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.
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.
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.
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.
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.
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.
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.
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.
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%.
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 virus, a Bunyavirusgenus member, is responsible for repeated epidemics in northern Brazil and northern South America.
The disease is associated with fever, headache, myalgia, arthralgia, and prostration, but no mortality.
The virus is maintained throughout its cycle with sloths, monkeys, jungle mosquitoes, humans, and midges. The primary vector is a midge, Culicoides paraennsis.
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.
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.
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.
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.
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.
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 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,
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.
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.
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.