The Praedico has issued a Translocation Advisory for an epizootic of Venezuelan Equine Encephalitis in Panama. Detailed report may be found here.
While the
world was busy dealing with the spread of pH1N1 in 2009, Mother Nature did not
sleep. We handled several events
that could have posed an additional unwanted distraction to the global public
health community in the midst of pandemic response. Below is one example.
Introduction:
Venezuelan Equine Encephalitis
Venezuelan Equine
Encephalitis (VEE) is a zoonotic,
mosquito-borne, aerosol-transmitted viral disease affecting humans and equines,
the latter of which serve as amplifying hosts. The VEE virus is an RNA
virus in the genus Alphavirus of the
family Togaviridae, and is serologically classified into six antigenic subtypes
(I–VI) and five antigenic variants (types AB-F).1 Subtypes IAB and IC are the only ones
associated with significant human and equine epidemics. VEE is considered
endemic to many areas of Central and South America. 1,2
Epidemics of VEE have occurred periodically in humans and
equines in Latin America since the early 1920s. The largest documented epidemic
began in Colombia in 1967 and spread by land to Ecuador and Venezuela, then
moved northward through Central America and Mexico until it reached Texas in
1971. It is believed aggressive
mosquito control and vaccination prevented the virus from spreading further
into the United States. The
epidemic involved close to 231,000 human cases in Colombia and Ecuador alone,
with at least 310 deaths documented in the latter country.2,3 Although epidemic VEE has not been
diagnosed in the United States since its last appearance in 1971, there remains
concern that VEE could be used effectively as a bioterrorism agent.4-6
The 1995
Epidemic of Venezuelan Equine Encephalitis
In 1995,
an epidemic of Venezuelan equine encephalitis (VEE) occurred in South America,
resulting in 75,000 to 100,000 human cases of the disease and more than 300
deaths in Venezuela and Colombia.7,8 The actual number of human cases is
unknown because of poor reporting from indigenous groups located in the Guajira
peninsula shared by Venezuela and Colombia. 1,5 Likewise, equine deaths due to the
disease were reportedly significant, but reliable estimates of the number of
horses affected are unavailable. 7
In April 1995, the epidemic began in equines in Falcón
state, located along the northern coastline of Venezuela. By the end of July, human transmission
had been documented, with cases detected south and west of Falcón in the states
of Lara, Carabobo, Yaracuy, and Zulia. By August, the epidemic had already
spread to the Guajira peninsula in the far west of Venezuela on the border with
Colombia. Through the end of 1995, scattered cases continued to appear in the
southern and western Venezuelan states of Trujillo, Portuguesa, Cojedes, and
Guarico. 7 The epidemic
in Venezuela is estimated to have spread at a rate of 5 km per day, ultimately
covering a geographic area of approximately 200,000 km2. 7-9
Overall, the state of Zulia was hardest hit, with
approximately 10,000 human cases, 101 of which were confirmed by virus
isolation. 2,7 At the
time of the epidemic, emergency control measures, including restriction of
equine movement, equine vaccination, and insecticide fumigation, were enacted
to stop the spread. 4,9-11
Coincidentally, analysis of satellite imagery indicated
enviro-climatic conditions had declined during this time as well, which was the
beginning of the dry season. It is
believed the geography of the area contributed to inhibiting spread of the
virus, where the Cordillera de Mérida mountain range with peaks as high as
16,342 feet formed a perimeter around the epidemic zone. Most of the range is above treeline. The snow season of this mountain range
coincided with the peak of the epidemic in July-August. Where the last stand of epidemic
containment occurred, the Guajira peninsula, the Montes de Oca and Serrania del
Perija mountain ranges form a valley with the Sierra Nevada de Santa Marta
mountain range on the Venezuelan border.
This could have served as a “funnel”, channeling the epidemic deep into
the heart of Colombia, where potentially millions could have been infected.
Although the origin of this particular epidemic has yet to
be determined, several theories were proposed to explain the periodic emergence
of VEE: (1) evolution of epidemic strains from enzootic progenitors, (2)
circulation of epidemic viruses as subpopulations within enzootic strains, (3)
continuous circulation of epidemic viruses in cryptic cycles, (4) reemergence
of epidemic strains from latent infections, and (5) reemergence of epidemic
strains from incompletely inactivated vaccines. Additionally, there were speculation at the time that the
1995 epidemic was caused by an accidentally released laboratory strain. 1
Several key conditions in Venezuela contributed to the 1995
epidemic, including diminished equine vaccination coverage, lack of
surveillance, limited knowledge of equine encephalitis, and increased viral
activity following smaller VEE epidemics in Trujillo and Zulia in 1993. 2,3,12
Furthermore, unusually heavy rainfall was noted in both Venezuela and
Colombia, the highest in 18 years. The heavy precipitation, coinciding with the
apparent 15- to 20-year periodicity of major VEE epidemics in Venezuela and
Colombia, appears to have favored an overproliferation of Aedes taeniorhynchus, Psorophora confinnis, and Anopheles aquasalis vector mosquitoes by enhancing their breeding
sites. 7-11,13,14
In 1995, the total annual number of inbound
passengers from Venezuela to the United States was 749,274, a 100 percent
increase over the number in 1990.
A seasonal peak of inbound air traffic was observed in August 1995. This seasonality was noted for 1990 to
2003, inclusive, as well. 15
Caracas was the main source of traffic to the United States
in 1995 (641,975 annual inbound passengers), followed by Maracaibo (81,923) and
Porlamar (16,938). Of particular note, Maracaibo was proximal to the epicenter
of the 1995 epidemic and was a potential source of disease translocation to the
United States. In addition, although international statistics identify Caracas
as the main traffic source, the data fail to account for passengers who
traveled to Caracas from other areas of Venezuela, then continued abroad. The
top destinations in the United States were Miami, New York City, and Puerto
Rico, with 572,380, 114,896, and 49,698 annual inbound passengers received from
Caracas, respectively.
These statistics suggest that the United States was
vulnerable to the translocation of a serious pathogen in 1995, much as New York
City was vulnerable to West Nile virus in 1999. However, no signs of such
translocation were reported. A
variety of factors may account for this circumstance. First, it is possible that the pathogen never arrived,
because no infected mosquito, equine, or human being was ever transported to
the United States. Second, it is possible
the pathogen was transported to the United States, but did not cause VEE,
because the number of horses infected was insufficient to sustain an epidemic,
because an infected human who did come to the United States was never bitten by
a transmission-competent mosquito. Third, it is possible that the pathogen was transported to
the United States and did cause VEE, but there were no syndromic surveillance
systems in 1995 that could detect it.
We had no indication if or when Miami Dade county or the Florida State
Epidemiologist were aware of the events in Venezuela. Regardless, it is our conclusion that the United States was
fortunate to have escaped an introduction of this virus.
It remains our assessment that as far as the United States
and Canada are concerned, VEE represents another potential next-West Nile virus
translocation threat. The concern
is not just whether the virus is capable of translocating and triggering an
epizootic in the receiving localities, but also may gain ecological establishment. We are fortunate an equine vaccine
exists to assist in epizootic control should this occur.
Outbreak
of Equine Encephalitis in Colombia (2009)
On June 8, 2009, we reported implementation of
countermeasures for equine encephalitis in Río Viejo, Bolívar State,
Colombia. These countermeasures
were implemented on June 5th; it was unknown precisely how long the
outbreak had been present. Sources noted health officials were involved in
addition to veterinarians.
Countermeasures reportedly included fumigation efforts, a vaccination
campaign, distribution of mosquito nets, and an education campaign directed for
people who lived near the farms where positive test samples were identified.
The vaccination campaign was specifically targeted towards the local
horse, mule, and donkey population.
The exact type of equine encephalitis was not specified,
although a 2001 epidemiological bulletin by the Colombian Ministry of Health
noted that outbreaks of VEE occurred in Colombia in 1995, 1998, and 2001.
Colombian agricultural officials had an established routine cycle of VEE
vaccinations for the local equine population that occurred every two years
during the months of July and August. The Colombian government in May
2007 noted four cases of equine encephalitis in Bolívar State were recorded in
2006 and indicated Río Viejo was one of the municipalities most affected by
vector transmitted encephalitis in Bolívar State. The diagnostic etiology
of equine encephalitis recorded in Bolívar State in 2006 was not specified.
Outbreak
of Equine Encephalitis in Belize (2009)
We reported on 3 September the Belize Ministry of Health had
increased vector control activities in Belize, Cayo, and Stann Creek districts
due to Venezuelan equine encephalomyelitis (VEE) activity on 31 August. The sources reported a
"surge" of VEE activity specifically in the Cayo District between
July and August 2009. Four
villages in the Cayo District reported cases of equine VEE, although exact
locations and case counts were not specified. Countermeasures were implemented quickly: 224 horses in Cayo
District have been vaccinated along with 19 horses in Belize District and 19
horses in Stann Creek District.
Response efforts also included animal movement control and "control
of wildlife reservoirs."
According to a Veterinary Officer of the Belize Agricultural
Health Authority, there were "a few" cases of equine
encephalomyelitis in Belize every year, although information regarding the
current incident was released due to an increase in the number of identified
cases. In addition to an above
normal number of cases, the sources note that the current distribution of cases
is also greater than normal. Sources reported one isolated case was identified
in Belize District in January 2009, while another isolated case was identified
in Stann Creek District in April 2009.
The National Veterinary Services Laboratory, a reference laboratory for
the World Organization of Animal Health (OIE), had confirmed an unspecified
number of cases in Belize, Cayo, and Stann Creek districts.
Additional reporting by the Belize Ministry of Agriculture
and Fisheries recommended that all horse owners in Belize vaccinate their
horses against equine encephalomyelitis.
The source reported that the United States Department of Agriculture,
National Veterinary Services Laboratory had confirmed that both VEE and Eastern
equine encephalomyelitis viruses were currently circulating in Belize. The report specifically cited outbreaks
in the Belize, Stann Creek, and Cayo Districts, although the number of cases is
not reported. The source noted
that additional cases were expected due to the current rainy season in Belize
occurred between June and November.
The Belize Agricultural Health Authority had previously identified
outbreaks of equine encephalomyelitis in 2007 and 2005, although specific
information regarding the prior outbreaks was not reported. The OIE had also previously reported an
outbreak of Eastern equine encephalomyelitis between October and November 2005
that infected one horse in Teakettle, Cayo District.
On 16 September the Quintana Roo State Committee of Animal
Health across the border in Mexico went on alert due to the situation in
Belize. Officials moved to
implement preventive countermeasures to prevent the introduction of equine
encephalitis to the state. Sources
at the time noted no cases of equine encephalitis had been detected on the
Mexican side of the border. Response
measures included increased surveillance efforts along the border with Belize
and the implementation of "health cordons." Sources indicated that health documents were required to
enter Mexico, although it was unclear if this measure applied to horses,
humans, or both.
Outbreak
of VEE in Costa Rica (2009)
On 3 September, we reported the Director General of the
Costa Rican Ministry of Agriculture and Livestock, National Animal Health
Service, had confirmed five equine cases of Venezuelan equine encephalomyelitis
(VEE) on a farm in Liberia, Liberia County, Guanacaste Province, including one
fatal case on 31 August. According to the sources, a total of nine susceptible
horses were located at the farm, although only five confirmed cases were
reported. The first confirmation
of the Liberia event was received on 25 August, although the start date of the
event was reported as 28 July 2009.
The diagnostic test results were received from the Laboratory of
Virology at the Veterinary School of the National University in Costa Rica. The sources did not report the strain
of VEE involved in the incident. In response to the cases, health officials had
implemented quarantine efforts, movement control measures, vector control
measures, and vaccination measures.
A total of 150 horses have been vaccinated in Guanacaste Province in
response to current VEE activity in Guanacaste Province. Information regarding
the cases was reported in conjunction with information on three additional
equine VEE cases at two additional locations. The additional cases were identified in Capulín (2), and
Rodeíto (1), both in Liberia County.
VEE Threat
Assessment Process
We were concerned about several factors:
1. Connectivity
to the US by direct, non-stop air traffic:
-Multiple cities in Colombia are connected to the US by
direct, non-stop air traffic: Barranquilla, Bogota, Cali, Cartagena, Medellin,
and Pereira. These US cities are
the recipients of this traffic: Atlanta, Fort Lauderdale, Houston, Los Angeles,
Miami, New York, and Newark. Key
traffic nodes are Bogota and Miami in terms of number of unique connections.
-Belize and neighboring Quintana Roo State, Mexico are major
international tourism sites. Atlanta,
Dallas/Ft. Worth, Charlotte, Houston, and Miami are all connected to Belize
City by direct, non-stop air traffic.
-San Jose, Costa Rica is connected to Charlotte, Los
Angeles, Phoenix, Newark, Dallas/Ft. Worth, New York, Atlanta, Houston, and
Miami. Liberia, Costa Rica (where
VEE was confirmed) is connected to Dallas/Ft. Worth, Atlanta, Houston, and
Miami.
2. Endemic
mosquito transmission competency at the potential receiving sites. Particularly in the state of Florida
and coastal Texas (Houston, Galveston, Corpus Christi and points south), VEE
transmission competent mosquitoes are present.
3. Presence of
equine populations at the potential receiving sites.
4.
Environmental synchronization of the recipient sites. Transmission of VEE is a
temperature-dependent process, and the temperature profiles of many of the
receiving cities were optimizing or fully optimized for transmission.
5. Unsensitized
public health and medical community.
By “unsensitized”, we were aware the majority of the US public health
and medical establishment were primarily sensitized to pH1N1, not other exotic
biological threats. Further, we
were well aware (as evidenced by the pandemic warning experience) that the
tactical warning process was flawed- we believed it a challenge to fully
sensitize Florida in particular if the need presented it. It was reassuring to see Miami/Dade
County did have VEE on its notifiable disease list, however it is highly
debatable if the medical community would be sensitive to report pediatric viral
encephalitis without a prior sensitization step provided through an
advisory. More likely to get such
reporting from equine veterinarians at the race tracks.
We notified CDC, PAHO, and OIE of these events, as well as
other NGO ground partners in Colombia, Belize, and Mexico in an effort to
sensitize the community to be watchful for indications of an expanding epizootic. This notification was a “for your
information” as opposed to a full warning. We believed it probable the involved strain of VEE was
enzootic- specifically serotype IE- and not epizootic, and equine herd immunity
in Colombia was likely high enough to inhibit transmission, especially if
additional vaccinations, mosquito control, and heightened surveillance were
occurring. Evidence of an
expanding epizootic (i.e. loss of containment) that included human infections
would have prompted more aggressive steps in the warning process. It is fortunate these indicators were
not observed. We were sensitive to
the profound crisis fatigue already seen in the public health and medical
community and did not believe it prudent to add unnecessary stress.
As a final key point, no laboratory test results were disclosed
regarding the serotypes in any of these events. Current reporting requirements to OIE should be expanded to
include serotype analysis of VEE to assist in time-sensitive threat
assessments.
1.
Brault AC, Powers AM, Medina G, Wang E, Kang W, Salas
RA, De Siger J, Weaver SC. “Potential sources of the 1995 Venezuelan equine
encephalitis subtype IC epidemic.” Journal of Virology, July 2001. Vol. 75, No. 13, 5823-5832.
2. Ruiz A. “Brote de encefalitis equina.” Revista
Panamericana de Salud Publica,
January 1997. Vol. 1, No. 1, 78-83.
3. Pan
American Health Organization. “Outbreak of Venezuelan equine encephalitis,
1995.” Epidemiological Bulletin,
December 1995. Vol. 16, No. 4.
4. Weaver SC, Ferro C, Barrera R, Boshell J, Navarro JC.
“Venezuelan equine encephalitis.” Annu Rev Entomol, 2004. Vol. 49,
141-174.
5. Hawley RJ,
Eitzen EM Jr. “Biological weapons—a primer for microbiologists.” Annual
Review of Microbiology, 2001. Vol. 55, 235-253.
6. Bronze MS, Huycke MM, Machado LJ, Voskuhl GW, Greenfield RA. “Viral
agents as biological weapons and agents of bioterrorism.” American Journal of the Medical Sciences, June 2002. Vol. 323, No.
6, 316-325.
7. Weaver SC,
Salas R, Rico-Hesse R, Ludwig GV, Oberste MD, et al. “Re-emergence of epidemic
Venezuelan equine encephalomyelitis in South America.” VEE Study Group. Lancet, 1996. Vol. 348, 436-440.
8. Rivas F, Diaz LA, Cardenas VM, Daza E, Bruzon L,
Alcala A, De la Hoz O, Caceres FM, Aristizabal G, Martinez JW, Revelo D, De la
Hoz F, Boshell J, Camacho T, Calderon L, Olano VA, Villarreal LI, Roselli D,
Alvarez G, Ludwig G, Tsai T. “Epidemia equine encephalitis in La Guajira,
Colombia, 1995.” Journal of
Infectious Diseases, April 1997. Vol. 175, No. 4, 828-832.
9. CDC. “Venezuelan equine
encephalitis: Colombia, 1995.” Morbidity and Mortality Weekly Report (MMWR), October 20, 1995. Vol. 44, No.
41.
10. CDC. “Venezuelan equine
encephalitis: Colombia, 1995.” Morbidity and Mortality Weekly Report (MMWR), October 6, 1995. Vol. 44, No. 39.
11. WHO/PAHO.
“Outbreak of Venezuelan equine encephalitis in Colombia and Venezuela.” Weekly Epidemiological Record, October
6, 1995. 40.
12. Rico-Hesse R, Weaver SC, de
Siger J, Medina G, Salas RA. “Emergence of a new
epidemic/epidemic encephalitis virus in South America.” Proceedings of the National
Academy of Sciences, June 6, 1995. Vol. 92, No. 12, 5278-5281.
13. Turell MJ.
“Vector competence of three Venezuelan mosquitoes (Diptera: Culicidae) for an
epidemic IC strain of Venezuelan equine encephalitis virus.” Journal of Medical Entomology, July
1999. Vol. 36, No. 4, 407-409.
14. Wilson JM,
Tucker CJ. “Use of remote sensing in epidemic surveillance and response.” World Meteorological Organization Bulletin.
2002. Vol. 51, No. 2, 136-139.
15.
DOT. “Bureau of Transportation
Statistics, Intermodal Transportation Database [online].” Available at http://www.transtats.bts.gov/ [accessed April 26,
2005]
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