Stakeholder Insights from Zika Virus Infections in Houston, Texas, USA, 2016–2017

Responding to Zika virus infections in Houston, Texas, USA, presented numerous challenges across the health system. As the nation’s fourth-largest city, in a subtropical region with high travel volume to Latin America and the Caribbean, Houston was an ideal location for studying experiences encountered by clinicians and public health officials as they responded to the Zika virus crisis. To identify the challenges encountered in the response and to explore strategies to improve future responses to emerging infectious diseases, we interviewed 38 key stakeholders who were clinical, scientific, operational, and public health leaders. From the responses, we identified 4 key challenges: testing, travel screening, patient demographics and immigration status, and insufficient collaboration (between public health officials and clinicians and among clinical providers). We also identified 5 strategic areas as potential solutions: improved electronic health record support, specialty centers and referral systems, standardized forms, centralized testing databases, and joint academic/public health task forces

Safety and tolerance of intermittent intravenous and oral zidovudine therapy in human immunodeficiency virus-infected pediatric patients

Thirty-five children with symptomatic human immunodeficiency virus infection were enrolled in a 12-week, three-center phase I study of intravenous and oral zidovudine therapy. At enrollment the children ranged in age from 5 months to 13 years, with a median age of 3 1/2 years. Twenty-one children (60%) had acquired immunodeficiency syndrome and 14 (40%) had the related complex; 20 children had <0.5 10 9 CD4+ lymphocytes per liter (<500 cells/mm 3) at entry. Zidovudine was administered in one of three escalating dose regimens. One or two months of intravenous treatment with zidovudine every 6 hours was followed by orally administered drug on the same schedule; zidovudine was infused at 80, 120, or 160 mg/m 2/dose, and the oral dose was one and one-half times the intravenous dosage. Adverse events were similar to those observed in adults. Neutropenia (absolute neutrophil count <0.75 10 9/L (750 cells/mm 3)) occurred in nine patients. The median neutrophil count fell from 2.50 10 9/L at entry to 1.72 10 9/L at the end of the study. Anemia requiring transfusion occurred in seven patients; the median hemoglobin level among nontransfused patients decreased from an entry value of 108 to 105 gm/L (10.8 to 10.5 gm/dl). Dosage adjustments were made in 15 patients, in 12 because of anemia or neutropenia

Clinical Importance of Placental Testing among Suspected Cases of Congenital Zika Syndrome

Contemporaneous Zika virus (ZIKV) strains can cause congenital Zika syndrome (CZS). Current ZIKV clinical laboratory testing strategies are limited and include IgM serology (which may wane 12 weeks after initial exposure) and nucleic acid testing (NAT) of maternal serum, urine, and placenta for (+) strand ZIKV RNA (which is often transient). The objectives of this study were to determine if use of additional molecular tools, such as quantitative PCR and microscopy, would add to the diagnostic value of current standard placental ZIKV testing in cases with maternal endemic exposure and indeterminate testing. ZIKV RNA was quantified from dissected sections of placental villi, chorioamnion sections, and full cross-sections of umbilical cord in all cases examined. Quantitation with high-resolution automated electrophoresis determined relative amounts of precisely verified ZIKV (74-nt amplicons). In order to localize and visualize stable and actively replicating placental ZIKV in situ, labeling of flaviviridae glycoprotein, RNA ISH against both (+) and (&#8722;) ZIKV-specific ssRNA strands, and independent histologic examination for significant pathologic changes were employed. We demonstrate that the use of these molecular tools added to the diagnostic value of placental ZIKV testing among suspected cases of congenital Zika syndrome with poorly ascribed maternal endemic exposure