Rift Valley Fever
Rift Valley fever has long
been a devastating disease of ruminant livestock in Africa. It kills
livestock and induces abortion in pregnant ewes and cows. At the
time of such epidemics, a few cases of a nonlethal dengue-like illness
were observed in people who were exposed to the animals. In 1977
an epizootic occurred of large size in the Nile Valley which hundreds of
thousands of livestock cases and large numbers of f humans. The virus
was detected in eastern Africa in the late 1980's and caused hundreds of
human deaths.
Clinical Features
After a brief incubation period
of 2-6 days, fever, severe headache, retroorbital pain, photophobia,
and generalized myalgia begins. Patients tend to progress to
one of three final complications: mild encephalitis, retinitis, or
hemorrhagic fever.
Epidemiology
The natural vertebrate reservoir
of the the Rift Valley fever virus has not yet been precisely identified
but is suspected to be one or several wild ungulates. The virus remains
in a silent enzootic cycle for many years, and then, during a period of
heavy rainfall, it explodes in epizootics of great magnitude among sheep
and cattle. During such epizootics, the virus is transmitted by many
species of mosquitos and may also be transmitted by fomites, direct contact
and by arthropods. This epizootic cycle is closely tied to
the ecological niche of the Aedes mosquitos.. These mosquitoes
hatch from dormant eggs in dry depressions located in the grassy plateau
regions of sub-Saharan Africa with abundant rainfall and are infected
transovarily with the virus. The Aedes mosquitos thus being the epizootic
which is maintained by other species of mosquitos.
Control
Live attenuated and formalin
inactivated Rift Valley fever vaccines are available for livestock immunization.
Due to the large number of livestock, however, prevention of outbreaks
is unrealistic. No human vaccine is available. In the future
policing the international la movement of livestock may help to prevent
the spread of the disease. During an outbreak, mosquito control and
implementation of safer animal handling practices could help to decrease
the outbreak.
Sandfly Fever
Description of an acute illness
that is probably a representation of phlebotomus fever date back to the
time of the Napoleonic wars. Interest peaked in the phlebotomus fever
during World War II due to the occurrence of epidemics among the Allied
troops. Sandfly fever viruses continue to cause human infections
in North Africa and southwest Asia.
Clinical Features
Sandfly fever is a
common but nonlethal disease. The Human disease is a self limiting dengue-like
syndrome marked by fever, headache, myalgia, retroorbital pain, conjunctivitis,
and leukopenia.
Epidemiology
Concentrated
in the countries around the Mediterranean Sea and eastward to central Asia
and India, Sandfly fever is transmitted to humans by peridomestic sandflies.
A second focus of the disease occurs in Central and South America where
the virus is similarly transmitted by phlebotomines. Gerbils and
forest rodents are suspected as the vertebrate host, but no host other
than man has been definitely incriminated yet. As a result of childhood
infection indigenous people are typically immune; however, travelers are
at risk.
California Encephalitis
The
California serogroup viruses are transmitted by mosquitos. Each virus
has a very narrow range of mosquito and mammalian hosts and a limited geographic
distribution. La Crosse virus,, Tahyna virus, and snowshoe hare virus
(an antigenic variant of the La Crosse virus) have been studied most studied.
La Crosse Virus
La Crosse virus was isolated
from a fatal case of encephalitis in La Crosse, Wisconsin in 1960.
La Crosse is the primary cause of human encephalitis due to California
serogroup virus infection. The virus is endemic and associated with
about 100 cases of encephalitis annually, but surveys indicate that
about 300,000 human infections occur annually throughout the Midwest.
Clinical Disease
La Crosse virus produces a
classical acute encephalitis in children. The incubation period has
been estimated at about 7 days. The acute illness lasts around 10
days. The first symptoms of days 1-3 are nonspecific and are followed
by the appearance of signs and symptoms associated with the central
nervous system. These last around one week and include stiff neck,
lethargy, and seizures. The most significant sequelae of La Crosse
encephalitis are epilepsy and persistent paresis. Epilepsy occurs
in about 10% of children; persistent paresis occurs in 2%.
The mortality rate is about .3%.
Epidemiology
California encephalitis
is ironically concentrated geographically in the Midwest. Over 90%
of all cases in the US are reported from Minnesota, Wisconsin, Iowa, Illinois,
Indiana, and Ohio during the months of July, August, and September.
Individuals under the age of 20 are at greatest risk of exposure.
The principle vector, Aedes triseriatus, is a woodland mosquito
which needs tree holes for reproduction. The mosquito feeds primarily
on small woodland mammals which maintains the virus during the winter months.
Serological studies suggest that nearly 20% of Midwesterner are seropositive
to this virus by age 60 and that for every 1 reported case of La
Crosse infection in children under age 16,, there are more than 1000 unreported
cases.
Oropouche Fever
Oropouche virus, a
Bunyavirusgenus member, is responsible for repeated epidemics
in northern Brazil and northern South America.
Clinical Features
The disease is associated
with fever, headache, myalgia, arthralgia, and prostration, but no mortality.
Epidemiology
The virus is maintained
throughout its cycle with sloths, monkeys, jungle mosquitoes, humans, and
midges. The primary vector is a midge, Culicoides paraennsis.
Crimean-Congo Hemorrhagic
Fever
Recognized for many years in central Asia and
eastern Europe, Crimean hemorrhagic fever is a sever zoonotic disease which
affects people coming into contact with livestock or ticks. The range
of the CCHF virus is now known to extend from central Asia to India, Pakistan,
Afghanistan, Iran, Iraq, Persian Gulf countries, the Middle East, eastern
Europe, and to most of Saharan and sub-Saharan Africa.
Clinical Features
After an incubation period of approximately 3
to 6 days the abrupt onset of acute febrile illness occurs. The first
symptoms are similar to severe influenza and include fever, headache, severe
back and abdominal pain. The hemorrhagic fever manifestations
occur after several days of illnesses and include petechial rash, ecchymoses,
and bruises, hematemmesis, and melenna. Cases typically present with
some form of hepatitis. The mortality rate is 10--50% in different
outbreaks with deaths typically occurring during the second week of illness.
Epidemiology
The genus Hyalomma
of ixodid ticks is the most important vector of the CCHF virus. The
ticks work in a cycle involving transovarial/transtadial transmission of
the virus. Vertebrates including birds and small animals provide
excellent amplifier hosts of both the virus and the tick. The
virus can be transmitted to humans by direct contact with infected animals
(even subclinically infected animals) and from person to person.
CCHF is an increasing problem in the world with more cases being reported
every year and an increasing percentage of animals begin found seropositive.
Control
Tick control measure
need to be emphasized and utilized to prevent CCHF. This includes
spraying camp sites and, clothing, and danger areas with acaricides or
repellent. Strict isolation of patients with CCHF and a focus on
barrier nursing would help to prevent nosocomial spread. Presently
the vaccine is a dangerous mouse brain-derived version. Future development
of a vaccine would help to prevent human infection.
Sin Nombre Virus / Four Corner's Disease
The Sin Nombre virus was first recognized in 1993
when healthy young adults in the Four Corner's region of the United States
developed a severe pulmonary illness and died. A virus which causes
chronic infection in deer mice, SNV virus ranges throughout the North America
with a concentration west of the Mississippi River and south of central
Colorado. SNV typically infects people only after exposure to concentrated
fecal material from infected rodents and tends to occur during years of
high rain fall when local plants allow for rapid expansions of the rodent
population.
Clinical Features
The SNV, similar to the Prospect Hill virus, causes
hantaviral pulmonary syndrome. Beginning as a flue like illness that
includes fever myalgias, headaches, cough, and respiratory distress, HPS
is indistinguishable from HFRS in the first two days. With time the
respiratory symptoms progress towards respiratory failure and hemorrhagic
pneumonia resulting from interstitial fluids collecting in the lungs.
Other symptoms such nausea, vomiting, abdominal pain, headache, cough,
and dyspnea worsen. Hospitalization is typically required by day
4. Mortality due to HPS is 52% and death tends to occur during the
end of the first week of symptoms. Individuals who survive this critical
period recover without any sequelae.
Epidemiology
SNV infection affects humans when they come
into contact with rodent carriers of the virus or they inhale the aerosolized
particles of the rodent feces. This tends to occur either during
a year of high rodent population or as a result of a human entering an
area with a high concentration of rodents. The SNV outbreak in 1993
was associated with a year of high rainfall after years of drought which
resulted in a increase in the preferred food of the deer mouse, the piñon,
and an increase in the rodent population. According to local medicine
men, the oral tradition of the Navajo people suggests that this disease
occurred three time during the last century. Each of the reported
times correspond to a year of high rain fall and piñon bloom.
There is no evidence that human to human transmission occurred during this
time.
Control
Control of the SN virus is primarily achieved through
rodent population control with poison, cats, or traps. Periodic serological
testing of rodents determines the range of the virus and the number of
carriers in the rodent population. Preventative measures should be
taken by people who must work in an area of probable contamination.
During years of high rainfall, like this year of El Niño,
extra measures should be taken to control rodent populations around the
living area and to prevent exposure to rodent infested areas.
Viruses Causing HFRS: Hantaan, Puumala, Belgrade,
Seoul viruses.
During the Korean war, thousands of troops developed
a disease marked with fever, hemorrhagic complications, and acute renal
failure with shock. The mortality rate was 5-10%. The cause
of the disease remained a mystery until 1978 when a virus, Hantaan virus,
was isolated in Korea from a rodent and determined to be a bunyavirus.
After this time several other viruses associated with similar disease symptoms
and reservoir hosts were found in other areas throughout the world.
Clinical Features
Hemorrhagic Fever with Renal Syndrome (HFRS) is
a hemorrhagic fever associated with profound renal tubular involvement.
During the febrile phase lumbar abdominal pain and proteinuria are prominent.
Hemorrhage can occur in different places in different patients including
a petechial skin rash, massive gastrointestinal bleeding, or hemorrhagic
pneumonia. The Belgrade virus produces this severe syndrome in the
Balkans. Seoul virus tends to be more mild and cause more hepatic,
not renal, syndromes. Puumala virus is an even more mild virus of
Scandinavia and typically involves little hemorrhage and no shock.
Epidemiology
There are three distinct patterns of epidemiology
associated with the viruses causing HFRS: rural, urban, and laboratory-acquired.
The rural type is the most common. It is associated with the Hantaan
virus and field mouse Apodemus agrarius in China, Korea and Russia,
Hantaan and the field mouse Apodemus flavicollis in the Balkans,
Puumala virus and the bank vole Clethrionomys glareolus in Scandinavia.
All these species are field rodents and human infections tend to occur
in rural workers. The Seoul virus is most widespread among urban
rats Rattus norvegicus throughout the world. It is concentrated
at urban seaports and has been recognized as an occupational hazard for
animal caretakers and lab researchers.