• View in gallery
    Figure 1.

    Equine West Nile encephalitis deaths by place of occurrence and percent slope of areas, El Salvador, 2001–2003. Equine encephalitis deaths occurred throughout El Salvador in 12 separated and discrete geographic foci ranging from 1 to 36 deaths each. All were either within (10) or adjacent to (2) steeply sloped (15–50%) terrain broken by deep gullies of temporary watercourses. This figure appears in color at www.ajtmh.org.

  • 1

    CDC, 2003. West Nile Virus Activity in the United States (reported as of May 21, 2004). Available at http://www.cdc.gov/ncidod/dvbid/westnile/surv&controlCaseCount03_detailed.htm.

  • 2

    Campbell GL, Marfin AA, Lanciotti RS, Gubler DJ, 2002. West Nile virus. Lancet Infect Dis 2 :519–529.

  • 3

    Eidson M, Kramer L, Stone W, Hagiwara Y, Schmit K, and the New York State West Nile Virus Avian Surveillance Team, 2001. Dead bird surveillance as an early warning system for West Nile virus. Emerg Infect Dis 7 :631–635.

    • Search Google Scholar
    • Export Citation
  • 4

    Blitvich BJ, Fernandez-Salas I, Contreras-Cordero JF, Marlenee NL, Gonzalez-Rojas JI, Komar N, Gubler DJ, Calisher CH, Beaty BJ, 2003. Serologic evidence of West Nile virus infection in horses, Coahuila State, Mexico. Emerg Infect Dis 9: 853–856. Available at http://www.cdc.gov/ncidod/EID/vol9no7/03-0166.htm.

  • 5

    Loroño-Pino MA, Blitvich BJ, Farfán-Ale JA, Puerto FI, Blanco JM, Marlenee NL, Rosado-Paredes EP, Garcia-Rejon JE, Gubler DJ, Calisher CH, Beaty BJ, 2003. Serologic evidence of West Nile virus infection in horses, Yucatan State, Mexico. Emerg Infect Dis 9 :857–859.

    • Search Google Scholar
    • Export Citation
  • 6

    Estrada-Franco J, Navarro-Lopez R, Beasley DWC, Coffey L, Carrara AS, Travassos da Rosa APA, Clements T, Wang E, Ludwig GV, Cortes AC, Ramirez PP, Tesh RB, Barrett ADT, Weaver SC, 2003. Isolation of West Nile virus in Mexico and serologic evidence of widespread circulation since July 2002. Emerg Infect Dis 9 :1604–1607.

    • Search Google Scholar
    • Export Citation
  • 7

    Blitvich BJ, Fernández-Salas I, Contreras-Cordero JF, Loroño-Pino MA, Marlenee NL, Díaz FJ, González-Rojas JI, Obregón-Martínez N, Chiu-García JA, Black WC IV, Beaty BJ, 2004. Phylogenetic analysis of West Nile Virus, Nuevo Leon State, Mexico. Emerg Infect Dis 10 :1314–1317.

    • Search Google Scholar
    • Export Citation
  • 8

    Hinman AR, McGowan JE Jr, Henderson BE, 1971. Venezuelan equine encephalomyelitis: surveys of human illness during an epizootic in Guatemala and El Salvador. Am J Epidemiol 93 :130–136.

    • Search Google Scholar
    • Export Citation
  • 9

    Martin DA, Muth DA, Brown T, Johnson AJ, Karabatsos N, Roehrig JT, 2000. Standardization of immunoglobulin M capture enzyme-linked immunosorbent assays for routine diagnosis of arboviral infections. J Clin Microbiol 38 :1823–1826.

    • Search Google Scholar
    • Export Citation
  • 10

    Roehrig JT, Nash D, Maldin B, Labowitz A, Martin DA, Lanciotti RS, Campbell GL, 2003. Persistence of virus-reactive serum immunoglobulin M antibody in confirmed West Nile virus encephalitis cases. Emerg Infect Dis 9 :376–379.

    • Search Google Scholar
    • Export Citation
  • 11

    Autorino GL, Battisti A, Deubel V, Ferrari G, Forletta R, Giovannini A, Lelli R, Murri S, Scicluna MT, 2002. West Nile virus epidemic in horses, Tuscany Region, Italy. EID 8 :1372–1378.

    • Search Google Scholar
    • Export Citation
  • 12

    Murgue B, Murri S, Zientara S, Durand B, Durand JP, Zeller H, 2001. West Nile outbreak in horses in Southern France, 2000: the return after 35 years. Emerg Infect Dis 7 :692–696.

    • Search Google Scholar
    • Export Citation
  • 13

    Hadler J, Nelson R, McCarthy T, Andreadis T, Lis MJ, French R, Beckwith W, Mayo D, Archambault G, Cartter M, 2001. West Nile virus surveillance in Connecticut in 2000: an intense epizootic without high risk for severe human disease. Emerg Infect Dis 7 :636–642.

    • Search Google Scholar
    • Export Citation
  • 14

    Tesh RB, Travassos da Rosa A, Guzman H, Araujo TP, Xiao SY, 2002. Immunization with heterologous flavivirus protective against fatal West Nile encephalitis. Emerg Infect Dis 8 :245–251.

    • Search Google Scholar
    • Export Citation
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SEROLOGICAL EVIDENCE OF WEST NILE VIRUS ACTIVITY IN EL SALVADOR

LILIAN CRUZField Epidemiology Training Program, Ministry of Public Health and Social Welfare, San Salvador, El Salvador; University of Texas–Houston School of Public Health, El Paso Regional Campus, El Paso, Texas; University of Texas Medical Branch, Center for Biodefense and Emerging Infectious Diseases, and Department of Pathology, Galveston, Texas; Centers for Disease Control and Prevention, Division of Vector Borne Infectious Diseases, Fort Collins, Colorado; Centers for Disease Control and Prevention, Division of International Health, Atlanta, Georgia

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VICTOR M. CARDENASField Epidemiology Training Program, Ministry of Public Health and Social Welfare, San Salvador, El Salvador; University of Texas–Houston School of Public Health, El Paso Regional Campus, El Paso, Texas; University of Texas Medical Branch, Center for Biodefense and Emerging Infectious Diseases, and Department of Pathology, Galveston, Texas; Centers for Disease Control and Prevention, Division of Vector Borne Infectious Diseases, Fort Collins, Colorado; Centers for Disease Control and Prevention, Division of International Health, Atlanta, Georgia

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MAURICIO ABARCAField Epidemiology Training Program, Ministry of Public Health and Social Welfare, San Salvador, El Salvador; University of Texas–Houston School of Public Health, El Paso Regional Campus, El Paso, Texas; University of Texas Medical Branch, Center for Biodefense and Emerging Infectious Diseases, and Department of Pathology, Galveston, Texas; Centers for Disease Control and Prevention, Division of Vector Borne Infectious Diseases, Fort Collins, Colorado; Centers for Disease Control and Prevention, Division of International Health, Atlanta, Georgia

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TITO RODRIGUEZField Epidemiology Training Program, Ministry of Public Health and Social Welfare, San Salvador, El Salvador; University of Texas–Houston School of Public Health, El Paso Regional Campus, El Paso, Texas; University of Texas Medical Branch, Center for Biodefense and Emerging Infectious Diseases, and Department of Pathology, Galveston, Texas; Centers for Disease Control and Prevention, Division of Vector Borne Infectious Diseases, Fort Collins, Colorado; Centers for Disease Control and Prevention, Division of International Health, Atlanta, Georgia

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ROBERTO FLORES REYNAField Epidemiology Training Program, Ministry of Public Health and Social Welfare, San Salvador, El Salvador; University of Texas–Houston School of Public Health, El Paso Regional Campus, El Paso, Texas; University of Texas Medical Branch, Center for Biodefense and Emerging Infectious Diseases, and Department of Pathology, Galveston, Texas; Centers for Disease Control and Prevention, Division of Vector Borne Infectious Diseases, Fort Collins, Colorado; Centers for Disease Control and Prevention, Division of International Health, Atlanta, Georgia

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MARIO V. SERPASField Epidemiology Training Program, Ministry of Public Health and Social Welfare, San Salvador, El Salvador; University of Texas–Houston School of Public Health, El Paso Regional Campus, El Paso, Texas; University of Texas Medical Branch, Center for Biodefense and Emerging Infectious Diseases, and Department of Pathology, Galveston, Texas; Centers for Disease Control and Prevention, Division of Vector Borne Infectious Diseases, Fort Collins, Colorado; Centers for Disease Control and Prevention, Division of International Health, Atlanta, Georgia

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ROBERT E. FONTAINEField Epidemiology Training Program, Ministry of Public Health and Social Welfare, San Salvador, El Salvador; University of Texas–Houston School of Public Health, El Paso Regional Campus, El Paso, Texas; University of Texas Medical Branch, Center for Biodefense and Emerging Infectious Diseases, and Department of Pathology, Galveston, Texas; Centers for Disease Control and Prevention, Division of Vector Borne Infectious Diseases, Fort Collins, Colorado; Centers for Disease Control and Prevention, Division of International Health, Atlanta, Georgia

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DAVID W. C. BEASLEYField Epidemiology Training Program, Ministry of Public Health and Social Welfare, San Salvador, El Salvador; University of Texas–Houston School of Public Health, El Paso Regional Campus, El Paso, Texas; University of Texas Medical Branch, Center for Biodefense and Emerging Infectious Diseases, and Department of Pathology, Galveston, Texas; Centers for Disease Control and Prevention, Division of Vector Borne Infectious Diseases, Fort Collins, Colorado; Centers for Disease Control and Prevention, Division of International Health, Atlanta, Georgia

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AMELIA P. A. TRAVASSOS DA ROSAField Epidemiology Training Program, Ministry of Public Health and Social Welfare, San Salvador, El Salvador; University of Texas–Houston School of Public Health, El Paso Regional Campus, El Paso, Texas; University of Texas Medical Branch, Center for Biodefense and Emerging Infectious Diseases, and Department of Pathology, Galveston, Texas; Centers for Disease Control and Prevention, Division of Vector Borne Infectious Diseases, Fort Collins, Colorado; Centers for Disease Control and Prevention, Division of International Health, Atlanta, Georgia

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SCOTT C. WEAVERField Epidemiology Training Program, Ministry of Public Health and Social Welfare, San Salvador, El Salvador; University of Texas–Houston School of Public Health, El Paso Regional Campus, El Paso, Texas; University of Texas Medical Branch, Center for Biodefense and Emerging Infectious Diseases, and Department of Pathology, Galveston, Texas; Centers for Disease Control and Prevention, Division of Vector Borne Infectious Diseases, Fort Collins, Colorado; Centers for Disease Control and Prevention, Division of International Health, Atlanta, Georgia

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ROBERT B. TESHField Epidemiology Training Program, Ministry of Public Health and Social Welfare, San Salvador, El Salvador; University of Texas–Houston School of Public Health, El Paso Regional Campus, El Paso, Texas; University of Texas Medical Branch, Center for Biodefense and Emerging Infectious Diseases, and Department of Pathology, Galveston, Texas; Centers for Disease Control and Prevention, Division of Vector Borne Infectious Diseases, Fort Collins, Colorado; Centers for Disease Control and Prevention, Division of International Health, Atlanta, Georgia

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ANN M. POWERSField Epidemiology Training Program, Ministry of Public Health and Social Welfare, San Salvador, El Salvador; University of Texas–Houston School of Public Health, El Paso Regional Campus, El Paso, Texas; University of Texas Medical Branch, Center for Biodefense and Emerging Infectious Diseases, and Department of Pathology, Galveston, Texas; Centers for Disease Control and Prevention, Division of Vector Borne Infectious Diseases, Fort Collins, Colorado; Centers for Disease Control and Prevention, Division of International Health, Atlanta, Georgia

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GLORIA SUAREZ-RANGELField Epidemiology Training Program, Ministry of Public Health and Social Welfare, San Salvador, El Salvador; University of Texas–Houston School of Public Health, El Paso Regional Campus, El Paso, Texas; University of Texas Medical Branch, Center for Biodefense and Emerging Infectious Diseases, and Department of Pathology, Galveston, Texas; Centers for Disease Control and Prevention, Division of Vector Borne Infectious Diseases, Fort Collins, Colorado; Centers for Disease Control and Prevention, Division of International Health, Atlanta, Georgia

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Epizootics of encephalitis in El Salvador killed 203 equines between November 2001 and April 2003. During an investigation of the outbreaks, 18 (25%) of 73 serum samples collected from stablemates of deceased animals in 2003 had antibodies to West Nile virus. Ten of these infections were confirmed by plaque reduction neutralization tests, suggesting West Nile virus has extended its range and spread to Central America.

Since its introduction into North America in 1999, West Nile virus (WNV) has caused disease in thousands of humans, equines and birds.13 By the end of September 2004, the WNV epizootic/epidemic had spread to most of the continental United States and Puerto Rico.1 Recent reports also indicate that WNV is now widely distributed in Mexico.47 In March 2002, anecdotal reports of equine deaths in Berlin, Usulutan, El Salvador, prompted a field investigation by the El Salvador (Central America) Ministry of Health and Welfare’s Field Epidemiology Training Program (FETP). We report preliminary findings of the ongoing investigation of these epizootics.

Information gathered from horse owners confirmed the occurrence of equine deaths beginning in November 2001. By the second week of March 2002, equine deaths had been reported in 11 of the 19 villages of the municipality of Berlin, in the State of Usulutan, (Figure 1). A few weeks later, another outbreak was reported and investigated in Jutiapa, El Salvador. An estimated 10% of the equines in this area succumbed to encephalitis during the outbreak. Clinically, at least 70% of the equine deaths and the few reports of illness among surviving animals described physical signs consistent with ataxia (stumbling, staggering, incoordination), head tilt, muscular fasciculation, circling, or paralysis. El Salvador’s Ministry of Agriculture (MOA) initially suspected anthrax, whereas the Ministry of Health (MOH) suggested a viral etiology such as Venezuelan equine encephalitis virus (VEEV) as the cause of these deaths, because VEEV caused epizootics in Central America in 1969–1972.8 Because of the lack of confirmed equine or human VEEV infections (i.e., lack of virus isolation, demonstration of viral RNA, or serological evidence), the FETP obtained 60 serum samples from horses and 18 from humans exhibiting acute fever in Berlin at the time of the outbreak investigation and sent these to the University of Texas Medical Branch for analysis.

Forty-three equine serum samples were assayed by hemagglutination inhibition (HI) tests for antibodies to VEEV, eastern equine encephalitis virus (EEEV), and WNV. Eight (19%) of these had HI antibody titers, suggesting they were infected with WNV or another closely related virus. All but one of these serum samples also had lower levels of HI antibodies to Saint Louis encephalitis (SLEV) and Ilheus viruses. Two of those eight samples had titers ≥ 320 by 90% plaque reduction neutralization tests (PRNT90) with the NY99 WNV (strain 385-99); the other six had titers ranging from 20 to 160. No virus was isolated from the equine sera, nor from brain tissue from a recently deceased horse from the area. Five samples had HI antibodies to dengue virus serotypes 1–4 (< 1:160).

Surveillance activities were subsequently enhanced and weekly reports of equine deaths and field research results were prepared by FETP and MOA teams. By April 2003, 203 equine deaths were reported from 6 states. All occurred between November 2001 and March 2002 and between November 2002 and April 2003. According to estimates of the MOA, 60,000 equines were present in El Salvador in 2000. Reports were entered into a geo-referenced database (Epi2000) and analyses were performed using different layers (humidity, land use, etc.). Eight of the nine foci of equine deaths occurred in three areas: Berlin, Jutiapa, and near Tamanique (Figure 1). Entomological evaluations conducted by El Salvador MOH entomologists reported the presence of Culex nigripalpus and Culex quinquefasciatus in the premises where equines had died in Berlin. At the time of this report, no testing for WNV infection in mosquitoes had been conducted.

Equine encephalitis deaths occurred in only 23 of the 2079 townships across El Salvador. Equine deaths formed 12 separated and discrete geographic foci ranging from 1 to 36 deaths each (Figure 1). All were either within (N = 10) or adjacent to (N = 2) steeply sloped (15–50%) terrain broken by deep gullies of temporary watercourses. The most affected area was Berlin, Usulutan (25,000 inhabitants) (area A in Figure 1). In one village of Berlin, San Felipe, 90 horses were enumerated in 2002 during a census carried out on behalf of the MOA. By April of 2003, 54 horses had died.

Samples taken from stable mates of equines that had died of neurologic illness were sent to the Centers for Disease Control and Prevention in Ft. Collins, Colorado, and tested by enzyme-linked immunosorbent assay (ELISA) for IgG and IgM antibodies to WNV and VEEV and by PRNT90 for antibody against WNV and SLEV.9 Twenty-three samples (from a total of 30 tested) with positive results in the initial screen are shown in Table 1; these sera were further tested to elucidate the likely infecting flavivirus by PRNT90 against a panel of flaviviruses considered most prevalent in Central America (Table 2). Ten of the serum samples had results suggestive of WNV infection with the PRNT90 antibody titers 4-fold or more greater for WNV than for SLEV or other flaviviruses. However, none of the WNV-positive samples was IgM positive. In humans, IgM antibodies to WNV have been shown to have a half-life 6–8 months, but it is possible they do not persist long in infected horses.10 All VEEV positive samples were IgG but not IgM positive (Table 1).

To look for evidence of human infection with WNV, field investigations included limited serologic household surveys, including 26 serum samples taken from acutely ill fever patients residing in affected villages identified through door-to-door surveys, and examination of emergency room visits and hospital discharge records. However, these limited inquiries failed to identify CNS disease among humans as having been caused by WNV infection. Further human studies will be required to assess human WNV infection patterns in El Salvador.

The surveillance and serologic data presented herein suggests epizootic transmission of WNV in El Salvador. The pattern of occurrence of this epizootic is consistent with a seasonal component limited to the dry season, when Culex mosquitoes are believed to be more abundant in El Salvador. The discrete geographic foci and November to March season indicate the possibility of introduction of WNV by migratory birds from North America to a limited number of points scattered throughout a characteristic ecological zone. The isolation of WNV from a dead bird from southern Mexico in May 2003 indicates that it was present nearby.6 Our data represent a rapid response to a potential public health emergency and accordingly have several limitations. First, the data and specimens were collected at the end of the epizootics, mainly from unaffected equines. Virus isolation or antigen and IgM antibody detection would have been more productive during the initial rise and peak of the outbreak. Similarly, human disease and vector populations in March may not represent the situation earlier in the season. We also have serologic studies from only 3 of the largest foci of equine encephalitis outbreaks the others may not have given similar results. Although we demonstrated 4-fold or greater differences in 90% PRNT titer between WNV and the other flaviviruses (including members of the JE complex known to circulate in Central America), the remote possibility exists that another untested flavivirus was responsible for the reactivity to WNV. Finally, we were not able to obtain follow-up sera from the equines that we sampled to show changes in antibody titers. The low prevalence of IgG VEEV antibodies would not be unexpected since VEEV occasionally appears in Central America and Mexico and since the vaccine has been used in El Salvador. Eventually, the confirmation of WNV transmission in Central America will rest on antigen detection from appropriate human, equine, avian, or mosquito specimens collected during the peak, November–February season.

Epizootics of WNV have occurred in Europe and the United States without recognized disease in humans.1113 Although human surveillance was extremely limited during the equine outbreak in 2003 in El Salvador, the apparent absence of human cases of WNV encephalitis could be due to multiple factors. First, there may be a lack of awareness and familiarity with the clinical picture caused by WNV. Another explanation might be that humans living in this region are not often bitten by the local WNV vector(s); in contrast, horses that roam freely in the fields of villages such as San Felipe, in Berlin, Usulutan, in the hills of El Salvador could be bitten by mosquitoes that do not normally feed on humans. Further, immunity to other flaviviruses present in Central America may play a role in preventing severe human disease as suggested by one experimental study in hamsters.14 Although it is not certain that human infections did not occur, further investigations into the WNV ecology, pathogenesis, and education of local clinicians are warranted. At this point, it is unclear why these epizootics seem to have been limited to hilly terrains.

In summary, serologic results strongly suggest the spread of WNV infection to Central America by 2003. Our preliminary findings underscore the need for further field investigations, isolation of virus from vectors, equines, birds, and humans, enhanced regional WNV surveillance, and assessment of the potential impact to humans in tropical America.

Table 1

Results of testing for antibody against West Nile virus (WNV), Saint Louis encephalitis virus (SLEV), and Venezuelan equine encephalitis virus (VEEV) in equine serum samples from San Felipe, Usulutan, El Salvador, 2003

IgG P/N IgM P/N 90% Neutralization
Sample no. WNV VEEV WNV VEEV WNV SLEV Interpretation
Cutoff values (reactive) for IgG and IgM are P/N = 3; all P/N values less than 3 are considered negative and are denoted as (−). Any titer of 10 or more is considered positive for neutralization.
12–1A 14.95 (−) (−) (−) 40 40 undetermined
2–S2 13.42 (−) (−) (−) 320 < 10 WNV
10–S2 11.99 (−) (−) (−) ≥ 320 ≥ 320 undetermined
13–1A 11.16 7.82 (−) (−) 320 80 WNV
17–1A 10.87 (−) (−) (−) 80 < 10 WNV
7–S2 9.59 11.48 (−) (−) 160 ≥ 320 undetermined
5–1A 9.37 (−) (−) (−) 320 ≥ 320 undetermined
1–S2 9.03 (−) (−) (−) 320 40 WNV
10–1A 8.93 (−) (−) (−) 160 160 undetermined
9–1A 8.37 (−) (−) (−) 160 < 10 WNV
8–1A 8.10 (−) (−) (−) 160 40 WNV
8–S2 7.22 (−) (−) (−) ≥ 320 20 WNV
3–S2 7.06 (−) (−) (−) 320 < 10 WNV
18–1A 5.81 (−) (−) (−) 80 < 10 WNV
5–S2 5.49 (−) (−) (−) 80 < 10 WNV
4–1A 5.12 (−) (−) (−) < 10 10 undetermined
16–1A 4.79 (−) (−) (−) 80 80 undetermined
4–S2 4.64 (−) (−) (−) 80 80 undetermined
6–S2 4.21 (−) (−) (−) 20 < 10 undetermined
3–1A (−) (−) (−) (−) < 10 10 undetermined
6–1A (−) 25.52 (−) (−) < 10 10 undetermined
14–1A (−) 6.25 (−) (−) < 10 < 10 undetermined
15–1A (−) (−) (−) (−) 10 < 10 undetermined
Table 2

Results of 90% plaque reduction neutralization assays against flavivi-ruses known to exist in Central America for 10 equine sera with antibody to West Nile virus (WNV), San Felipe, Usulutan, El Salvador

Neutralization titers against
Sample/set WNV SLEV DENV-2 YFV BSQV ILHV
WNV, West Nile virus; ILHV, Ilheus virus; YFV, yellow fever virus; SLEV, Saint Louis encephalitis virus; BSQV, Bussuquara virus; DENV-2, dengue virus type 2; (−), neutralizing antibody < 10.
13/1A 320 40 (−) (−) (−) (−)
3/S2 320 (−) (−) (−) (−) (−)
8/1A 160 20 10 (−) (−) (−)
8/S2 160 10 (−) (−) (−) (−)
1/S2 80 20 (−) (−) (−) (−)
9/1A 80 (−) (−) (−) (−) (−)
17/1A 80 (−) (−) (−) (−) (−)
18/1A 80 (−) (−) (−) (−) (−)
2/S2 80 (−) (−) (−) (−) (−)
5/S2 80 (−) (−) (−) (−) (−)
Median titer 80 <10 (−) (−) (−) (−)
Figure 1.
Figure 1.

Equine West Nile encephalitis deaths by place of occurrence and percent slope of areas, El Salvador, 2001–2003. Equine encephalitis deaths occurred throughout El Salvador in 12 separated and discrete geographic foci ranging from 1 to 36 deaths each. All were either within (10) or adjacent to (2) steeply sloped (15–50%) terrain broken by deep gullies of temporary watercourses. This figure appears in color at www.ajtmh.org.

Citation: The American Journal of Tropical Medicine and Hygiene Am J Trop Med Hyg 72, 5; 10.4269/ajtmh.2005.72.612

Authors’ addresses: Victor M. Cardenas, UT School of Public Health, El Paso Regional Campus, 1100 N. Stanton Ave., Suite 110F, El Paso, TX 79902, E-mail: vcardenas@utep.edu; Lilian Cruz, Mauricio Abarca, Tito Rodriguez, Roberto Flores Reyna, Mario V. Serpas, and Gloria Suarez-Rangel, Calle Avce 827, San Salvador, El Salvador, Central America; Ann M. Powers, Division of Vector-Borne Infectious Diseases, Rampert Rd (Foothills Campus), P.O. Box 2087, Fort Collins, CO 80522, Robert E. Fontaine, Centers for Disease Control and Prevention, MS-C08, 1600 Clifton Road NE, Atlanta, GA 30333; David W. C. Beasley, Amelia P. A. Travassos Da Rosa, Scott C. Weaver, and Robert B. Tesh, Department of Pathology, UTMB, 1.116 Keiller Bldg., Galveston, TX 77555-0609.

Acknowledgments: The authors thank Mr. Jorge Escobar, entomologist, and Dr. Miguel Castro for their valuable assistance in data collection. The support of the Ministry of Public Health and Welfare (MSPAS), Ministry of Agriculture (MAG), and Ministry for the Environment and Natural Resources (MARN) of El Salvador, and the U.S. Agency for International Development Mission in El Salvador, is greatly appreciated. The authors thank Mr. Wilfredo Fuentes and Mr. Rene Osorio of the Environmental Information System at MARN for providing us with valuable geographic information. We thank Mr. Michael Bristow for his valuable assistance in preparing Figure 1. We also thank Ms. Janae Raetz for excellent technical assistance. This research was supported by contract N01-AI25489 from the National Institutes of Health.

REFERENCES

  • 1

    CDC, 2003. West Nile Virus Activity in the United States (reported as of May 21, 2004). Available at http://www.cdc.gov/ncidod/dvbid/westnile/surv&controlCaseCount03_detailed.htm.

  • 2

    Campbell GL, Marfin AA, Lanciotti RS, Gubler DJ, 2002. West Nile virus. Lancet Infect Dis 2 :519–529.

  • 3

    Eidson M, Kramer L, Stone W, Hagiwara Y, Schmit K, and the New York State West Nile Virus Avian Surveillance Team, 2001. Dead bird surveillance as an early warning system for West Nile virus. Emerg Infect Dis 7 :631–635.

    • Search Google Scholar
    • Export Citation
  • 4

    Blitvich BJ, Fernandez-Salas I, Contreras-Cordero JF, Marlenee NL, Gonzalez-Rojas JI, Komar N, Gubler DJ, Calisher CH, Beaty BJ, 2003. Serologic evidence of West Nile virus infection in horses, Coahuila State, Mexico. Emerg Infect Dis 9: 853–856. Available at http://www.cdc.gov/ncidod/EID/vol9no7/03-0166.htm.

  • 5

    Loroño-Pino MA, Blitvich BJ, Farfán-Ale JA, Puerto FI, Blanco JM, Marlenee NL, Rosado-Paredes EP, Garcia-Rejon JE, Gubler DJ, Calisher CH, Beaty BJ, 2003. Serologic evidence of West Nile virus infection in horses, Yucatan State, Mexico. Emerg Infect Dis 9 :857–859.

    • Search Google Scholar
    • Export Citation
  • 6

    Estrada-Franco J, Navarro-Lopez R, Beasley DWC, Coffey L, Carrara AS, Travassos da Rosa APA, Clements T, Wang E, Ludwig GV, Cortes AC, Ramirez PP, Tesh RB, Barrett ADT, Weaver SC, 2003. Isolation of West Nile virus in Mexico and serologic evidence of widespread circulation since July 2002. Emerg Infect Dis 9 :1604–1607.

    • Search Google Scholar
    • Export Citation
  • 7

    Blitvich BJ, Fernández-Salas I, Contreras-Cordero JF, Loroño-Pino MA, Marlenee NL, Díaz FJ, González-Rojas JI, Obregón-Martínez N, Chiu-García JA, Black WC IV, Beaty BJ, 2004. Phylogenetic analysis of West Nile Virus, Nuevo Leon State, Mexico. Emerg Infect Dis 10 :1314–1317.

    • Search Google Scholar
    • Export Citation
  • 8

    Hinman AR, McGowan JE Jr, Henderson BE, 1971. Venezuelan equine encephalomyelitis: surveys of human illness during an epizootic in Guatemala and El Salvador. Am J Epidemiol 93 :130–136.

    • Search Google Scholar
    • Export Citation
  • 9

    Martin DA, Muth DA, Brown T, Johnson AJ, Karabatsos N, Roehrig JT, 2000. Standardization of immunoglobulin M capture enzyme-linked immunosorbent assays for routine diagnosis of arboviral infections. J Clin Microbiol 38 :1823–1826.

    • Search Google Scholar
    • Export Citation
  • 10

    Roehrig JT, Nash D, Maldin B, Labowitz A, Martin DA, Lanciotti RS, Campbell GL, 2003. Persistence of virus-reactive serum immunoglobulin M antibody in confirmed West Nile virus encephalitis cases. Emerg Infect Dis 9 :376–379.

    • Search Google Scholar
    • Export Citation
  • 11

    Autorino GL, Battisti A, Deubel V, Ferrari G, Forletta R, Giovannini A, Lelli R, Murri S, Scicluna MT, 2002. West Nile virus epidemic in horses, Tuscany Region, Italy. EID 8 :1372–1378.

    • Search Google Scholar
    • Export Citation
  • 12

    Murgue B, Murri S, Zientara S, Durand B, Durand JP, Zeller H, 2001. West Nile outbreak in horses in Southern France, 2000: the return after 35 years. Emerg Infect Dis 7 :692–696.

    • Search Google Scholar
    • Export Citation
  • 13

    Hadler J, Nelson R, McCarthy T, Andreadis T, Lis MJ, French R, Beckwith W, Mayo D, Archambault G, Cartter M, 2001. West Nile virus surveillance in Connecticut in 2000: an intense epizootic without high risk for severe human disease. Emerg Infect Dis 7 :636–642.

    • Search Google Scholar
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  • 14

    Tesh RB, Travassos da Rosa A, Guzman H, Araujo TP, Xiao SY, 2002. Immunization with heterologous flavivirus protective against fatal West Nile encephalitis. Emerg Infect Dis 8 :245–251.

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Author Notes

Reprint requests: Victor M. Cardenas, M.D., M.P.H., Ph.D., El Paso Regional Campus, University of Texas–Houston School of Public Health, 1100 N. Stanton Ave., Suite 110F, El Paso, TX 79902.
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