnostic accuracy of this approach has not been established. The greatest challenge with serologic cross-reactivity arises from the “original antigenic sin” phenomenon105: for patients who have previously been exposed to a heterologous flavivirus by natural infection or vaccination, the antibody response to the previous infecting flavivirus will be more vigorous than the response to the current one.101,106 Even the PRNT cannot reliably establish a diagnosis in such patients. This is particularly problematic in areas in which dengue is endemic, where more than 90% of the population may have had previous exposure to dengue virus107 and dengue and Zika viruses may be cocirculating. Limited data suggest that Zika virus RNA can be detected longer in urine than in serum; if verified, this would extend the period during which a definitive diagnosis of Zika virus infection can be established by RT-PCR.74,108-110 Another large study that compared RT-PCR results in serum and saliva samples indicated that RT-PCR had higher sensitivity in saliva than in serum, although samples from some patients were positive in serum but not saliva, and testing of saliva did not extend the duration of detectability of viral nucleic acid after the onset of illness.111 Reliable testing regimens for the diagnosis of prenatal and antenatal Zika virus infection have not been established. Amniotic fluid has tested positive by RT-PCR in instances of congenital Zika virus infection; however, the sensitivity of RT-PCR in this context is unknown.40,53,54,94,95 At the time of delivery, cord blood can be tested by RT-PCR and MAC-ELISA, but the sensitivities of these tests for detecting prenatal Zika virus infection are unknown. RT-PCR and immunohistochemical testing have been useful in establishing Zika virus infection in tissues of fetal losses and full-term infants who died shortly after birth.55,94 Although microcephaly and other fetal abnormalities may be detected as early as 18 to 20 weeks of gestation,40,54,69,112 they are often not detected until later in pregnancy, in part because some cases do not occur earlier in pregnancy.69,113 Furthermore, the use of ultrasonography to detect microcephaly is dependent on clinical and technical factors,114 and ultrasonography is not a highly sensitive means of detecting microcephaly.115 Findings associated with Zika virus infection that have been noted on ultrasound have included, in addition to microcephaly, an absent corpus callosum, hydranencephaly, cerebral calcifications, ventricular dilatation, brain atrophy, abnormal gyration, hydrops fetalis, anhydramnios, and intrauterine growth retardation.40,69,94,116

CLINICAL ASPECTSAcute Febrile IllnessThe incubation period for Zika virus is unknown, but if it is similar to that of other mosquito-borne flaviviruses, it is expected to be generally less than 1 week. In one volunteer, a febrile illness of 4 days’ duration developed 82 hours after subcutaneous inoculation of Zika virus.67 Viremia was detected when symptoms were present, but not afterward. Among French Polynesian blood donors who tested positive for Zika virus by RT-PCR, 11 (26%) reported conjunctivitis, rash, arthralgia, or a combination of these symptoms 3 to 10 days after donation.64 Serosurvey results from Yap indicated that only 19% of persons who were infected had symptoms that were attributable to Zika virus.17 Common symptoms were macular or papular rash (90% of patients), fever (65%), arthritis or arthralgia (65%), nonpurulent conjunctivitis (55%), myalgia (48%), headache (45%), retro-orbital pain (39%), edema (19%), and vomiting (10%). No patient was hospitalized during the outbreak in Yap. These common symptoms occurred at frequencies similar to those in the Yap outbreak in a cohort of pregnant women with Zika virus infection in Brazil.69 The rash is generally maculopapular and pruritic,69 and fever, when present, is generally short-term and low-grade.69 Other symptoms that have been noted in association with acute infection include hematospermia,57,60 transient dull and metallic hearing,27 swelling of the hands and ankles,27,70 and subcutaneous bleeding.71 Neurologic ComplicationsA temporal and geographic relationship has been observed between Guillain–Barré syndrome and Zika virus outbreaks in the Pacific and the Americas.19,21,72-74 In the outbreak in French Polynesia, 38 cases of Guillain–Barré syndrome occurred among an estimated 28,000 persons who sought medical care.19 A case–control study in French Polynesia revealed a strong association (odds ratio, >34) between Guillain–Barré syndrome and previous Zika virus infection; the findings from electrophysiological studies were compatible with the acute motor axonal neuropathy subtype of Guillain–Barré syndrome.75 Meningoencephalitis76 and acute myelitis77 complicating Zika virus infection also have been reported. Adverse Fetal OutcomesThe full spectrum of fetal outcomes resulting from fetal Zika virus infection in humans is yet to be determined; however, the well-characterized effects of maternal infection with rubella virus and cytomegalovirus (CMV) may be instructive.78,79 Maternal rubella infections in the first 10 weeks of pregnancy can result in adverse fetal effects in up to 90% of infants and decrease thereafter, with a much lower risk after gestational week 18.80,81 The congenital anomalies associated with maternal rubella infection during pregnancy include sensorineural hearing loss, cataracts and other eye anomalies, cardiac anomalies, and neurologic effects, including intellectual disability, ischemic brain damage, and microcephaly.80,82 Similarly, maternal CMV infection can produce profound effects on the fetus, including sensorineural hearing loss, chorioretinitis, and neurologic effects, such as microcephaly, intellectual disability, and cerebral palsy.83 For primary infections with CMV, the risk of adverse fetal effects is highest during the first trimester, but the risk persists in the second and third trimester, with some adverse fetal outcomes noted in mothers who had seroconversion after gestational week 27.84 It is of particular concern that some infants without obvious adverse effects of congenital CMV infection at birth can have late-onset or progressive hearing loss that cannot be identified through screening of newborns.85 Other causes of microcephaly include some genetic syndromes, vascular disruption during brain development, nutritional deficiencies, and exposure to certain toxins, such as mercury.86 Microcephaly is a clinical finding of a small head size for gestational age and sex and is indicative of an underlying problem with the growth of the brain.87 The lack of consistent and standardized case definitions has challenged the accurate monitoring of microcephaly during the current Zika virus outbreak.39 Centers for Disease Control and Prevention (CDC) guidance has recommended that microcephaly be defined as an occipitofrontal circumference below the third percentile for gestational age and sex.88 The prevalence of microcephaly in the United States averages approximately 6 cases per 10,000 live births, with a range of about 2 to 12 cases per 10,000 live births.89 Because similar prevalences are expected in other countries, these figures may be suitable benchmarks for regions lacking accurate historical data. Microcephaly can occur as a result of fetal brain disruption sequence, a process in which, after relatively normal brain development in early pregnancy, collapse of the fetal skull follows the destruction of fetal brain tissue.90-92 Although previous case reports of maternal infection leading to fetal brain disruption sequence do not include information on the timing of maternal infection, some evidence indicates that this damage can occur late during the second trimester or even early in the third trimester.93 Initial case reports from Brazil have suggested that some of the infants with microcephaly related to Zika virus infection have a phenotype consistent with fetal brain disruption (Figure 4FIGURE 4Infants with Moderate or Severe Microcephaly Associated with Maternal Zika Virus Infection, as Compared with a Typical Newborn.).38,94,95 The findings of Zika virus RNA in the amniotic fluid of fetuses with microcephaly40,52,54 and in the brain tissue of fetuses and infants with microcephaly,55,94,95 as well as the high rates of microcephaly among infants born to mothers with proven antecedent acute Zika virus infection,69provide strong evidence linking microcephaly to maternal Zika virus infection. The timing of the Zika virus and microcephaly epidemics in Brazil96,97 and French Polynesia41 indicate that the greatest risk of microcephaly is in the first trimester. In case reports of microcephaly, documented maternal Zika virus infection most often occurred between 7 and 13 weeks of gestation, but in some cases it occurred as late as at 18 weeks of gestation.40,52,54,69,94 A preliminary report from Brazil indicated that fetal abnormalities detected by ultrasonography were present in 29% of women with Zika virus infection during pregnancy.69 Early fetal loss and fetal death have been noted in association with maternal infection that occurred between 6 and 32 weeks of gestation.54,69 Ocular anomalies have been reported among infants with microcephaly in Brazil.69,98-100 In the largest study with comprehensive ophthalmologic examinations of infants with microcephaly, ocular abnormalities were found in 10 of 29 patients (35%).100 The most common ocular abnormalities were focal pigment mottling, chorioretinal atrophy, and optic-nerve abnormalities (hypoplasia and severe cupping of the optic disk). Other ocular manifestations in this and other case studies have included foveal reflex loss, macular neuroretinal atrophy, lens subluxation, and iris coloboma. Whether ocular manifestations occur after congenital Zika virus infection in infants without microcephaly remains unknown.

ZIKA VIRUS TRANSMISSIONMosquito-borne TransmissionIn Africa, Zika virus exists in a sylvatic transmission cycle involving nonhuman primates and forest-dwelling species of aedes mosquitoes (Figure 2FIGURE 2Zika Virus Transmission Cycle.). In Asia, a sylvatic transmission cycle has not yet been identified. Several mosquito species, primarily belonging to the stegomyia and diceromyia subgenera of aedes, including A. africanus, A. luteocephalus, A. furcifer, and A. taylori, are likely enzootic vectors in Africa and Asia.42,43 In urban and suburban environments, Zika virus is transmitted in a human–mosquito–human transmission cycle (Figure 2). Two species in the stegomyia subgenus of aedes — A. aegypti and, to a lesser extent, A. albopictus44 — have been linked with nearly all known Zika virus outbreaks, although two other species, A. hensilli and A. polynesiensis, were thought to be vectors in the Yap45 and French Polynesia46 outbreaks, respectively. A. aegypti and A. albopictus are the only known aedes (stegomyia) species in the Americas. Despite the association of A. aegypti and A. albopictus with outbreaks, both were found to have unexpectedly low but similar vector competence (i.e., the intrinsic ability of a vector to biologically transmit a disease agent) for the Asian genotype Zika virus strain, as determined by a low proportion of infected mosquitoes with infectious saliva after ingestion of an infected blood meal.47 However, A. aegyptiis thought to have high vectorial capacity (i.e., the overall ability of a vector species to transmit a pathogen in a given location and at a specific time) because it feeds primarily on humans, often bites multiple humans in a single blood meal, has an almost imperceptible bite, and lives in close association with human habitation.48 Both A. aegypti and A. albopictus bite primarily during the daytime and are widely distributed throughout the tropical and subtropical world. A. albopictus can exist in more temperate areas thanA. aegypti, thus extending the potential range where outbreaks may occur. In the United States, A. aegypti is endemic throughout Puerto Rico and the U.S. Virgin Islands and in parts of the contiguous United States and Hawaii (Figure 3FIGURE 3Approximate Ranges of A. aegypti and A. albopictus in the United States (as of March 2016).).49 A. albopictus is widely distributed in the eastern United States and Hawaii. Nevertheless, in the contiguous United States, contemporary outbreaks of dengue, which has a transmission cycle similar to that of Zika virus, have occurred only in areas in which A. aegypti is endemic, which suggests that the potential for the transmission of Zika virus elsewhere is limited. In contrast, Hawaii has experienced contemporary dengue outbreaks in which A. albopictus was the vector.50,51 Zika virus has infrequently been identified in other mosquito species, such as A. unilineatus, Anopheles coustani, and Mansonia uniformis; however, vector-competence studies have indicated that these species have a low potential for transmission of the virus. It is notable that Zika virus has been reported only once in any culex species, which suggests that mosquitoes in this genus have a low vectorial capacity.42 Nonmosquito TransmissionSubstantial evidence now indicates that Zika virus can be transmitted from the mother to the fetus during pregnancy. Zika virus RNA has been identified in the amniotic fluid of mothers whose fetuses had cerebral abnormalities detected by ultrasonography,40,52-54 and viral antigen and RNA have been identified in the brain tissue and placentas of children who were born with microcephaly and died soon after birth,55 as well as in tissues from miscarriages.54,55 The frequency of and risk factors for transmission are unknown. Two cases of peripartum transmission of Zika virus have been reported among mother–infant pairs.56 Zika virus RNA was detected in both infants; one infant had a mild rash illness and thrombocytopenia, whereas the other was asymptomatic. Sexual transmission to partners of returning male travelers who acquired Zika virus infection abroad has been reported.57-59 In one instance, sexual intercourse occurred only before the onset of symptoms, whereas in other cases sexual intercourse occurred during the development of symptoms and shortly thereafter. The risk factors for and the duration of the risk of sexual transmission have not been determined. Replicative viral particles, as well as viral RNA — often in high copy numbers — have been identified in sperm, and viral RNA has been detected up to 62 days after the onset of symptoms.60-62 Although the transmission of Zika virus through a blood transfusion has yet to be reported, it is likely to occur, given the transmission of other, related flaviviruses through this route.63 During the Zika virus outbreak in French Polynesia, 3% of donated blood samples tested positive for Zika virus by reverse-transcriptase polymerase chain reaction (RT-PCR).64 One case of Zika virus transmission occurred after a monkey bite in Indonesia, although mosquito-borne transmission could not be ruled out.65 Two infections in laboratories have been reported.16,66A volunteer became infected after subcutaneous injection of infected mouse brain suspension.67Transmission through breast milk has not been documented, although the breast milk of a woman who became symptomatic with Zika virus infection on the day of delivery contained infective Zika viral particles in high titer.68

EPIDEMIOLOGYZika virus is a flavivirus, in the family Flaviviridae. Although Zika virus was isolated on several occasions from Aedes africanus mosquitoes after its discovery in 1947,4 there initially was no indication that the virus caused human disease. Nevertheless, a serosurvey involving residents of multiple areas of Uganda revealed a 6.1% seroprevalence of antibodies against Zika virus, which suggested that human infection was frequent.5 Additional serosurveys indicated a much broader geographic distribution of human infection, including Egypt,6 East Africa,7 Nigeria,8 India,9Thailand,10 Vietnam,10 the Philippines,11 and Malaysia (near Kuala Lumpur and in East Malaysia [Sabah and Federal Territory of Labuan]).12 Human illness caused by Zika virus was first recognized in Nigeria in 1953, when viral infection was confirmed in three ill persons.8 Despite recognition that Zika virus infection could produce a mild, febrile illness, only 13 naturally acquired cases were reported during the next 57 years.13-16Thus, it came as a great surprise when a 2007 outbreak on several islands in the State of Yap, Federated States of Micronesia, resulted in an estimated 5000 infections among the total population of 6700.17 Subsequently, an outbreak in French Polynesia in 2013 and 2014 is estimated to have involved 32,000 persons who underwent evaluation for suspected Zika virus infection.18-20 Although most of the illnesses appeared similar to those seen in Yap, cases of Guillain–Barré syndrome were also noted.19,21 Subsequent outbreaks occurred on other Pacific islands, including New Caledonia (in 2014),22 Easter Island (2014),23 Cook Islands (2014),24 Samoa (2015), and American Samoa (2016) (Figure 1FIGURE 1Areas in Which Zika Virus Infections in Humans Have Been Noted in the Past Decade (as of March 2016).). In stark contrast to these outbreaks, in the past 6 years, only sporadic cases of Zika virus infection have been reported in Thailand,25,26 East Malaysia (Sabah),27 Cambodia,28 the Philippines,29 and Indonesia.30,31 Zika virus was first identified in the Americas in March 2015, when an outbreak of an exanthematous illness occurred in Bahia, Brazil.32,33Epidemiologic data indicate that in Salvador, the capital of Bahia, the outbreak had begun in February and extended to June 2015.34 By October, the virus had spread to at least 14 Brazilian states,35 and in December 2015, the Brazil Ministry of Health estimated that up to 1.3 million suspected cases had occurred.36 In October 2015, Colombia reported the first autochthonous transmission of Zika virus outside Brazil,35 and by March 3, 2016, a total of 51,473 suspected cases of Zika virus had been reported in that country.37 By March 2016, the virus had spread to at least 33 countries and territories in the Americas (Figure 1).36,37 By September 2015, investigators in Brazil noted an increase in the number of infants born with microcephaly in the same areas in which Zika virus was first reported,38 and by mid-February 2016, more than 4300 cases of microcephaly had been recorded, although overreporting and misdiagnosis probably inflated this number.39 Subsequently, French Polynesian investigators retrospectively identified an increased number of fetal abnormalities, including microcephaly, after the Zika virus outbreak in that country.40,41

In 1947, a study of yellow fever yielded the first isolation of a new virus, from the blood of a sentinel rhesus macaque that had been placed in the Zika Forest of Uganda.1 Zika virus remained in relative obscurity for nearly 70 years; then, within the span of just 1 year, Zika virus was introduced into Brazil from the Pacific Islands and spread rapidly throughout the Americas.2 It became the first major infectious disease linked to human birth defects to be discovered in more than half a century and created such global alarm that the World Health Organization (WHO) would declare a Public Health Emergency of International Concern.3 This review describes the current understanding of the epidemiology, transmission, clinical characteristics, and diagnosis of Zika virus infection, as well as the future outlook with regard to this disease.

REVIEW ARTICLE Lindsey R. Baden, M.D., editor Zika VirusLyle R. Petersen, M.D., M.P.H., Denise J. Jamieson, M.D., M.P.H., Ann M. Powers, Ph.D., and Margaret A. Honein, Ph.D., M.P.H. March 30, 2016DOI: 10.1056/NEJMra1602113 SOURCE INFORMATIONFrom the Division of Vector-Borne Diseases, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Fort Collins, CO (L.R.P., A.M.P.); and the Division of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion (D.J.J), and the Division of Congenital and Developmental Disorders, National Center on Birth Defects and Developmental Disabilities (M.A.H), Centers for Disease Control and Prevention, Atlanta. Address reprint requests to Dr. Petersen at the Division of Vector-Borne Diseases, Centers for Disease Control and Prevention, 3156 Rampart Rd., Fort Collins, CO 80521, or at [email protected]. http://www.nejm.org/doi/full/10.1056/NEJMra1602113?query=featured_home

Map Update https://www.google.com/maps/d/u/0/edit?hl=en&hl=en&authuser=0&authuser=0&mid=zv94AJqgUct4.kT4qLMXp3SLU

As of Thursday, March 31, VDH has reported 9 cases of Zika virus disease in Virginia residents to the CDC (2 in Northwest Region, 3 in Northern Region, 1 in Eastern Region, 1 in Central Region and 2 in Southwest Region). http://www.vdh.virginia.gov/

As of Thursday, March 31, VDH has reported 9 cases of Zika virus disease in Virginia residents to the CDC (2 in Northwest Region, 3 in Northern Region, 1 in Eastern Region, 1 in Central Region and 2 in Southwest Region).

Latest Facts and Advisories as of 3/30/2016 [ Español (PDF)]Reported cases of Zika in New York City: 25 Three of the twenty-five cases were pregnant at the time of diagnosis;All cases contracted Zika while visiting other countries; andAll patients have recovered.

CASE REPORTA 33-year-old Finnish woman who was in the 11th week of gestation was on holiday in Mexico, Guatemala, and Belize with her husband in late November 2015. (Details are provided in Section 1.0 of the Supplementary Appendix, available with the full text of this article at NEJM.org.) During their travels, she and her husband recalled being bitten by mosquitoes, particularly in Guatemala. One day after her arrival at her current residence in Washington, D.C., she became ill with ocular pain, myalgia, and mild fever (maximum, 37.5°C), which lasted for 5 days. On the second day of fever, a rash developed (Figure 1FIGURE 1Timeline of Symptoms and Radiographic and Laboratory Studies., and Fig. S5 in the Supplementary Appendix). Her husband was concomitantly reporting similar symptoms. Serologic analysis that was performed 4 weeks after the onset of illness while she was on a trip to her native Finland was positive for IgG antibodies and negative for IgM antibodies against dengue virus. Subsequent serologic analysis was positive for both IgG and IgM antibodies against ZIKV, findings that were compatible with acute or recent ZIKV infection. Serologic analysis for the presence of chikungunya virus was negative. The patient had been vaccinated against tick-borne encephalitis and yellow fever more than 10 years earlier. Fetal ultrasonography that was performed at 13, 16, and 17 weeks of gestation (1, 4, and 5 weeks after the resolution of symptoms) showed no evidence of microcephaly or intracranial calcifications. However, there was a decrease in the fetal head circumference from the 47th percentile at 16 weeks to the 24th percentile at 20 weeks. At 16 weeks of gestation, the presence of flavivirus in serum was detected on nested reverse-transcriptase–polymerase-chain-reaction (RT-PCR) assay, and sequencing showed identity to Central American epidemic strains of ZIKV. The finding was confirmed with a specific ZIKV quantitative RT-PCR assay (Table S2 in the Supplementary Appendix). The Division of Vector-Borne Diseases Arbovirus Diagnostic Laboratory at the CDC reported serologic evidence of infection at 17 weeks of gestation, with serum positivity for ZIKV IgM and a titer of more than 1:2560 on a plaque-reduction neutralization test. On the basis of these results, the patient sought more thorough assessment of the fetus. Fetal ultrasonography at 19 weeks of gestation showed abnormal intracranial anatomy (Figure 2FIGURE 2Fetal Ultrasonography at 19 Weeks of Gestation., and Fig. S1 in the Supplementary Appendix). The cerebral mantle appeared to be thin with increased extra-axial spaces. Both frontal horns were enlarged with heterogeneous, predominantly echogenic material present in the frontal horn and body of the left lateral ventricle, a finding that raised concern about intraventricular hemorrhage. Dilation and upward displacement of the third ventricle, dilation of the frontal horns of the lateral ventricles, concave medial borders of the lateral ventricles, and the absence of the cavum septum pellucidum suggested agenesis of the corpus callosum. No parenchymal calcifications were seen. The head circumference measured in the 24th percentile for gestational age. The remainder of the fetal anatomy was normal. Fetal MRI at 20 weeks of gestation showed diffuse atrophy of the cerebral mantle, which was most severe in the frontal and parietal lobes, with the anterior temporal lobes least affected (Figure 3FIGURE 3Magnetic Resonance Imaging of the Fetal Brain at 19 Weeks of Gestation.). The normal lamination pattern of the cerebral mantle was absent, and the subplate zone was largely undetectable. The corpus callosum was significantly shorter than expected for gestational age, with an anterior–posterior length of 14 mm (expected range, 18 to 22).18,19 The cavum septum pellucidum was very small. The lateral ventricles were mildly enlarged, as was the third ventricle, with a transverse diameter measuring 2.5 mm (average measurement at gestational age, 1.75 mm [range, 1.1 to 2.3]).18 The fourth ventricle was normal. The volume of the choroid plexus was unusually prominent, without evidence of hemorrhage. No focal destructive lesions were identified within the cerebral cortex or white matter. The cerebellum was normal in appearance and size. Given the grave prognosis, the patient elected to terminate the pregnancy at 21 weeks of gestation.

CASE REPORTA 33-year-old Finnish woman who was in the 11th week of gestation was on holiday in Mexico, Guatemala, and Belize with her husband in late November 2015. (Details are provided in Section 1.0 of the Supplementary Appendix, available with the full text of this article at NEJM.org.) During their travels, she and her husband recalled being bitten by mosquitoes, particularly in Guatemala. One day after her arrival at her current residence in Washington, D.C., she became ill with ocular pain, myalgia, and mild fever (maximum, 37.5°C), which lasted for 5 days. On the second day of fever, a rash developed (Figure 1FIGURE 1Timeline of Symptoms and Radiographic and Laboratory Studies., and Fig. S5 in the Supplementary Appendix). Her husband was concomitantly reporting similar symptoms. Serologic analysis that was performed 4 weeks after the onset of illness while she was on a trip to her native Finland was positive for IgG antibodies and negative for IgM antibodies against dengue virus. Subsequent serologic analysis was positive for both IgG and IgM antibodies against ZIKV, findings that were compatible with acute or recent ZIKV infection. Serologic analysis for the presence of chikungunya virus was negative. The patient had been vaccinated against tick-borne encephalitis and yellow fever more than 10 years earlier. Fetal ultrasonography that was performed at 13, 16, and 17 weeks of gestation (1, 4, and 5 weeks after the resolution of symptoms) showed no evidence of microcephaly or intracranial calcifications. However, there was a decrease in the fetal head circumference from the 47th percentile at 16 weeks to the 24th percentile at 20 weeks. At 16 weeks of gestation, the presence of flavivirus in serum was detected on nested reverse-transcriptase–polymerase-chain-reaction (RT-PCR) assay, and sequencing showed identity to Central American epidemic strains of ZIKV. The finding was confirmed with a specific ZIKV quantitative RT-PCR assay (Table S2 in the Supplementary Appendix). The Division of Vector-Borne Diseases Arbovirus Diagnostic Laboratory at the CDC reported serologic evidence of infection at 17 weeks of gestation, with serum positivity for ZIKV IgM and a titer of more than 1:2560 on a plaque-reduction neutralization test. On the basis of these results, the patient sought more thorough assessment of the fetus. Fetal ultrasonography at 19 weeks of gestation showed abnormal intracranial anatomy (Figure 2FIGURE 2Fetal Ultrasonography at 19 Weeks of Gestation., and Fig. S1 in the Supplementary Appendix). The cerebral mantle appeared to be thin with increased extra-axial spaces. Both frontal horns were enlarged with heterogeneous, predominantly echogenic material present in the frontal horn and body of the left lateral ventricle, a finding that raised concern about intraventricular hemorrhage. Dilation and upward displacement of the third ventricle, dilation of the frontal horns of the lateral ventricles, concave medial borders of the lateral ventricles, and the absence of the cavum septum pellucidum suggested agenesis of the corpus callosum. No parenchymal calcifications were seen. The head circumference measured in the 24th percentile for gestational age. The remainder of the fetal anatomy was normal. Fetal MRI at 20 weeks of gestation showed diffuse atrophy of the cerebral mantle, which was most severe in the frontal and parietal lobes, with the anterior temporal lobes least affected (Figure 3FIGURE 3Magnetic Resonance Imaging of the Fetal Brain at 19 Weeks of Gestation.). The normal lamination pattern of the cerebral mantle was absent, and the subplate zone was largely undetectable. The corpus callosum was significantly shorter than expected for gestational age, with an anterior–posterior length of 14 mm (expected range, 18 to 22).18,19 The cavum septum pellucidum was very small. The lateral ventricles were mildly enlarged, as was the third ventricle, with a transverse diameter measuring 2.5 mm (average measurement at gestational age, 1.75 mm [range, 1.1 to 2.3]).18 The fourth ventricle was normal. The volume of the choroid plexus was unusually prominent, without evidence of hemorrhage. No focal destructive lesions were identified within the cerebral cortex or white matter. The cerebellum was normal in appearance and size. Given the grave prognosis, the patient elected to terminate the pregnancy at 21 weeks of gestation.

CASE REPORTA 33-year-old Finnish woman who was in the 11th week of gestation was on holiday in Mexico, Guatemala, and Belize with her husband in late November 2015. (Details are provided in Section 1.0 of the Supplementary Appendix, available with the full text of this article at NEJM.org.) During their travels, she and her husband recalled being bitten by mosquitoes, particularly in Guatemala. One day after her arrival at her current residence in Washington, D.C., she became ill with ocular pain, myalgia, and mild fever (maximum, 37.5°C), which lasted for 5 days. On the second day of fever, a rash developed (Figure 1FIGURE 1Timeline of Symptoms and Radiographic and Laboratory Studies., and Fig. S5 in the Supplementary Appendix). Her husband was concomitantly reporting similar symptoms. Serologic analysis that was performed 4 weeks after the onset of illness while she was on a trip to her native Finland was positive for IgG antibodies and negative for IgM antibodies against dengue virus. Subsequent serologic analysis was positive for both IgG and IgM antibodies against ZIKV, findings that were compatible with acute or recent ZIKV infection. Serologic analysis for the presence of chikungunya virus was negative. The patient had been vaccinated against tick-borne encephalitis and yellow fever more than 10 years earlier. Fetal ultrasonography that was performed at 13, 16, and 17 weeks of gestation (1, 4, and 5 weeks after the resolution of symptoms) showed no evidence of microcephaly or intracranial calcifications. However, there was a decrease in the fetal head circumference from the 47th percentile at 16 weeks to the 24th percentile at 20 weeks. At 16 weeks of gestation, the presence of flavivirus in serum was detected on nested reverse-transcriptase–polymerase-chain-reaction (RT-PCR) assay, and sequencing showed identity to Central American epidemic strains of ZIKV. The finding was confirmed with a specific ZIKV quantitative RT-PCR assay (Table S2 in the Supplementary Appendix). The Division of Vector-Borne Diseases Arbovirus Diagnostic Laboratory at the CDC reported serologic evidence of infection at 17 weeks of gestation, with serum positivity for ZIKV IgM and a titer of more than 1:2560 on a plaque-reduction neutralization test. On the basis of these results, the patient sought more thorough assessment of the fetus. Fetal ultrasonography at 19 weeks of gestation showed abnormal intracranial anatomy (Figure 2FIGURE 2Fetal Ultrasonography at 19 Weeks of Gestation., and Fig. S1 in the Supplementary Appendix). The cerebral mantle appeared to be thin with increased extra-axial spaces. Both frontal horns were enlarged with heterogeneous, predominantly echogenic material present in the frontal horn and body of the left lateral ventricle, a finding that raised concern about intraventricular hemorrhage. Dilation and upward displacement of the third ventricle, dilation of the frontal horns of the lateral ventricles, concave medial borders of the lateral ventricles, and the absence of the cavum septum pellucidum suggested agenesis of the corpus callosum. No parenchymal calcifications were seen. The head circumference measured in the 24th percentile for gestational age. The remainder of the fetal anatomy was normal. Fetal MRI at 20 weeks of gestation showed diffuse atrophy of the cerebral mantle, which was most severe in the frontal and parietal lobes, with the anterior temporal lobes least affected (Figure 3FIGURE 3Magnetic Resonance Imaging of the Fetal Brain at 19 Weeks of Gestation.). The normal lamination pattern of the cerebral mantle was absent, and the subplate zone was largely undetectable. The corpus callosum was significantly shorter than expected for gestational age, with an anterior–posterior length of 14 mm (expected range, 18 to 22).18,19 The cavum septum pellucidum was very small. The lateral ventricles were mildly enlarged, as was the third ventricle, with a transverse diameter measuring 2.5 mm (average measurement at gestational age, 1.75 mm [range, 1.1 to 2.3]).18 The fourth ventricle was normal. The volume of the choroid plexus was unusually prominent, without evidence of hemorrhage. No focal destructive lesions were identified within the cerebral cortex or white matter. The cerebellum was normal in appearance and size. Given the grave prognosis, the patient elected to terminate the pregnancy at 21 weeks of gestation.

CASE REPORTA 33-year-old Finnish woman who was in the 11th week of gestation was on holiday in Mexico, Guatemala, and Belize with her husband in late November 2015. (Details are provided in Section 1.0 of the Supplementary Appendix, available with the full text of this article at NEJM.org.) During their travels, she and her husband recalled being bitten by mosquitoes, particularly in Guatemala. One day after her arrival at her current residence in Washington, D.C., she became ill with ocular pain, myalgia, and mild fever (maximum, 37.5°C), which lasted for 5 days. On the second day of fever, a rash developed (Figure 1FIGURE 1Timeline of Symptoms and Radiographic and Laboratory Studies., and Fig. S5 in the Supplementary Appendix). Her husband was concomitantly reporting similar symptoms. Serologic analysis that was performed 4 weeks after the onset of illness while she was on a trip to her native Finland was positive for IgG antibodies and negative for IgM antibodies against dengue virus. Subsequent serologic analysis was positive for both IgG and IgM antibodies against ZIKV, findings that were compatible with acute or recent ZIKV infection. Serologic analysis for the presence of chikungunya virus was negative. The patient had been vaccinated against tick-borne encephalitis and yellow fever more than 10 years earlier. Fetal ultrasonography that was performed at 13, 16, and 17 weeks of gestation (1, 4, and 5 weeks after the resolution of symptoms) showed no evidence of microcephaly or intracranial calcifications. However, there was a decrease in the fetal head circumference from the 47th percentile at 16 weeks to the 24th percentile at 20 weeks. At 16 weeks of gestation, the presence of flavivirus in serum was detected on nested reverse-transcriptase–polymerase-chain-reaction (RT-PCR) assay, and sequencing showed identity to Central American epidemic strains of ZIKV. The finding was confirmed with a specific ZIKV quantitative RT-PCR assay (Table S2 in the Supplementary Appendix). The Division of Vector-Borne Diseases Arbovirus Diagnostic Laboratory at the CDC reported serologic evidence of infection at 17 weeks of gestation, with serum positivity for ZIKV IgM and a titer of more than 1:2560 on a plaque-reduction neutralization test. On the basis of these results, the patient sought more thorough assessment of the fetus. Fetal ultrasonography at 19 weeks of gestation showed abnormal intracranial anatomy (Figure 2FIGURE 2Fetal Ultrasonography at 19 Weeks of Gestation., and Fig. S1 in the Supplementary Appendix). The cerebral mantle appeared to be thin with increased extra-axial spaces. Both frontal horns were enlarged with heterogeneous, predominantly echogenic material present in the frontal horn and body of the left lateral ventricle, a finding that raised concern about intraventricular hemorrhage. Dilation and upward displacement of the third ventricle, dilation of the frontal horns of the lateral ventricles, concave medial borders of the lateral ventricles, and the absence of the cavum septum pellucidum suggested agenesis of the corpus callosum. No parenchymal calcifications were seen. The head circumference measured in the 24th percentile for gestational age. The remainder of the fetal anatomy was normal. Fetal MRI at 20 weeks of gestation showed diffuse atrophy of the cerebral mantle, which was most severe in the frontal and parietal lobes, with the anterior temporal lobes least affected (Figure 3FIGURE 3Magnetic Resonance Imaging of the Fetal Brain at 19 Weeks of Gestation.). The normal lamination pattern of the cerebral mantle was absent, and the subplate zone was largely undetectable. The corpus callosum was significantly shorter than expected for gestational age, with an anterior–posterior length of 14 mm (expected range, 18 to 22).18,19 The cavum septum pellucidum was very small. The lateral ventricles were mildly enlarged, as was the third ventricle, with a transverse diameter measuring 2.5 mm (average measurement at gestational age, 1.75 mm [range, 1.1 to 2.3]).18 The fourth ventricle was normal. The volume of the choroid plexus was unusually prominent, without evidence of hemorrhage. No focal destructive lesions were identified within the cerebral cortex or white matter. The cerebellum was normal in appearance and size. Given the grave prognosis, the patient elected to terminate the pregnancy at 21 weeks of gestation.

BiomedicineZika Attacked a Baby’s Brain as Doctors WatchedU.S. and Finnish doctors caught the brain-shrinking virus in action, and say tests are possible. by Antonio Regalado March 30, 2016Doctors used MRIs and blood tests to watch, in nearly real-time, as the Zika virus destroyed the brain of a fetus whose mother had been infected during a vacation in Latin America. The nine-week ordeal of a Finnish woman who was bitten by mosquitoes during a trip to Mexico, Guatemala, and Belize is described in the New England Journal of Medicine. The Zika virus began spreading quickly in the Americas last year and, by last fall, doctors in northeast Brazil were linking the infection to microcephaly, a devastating, life-altering birth defect in which babies are born with shrunken heads and brains. That link is now a fact. “What we do know for sure is if the fetal brain is infected, that this appears to be a very bad situation,” said Adre du Plessis, director of the Fetal Medicine Institute at the Children’s National Health System in Washington, D.C. The woman, who lives in Washington, D.C., was 33 and three months pregnant at the time she got infected with Zika. She suffered a mild fever and rash, but became concerned after reading news reports of Zika’s link to microcephaly. Over Christmas she had her blood tested in Finland during a trip to her home country. The test, which looks for the virus’s genetic material, came back positive. But at first, ultrasound exams didn’t show any abnormality, leading Du Plessis to caution that such widely used tests may not be picking up problems. The woman later underwent a series of MRIs, which offered a detailed and frightening picture of the baby’s brain “turning to liquid,” says Olli Vapalahti, who runs an arbovirus research center at the University of Helsinki and is the senior author of the case report. People infected with Zika usually clear the virus in seven days, sometimes a little longer. In this case, the woman kept testing positive for the virus for just over two months. Vapalahti believes the tests were picking up the virus replicating inside the fetus’s brain tissue. “We tracked it in real time in a way,” he says. “Our study brings hope that maybe we can screen pregnant mothers with a viral test, and then do MRI studies.” Given the guarantee of severe disability, the woman chose to have an abortion at week 20. The bigger problem is how to counsel women in less affluent parts of Latin America who won’t have access to repeated MRIs or multiple tests. In many Latin countries, access to abortion is restricted. Infection during pregnancy doesn’t always cause a birth defect; the factors that determine when microcephaly results from a Zika infection still aren’t known. The threat of Zika seems almost existential. Yet eventually the virus may become less of a danger due to a phenomenon called “herd immunity.” That is because it’s believed that once infected, people become immune to it. That means girls and women infected now probably won’t be at risk if they get pregnant later. Also, as fewer and fewer people are susceptible and able to spread Zika, the virus may retreat back to the forest. https://www.technologyreview.com/s/601153/zika-attacked-a-babys-brain-as-doctors-watched/#/set/id/601150/

· Posted just now · Report post The evidence that Zika causes fetal brain damage is now 'awfully strong' A report describes an abnormal pregrancy following a Zika infection By Arielle Duhaime-Ross on March 30, 2016 05:00 pm Email @ArielleDRoss Share on Facebook (31) Tweet Share (2) Pin (2)A fetus that was aborted weeks after the mother was infected with Zika provides striking evidence that the virus causes fetal brain abnormalities, researchers say. The report, published today in the New England Journal of Medicine, isn't the first to document a case of a mother passing on the virus to a fetus, but it does provide the most detailed look yet at changes that occurred in the fetus' brain following a mother's Zika infection. In the study, researchers describe the case of a 33-year-old Finnish woman who was almost three months pregnant when she became infected with Zika during a trip to Guatemala. Fetal ultrasounds later showed that her fetus' head wasn't growing at a normal rate; its brain also began to display abnormal anatomy, researchers say. After the pregnancy was terminated, scientists found Zika virus in the fetus' brain, as well as in the umbilical cord and placenta. Because researchers were able to follow the pregnancy every step of the way, scientists think this case lends strong support to the idea that Zika virus causes fetal brain damage. "THAT’S PRETTY MUCH A SMOKING GUN." "What makes this study so convincing is that this one case was so thoroughly studied from the time of infection to the ultrasound studies," says Lee Norman, an intelligence officer in disaster medicine planning in the United States Army National Guard, who didn’t work on the study. Because the woman was so closely followed by doctors, researchers were able to eliminate other factors that could have played a role in the fetal brain abnormalities and focus in on the Zika virus. "Finding the virus in the brain of the fetus in the NEJM study — that’s pretty much a smoking gun," he says. In most cases, the Zika virus isn't dangerous. About 80 percent of people infected with the virus never develop symptoms, which resemble the flu and last no more than a week. But an outbreak of the virus in Brazil has caused concern among health officials who suspect Zika might be responsible for stillbirths, problems with the placenta that may harm a developing fetus, and a birth defect that can affect the brain size of newborns, microcephaly. There's no cure or treatment for the virus. And even though Zika is mostly transmitted through mosquito bites, it is possible to become infected through sexual contact. Because of this, the US government recommends that women with Zika should wait eight weeks before trying to conceive, and men should wait at least six months after their symptoms first appear to have unprotected sex. Both recommendations were made despite the fact that scientists have yet to demonstrate a definitive link between Zika and fetal brain abnormalities. Now, scientists are working to document the effects of the virus in expecting mothers. THE ANATOMY OF THE FETUS' BRAIN WAS ABNORMAL The woman's pregnancy was normal prior to her Zika infection. But three months in, during a trip to Guatemala, she began to show Zika-like symptoms. Four weeks after she had recovered, the woman tested positive for antibodies that fight off Zika; another batch of tests eliminated other possible culprits, like dengue. Then, between her 16th and 19th week of pregnancy, the fetus' head stopped growing at a normal rate; its head went from being in the 47th percentile to the 24th percentile, meaning that only 24 percent of fetuses have a head that size or smaller at that stage. A fetal ultrasound also showed that the anatomy of the fetus' brain was abnormal. "Given the grave prognosis," the mother decided to have an abortion, the researchers wrote in the study; she was five months pregnant by then. "I THINK THAT THE EVIDENCE IS NOW AWFULLY STRONG." The report provides "very striking evidence" that Zika virus infection causes severe abnormalities, says Sara Cherry, a microbiologist at the University of Pennsylvania who didn't work on the study. But a single case isn't enough to prove Zika's role in fetal brain abnormalities, she says. What matters is the picture that data from this study and others paint. Emerging and aggregate data "really do show that Zika virus infection can lead to developmental defects in the fetus," she says. Harvard University immunologist Eric Rubin put things more bluntly. The study "doesn't prove the link between Zika and microcephaly," he told The Verge. "However, particularly given the other recently published study, that shows that women who develop Zika during pregnancy are at high risk for fetal abnormalities, I think that the evidence is now awfully strong." Earlier this month, another study showed that women who are infected with Zika during the first trimester of pregnancy face a 1 in 100 chance that their fetus will develop microcephaly. According to Hongjun Song, a neuroscientist at Johns Hopkins University, the only way scientists will be able to definitely prove that Zika causes fetal brain abnormalities is by conducting a large, controlled study. Norman, for his part, says scientists need to test the effects of Zika on animals. http://www.theverge.com/2016/3/30/11332044/zika-fetus-brain-damage-evidence-abnormalities

The evidence that Zika causes fetal brain damage is now 'awfully strong' A report describes an abnormal pregrancy following a Zika infection By Arielle Duhaime-Ross on March 30, 2016 05:00 pm Email @ArielleDRoss Share on Facebook (31) Tweet Share (2) Pin (2)A fetus that was aborted weeks after the mother was infected with Zika provides striking evidence that the virus causes fetal brain abnormalities, researchers say. The report, published today in the New England Journal of Medicine, isn't the first to document a case of a mother passing on the virus to a fetus, but it does provide the most detailed look yet at changes that occurred in the fetus' brain following a mother's Zika infection. In the study, researchers describe the case of a 33-year-old Finnish woman who was almost three months pregnant when she became infected with Zika during a trip to Guatemala. Fetal ultrasounds later showed that her fetus' head wasn't growing at a normal rate; its brain also began to display abnormal anatomy, researchers say. After the pregnancy was terminated, scientists found Zika virus in the fetus' brain, as well as in the umbilical cord and placenta. Because researchers were able to follow the pregnancy every step of the way, scientists think this case lends strong support to the idea that Zika virus causes fetal brain damage. "THAT’S PRETTY MUCH A SMOKING GUN." "What makes this study so convincing is that this one case was so thoroughly studied from the time of infection to the ultrasound studies," says Lee Norman, an intelligence officer in disaster medicine planning in the United States Army National Guard, who didn’t work on the study. Because the woman was so closely followed by doctors, researchers were able to eliminate other factors that could have played a role in the fetal brain abnormalities and focus in on the Zika virus. "Finding the virus in the brain of the fetus in the NEJM study — that’s pretty much a smoking gun," he says. In most cases, the Zika virus isn't dangerous. About 80 percent of people infected with the virus never develop symptoms, which resemble the flu and last no more than a week. But an outbreak of the virus in Brazil has caused concern among health officials who suspect Zika might be responsible for stillbirths, problems with the placenta that may harm a developing fetus, and a birth defect that can affect the brain size of newborns, microcephaly. There's no cure or treatment for the virus. And even though Zika is mostly transmitted through mosquito bites, it is possible to become infected through sexual contact. Because of this, the US government recommends that women with Zika should wait eight weeks before trying to conceive, and men should wait at least six months after their symptoms first appear to have unprotected sex. Both recommendations were made despite the fact that scientists have yet to demonstrate a definitive link between Zika and fetal brain abnormalities. Now, scientists are working to document the effects of the virus in expecting mothers. THE ANATOMY OF THE FETUS' BRAIN WAS ABNORMAL The woman's pregnancy was normal prior to her Zika infection. But three months in, during a trip to Guatemala, she began to show Zika-like symptoms. Four weeks after she had recovered, the woman tested positive for antibodies that fight off Zika; another batch of tests eliminated other possible culprits, like dengue. Then, between her 16th and 19th week of pregnancy, the fetus' head stopped growing at a normal rate; its head went from being in the 47th percentile to the 24th percentile, meaning that only 24 percent of fetuses have a head that size or smaller at that stage. A fetal ultrasound also showed that the anatomy of the fetus' brain was abnormal. "Given the grave prognosis," the mother decided to have an abortion, the researchers wrote in the study; she was five months pregnant by then. "I THINK THAT THE EVIDENCE IS NOW AWFULLY STRONG." The report provides "very striking evidence" that Zika virus infection causes severe abnormalities, says Sara Cherry, a microbiologist at the University of Pennsylvania who didn't work on the study. But a single case isn't enough to prove Zika's role in fetal brain abnormalities, she says. What matters is the picture that data from this study and others paint. Emerging and aggregate data "really do show that Zika virus infection can lead to developmental defects in the fetus," she says. Harvard University immunologist Eric Rubin put things more bluntly. The study "doesn't prove the link between Zika and microcephaly," he told The Verge. "However, particularly given the other recently published study, that shows that women who develop Zika during pregnancy are at high risk for fetal abnormalities, I think that the evidence is now awfully strong." Earlier this month, another study showed that women who are infected with Zika during the first trimester of pregnancy face a 1 in 100 chance that their fetus will develop microcephaly. According to Hongjun Song, a neuroscientist at Johns Hopkins University, the only way scientists will be able to definitely prove that Zika causes fetal brain abnormalities is by conducting a large, controlled study. Norman, for his part, says scientists need to test the effects of Zika on animals. http://www.theverge.com/2016/3/30/11332044/zika-fetus-brain-damage-evidence-abnormalities

Pregnant Missouri Woman Contracts Zika VirusMarch 30, 2016 7:54 PMFiled Under: Honduras, microcephaly, Missouri, Zika (Photo by Mario Tama/Getty Images) 2JEFFERSON CITY (KMOX) — The Missouri Department of Health and Senior Services confirms a second Missouri resident has tested positive for the Zika virus. She’s pregnant. Department spokesman Ryan Hobart says the effects of Zika on unborn children are still being studied. “There is a birth defect called ‘microcephaly’ that results in babies having smaller than normal head sizes and brains that might not have developed properly,” he says. The woman traveled to Honduras, but Hobart wouldn’t say when she traveled, where in Missouri she lives or whether she’s still infected. The disease is typically transmitted through a mosquito bite, sexual contact or blood transfusions. http://stlouis.cbslocal.com/2016/03/30/pregnant-missouri-woman-contracts-zika-virus/

March 30, 2016 CDC test confirms Missouri traveler infected with Zika virusThe Centers for Disease Control and Prevention (CDC) confirmed a case of Zika virus in a pregnant Missouri woman who had travelled to Honduras, a known area of Zika transmission. This is the second confirmed case of Zika virus infection reported in a Missouri resident. Nearly 80 percent of people infected with the virus will have no symptoms. Typically, symptoms are mild and include fever, rash, joint soreness and/or redness of eyes. International health officials are examining the connection between pregnant women contracting the virus and a birth defect called microcephaly in their newborn infants. According to the CDC, babies with microcephaly often have smaller head sizes and brains that might not have developed properly. According to the CDC, Zika virus has the potential to be spread through a mosquito bite, through unprotected sexual contact, through blood transfusion and an infected pregnant woman can pass Zika virus to her fetus during pregnancy. There is not currently a vaccine for Zika virus. The best prevention measure is to avoid mosquito bites in areas with ongoing transmission. There have been no reported cases of Zika virus contracted from a mosquito bite in Missouri. Ways to avoid mosquito bites while outdoors include wearing EPA-registered insect repellent with DEET, wearing pants and long sleeves, or remaining indoors in an air conditioned environment. The CDC is recommending pregnant women avoid traveling to Zika-affected areas which include countries ranging from Mexico into the Caribbean, Central American and South America. Since the beginning of the year, DHSS has regularly updated health care providers and the public about Zika virus in addition to coordinating the approval of Missourians for testing by the CDC. Please consult CDC resources for a listing of all areas and other information about Zika virus:http://www.cdc.gov/zika/

Map Update https://www.google.com/maps/d/u/0/edit?hl=en&hl=en&authuser=0&authuser=0&mid=zv94AJqgUct4.kT4qLMXp3SLU

The Centers for Disease Control and Prevention (CDC) confirmed a case of Zika virus in a pregnant Missouri woman who had travelled to Honduras, a known area of Zika transmission. http://health.mo.gov/information/news/2016/zika33016

Pregnant Women May Be Able To Get Answers About Zika EarlierFacebookTwitterGoogle+EmailMarch 30, 20165:00 PM ETMICHAELEEN DOUCLEFFTwitteriA pregnant woman gets an ultrasound in Guatemala City on Feb. 2, monitoring for the birth defect microcephaly. Johan Ordonez/AFP/Getty ImagesLast November, a couple from Washington, D.C., took a weeklong vacation. They visited Mexico, Guatemala and Belize. And got bitten by plenty of mosquitoes. Two days after they returned home, the woman — who was pregnant — fell ill. She had muscle pain, a fever and a rash. "At first she didn't think much about it," says OB-GYN Rita Driggers, who saw the woman at Johns Hopkins University School of Medicine. "But then all the news started coming out about Zika, so the woman went and got tested." The test came back positive. And then the big question became: Was her baby going to be OK? At first, everything looked good on a standard ultrasound, Driggers says. Even during the 20th week of the pregnancy, the fetus didn't have microcephaly or calcifications in the brain — two telltale signs of a Zika infection. But when doctors ran MRI on the fetus, the good news quickly faded. "There were severe abnormalities within the brain," Driggers says. "The width of the brain was very, very thin. ... Some structures were completely missing." The woman decided to terminate the pregnancy. And she allowed Driggers and her colleagues to study the baby. The case — published Wednesday in The New England Journal of Medicine — offers insights into how Zika infects a fetus and suggests ways women may be able to find out earlier whether babies will have birth defects. First, the virus lingered in the patient's blood for months after she got sick. Usually a person's immune system clears out Zika in a week or so. But in this case, Driggers thinks the virus was hiding out inside the fetus — and repeatedly infecting the mother. "So if you're seeing the virus in the mom's blood more than a week after symptoms," Driggers says, "then perhaps what's going on is that the baby is infected with Zika." GOATS AND SODAThe Poignant Cry Of Babies With Birth Defects Linked to ZikaSecond, looking only for microcephaly isn't enough. Right now the Centers for Disease Control and Prevention recommends doctors measure the size of the fetus's head with an ultrasound near the 20th week of the pregnancy to check for Zika-related problems. But with this new case, doctors could see brain abnormalities by MRI before there were signs of microcephaly. "This is very alarming," says Dr. Carla Janzen, a maternal-fetal medicine specialist at UCLA, who wasn't involved in the study. "If we see more cases like this, the [CDC's] guidelines will probably have to change" to include MRI screening or more intensive ultrasound tests. http://www.npr.org/sections/goatsandsoda/2016/03/30/472307332/one-woman-s-case-may-change-zika-screening-for-expectant-mothers?utm_source=twitter.com&utm_campaign=health&utm_medium=social&utm_term=nprnews