To assess the impact of
continuing circulation of VEE virus (VEEV) on human and animal populations,
serologic and viral isolation studies were conducted in 2000 to 2001
in Chiapas State.
Human serosurveys and risk analyses indicated that
long-term endemic transmission of VEEV occurred among villages with
seroprevalence levels of 18% to 75% and that medical personnel had a
high risk for VEEV exposure.
Seroprevalence in wild animals suggested
cotton rats as possible reservoir hosts in the region.
Virus isolations
from sentinel animals and genetic characterizations of these strains
indicated continuing circulation of a subtype IE genotype, which was
isolated from equines during the recent VEE outbreaks.
These data indicate
long-term enzootic and endemic VEEV circulation in the region and continued
risk for disease in equines and humans
Venezuelan equine encephalitis (VEE) epidemics or epizootics involving
hundreds of thousands of equine and human cases have occurred in the Americas
since the 1930s ( 1,2 ).
In Mexico, human VEE was first
recognized during the 1960s along the Atlantic coast ( 3?5 ).
In 1962, a total of 13 human cases were detected by serologic testing
in Campeche and Champoton, state of Campeche ( 3,6 ); 5
deaths occurred (38% case-fatality rate), and 3 patients exhibited neurologic
disease ( 3 ).
A more extensive serosurvey in 1962?1964
in four southeastern states found 23 of 770 serum specimens had antibodies
against VEE virus (VEEV; Togaviridae: Alphavirus) ( 4 ).
Although clinical cases were not detected during that study, the findings
implied extensive VEEV circulation.
During 1963, VEEV subtype IE was recovered
from a sentinel hamster and mosquitoes collected in southeastern Veracruz
State ( 7 ).
In 1965, a fatal human case occurred in the
village of Jaltipan, Veracruz State ( 5 ).
Almost simultaneously,
equine epizootics were reported in 1966 in Tamaulipas State and in northern
Veracruz State ( 8 ).
Although no virus isolations were
made, a VEEV etiology was suggested by serosurveys
In 1969?1972, a major VEE outbreak began on the Guatemala-El Salvador
border soon after an epizootic occurred in Ecuador and Peru.
The Central
American outbreak affected tens of thousands of equines and humans as
it spread northward into Mexico.
The first equine deaths were reported
in 1969 in mountainous areas in La Trinitaria and La Concordia, Chiapas
State, close to the Guatemalan border ( 8 ).
By 1970, the
epidemic and epizootic had caused 10,000 equine deaths and many unconfirmed
human cases in the states of Chiapas and Oaxaca.
By the end of 1972, nearly
50,000 equine deaths and 93 confirmed human deaths, as well as several
hundred nonfatal human cases, had occurred in Mexico ( 9,10 ).
The epidemic and epizootic eventually reached southern Texas, where ≈1,500
horses died and several hundred human cases occurred ( 11 ).
This epizoodemic was caused by a subtype IAB strain and may have been
halted in Texas by equine vaccination, insecticide spraying ( 12 ),
and possibly by preexisting natural immunity to other alphaviruses in
the equine population ( 13 ).
Between 1973 and 1992, no
VEE outbreaks were reported anywhere, prompting speculation that epizootic
strains of VEEV had become extinct ( 12 ).
However, reemerging
VEEV activity in the early and mid-1990s in Venezuela and Colombia ( 13,14 )
and on the Pacific coast of southern Mexico ( 15 ) underscores
the continued threat of VEE in the Americas
Two equine epizootics occurred on the Pacific coast of Mexico in 1993
and 1996.
In the summer of 1993 in coastal areas of Chiapas State, an
outbreak affecting125 horses, with 63 deaths, was documented.
Three years
later, during the summer of 1996 in the adjacent State of Oaxaca, another
equine epizootic involved 32 horses with 12 deaths ( 15 ).
Both outbreaks were caused by a subtype IE VEEV strain.
However, no human
cases were documented during either outbreak.
VEEV strains isolated from
encephalitic horses during 1993 and 1996 produced little evidence of viremia
in experimentally infected horses, although the strains had caused encephalitis
( 16 ).
Viremia titers were similar to those generated
by enzootic VEEV strains, which indicates that equines were probably not
important amplifying hosts during either Mexican epizootic
Isolation of VEEV Strains.
. Of a total of 14 hamsters exposed in La Encrucijada during July, 2001
(98 hamster-days), 10 became ill or died.
. Using a combination of human serosurveys, wild and domestic animal serosurveys,
and detection of virus circulation with sentinel hamsters, we obtained
evidence that VEEV circulated in the La Encrucijada area of coastal Chiapas
State for at least several decades before the 1993 epizootic and continues
to circulate in an undescribed transmission cycle.
Satellite imagery ( Figure
1 ) and visual inspections indicate that lowland tropical forest habitats
characteristic of VEEV enzootic foci, including of subtype IE viruses
in other areas of Mexico and the nearby Pacific coast of Guatemala ( 31,32 ),
have been almost completely destroyed for the purposes of cattle ranching
and other agricultural activities.
Mosquito collections in La Encrucijada
have indicated an extremely low abundance of Culex (Melanoconion)
taeniopus, the proven enzootic vector in a coastal Guatemalan subtype
IE VEEV focus ( 33 ).
This indicates that VEEV is likely
using a different mosquito species as its enzootic vector in coastal Chiapas
State.
Experimental studies indicate that adaptation of the Mexican VEEV
strains for efficient infection of Ochlerotatus taeniorhynchus
mosquitoes, through a mutation in the E2 envelope glycoprotein, may have
contributed to epizootic transmission ( 34 ).
. Seroprevalence in wild animals suggests a possible role for cotton rats
(S. hispidus), implicated previously as a VEEV reservoir host in
other parts of Mexico ( 28 ) and in Panama ( 35,36 ).
Although the number of animals tested was small, our data also suggest
a possible role for rice rats (Oryzomys alfaroi) and opossums (Didelphis
marsupialis and Philander opposum) as vertebrate reservoir
hosts required to maintain horizontal transmission or amplification hosts
involved in increased circulation, resulting in equine cases.
Other domestic
animals, including dogs, cattle, and birds, are also exposed to VEEV in
Chiapas State.
Previous experimental studies of dogs ( 37 )
and cattle ( 38 ) indicate that low levels of viremia
or none develops in those animals after VEEV infection and, therefore,
they are probably not important as enzootic hosts.
Larger sample sizes
and experimental infections to assess viremia levels are needed before
conclusions can be drawn regarding the relative importance of different
animals as reservoir or amplification hosts of VEEV in Mexico
The vertebrate amplification hosts responsible for increased circulation
of VEEV and its transmission to equines during 1993 and 1996 remain unidentified,
since equines inefficiently amplify the etiologic VEEV strains of the
subtype isolated during the outbreaks ( 16 ).
Human Risk and Disease.
Although our data indicate that persons are regularly infected with VEEV
in coastal Chiapas State, the effect of endemic transmission on human
health is unknown.
Most undifferentiated febrile illness in the region
is clinically diagnosed as dengue or flulike febrile illness, and currently
no diagnostic tools are in place to test for human VEEV infections.
We
identified the occupations of La Encrucijada inhabitants and the ecologic
habitats where they live and work as risk factors for VEEV infection.
We detected no risk differences between the sexes.
A possible explanation
is that, in this region, female homemakers often accompany male farm laborers
to sites where VEEV may circulate
Ecologic
studies of Venezuelan encephalitis virus in southeastern Mexico.
Viruses
of the Venezuelan equine encephalomyelitis complex.
Dengue and dengue hemorrhagic fever: its history and resurgence
as a global public health problem.
Dengue and
dengue hemorrhagic fever.