Epidemiological Bulletin
      Vol. 16, No. 4
December 1995  


Venezuelan equine encephalitis (VEE) is a disease of horses, mules, and donkeys caused by an 2alphavirus, which is known to occur only in this hemisphere. The virus of VEE can be transmitted to humans by mosquito bites and occasionally causes epizootics and epidemics.

Through serologic test, the VEE virus has been classified in six subtypes I to VI, as shown in table 1. The subtype I has seven recognized variants, which include the vaccinal strain TC-83. The variants A, B and C of the subtype I are the main cause of epizootics and epidemics. (20)

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Since the isolation of the VEE virus in 1938 in the state of Aragua, Venezuela, several outbreaks, and epizootic-epidemics (Epizoodemics) have been notified in 12 countries in the Americas: Peru, Ecuador, Colombia, Venezuela, Trinidad and Tobago, Costa Rica, Nicaragua, Honduras, El Salvador, Guatemala, Mexico, and the United States.

During the period 1935-1961 outbreaks were reported in eleven years occurring mostly in Colombia and Venezuela, but also in Trinidad and Tobago, and Peru. Between 1962 and 1973 outbreaks occurred every year except in 1965.

Trends in proportional mortality from external causes (% based on deaths from defines causes), the largest epizooticand epidemic was caused by the subtype I variant B. It was initiated in Colombia in 1967 and extended to Ecuador, Venezuela, Central America, Mexico, and finally reached Texas in the United States in 1971. During this epizoodemic a number of 38,000 to 50,000 equine deaths were reported; close to 31,000 human cases and 310 deaths were notified in Ecuador and 200,000 human cases in Colombia. (1) (10)

2 After this epizoodemic, the surveillance of equine encephalitides has declined in most of the countries of Latin America and the Caribbean, particularly in the last 18 years. The few countries that reported clinical cases consistent with equine encephalitides obtain no laboratory confirmation. In Latin America and the Caribbean, laboratory diagnosis of equine encephalitides has practically ceased.

Some countries have continued to utilize the weekly information system of the Pan American Foot-and-Mouth Disease Center (PANAFTOSA), which reports by quadrants the occurrence of syndromes compatible with equine encephalitis of viral origin, locating the site of occurrence in the Cartesian coordinates of every country. Table 1 presents a summary of the information received from the countries during the period 1989-1994. The limited participation of the countries is evident, since only Argentina, Bolivia, Brazil, Colombia, Ecuador, El Salvador, Guatemala, Paraguay, and Venezuela reported. In 1994, Panama and Peru started reporting. (13), (16).

With the limited information provided during the period October 1989-December 1994, it has been possible to confirm the existence of enzootic areas in various countries where clinical episodes of equine encephalitides were frequently reported like some of these areasin Colombia and Venezuela.

Table 1
Occurence of Reported Foci of Syndroms Consistent with Equine Encephalitides and Number
of Weeks reported, 1989-1994

Country 1989 1990 1991 1982 1993 1994
El Salvador
0/10 (1)

(1) Number of occurence of foci/number of weeks reported
(2) Did not report (NI)

Source: Pan American Foot-and Mouth Disease Center (PANAFTOSA)

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Outbreak of Venezuelan Equine Encephalitis (VEE) 1995

The 1995 outbreak of VEE occurring in Venezuela and Colombia was originated through an increased viral activity in the areas where the disease was observed since 1993 in a susceptible equine population. Unfortunately, because of the lack of laboratory diagnostic services, typing of the VEE virus was not made on previous outbreaks.

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The Outbreak in Venezuela

Between December 1992 and January 1993, the sanitary officers of Venezuela reported an outbreak of VEE in the State of Trujillo. Twenty eight equine clinical cases and 12 deaths were recorded. The localities involved were: La Catalina, Zapatero, La Urbina Rio Seco, Agua Caliente, and Albaricol, all of them neighboring the Agua Viva dam that was filled in August 1992. Thirty nine human febrile cases were also reported. In this occasion isolation of the VEE virus showed involvement of the enzootic subtype ID. (15) (18)

In June 1993, outbreaks were also reported in the State of Zulia, involving 55 human cases and 66 equines.

Following these outbreaks, vaccination campaigns were developed in the western states of Venezuela. No outbreaks were reported in 1994.

In May 23, 1995 a report of a syndrome compatible with equine encephalitiswas made in the localities of Cacique Manaure and Monseñor Iturriza in the State of Falcon at the northwest of the country. This outbreak continued spreading toward the northwest, but also to the south. The disease appeared in the north of the State of Yaracuy in June 7, in the localities Aroa, Yumare and Socremo of the municipality of Bolivar. At this time, vaccination of 1,435 equine was initiated in the neighbor state of Lara. In the last fifteen days of August reports of sick and dead horses preceded a report of nine human cases in the municipality of Urdaneta at the northeast of the state of Lara. Investigation of the report showed 15 human suspected cases and 29 equine deaths. (15)

The disease progressed through the north of the State of Lara as well as through the north of the state of Falcon toward the Lake of Maracaibo, reaching the east side of Zulia state at the end of August.

The disease was first reported in the west side of Zulia state in August 28, affecting the districts of Mara and Paez located at the northwest of Maracaibo Lake.(7) In these districts most of the febrile human cases were reported. Isolation of the virus was made at the National Institute of Hygiene and later it was typified by the University of Texas and University of Yale. The identified VEE virus was the subtype I variant C. (5) (2)

During September, outbreaks were reported in the state of Carabobo, neighbor to Yaracuy state which notified increased incidence of human febrile cases. VEE virus isolation was made from two human cases. (8) During October, reports and confirmation of VEE causing sick and dead equine have been made in two additional states: Cojedes and Guarico. In summary the geographical extension of the epizootic-epidemic in Venezuela covered seven states: Zulia (50% of its territory), Falcon (100%); Lara (15%), Yaracuy (100%); Carabobo (15%), Cojedes (less than 5%) and Guarico (recent outbreak). (6)

Since the beginning of the epidemic to October 31, national authorities reported 11,390 human febrile cases compatible to VEE and 16 deaths. The disease has been confirmed in 185 human cases through viral isolation and/or hemagglutination inhibition test. About 500 clinical equine cases and 475 dead animals, including horses, mules and donkeys have been notified (Table 2). (6) (7)

Table 2

Human and Equine Cases Reported in Venezuela(*)

  Human Cases Equine Cases
Department Date of Fist



May 23
June 10
July 23
Aug. 28
Sept. 10
Oct. 10
Oct 23
TOTAL 11.390 185 16 504 474(1)

* Data up to October 31, 1995
- No information
(1) Global data provided

Venezuelan equine encephalitis was most striking in the state of Zulia causing more than 10,000 human cases including few cases in the city of Maracaibo and 272 equine cases were reported.

Control measures have consisted on:

  1. Quarantine of affected states which included: Zulia, Falcon, Yaracuy, Carabobo, Cojedes and Guarico. This quarantine, implies restriction of movement of solidungulates within and outside states.

  2. Equine vaccination. Since the beginning of the epizootic, a number of 163,214 equine (horse, mules and donkeys) have been vaccinated which represent 69.3% of the population in affected states and a total of 206,208 equine in the country (27.4%) (6) (8).

  3. Spraying insecticides for vector control.

  4. Medical care to human febrile cases. Treatment has been symptomatic. Those patients presenting nervous signs are being hospitalized.

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VEE in Colombia

During the first week of September, rural health services of the localities of Mayapo, Manaure and El Pajaro in the department of La Guajira reported an increased number of patients having fever, headaches, muscle pain, prostration and vomiting. Few patients developed convulsions and other neurologic symptoms.

The disease spread to the southwest following particularly the Caribbean Sea seashore and bordering localities with Venezuela. A natural barrier, the Sierra Nevada of Santa Marta prevents a direct southern spread and helped in establishing preventive immune equine barriers through vaccination along these only passways to the departments of Magdalena and El Cesar. Sick and dead equine cases were preceding the epidemic of febrile human cases.

From the beginning of the epizootic epidemic to October 31 the disease was confined to the department of La Guajira, except by the occurrence of a recent outbreak in equine in the northern locality of Guachaca in department of Magdalena. (2) (9).

To October 31 a total of 14,156 human cases compatible with VEE were reported. From that number, 1,258 required hospitalization and 26 were reported dead as a result of VEE. (Table 3). (10) (11).

Based on random survey in the hospitals of Manaure, Riohacha, Uribia and Maicao, it was observed that all age groups were equally affected. The case fatality rate was estimated as 0.7% and only 4% of the acute illness patients developed neurologic symptoms, primarily among children. (9) (19)

Table 3
Cases Reported in La Guajira, Colombia* 1995

Date of First
Number of
Total Suspected
Number of
Sept. 12
Sept. 15
Sept. 10
Sept. 14
Total 28,142 14,156 1,258 26

* Data up to Octobre 31, 1996

The Control Measures Taken in Colombia

Consisted on:

  1. Emergence medical care to ill to avoid deaths, was developed, mobilizing medical doctors, nurses and Red Cross volunteers to reinforce local health personnel. Symptomatic treatment was undertaken and patient having neurologic signs were hospitalized.

  2. Restriction of movement from and within the department, of La Guajira. Equine concentrations, as commercial, exhibitions and sports were restrained in the rest of the country.

  3. Equine vaccination. National authorities, reported vaccination of 29,700 horses, mules and donkeys in La Guajira, representing almost the totality of the population (96.0%). Authorities proceeded with the equine vaccination in the entire country, reporting a total of 860,000 vaccinations, covering 59.6% of the total equine population of the country. (3) (17)

  4. Vector control. Entomologic surveys in affected areas detected large numbers of Aedes taeniorhynchus, Psorophora confinnis and Deinoceritis sp. Campaigns to eradicate mosquito vector consisted in spraying with malathion and larvicide treatment of breeding sites. (2) (11)

  5. Public awareness through massive media, was undertaken

  6. Epidemiological surveillance of human and equine was reestablished for the affected Department and the rest of the Colombian territory through a daily report of human and equine cases having signs consistent to equine encephalitides.

Associated Factors for the 1995 VEE Outbreak Occurrence

The 1995 VEE outbreak in Colombia and Venezuela was the result of several associated factors that act interdependently.

  1. Diminished equine vaccination. Information obtained in the affected areas of La Guajira showed that no vaccination was made in a period of three years in most places. While in Venezuela, vaccination coverage was very low in some states, like in Guarico where out of an equine population of 94,000 only 3% were vaccinated (8) (17).

  2. Lack of sustained epidemiological surveillance. As it was mentioned in the background of this paper, the epidemiological surveillance almost disappeared from the countries. The laboratory diagnostic services were limited and practically absent in Colombia. This situation contributed to discourage the field services in sending samples for laboratory analysis.(17).

    The poor intersectoral coordination of the health and Veterinary services finally outbursted when restructuring the official diseases surveillance and control services, in the countries. The information was unnotified among the national and local institutions, preventing the adoption of appropriate prevention and control measures.

  3. Limited knowledge on the ecology of equine encephalitides. This epizootic - epidemic like others in the past were associated with heavy rains and flooding, favoring reproduction of a wide variety of arthropods insects, particularly mosquitos, vector of diseases. Psorophora sp and Aedes taeniorhynchus were found abundant in Colombia and VEE virus was isolated from pools of there vectors (21) (10).

    Mosquito population not only might increase under favorable climatic conditions, but also they might be displaced by air currents, flooding and other environmental phenomena. Diseases also are displaced with them.

    Additionally, other mosquitos have been recognized as transmitters for VEE virus in Colombia and Venezuela, establishing a wide variety of vectors, that probably are using equal variety of vertebrate hosts for their intrinsic viral cycles.

    Since the largest epizootic-epidemic of 1969-1973 no other major outbreaks had been recognized in the area of Zulia, Venezuela and La Guajira, Colombia, suggesting that the main epizootic viral strains (subtype A, B, C) were almost extinct. However, the outbreak that occurred in Trujillo in 1993, that was caused by the enzootic VEE virus ID showed serological relation to virus IC and some genomic homogeneity (14). These findings might be indicative of mutagenic activity in local viruses resulting also in modifications of their pathogenic behaviors. (14) (18).

    However, the recent VEE subtype IC virus strain isolated during this outbreak has similarities with the past IC isolated in 1963. (23)

    The VEE virus has been isolated from rodents considering as reservoirs of the disease in wildlife, particularly because of their short life and high reproduction capacity might perpetuate the virus in a susceptible population, which is constantly renewed. Population reservoirs, particularly rodents which are able to maintain an enzootic cycle of the VEE virus suffer changes as well in population numbers, diseases resistance or susceptibility and population displacements.

  4. Increased viral activity was advertised through minor outbreaks occurring in same districts, as it was reported to PANAFTOSA, since 1993. (13)

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Bibliographic References

  1. Acha P., Szyfres B. Zoonosis and Communicable Diseases Common to Man and Animals. PAHO Scientific Publication No. 503 2nd ed. 1987

  2. CDC. Venezuelan Equine Encephalitis - Colombia, 1995. In: Morbidity and Mortality Weekly Report (MMWR). Vol. 44/Nº 39, Oct. 1995.

  3. Cardenas, J. Situación de encefalitis equina venezolana en Colombia. Vacunación equina. División Nacional de Sanidad Animal, Instituto Colombiano Agropecuario (ICA), Bogotá, Colombia. Comunicación Personal 1995.

  4. Instituto Nacional de Higiene, "Rafael Rangel". Informe sobre el brote de encefalomielitis equina venezolana en el Estado de Trujillo 1993.

  5. Ministerio de Agricultura y Cría. Dirección de Sanidad Animal. Situación de encefalitis equina en Venezuela. Informe oficial. 1993.

  6. Ministerio de Salubridad y Asistencia Social - Ministerio de Agricultura y Cría. Reporte epidemiológico semanal para el nivel gerencial. Encefalitis Equina Venezolana. En Alerta. Semana No. 41, Caracas, Venezuela 1995.

  7. Ministerio de Salubridad y Asistencia Social - Ministerio de Agricultura y Cría. Reporte epidemiológico semanal para el nivel gerencial. Encefalitis Equina Venezolana. En Alerta. Semana Nº 39, Caracas, Venezuela 1995.

  8. Ministerio de Salubridad y Asistencia Social de Venezuela: Situación epidemiológica de EEV. Boletín Epidemiológico Semanal Nº 43, Caracas, Venezuela. Nov. 6, 1995.

  9. Ministerio de Salud de Colombia. Situación de Encefalitis Equina Venezolana. Informe hasta 31 octubre, 1995. Fax OPS/OMS, Nov. 6, 1995.

  10. Ministerio de Salud de Colombia. Encefalitis Equina Venezolana (EEV) en la Guajira. Colombia, Septiembre 1995 IQCB Nº 3, Vol. 1, Sept. 30, 1995.

  11. Ministerio de Salud de Colombia. Actualización sobre la epizoodemia de encefalitis equina venezolana. IQCB Nº 4, Vol. 1, Oct. 15, 1995.

  12. PAHO/WHO. Situación of Equine Encephalitides in The Americas, 1989-1994, IX Inter-American Meeting, at the Ministerial Level, on Animal Health (IX RIMSA), Washington, D.C. April 25-27, 1995.

  13. PANAFTOSA. Informe epidemiológico sobre encefalitis equinas, 1989-1994.

  14. Rico-Hesse, R; Weaver, S.L.; de Siger, J.; Medina, G.; Salas, R.A. Emergence of a new epidemic/epizootic venezuelan equine encephalitis virus in South America. Pro. Nat. Acad. Sc. USA. 92 p, 1995.

  15. Rivera, E.; Ruiz, L; Mosquera, O; Rumbos, A.T.; De Vásquez, H.; Rangel, R. Informe técnico sobre las acciones realizadas para impedir la propagación del brote de encefalitis equina venezolana al Estado de Lara, proveniente de las Entidades Falcón y Yaracuy. Barquisimeto, Venezuela, Sept. 4, 1995.

  16. Ruíz, A. Situation of Equine Encephalitides in the Americas, 1989-1993. VIII Inter-American Meeting, at the Ministerial Level, on Animal Health (VIII RIMSA), Washington, DC, 27-29 abril 1993.

  17. Ruíz, A. Informe de viaje a Colombia. Septiembre 29-Octubre 10, 1995. Documento oficial, Organización Panamericana de la Salud, 1995.

  18. Salas Mora, R.A. Monitoreo de la circulación de cepas enzoóticas del virus de la EEV. Propuesta de investigación. Instituto Nacional de Higiene "Rafael Rangel", Caracas, Venezuela 1994.

  19. San Martin, C.; MacKenzie, R. B.; Trapido, H; et al: Equine Encephalitis in Colombia 1967. Bol. Ofic. Sanitaria Panamericana. 74, 1973.

  20. Sanmartin, C. Encefalitis Equina Americana por virus transmitida por antrópodos. Material informativo para capacitación sobre vigilancia de las encefalitis equinas. ICA, Colombia, 1992.

  21. Sanmartin, C. Informe Final de la consultoría para la instrumentación del diagnóstico serológico en las encefalitis equinas en Colombia. OPS/OMS, 1992.

  22. Smith, J.; Ludwig, G..; Roberts, B. Isolates obtained for the VEE outbreak in Colombia, USAMRIID. Personal communication. 1995.

  23. Smith , J., et al: Genetic relatedness of VEE isolates from the recent outbreak of VEE in Colombia. USAMRIID. Personal communication. 1995.

  24. Weaver, S.G.; Bellew, L. A and Rico-Hesse, R. Phyhogenetic analysis of alphaviruses in the VEE complex and identification of the source of epizootic viruses. Virology 191, 282-290, 1992.

Source: Division of Disease Prevention and Control, Veterinary Public Health Program, HCP/HCV, PAHO.

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