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Updated: Jun 2, 2026

12:48
Blood Collection from the American Horseshoe Crab, Limulus Polyphemus
Published on: October 13, 2008
The crab hole mosquito blues.
Karl M Johnson1, Douglas F Antczak, William H Dietz
1Cornell University, Ithaca, New York, USA.
Emerging Infectious Diseases
|May 3, 2011
Summary
Venezuelan equine encephalomyelitis (VEE) viruses have a long history of outbreaks in South America. A 1969 movement of VEE virus to Central America and beyond impacted equids and humans.
Area of Science:
- Veterinary Virology
- Epidemiology
- Molecular Biology
Background:
- Venezuelan equine encephalomyelitis (VEE) has caused recurrent epizootics in South America since the 1920s.
- VEE virus was first isolated in 1937, distinguishing it from North American equine encephalomyelitis viruses.
- Distinct epizootic and sylvatic strains of VEE virus were identified in different ecosystems.
Observation:
- Epizootic VEE virus strains were classified as subtype I (variants A/B, C).
- Sylvatic (enzootic) VEE virus strains were classified as subtype I (variants D, E, F) and subtypes II, III, IV.
- In 1969, VEE variant I-A/B spread from South America to Central America, affecting multiple countries.
Findings:
- The 1969 VEE outbreak represented an unprecedented geographic expansion of the virus.
- This epizootic event involved the movement of VEE virus from South America to Central America and into Mexico and the United States.
- The VEE outbreak continued to affect equids and humans until 1972.
Implications:
- Understanding VEE virus ecology and strain diversity is crucial for predicting and controlling future outbreaks.
- The 1969 event highlights the potential for rapid, long-range dissemination of VEE virus.
- Effective surveillance and response strategies are necessary to mitigate the impact of VEE on animal and human health.
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