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Intrauterine West Nile Virus Infection --- New York, 2002

West Nile virus (WNV), a mosquito-borne flavivirus and human neuropathogen, is epidemic in the United States (1). In 2002, newly recognized mechanisms of person-to-person WNV transmission were described, including possible transmission from mother to infant through breast milk (2,3). WNV has not been previously associated with intrauterine infection or adverse birth outcomes. This report describes a case of transplacental WNV transmission. Pregnant women should take precautions to reduce their risk for WNV or other arboviral infection and should undergo diagnostic testing when clinically appropriate.

On August 29, 2002, a previously healthy woman aged 20 years in the estimated 27th week of pregnancy was admitted to a New York hospital with a 2-day history of fever, severe headache, blurred vision, abdominal and back pain, and vomiting. On examination, she had a fever of 102.7º F (39.3º C); the fetal heart rate was elevated. A computerized tomographic scan of the patient's head, a fetal sonogram, and routine analyses of blood and amniocentesis fluid were normal. A urine culture grew Proteus mirabilis and Escherichia coli. Intravenous antibiotics were administered.

Four days after admission, the fever had resolved, and the patient had pain and weakness of the legs. Neurologic examination indicated symmetric weakness of the legs and hyporeflexia of the legs and arms. No cranial nerve abnormalities were noted. Electromyelography (EMG) was not completed. On September 14, despite persistent lower extremity paresis, she left the hospital against medical advice.

On September 16, the patient was readmitted following a fall. She was afebrile, but physical examination revealed weakness in both legs. Fetal monitoring results were normal. Serum was positive for IgG antibodies to rubella virus and herpes simplex virus (HSV), and laboratory tests showed no evidence of syphilis or infection with human immunodeficiency virus (HIV). Serum also was positive for flavivirus IgM and IgG by immunofluorescence assay. Additional serum and CSF specimens were obtained during the week ending October 12. Serum was positive for WNV-specific IgM antibodies. CSF analysis indicated lymphocytic pleocytosis (11 white blood cells/mm3, 87% lymphocytes, 8% monocytes, and 5% neutrophils), elevated protein (63 mg/dL), and the presence of WNV-specific IgM antibodies. Polymerase chain reaction (PCR) tests of CSF for WNV, enterovirus (EV), and HSV were negative. EMG studies indicated widespread involvement of the lower motor neurons or their proximal axons, with the legs affected more severely than the arms. A diagnosis of meningoencephalitis was made.

Approximately 5 weeks later, the patient delivered a live infant (estimated gestational age: 38 weeks). Serum obtained from the mother at the time of birth was positive for WNV-specific IgM and neutralizing antibodies. The infant's birth weight and general clinical examination were normal. An ophthalmologic examination revealed bilateral chorioretinitis, and MRI of the brain indicated severe cerebral abnormalities, including severe bilateral white-matter loss in the temporal and occipital lobes and cystic change in one temporal lobe consistent with focal cerebral destruction. Cord blood and infant heel-stick blood samples were positive for WNV-specific IgM and neutralizing antibodies. CSF was WNV-specific IgM antibody--positive but was contaminated with red blood cells. The presence of WNV-specific IgM antibody in the infant's serum and CSF confirmed intrauterine infection with WNV. Serum was cytomegalovirus (CMV) IgM antibody--negative but IgG-positive, and serologic tests were negative for lymphocytic choriomeningitis virus infection and toxoplasmosis. PCR tests of CSF for WNV, EV, and HSV were negative. Urine CMV culture was negative. Gross and histopathologic examinations of the placenta, umbilical cord, and amniotic membranes were normal. The placenta was WNV PCR--positive at one of two reference laboratories. The umbilical cord tissue was WNV-positive and -equivocal by PCR, respectively, at the same two laboratories. Viral cultures of umbilical cord tissue were negative; viral cultures of CSF and placenta are pending.

Reported by: Q Nguyen, MD, C Morrow, MD, L Novick, MD, Onondaga County Health Dept; C Cambareri, MSN, B Olson, MD, R Aubry, MD, J Snedeker, MD, Univ Hospital at Syracuse, Syracuse; M Anand, C Huang, PhD, D Morse, MD, B Rosen, PhD, B Wallace, MD, S Wong, PhD, P Smith, MD, State Epidemiologist, New York State Dept of Health. D O'Leary, DVM, A Marfin, MD, G Campbell, MD, R Lanciotti, PhD, Div of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, CDC.

Editorial Note:

On the basis of the presence of WNV-specific IgM in the mother and infant, this is the first report of transplacental transmission of WNV in humans. Intrauterine infections with Japanese encephalitis and dengue, two mosquito-borne flaviviruses closely related to WNV, have been associated with spontaneous abortion and severe dengue fever in the infant, respectively (4--7). Although the single case reported here demonstrates intrauterine WNV infection in an infant who had evidence of congenital abnormalities, it does not prove a causal relation between such an infection and these abnormalities.

Pregnant women should take precautions to reduce their risk for WNV and other arboviral infections by avoiding mosquitoes and by using protective clothing and repellents containing N,N-diethyl-m-toluamide (DEET) per manufacturers' directions. When WNV transmission is occurring in an area, pregnant women who have an illness that is clinically consistent with acute WNV infection should undergo appropriate diagnostic testing. Screening of asymptomatic pregnant women or newborns for evidence of WNV infection is not recommended because no specific treatment for this infection is available, and because WNV IgM antibody might persist for more than a year, tests of a single serum sample cannot accurately determine the timing of infection (8). CDC has initiated a voluntary registry to monitor birth outcomes among WNV-infected women. In the event of an adverse birth outcome, maternal and fetal or newborn samples should be submitted to a state public health laboratory or CDC for testing. Additional information and consultation about WNV are available from CDC's Division of Vector-Borne Infectious Diseases, telephone 970-221-6400 and 970-266-3592 or at http://www.cdc.gov/ncidod/dvbid/westnile.

References

  1. CDC. Provisional surveillance summary of the West Nile virus epidemic --- United States, January--November 2002. MMWR 2002;51: 1129--33
  2. CDC. Update: investigations of West Nile virus infections in recipients of organ transplantation and blood transfusion---Michigan, 2002. MMWR 2002;51:879.
  3. CDC. Possible West Nile virus transmission to an infant through breast-feeding---Michigan, 2002. MMWR 2002;51:877--8.
  4. Asha M, Tandon HO, Mathur KR, et al. Japanese encephalitis virus infection during pregnancy. Indian J Med Res 1985;81:9--12.
  5. Charuvedi UC, Mathur A, Chandra SK, et al. Transplacental infection with Japanese encephalitis virus. J Infect Dis 1980;141:712--5.
  6. Chye JK, Lim CT, Ng KB, et al. Vertical transmission of dengue. Clin Infect Dis 1997;25:1374--7.
  7. Thaithumyanon P, Thisyakorn U, Deerojnawong J, et al. Dengue infection complicated by severe hemorrhage and vertical transmission in a parturient woman. Clin Infect Dis 1994;18:248--9.
  8. Roehrig JT, Nash D, Maldin B, et al. Persistence of virus-reactive serum IgM antibody in confirmed West Nile virus encephalitis cases. Emerg Infect Dis (in press).

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