LaWanda Morgan
WCH
Disease
Rift Valley Fever (RVF)
Causative Agents
The RVF virus causes Rift Valley fever. It is a member of the Bunyaviridae family, of the genus Phlebovirus. The virus is an enveloped, single-stranded RNA virus. Their size ranges from 80-120 nanometers (def).
Epidemiology
Visitors to some parts of Africa are exposed to Rift Valley Fever, a zoonotic (def) disease that primarily affects sheep and cattle. The domesticated animals that are most affected by this disease are camels, goat, sheep, and cattle. It is also known as Infectious Enzootic Hepatitis of Sheep and Cattle. Israel’s former Chief Veterinary Officer (1974-1999), Arnon Shimshony, DVM, states, “the disease was described in sheep since the beginning of the 20th century in the Rift Valley area of Kenya”. The actual name Rift Valley Fever was created in 1931 after a viral outbreak occurred amongst sheep on a farm in Kenya’s Rift Valley area.
Rift Valley fever is normally found in Africa’s southern and eastern regions (Madagascar), including sub-Saharan areas, and North Africa. Throughout the El Nino/Southern Oscillation (ENSO) (def) phenomenon, the greatest outbreaks of RVF take place in East Africa. This time of extreme amounts of rainfall, allow for the swift population increase as the infected mosquito eggs hatch when the rain levels their nesting areas. RVF Outbreaks are not frequent; they depend on the mosquito population, the number of pre-vaccinated livestock, and the blood handling practices of people around animals. Every five to fifteen years, in partially dry savannah grasslands, outbreaks of RVF will usually arise.
A drastic outbreak of the virus occurred in 1997-1998 in Somalia, Tanzania, and Kenya. In September of 2000, the first account of RVF outside of Africa was validated in Yemen and Saudi Arabia. According to the United Nations World Health Organization (WHO), as of March 31, 2010, there were 63 reported cases of RVF (two deaths) in South Africa, as established by Johannesburg’s National Institute of Communicable Diseases (NICD). Those who were in direct contact with this major outbreak of infected livestock were either farm workers or veterinarians. Widespread animal deaths were reported on March 29, 2010, from eighty farms in Africa. Over 20,000 farm animals were infected in the same area between 1974 and 1976, where the last major outbreak prior to the March 31, 2010 happened. Proof of an RVF epidemic in a metropolitan area has never been confirmed, as the disease has never been reported to spread by human-to-human contact.
Transmission
When large numbers of domesticated livestock are affected, an RVF epizootic (def) epidemic occurs due to an outbreak in the human population. Bitten livestock acquire the disease from (arthropods) mosquitoes of the genus Aedes. The mosquitoes are biologically infected with the RVF virus as it passes from the female Aedes mosquito to her eggs. Other mosquito species that feed on infected livestock contract the disease, as well as other insects that bite the infected livestock.
The human population contracts the disease from bites from any infected insect or mosquito. The disease is spread by any type of human-to-animal contact involving: laboratory aerosol transmission, body fluids, blood, infected animal tissues, slaughter, or veterinary practices. Data supports that humans who consume uncooked or unpasteurized milk from contaminated animals will possibly contract RVF.
Signs and Symptoms
There is a two to six day incubation of RVF. At the start of the disease, infected persons may suffer from severe weight loss, appetite loss with vomiting, neck stiffness, fever, back pain, light sensitivity, weakness and/or dizziness. Patients exhibiting these RVF early stage symptoms are often falsely diagnosed as having meningitis. In general, those infected may exhibit no warning signs of any illness. In mild cases, the symptoms last from two to seven days. Soon afterwards, the virus steadily vanishes from the blood due to the presence of antibodies from the body’s immune reaction.
Meningoencephalitis
In severe cases, RVF evolves into meningoencephalitis (def), causing seizures, headaches, comas, disorientation, vertigo, confusion, and memory loss that transpires in one to four weeks after the first symptoms. Later meningoencephalitis complications (sixty days or greater) include a lasting neurological shortage.Ocular disease
Other severe, possible complications such as ocular disease (def) occur when the retina (def) of the eye is inflamed. After the first symptoms appear, visual impairments due to retinal lesions occur within one to three weeks. There is a 1% - 10% chance that lesions in the macula (def) will cause lasting vision loss. Death rarely occurs in those with Ocular disease.Hemorrhagic fever
Hemorrhagic fever (def) is an additional severity that can occur with RVF within two to four days after its inception. Patients may contract a fever along with jaundice (def), a liver defect. Other symptoms include blood in the feces, bleeding from the gums, nose, and venipuncture sites (def), and menorrhagia (def). Infected individuals with the icterus (def) form of Hemorrhagic fever, the most fatal of the three severe forms of RVF, may die within three to six days after symptoms first appear because the hemorrhages lead to shock and death.
The patient percentages for each of the three major severe RVF syndromes are: hemorrhagic fever (less than 1%), ocular disease (0.5-2%), and meningoencephalitis (less than 1%). There is a 50% increase in the case fatality rate of hemorrhagic fever. The number of infected people who actually die with this disease is less than 1% of all documented cases.
The greatest fatalities at 100% are the fetuses of infected, pregnant livestock. The age and type of animal are the leading determinants in which ones will contract the disease. Lambs are 90% more likely to die from this disease, whereas only 10% of adult sheep will die. There is a lower risk in other domesticated animals such as adult cattle who are 10% less likely to contract the disease (calves 10% - 20%). Animals exhibit intestinal and gastric hemorrhages, nasal drainage, liver lesions, and jaundice. There is 12-36 hour incubation period in lambs.
Prevention and Treatment
Asymptomatic and supportive therapy are the leading treatments for severe RVF in humans. There is no precise treatment for the average infected person because of RVF’s mild symptoms and short duration. There is an inactivated virus (def) vaccine for human infections, however; it is not licensed or available to the public. The experimental vaccine is mainly used for those at risk of contracting RVF while working in the veterinarian or lab personnel fields. Those infected with RVF may benefit from therapy involving, convalescent-phase plasma (def), interferon (def), and immune modulators (def). A possible future treatment for humans is currently underway. The antiviral drug, ribavirin, currently tested on monkeys, has showed positive results. Ribavirin works by using lethal mutagenesis (def) towards the genomes of RNA viruses.
Domesticated animals receive long-term protection from RVF if the disease can be prevented before an outbreak occurs. This process involves using continuous, modified inactivated virus and live attenuated virus (def) vaccines. Several doses of the inactivated vaccine dosage are required, whereas; the live attenuated virus is given in a single dose. Vaccinations after the outbreak often lead to additional animals becoming infected if the same vials and syringes are used on multiple animals. Some vaccinations cause abortions or birth defects in animals. For domestic animals, laboratory trials showed potential results of MP-12, the human live attenuated vaccine. Testing is still currently underway on the MP-12 vaccine and other vaccines. The epidemic of RVF will possibly be slowed if the uninfected animals are isolated away from the infected animals. In addition, a Public Health warning to alert people to be more vigilant in preparing their foods properly for consumption in order to not contract the disease should be mandatory. This is especially true because the spread of RVF is predominant in animals, not humans.
Managing the vector (Aedes mosquito) by Larvicide (def) is the most successful way of dealing with the larval habitats of the infected mosquitoes. This allows the mosquito population to be controlled, but only if the larval grounds are extremely noticeable, and in a small area. Public Health messages to prevent mosquito bites should extol the benefits of using repellants and netting, wearing long-sleeved/leg, light colored clothing, and limiting outdoor time that coincides with that of mosquitoes. Calculating the outbreak of RVF by climate forecasting and comparing it to a common link between above average rainfall areas, permits a Remote Sensing Satellite Imagery to observe and gauge rainfall in order to estimate future outbreaks. The public can then be pre-warned and Public Health can employ the possible epidemic preventative measures that will lessen the threat of RFV outbreak.
Public Health messages and educational seminars should be given to those who are at risk of receiving RVF. These practices should concentrate on the dangers of transmission thru hazardous slaughtering and veterinarian practices that involve contact with infected animal tissues and blood. Workers should also clothe themselves with gloves and the proper attire for their profession in order to lessen their chances of disease. For those workplaces implementing the average preventative measures to control infection, there have been no accounts of RVF being transferred to their health care workers. There are no recorded instances in which RVF has been transferred from human-to-human contact. RVF epidemics will only be forestalled through the conjoined efforts of premature forecasting of RVF epidemics, a thorough safety plan, and International Health Regulations (2005).
Bibliography
CDC. Centers for Disease Control. Special Pathogens Branch. Rift Valley Fever Fact Sheet. Retrieved April 7, 2010 from http://www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/Fact_Sheets/Rift%20Valley%20Fever%20Fact%20Sheet.pdf
MedicineNet.com. Retrieved April 17, 2010 from http://www.medterms.com/script/main/art.asp?articlekey=3890.
Shimshony DVM, Arnon. Emerging Diseases: Rift Valley Fever: A Health Risk in Africa. Infectious Disease News. Posted July 1, 2009. Retrieved April 8, 2010 from http://www.infectiousdiseasenews.com/article/41608.aspx.
The Center for Food Security & Public Health. Selected Viral Families, Viruses and Species Affected. Retrieved April 18, 2010 from http://student.ccbcmd.edu/courses/bio141/lecguide/unit3/viruses/Viralfamilies_table_asm.pdf.
U.S. National Library of Medicine. National Institutes of Health. Ribavirin’s Antiviral Mechanism of Action: Lethal Mutagenesis. Retrieved April 18, 2010 from http://www.ncbi.nlm.nih.gov/pubmed/11907645.
United Nations News Centre. Outbreak of Rift Valley Fever Affecting Humans in South Africa – UN Agency. Retrieved April 18, 2010 from http://www.un.org/apps/news/story.asp?NewsID=34253.
WHO. World Health Organization Media Centre. Rift Valley Fever. Retrieved April 7, 2010 from http://www.who.int/mediac entre/factsheets/fs207/en/.
Wikipedia. Retrieved April 18, 2010 from http://en.wikipedia.org/wiki.