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93 Newly Recognized Focus of La Crosse Encephalitis in Tennessee Timothy F. Jones, Allen S. Craig, Roger S. Nasci, Lori E. R. Patterson, Paul C. Erwin, Reid R. Gerhardt, Xilla T. Ussery, and William Schaffner From the Epidemic Intelligence Service, Centers for Disease Control and Prevention, Atlanta, Georgia; Tennessee Department of Health, and Departments of Preventive Medicine and Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee; Division of VectorBorne Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado; and East Tennessee Children’s Hospital, East Tennessee Regional Department of Health, and University of Tennessee, Knoxville, Tennessee La Crosse virus is a mosquito-borne arbovirus that causes encephalitis in children. Only nine cases were reported in Tennessee during the 33-year period from 1964 – 1996. We investigated a cluster of La Crosse encephalitis cases in eastern Tennessee in 1997. Medical records of all suspected cases of La Crosse virus infection at a pediatric referral hospital were reviewed, and surveillance was enhanced in the region. Previous unreported cases were identified by surveying 20 hospitals in the surrounding 16 counties. Mosquito eggs were collected from five sites. Ten cases of La Crosse encephalitis were serologically confirmed. None of the patients had been discharged from hospitals in the region with diagnosed La Crosse encephalitis in the preceding 5 years. Aedes triseriatus and Aedes albopictus were collected at the case sites; none of the mosquitos had detectable La Crosse virus. This cluster may represent an extension of a recently identified endemic focus of La Crosse virus infection in West Virginia. La Crosse virus, one of the California serogroup bunyaviruses, is the primary cause of pediatric arboviral encephalitis in the United States [1]. In areas of endemicity, incidence rates for La Crosse encephalitis approximate those of bacterial meningitis of all causes [2, 3]. In Minnesota from 1967 to 1972, La Crosse virus accounted for 18% of acute CNS infections of known etiology [4]. La Crosse encephalitis occurs in an endemic pattern. Since 1964, an average of 73 cases per year (range, 29–139 cases per year) have been reported to the Centers for Disease Control and Prevention (CDC) from 23 different states (G. L. Campbell, Arbovirus Diseases Branch, Division of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, CDC; personal communication). Over this same 33-year period, only nine cases were reported in Tennessee. In September 1997, an apparent cluster of La Crosse encephalitis was reported by a children’s hospital in eastern Tennessee, and an investigation was undertaken by the state and regional health departments. Patients and Methods Hospital A served as the primary pediatric referral center in eastern Tennessee. Medical records of all children at hospital A with suspected viral encephalitis from 15 July through 15 Received 27 May 1998; revised 31 August 1998. Reprints or correspondence: Dr. Timothy Jones, Tennessee Department of Health, CEDS, 4th Floor, Cordell Hull Building, 425 5th Avenue North, Nashville, Tennessee 37247 ([email protected]). Clinical Infectious Diseases 1999;28:93–7 q 1999 by the Infectious Diseases Society of America. All rights reserved. 1058–4838/99/2801–0014$03.00 / 9c5e$$ja36 12-27-98 19:19:28 October 1997 were reviewed. Serum specimens from some patients were tested with a ‘‘meningoencephalitis panel’’ that measured antibodies to 28 viruses; this was performed at a private referral laboratory. All available serum and CSF specimens were sent to the CDC Arbovirus Diseases Laboratory (Fort Collins, Colorado) for arbovirus antibody testing. Convalescent serum specimens were collected 3 to 6 weeks after hospitalization. The CDC surveillance case definition for arboviral encephalitis was used to classify cases [5]. Patients with a symptomatic, physician-diagnosed, nonbacterial infection of the CNS and with serological evidence of recent La Crosse virus infection were included as cases. Confirmed diagnoses required a fourfold or greater change in serum antibody titers by use of indirect fluorescent antibody test (IFA) [6] between acute and convalescent sera, or single specimens of CSF or serum with specific IgM antibody by ELISA [7]. Serum and CSF IgM antibodies were confirmed by demonstration of antibodies with use of serum dilution – plaque reduction neutralization testing [8, 9]. Enhanced surveillance for potential cases of La Crosse encephalitis was undertaken from mid-September through mid-October, 1997. Emergency room personnel and medical staff at hospital A were asked to report all possible cases of viral CNS infection to the institution’s infection control personnel. Laboratory records were reviewed for all CSF or serum specimens tested for viral antibodies or sent to a referral laboratory for a ‘‘meningoencephalitis panel’’ in the preceding 3 months. Diagnoses of all patients who underwent lumbar puncture at the hospital were reviewed. Infection control personnel at all hospitals in the metropolitan area and the surrounding 16 counties were asked to immediately report any possible cases of viral encephalitis to the regional cida UC: CID 94 Jones et al. CID 1999;28 (January) Figure 1. Confirmed cases of La Crosse encephalitis according to week of onset, eastern Tennessee, 1997. health department. They were also asked to review hospital records for possible unreported cases in the preceding 3 months. To assess possible previously unreported cases, 20 hospitals in the region surrounding and including hospital A were asked to provide information concerning all hospital discharges of children and adults with viral encephalitis or related diagnoses in the preceding 5 years. The discharge diagnoses requested included La Crosse, California, mosquito-borne, or arboviral encephalitis; arboviral meningitis, encephalitis, viral encephalitis, viral meningoencephalitis, and aseptic meningitis. Mosquito eggs were collected from five sites in areas where patients were likely to have been exposed before their illnesses. Ten standard ovitraps [10] were placed Ç10 m apart at each site and collected after 7 to 10 days. Homesites of three patients were formally evaluated for potential mosquito-breeding habitats, including counting permanent and temporary manmade containers on the property and measuring the distance from the home to forested areas. Mosquito eggs were sent to the CDC for counting, identification, hatching, rearing, and examination for viruses by Vero-cell plaque assay [9]. Results During the period from 15 July to 15 October 1997, a total of 27 patients admitted to hospital A had illnesses consistent with possible La Crosse encephalitis on initial presentation. After further evaluation, nine patients were given other diagnoses by their physicians, including viral meningitis (7 patients), idiopathic seizures (1), and severe nonspecific headache (1), and had no further testing for arboviral antibodies. Of the remaining 18 patients, 10 had confirmed La Crosse encephalitis (figure 1) and eight patients with compatible symptoms were negative for La Crosse virus antibodies (table 1). Of the 10 patients with La Crosse virus infections, diagnoses were confirmed for seven patients by demonstration of a four- / 9c5e$$ja36 12-27-98 19:19:28 fold or greater increase in antibody titers between acute and convalescent sera. One patient had IgM demonstrated in CSF and a twofold change in serum IgM titer. The other two patients had serum specimens positive for IgM antibodies by use of IgM-capture ELISA, with positive plaque reduction neutralization tests; one of these patients had a twofold change in serum titers, and the other had only one specimen available for testing. All 10 of these patients had negative CSF viral cultures. A panel of 28 antibody tests was performed on single-serum spec- Table 1. Clinical characteristics of patients with viral CNS infections who were evaluated for La Crosse infection, eastern Tennessee, 1997. Characteristic Mean age, y (range) Male sex Fever (temperature, ú100.07F) Headache Vomiting Photophobia Behavioral change Altered consciousness Seizures Meningismus Neurologic sequelae Abnormal electroencephalogram Mean duration of symptoms before hospitalization, d (range) Mean CSF WBC count per mm3 (range) Serologically confirmed La Crosse (n Å 10) No La Crosse* (n Å 8) 6.9 (3 – 14) 7 (70) 10 (100) 9 (90) 7 (70) 4 (40) 7 (70) 7 (70) 8 (80) 1 (10) 1 (10) 9 (90) 7 (1 – 12) 6 (75) 8 (100) 6 (75) 7 (89) 2 (25) 5 (63) 3 (38) 3 (38) 1 (13) 1 (13) 3/5 (60) 3.1 (1 – 7) 2.8 (1 – 7) 205 (42 – 590) 203 (21 – 880) NOTE. Data are no. (%) of patients unless otherwise indicated. * There were no statistically significant differences between the two groups for any of the variables listed. cida UC: CID CID 1999;28 (January) La Cross Encephalitis in Tennessee imens from 10 and on CSF specimens from 6 of the 17 patients who did not have serologically documented La Crosse virus infections, and no other specific viral etiologies of their illnesses were identified serologically. Subsequently, viral cultures of CSF from two of the patients who did not have complete La Crosse virus antibody testing yielded coxsackievirus. Seven of the 10 patients with La Crosse virus infections were boys (table 1). The 10 patients were ages 3 to 14 years. Signs and symptoms were consistent with previous reports of La Crosse encephalitis: nine had headache, eight had seizures, seven had altered consciousness, and nine had abnormal electroencephalograms (EEGs). At the time of discharge from the hospital, diagnoses included viral meningoencephalitis (6 patients), viral meningitis (2), and encephalitis (2). None of the patients were discharged with a diagnosis indicating La Crosse virus as the etiologic agent. One patient was discharged from the hospital with persistent deficits including ptosis, right abducens palsy, slowed speech, residual gait ataxia, and intention tremors at 12 days after presentation. None of the clinical characteristics examined differed significantly between the patients with confirmed La Crosse encephalitis and those who did not have antibodies to La Crosse virus. On the basis of the patients’ histories and a reported incubation period of 5 to 15 days, of the 10 confirmed cases of La Crosse encephalitis, 9 were thought likely to have been infected within 50 miles of hospital A. No other hospitals in the area reported cases of pediatric or adult La Crosse encephalitis during this period. Evaluation of the homes of three patients with confirmed La Crosse encephalitis revealed 2, 7, and 16 permanent and 5, 16, and 22 disposable containers that could hold standing water in the yards. Two houses were within 50 to 100 feet of a forest line, and one was also 100 feet from a large pond of standing water. A total of 7,279 mosquito eggs were collected from 50 traps at five sites, including the yards of three patients with confirmed La Crosse virus infections. Of the 4,493 mosquitos that were successfully reared, 3,591 (80%) were identified as A. triseriatus, and 902 (20%) as A. albopictus. None of the mosquitos reared were found to harbor La Crosse virus. All 20 hospitals in the counties surrounding hospital A responded to the survey of discharge diagnoses in the preceding 5 years. There were no cases with discharge diagnoses of mosquito-borne, arboviral, La Crosse, or California encephalitis reported from these hospitals during this period. The highest number of cases of nonspecific viral CNS disease were seen in the third quarter (July through September) of each year, with 20 to 49 cases reported annually during that quarter. Discussion This cluster of 10 cases of La Crosse encephalitis is the largest ever reported in Tennessee, surpassing the total number of cases reported in the entire state over the preceding 33 years. / 9c5e$$ja36 12-27-98 19:19:28 95 Because not all patients with suspected La Crosse encephalitis had complete testing, these 10 cases represent a minimum estimate of the number of cases seen at this hospital. In the past, La Crosse encephalitis has been primarily an infection occurring in the upper midwestern United States, with most cases reported from Illinois, Indiana, Iowa, Minnesota, Ohio, and Wisconsin. Since 1993, however, West Virginia has had more reported cases than any other state, and, in 1996, West Virginia accounted for more than half of all cases reported in the country (figure 2) (G. L. Campbell, Arboviruses Disease Branch, Division of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, CDC; personal communication). This is the first report of a possible extension of the West Virginia endemic focus. Studies have suggested that there may be 300,000 human La Crosse virus infections per year in the United States, with more than 1,000 asymptomatic or mildly symptomatic infections per reported case [1,11, 12]. Estimates of ratios of inapparent-to-apparent infections in children have ranged from 26:1 [12] to 1,571:1 [11]. In highly endemic areas, seropositivity increases with age, and antibody prevalence can reach 35% by adulthood [12 – 18]. La Crosse virus infections are difficult to distinguish from other viral infections of the CNS. Most infections are not recognized clinically, and those that are can have diverse manifestations, ranging from nonspecific viral illness to aseptic meningitis or frank encephalitis. Specific laboratory testing is required to differentiate La Crosse virus from other causes of CNS infection. Viral-specific IgM antibody in the CSF is diagnostic of La Crosse virus infection, but the serum IgM antibody levels may remain elevated for ú9 months in over half of patients [3]. Serological diagnosis, therefore, requires demonstration of a fourfold or greater change in serum antibody titer or confirmation of serum IgM antibodies by demonstration of IgG antibodies with use of another serological assay [5]. Reliance on laboratory confirmation for diagnosis precludes the quantification of the extent of undetected illness before this outbreak. Some of the patients discharged in previous years with diagnoses of viral encephalitis or encephalitis of unknown etiology may have had La Crosse virus infections. All of the patients in this cluster who eventually were shown to have La Crosse virus infections were discharged from the hospital with diagnoses of nonspecific viral CNS illnesses during the period when annual peaks are seen for these diagnoses. Our review of hospital discharge data did not reveal specific examples of underreporting of documented La Crosse virus infections. This cluster of infections could represent a new southern endemic focus or a newly recognized focus elucidated by increased surveillance and testing. The La Crosse virus is transmitted to humans by the eastern treehole mosquito, A. triseriatus (Say). The virus is passed transovarially (vertically) in mosquitos and can survive the winter in eggs [19, 20], although it is amplified horizontally in small mammals as well [3]. Several previous cida UC: CID 96 Jones et al. CID 1999;28 (January) Figure 2. Geographic distribution according to county of La Crosse encephalitis cases reported to the Centers for Disease Control and Prevention, 1990 – 1997. Data are from: G. L. Campbell, Arbovirus Diseases Branch, Division of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, personal communication; and personal communications from departments of health in states reporting cases during these years. 1997 data reflect cases reported to the CDC as of 8 January 1998. studies have isolated La Crosse virus from only 0.2% to 0.6% of mosquitos collected in the field in areas of endemicity [19 – 21]. Endemic foci may be quite localized [18, 22], with possible ‘‘island’’ populations of mosquitos in shaded areas surrounding human habitats and discarded containers [23]. A. triseriatus typically breeds in treeholes or manmade containers and is difficult to control with the pesticide spraying usually used to eliminate pestiferous species [21]. Programs to prevent disease by filling treeholes, removing discarded tires, and educating the community have met with mixed success [17, 24]. A. triseriatus is generally a daytime biter [23, 25]. Persons potentially at risk in areas of endemicity should be encouraged to use adequate personal protective measures including insect repellents, protective clothing, and avoidance of infested areas when possible. This is the largest cluster of La Crosse encephalitis ever reported in Tennessee. Since 1994, West Virginia has reported more cases of La Crosse encephalitis than any other state. This cluster may represent a newly recognized endemic focus in the southeastern United States. Underdiagnosis is probably common. In endemic areas, physicians should be alerted to the broad spectrum of clinical manifestations of La Crosse virus infection and report all cases to local health departments. Further surveillance is warranted to help define shifts in endemicity of the disease. Acknowledgments The authors thank Alan Dupuis, Denise Martin, and Nick Karabatsos of the CDCs Arbovirus Disease Laboratory for laboratory testing of specimens; Grant L. Campbell, MD, PhD, at the CDC (Fort Collins) for updated surveillance information; Sandy Halford, Frank Bristow, Jan Fowler, Stephanie Hall, MD, Dan Jorgensen, MD, and the staffs of the Knoxville/Knox County and East Tennes- / 9c5e$$ja36 12-27-98 19:19:28 see Regional Health Departments for help with the investigation and patient follow-up; Kristy Gottfried of the University of Tennessee for assistance with mosquito surveillance; Jim Moore for information on A. albopictus in Tennessee; Pat Turri of the Tennessee Department of Health for assistance with mapping; and Laura Fehrs, MD, MPH, of the Epidemiology Program Office at the CDC for her thoughtful review of the manuscript. References 1. Calisher CH. Medically important arboviruses of the United States and Canada. Clin Microbiol Rev 1994; 7:89 – 116. 2. Centers for Disease Control and Prevention. La Crosse encephalitis in West Virginia. MMWR Morb Mortal Wkly Rep 1988; 37:79 – 82. 3. Tsai TF. Arboviral infections in the United States. Infect Dis Clin North Am 1991; 5:73 – 103. 4. Balfour HH, Siem RA, Bauer H, Quie PG. California arbovirus (La Crosse) infections. I. Clinical and laboratory findings in 66 children with meningoencephalitis. Pediatrics 1973; 52:680 – 91. 5. Centers for Disease Control and Prevention. Case definitions for infectious conditions under public health surveillance. MMWR Morb Mortal Wkly Rep 1997; 46:12 – 3. 6. Beaty BJ, Casals J, Brown KL, et al. Indirect fluorescent-antibody technique for serological diagnosis of La Crosse (California) virus infections. J Clin Microbiol 1982; 15:429 – 34. 7. Calisher CH, Pretzman CI, Muth DJ, Parsons MA, Peterson ED. Serodiagnosis of La Crosse virus infections in humans by detection of immunoglobulin M class antibodies. J Clin Microbiol 1986; 23:667 – 71. 8. Lindsey HS, Calisher CH, Mathews HH. Serum dilution neutralization test for California group virus identification and serology. J Clin Microbiol 1976; 4:503 – 10. 9. Beaty BJ, Calisher CH, Shope RS. Arboviruses. In: Schmidt NJ, Emmons RW, eds. Diagnostic procedures for viral, rickettsial and chlamydial infections. Washington, DC: American Public Health Association, 1989: 797 – 856. 10. Loor KA, DeFoliart GR. An oviposition trap for detecting presence of Aedes triseriatus (Say). Mosquito News 1969; 29:487 – 8. 11. Grimstad PR, Barrett RL, Humphrey RL, Sinsko MJ. Serologic evidence for widespread infection with La Crosse and St. Louis encephalitis cida UC: CID CID 1999;28 (January) 12. 13. 14. 15. 16. 17. La Cross Encephalitis in Tennessee viruses in the Indiana human population. Am J Epidemiol 1984; 119: 913 – 30. Kappus KD, Monath TP, Kaminski RM. Reported encephalitis associated with California serogroup infections in the United States, 1963 – 1981. Prog Clin Biol Res 1983; 123:31 – 41. Szumlas DE, Apperson CS, Hartig PC, Francy DB, Karabatsos N. Seroepidemiology of La Crosse virus infection in humans in western North Carolina. Am J Trop Med Hyg 1996; 54:332 – 7. Thompson WH, Evans AS. California encephalitis virus studies in Wisconsin. Am J Epidemiol 1965; 81:230 – 44. Monath TP, Nuckolls JG, Berall J, Bauer H, Chappell WA, Coleman PH. Studies on California encephalitis in Minnesota. Am J Epidemiol 1970; 92:40 – 50. Parkin WE, Hammon WM, Sather GE. Review of current epidemiologic literature on viruses of the California arbovirus group. Am J Trop Med Hyg 1972; 14:964 – 78. Thompson WH, Gundersen CB. La Crosse encephalitis: occurrence of disease and control in a suburban area. Prog Clin Biol Res 1983; 123: 225 – 36. / 9c5e$$ja36 12-27-98 19:19:28 97 18. Rowley WA, Wong YW, Dorsey DC, Hausler WJ, Currier RW. California serogroup viruses in Iowa. Prog Clin Biol Res 1983; 123:237 – 46. 19. Thompson WH. Vector-virus relationships. Prog Clin Biol Res 1983; 123: 57 – 66. 20. Balfour HH, Edelman CK, Cook FE, et al. Isolates of California encephalitis (La Crosse) virus from field-collected eggs and larvae of Aedes triseriatus: identification of the overwintering site of California encephalitis. J Infect Dis 1975; 131:712 – 5. 21. Craig GB. Biology of Aedes triseriatus: some factors affecting control. Prog Clin Biol Res 1983; 123:329 – 41. 22. LeDuc JW. The ecology of California group viruses. J Med Entomol 1979; 16:1 – 17. 23. Francy DB. Mosquito control for prevention of California (La Crosse) encephalitis. Prog Clin Biol Res 1983; 123:365 – 75. 24. Fish D. A systems approach to the control of La Crosse virus. Prog Clin Biol Res 1983; 123:343 – 53. 25. Woodruff BA, Baron RC, Tsai TF. Symptomatic La Crosse virus infections of the central nervous system: a study of risk factors in an endemic area. Am J Epidemiol 1992; 136:320 – 7. cida UC: CID