Birth outcomes following West Nile Virus infection of pregnant women in the United States: 2003-2004.

BACKGROUND: Congenital West Nile virus (WNV) infection was first described in a single case in 2002. The proportion of maternal WNV infections resulting in congenital infection and clinical consequences of such infections are unknown. METHODS: In 2003 and 2004, women in the United States who acquired WNV infection during pregnancy were reported to the Centers for Disease Control and Prevention by state health departments. Data on pregnancy outcomes were collected. One of the maternal WNV infections was identified retrospectively after the infant was born. Maternal sera, placenta, umbilical cord tissue, and cord serum were tested for WNV infection by using serologic assays and reverse-transcription polymerase chain reaction. Infant health was assessed at delivery and through 12 months of age. RESULTS: Seventy-seven women infected with WNV during pregnancy were clinically followed in 16 states. A total of 71 women delivered 72 live infants; 4 women had miscarriages, and 2 had elective abortions. Of the 72 live infants, 67 were born at term, and 4 were preterm; gestational age was unknown for 1. Of 55 live infants from whom cord serum was available, 54 tested negative for anti-WNV IgM. One infant born with umbilical hernia and skin tags had anti-WNV IgM in cord serum but not in peripheral serum at age 1 month. An infant who had no anti-WNV IgM in cord blood, but whose mother had WNV illness 6 days prepartum, developed WNV meningitis at age 10 days. Another infant, whose mother had acute WNV illness at delivery, was born with a rash and coarctation of the aorta and had anti-WNV IgM in serum at 1 month of age; cord serum was not available. A fourth infant, whose mother had onset of WNV illness 3 weeks prepartum that was not diagnosed until after delivery, had WNV encephalitis and underlying lissencephaly detected at age 17 days and subsequently died; cord serum was not available. The following major malformations were noted among live-born infants: aortic coarctation (n = 1); cleft palate (n = 1); Down syndrome (n = 1); lissencephaly (n = 1); microcephaly (n = 2); and polydactyly (n = 1). One infant had glycogen storage disease type 1. Abnormal growth was noted in 8 infants. CONCLUSIONS: Of 72 infants followed to date in 2003 and 2004, almost all seemed normal, and none had conclusive laboratory evidence of congenital WNV infection. Three infants had WNV infection that could have been congenitally acquired. Seven infants had major malformations, but only 3 of these had defects that could have been caused by maternal WNV infection based on the timing of the infections and the sensitive developmental period for the specific malformations, and none had any conclusive evidence of WNV etiology. However, the sensitivity and specificity of IgM testing of cord blood to detect congenital WNV infection are currently unknown, and congenital WNV infection among newborns with IgM-negative serology cannot be ruled out. Prospective studies comparing pregnancy outcomes of WNV-infected and -uninfected women are needed to better define the outcomes of WNV infection during pregnancy.

Sensitivity of second-generation enzyme immunoassay for detection of hepatitis C virus infection among oncology patients.

BACKGROUND: The second-generation hepatitis C virus (HCV) enzyme immunoassay (EIA 2), an antibody-detection test, has high sensitivity and is one of the recommended screening tests for detecting HCV infection in the United States. However, its sensitivity among oncology patients is unknown. OBJECTIVE: Assess the EIA 2 sensitivity among a group of oncology patients at a Nebraska clinic where an HCV outbreak occurred during 2000-2001 using nucleic acid testing (NAT) and recombinant immunoblot assay (RIBA) as the gold standards. STUDY DESIGN: Serum specimens were collected from patients 16 months after transmission had stopped. We tested the specimens using EIA 2 (Abbott HCV EIA 2.0), a NAT assay based on transcription-mediated amplification (TMA) (Gen-Probe TMA assay) and RIBA (Chiron RIBA HCV 3.0 SIA). HCV infection was defined as a positive RIBA or TMA test in an oncology patient. Alanine aminotransferase (ALT) levels were determined in EIA 2-negative/TMA-positive samples. RESULTS: A total of 264 samples were included in the study. We identified 92 HCV infections, 76 of which were Abbott EIA 2 positive. Abbott EIA 2 sensitivity was 83% (76/92), lower than that reported among healthy adults (90%) (p=0.01) and poor sensitivity was associated with receipt of chemotherapy during the outbreak period (p=0.02). Only 1 (6%) of the 16 EIA 2-negative cases had elevated ALT. CONCLUSIONS: In this study, EIA 2 sensitivity among oncology patients was lower than that previously reported among immunocompetent persons. Impaired antibody production related to cancer and/or chemotherapy might explain the reduced sensitivity. These findings indicate that, when assessing HCV status in oncology patients, a NAT test should be routinely considered in addition to EIA.

An outbreak of hepatitis C virus infections among outpatients at a hematology/oncology clinic.

BACKGROUND: Approximately 2.7 million persons in the United States have chronic hepatitis C virus (HCV) infection. Health care-associated HCV transmission can occur if aseptic technique is not followed. The authors suspected a health care-associated HCV outbreak after the report of 4 HCV infections among patients at the same hematology/oncology clinic. OBJECTIVE: To determine the extent and mechanism of HCV transmission among clinic patients. DESIGN: Epidemiologic analysis through a cohort study. SETTING: Hematology/oncology clinic in eastern Nebraska. PARTICIPANTS: Patients who visited the clinic from March 2000 through December 2001. MEASUREMENTS: HCV infection status, relevant medical history, and clinic-associated exposures. Bivariate analysis and logistic regression were used to identify risk factors for HCV infection. RESULTS: Of 613 clinic patients contacted, 494 (81%) underwent HCV testing. The authors documented infection in 99 patients who lacked previous evidence of HCV infection; all had begun treatment at the clinic before July 2001. Hepatitis C virus genotype 3a was present in all 95 genotyped samples and presumably originated from a patient with chronic hepatitis C who began treatment in March 2000. Infection with HCV was statistically significantly associated with receipt of saline flushes (P < 0.001). Shared saline bags were probably contaminated when syringes used to draw blood from venous catheters were reused to withdraw saline solution. The clinic corrected this procedure in July 2001. LIMITATION: The delay between outbreak and investigation (>1 year) may have contributed to an underestimate of cases. CONCLUSIONS: This large health care-associated HCV outbreak was related to shared saline bags contaminated through syringe reuse. Effective infection-control programs are needed to ensure high standards of care in outpatient care facilities, such as hematology/oncology clinics.

West Nile virus blood transfusion-related infection despite nucleic acid testing.

BACKGROUND: A case of West Nile virus (WNV) encephalitis associated with transfusion of blood that did not react when tested for WNV by minipool (MP) nucleic acid testing (NAT) is described. A Nebraska man developed clinical encephalitis 13 days after surgery and transfusion of 26 blood components. Antibody testing confirmed WNV infection. An investigation was initiated to determine the source of this infection. STUDY DESIGN AND METHODS: The patient's family members were interviewed to identify risk factors for WNV infection. Residual samples were retested for WNV RNA using transcription-mediated amplification (TMA) assay and two polymerase chain reaction (PCR) assays. Blood donors' follow-up serum samples were collected. All samples were tested for WNV-specific immunoglobulin M antibodies. RESULTS: The patient's family denied recent mosquito exposure. The 20 blood components collected after July 2003 did not react when tested for WNV in a six-member MP-NAT at the time of donation. Retrospective individual testing identified one sample as WNV-reactive by the TMA assay and one of the PCR assays. Seroconversion was demonstrated in the donor associated with this sample. CONCLUSION: WNV RNA detection by individual donation NAT demonstrates viremic blood escaping MP-NAT and supports transfusion-related WNV transmission. MP-NAT may not detect all WNV-infected blood donors, allowing WNV transmission to continue at low levels. WNV NAT assays might vary in sensitivity and pooling donations could further impact test performance. Understanding MP NAT limitations can improve strategies to maintain safety of the blood supply in the United States.