Atypical West Nile virus infection in a child

West Nile virus infections in North America are increasing rapidly, but relatively little is known about the spectrum of illness in children. This report describes a West Nile virus infection in a child during the Ontario 2002 outbreak that was unusually severe and followed a more protracted course than that typically described in children. West Nile virus (WNV) was first identified in 1937, but the first recognized human cases in the Western Hemisphere were not reported until 1999. 1 Since the 1999 outbreak in New York City involving 62 people, WNV has spread throughout much of North America. In Ontario in 2002, 389 cases were confirmed by public health authorities. 2 Few reports of its impact on children have been published. Case presentation. A previously healthy 5-year-old boy was transferred to the Hospital for Sick Children in Toronto in August 2002 with meningoencephalitis. He had been vacationing in the Huntsville, Ontario area and had been well until 5 days before admission when fever and sore throat developed. Four days before admission a rash on the face and extremities was noticed, and he was evaluated at a local hospital because of increasing headache and confusion on the day before transfer. The white blood cell (WBC) count was 14.6 × 109/l with lymphocytopenia (0.6 × 109/l). He became lethargic, and a brief seizure involving the right arm ensued. Lumbar puncture revealed 322 × 106 WBC/l (83% polymorphonuclear leukocytes), 60 × 106/l red blood cells and normal cerebrospinal fluid (CSF) glucose and protein values. Intravenous ceftriaxone and acyclovir were administered, and he was transferred for ongoing management. Tympanic temperature was 38.6°C and the Glasgow Coma Scale value was 13. Physical examination was notable for severe meningismus, photophobia, a maculopapular rash on the face and trunk and insect bite marks. Mild generalized weakness was apparent with normal reflexes. Enhanced computerized tomography images of the head were normal. Blood and CSF bacterial cultures were negative, and herpes simplex virus DNA and enterovirus RNA were not detected in the CSF by PCR. Serology for herpes simplex viruses 1 and 2, cytomegalovirus, measles, mumps, Bartonella henselae and Mycoplasma pneumoniae was negative. Serology was indicative of past infection with human herpesvirus 6, varicella zoster virus, Epstein-Barr virus and parvovirus. Respiratory viruses including parainfluenza and influenza viruses, adenovirus and respiratory syncytial virus were not detected by immunofluorescence on nasopharyngeal swab material, and M. pneumoniae DNA was not detected by PCR on throat swab material. Serology for arboviruses (West Nile, dengue, St. Louis, east equine, west equine and Powassan) was sent. Antimicrobials were discontinued, and the subsequent 10-day hospitalization was notable for gradual but slow resolution of the meningismus and photophobia. Ambulatory physiotherapy was continued because of mild but persistent truncal weakness. Two months after his initial hospitalization, fever, neck stiffness and vomiting recurred. Physical examination revealed only meningismus. A lumbar puncture showed 78 WBC × 106/l (28% polymorphonuclear leukocytes, 43% lymphocytes, 29% monocytes), 0 red blood cells and an elevated CSF protein (0.75 g/l; normal range, 0.15 to 0.40 g/l). Magnetic resonance images of the head were normal. Results of microbiologic and serologic studies were similar to those of his previous admission. He recovered after 48 h, and the weakness resolved during the next 2 months. In mid-December notification was received from the provincial laboratory of an IgG antibody titer of 1/160 by hemagglutination inhibition test and positive WNV IgM-specific antibody by enzyme-linked immunosorbent assay (ELISA) on the serum sample from his initial hospitalization. Serology for the other tested arboviruses was negative. A titer of 1/640 was found on subsequent testing 4 months after his initial illness, confirming acute infection with WNV. Discussion. WNV, an arbovirus in the Flaviviridae family, is transmitted between natural bird hosts by mosquito vectors and transmitted to humans by an infected mosquito. Humans are dead-end hosts because the viremia ensuing after infection is considered insufficient for the continuation of the transmission cycle. 3 The virus can also be acquired through infected blood transfusions or donated organs. 4 WNV activity in temperate climates occurs during the warmer months, but it can recur in subsequent years by overwintering (possibly by infected mosquitoes in protected underground sites) or through reintroduction by migrating birds. 5 Most infections are asymptomatic. Based on seroepidemiologic data during the 1999 New York epidemic, it was estimated that for every diagnosed meningoencephalitis case, 140 asymptomatic or mild infections occurred. 6 However, the report of the 1999 outbreak included only one 5-year-old child who had an uncomplicated aseptic meningitis, 1 and WNV infection during childhood has, in the past, been reported as mild. Of the 24 children diagnosed with WNV infection during a 2000 outbreak in Israel, only 1 child, who was immunocompromised, had a severe illness. 7 The most commonly recognized manifestation of WNV infection is an influenza-like febrile illness that occurs after an incubation period of 2 to 14 days. Other reported symptoms include sore throat, cough, conjunctivitis, nausea, diarrhea and a maculopapular rash. 8 Neurologic symptoms most commonly occur in older patients and include meningitis, encephalitis, meningoencephalitis and polyradiculitis. Prolonged weakness resembling Guillain-Barré syndrome can occur with fatalities generally in patients older than 50 years. 1 ELISAs for IgM and IgG antibodies in serum are the screening test of choice and should be verified by the more specific plaque reduction neutralization test. 9 ELISA for IgM antibodies and PCR for viral nucleic acid in CSF can be done for patients with encephalitis, although PCR specimens may be positive only in 50 to 60% of serologically proved infections. 10 The most important measure in preventing infection with WNV is avoidance of mosquito bites. Ribavirin has in vitro activity against the virus 11 and has been used in some cases, 7 but its role has yet to be defined. Given the increasing numbers of recognized WNV infections in North America and the suggestion that more virulent strains are involved in recent outbreaks, 12 the case described here illustrates that health care providers must be alert to the possibility of increased incidence and severe disease in children. Lymphocytopenia, rash and muscle weakness which were seen in our patient may be clues to WNV infection in the child with meningoencephalitis. Muscle weakness in particular has been a marker of WNV meningoencephalitis in adults, 13 but recurrence of symptoms after recovery from the initial illness has not been previously described. Although no other cause for the child’s recurrence of symptoms was found and is hypothesized to be related to recent WNV infection, confirmatory testing (plaque reduction neutralization test and PCR for viral nucleic acid on cerebrospinal fluid) was not readily available because of the inability of provincial and national laboratories to cope with the large number of suspected cases during the 2002 outbreak in Canada. 14 Our patient’s relatively long recovery time and weakness are features that also have not been emphasized in children and may portend more serious illness than had been previously predicted. Counseling caregivers about the realistic risks of WNV infection in children and prudent steps to avoid mosquito bites are topics that will likely assume greater importance in subsequent summers.

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