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Ebola and Other Tropical Viruses

Definition:
Ebola and other tropical viruses are related viruses that cause hemorrhagic fevers — illnesses marked by severe bleeding (hemorrhage), organ failure and, in many cases, death.

There are five types of Ebola and while infection with some (such as Ebola Reston, found in the Western Pacific) are so mild that people rarely get symptoms, other types such as Ebola Zaire (found in Africa) may be rapidly deadly.

Ebola was identified for the first time in 1976 in the Democratic Republic of Congo, and in Southern Sudan. It is one of about 30 new diseases to affect humans over the past few decades.

Both Ebola virus and Marburg virus are native to Africa, where sporadic outbreaks have occurred for decades. No human cases of Ebola virus have been reported in the United States.

Ebola and Marburg viruses live in one or more animal hosts, and humans can contract the viruses from infected animals. After the initial transmission, the viruses can spread from person-to-person through contact with body fluids or contaminated needles.

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Ebola was identified for the first time in 1976 in the Democratic Republic of Congo, and in Southern Sudan. It is one of about 30 new diseases to affect humans over the past few decades.

Theories on the origins of these diseases are widespread but many of the most frightening appear to have emerged from sub-Saharan Africa. HIV, which leads to Aids, has been linked to a similar virus common in West African monkeys, and the first ever recorded HIV sample was taken from a man in what is now the Democratic Republic of Congo in 1959.

Ebola and a few other haemorrhagic fevers have been responsible for a tiny number of deaths compared to Aids, and the number of symptomatic cases reported outside Africa has been miniscule. But the devastating speed at which they strike and the far higher possibility of transmission from human to human have made the thought of a major outbreak a terrifying prospect.

However, Ebola is not the only viral haemorrhagic fever which claims lives in Africa, and beyond. Marburg fever gets its name from the town in Germany in which it broke out in 1967 and shares its symptoms with Ebola. It claimed seven lives from the 25 people infected in Marburg and Frankfurt. Those initially infected were laboratory workers exposed to African green monkeys which had been imported for research. But the majority of cases occur in Africa.

Other well-known haemorrhagic fevers are:

*Lassa fever – first noticed in the 1960s after an outbreak in Nigeria
*Rift Valley fever – mainly found in sub-Saharan Africa
*Congo-Crimean haemorrhagic fever – found in many parts of Africa, the Middle East and even warmer parts of the former Soviet Union, in which an outbreak is ongoing.

No effective therapy exists for the hemorrhagic fevers caused by Ebola virus and Marburg virus. People diagnosed with Ebola virus or Marburg virus receive supportive care and treatment for complications.

Symptoms;
Signs and symptoms of hemorrhagic fevers caused by Ebola virus and Marburg virus start abruptly within a few days to a week or more after infection. Early signs and symptoms include:

*Fever
*Severe headache
*Joint and muscle aches
*Chills
*Sore throat
*Weakness

Over time, symptoms become increasingly severe and may include:

*Nausea and vomiting
*Diarrhea (may be bloody)
*Red eyes
*Raised rash
*Chest pain and cough
*Stomach pain
*Severe weight loss
*Confusion, irritability or aggression
*Massive hemorrhaging from many sites, including nose, mouth, rectum, eyes and ears

Causes:
Scientists first became aware of the potential of Ebola to destroy whole communities in the mid 1970s, when severe outbreaks in Sudan and the former Zaire killed a total of approximately 440 people. The Zaire strain of the virus is the most deadly to date, proving fatal in just under 90 per cent of those who contract it.

The virus is passed on through contact with blood, secretion or bodily fluids of an infected person – those with the disease start to haemorrhage and cough up or vomit blood, so in outbreaks the disease often spreads from patients to the health care workers looking after them.

Symptoms start to appear anytime from two to 21 days later.

However, how and why each outbreak starts is completely unknown. One theory is that there is a reservoir of the virus in bats, which are unaffected by it, and the virus passes from here to non-human primates such as chimpanzees who in turn pass it on to humans who come into contact with them.

By the time symptoms appear, the virus will have reproduced itself many times and spread through the blood to many organs. The major organs it affects are the liver, kidneys, spleen and reproductive organs.

Of the other haemorrhagic fevers, Lassa fever is spread from rodents which are the natural host. Rift Valley fever is spread by mosquitoes, whilst Congo-Crimean haemorrhagic fever is spread by ticks

Risk factors:-

For most people — including international travelers — the risk of getting Ebola or Marburg hemorrhagic fever is low. The risk increases if you:

*Travel to or work in areas where Ebola virus or Marburg virus outbreaks have occurred, such as Democratic Republic of Congo (DRC), Sudan, Gabon, Cote d’Ivoire and Angola

*Conduct animal research, especially in tropical African forests, or handle primates infected with Ebola virus or Marburg virus

*Provide medical or personal care for people with Ebola hemorrhagic fever or Marburg hemorrhagic fever

*Prepare people who have died of Ebola hemorrhagic fever or Marburg hemorrhagic fever for burial

Complections:
Ebola and other tropical viruses are hemorrhagic fevers lead to death for a high percentage of people who are affected. As the illness progresses, it can cause:

*Multiple organ failure
*Severe bleeding
*Jaundice
*Delirium
*Seizures
*Coma
*Shock

Death often occurs less than 10 days from the start of signs and symptoms.

One reason the viruses are so deadly is that they interfere with the immune system’s ability to mount a defense. But scientists don’t understand why some people recover from Ebola and Marburg and others don’t.

For people who survive, recovery is slow. It may take months to regain weight and strength, and the viruses remain in the body for many weeks. People may experience:

*Hair loss
*Sensory changes
*Liver inflammation (hepatitis)
*Weakness
*Fatigue
*Headaches
*Eye inflammation
*Testicular inflammation
Diagnosis:
Ebola and other tropical viruses fevers are difficult to diagnose because many of the early signs and symptoms resemble those of other infectious diseases, such as typhoid and malaria. But if doctors suspect that you have been exposed to Ebola virus or Marburg virus, they use laboratory tests that can identify the viruses within a few days.

Most people with Ebola or Marburg hemorrhagic fever have high concentrations of the virus in their blood. Blood tests known as enzyme-linked immunosorbent assay (ELISA) and reverse transcriptase polymerase chain reaction (PCR) can detect specific genes or the virus or antibodies to them.
Treatment
There is still no specific treatment for Ebola – no standard anti-viral therapies such as interferon have any effect. A vaccine has been produced that was 100 per cent effective in protecting a group of monkeys from the disease, but attempts to replicate the success in humans have so far proved unsuccessful. At present if someone beats Ebola, they do it by themselves, albeit with intensive medical support with intravenous fluids, and/or blood transfusions, or oral rehydration with electrolyte solutions. Survivors can be expected to make a full recovery, although occasionally reversible personality changes have been noted in such lucky patients.

Careful barrier nursing and avoidance of contamination with infected body fluids is still the best way to limit an outbreak.

Treatments in development
Scientists have developed vaccinations against both Ebola and Marburg which work on laboratory animals, and there are promising signs of some therapies that can be used on people affected. Some experiments use antibodies from the marrow of Ebola survivors. Much of the scientific work underway is focused on finding the original source of the disease – the reservoir. One project examined thousands of animals in the rainforests of West Africa in a bid to isolate those hosting the virus.

Some scientists say that the growing numbers of so-called emerging diseases are due to increasing forays by humans into the tropical forests. This brings them into contact with new creatures – and new infections – making it possible there could be even more powerful viruses waiting to play havoc in the human body.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/ebola_tropical_diseases.shtml
http://www.viviennebalonwu.com/health-notes/656/ebola-and-other-tropical-viruses-2/
http://www.mayoclinic.com/health/ebola-virus/DS00996

http://microvet.arizona.edu/Courses/JC-MIC205/S08/MIC205%20NEWS/ebola.html

http://www.thelancetstudent.com/2010/11/30/the-lancet-seminar-ebola-haemorrhagic-fever/

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Rift Valley Fever

Rift Valley fever
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Defibition:
Rift Valley Fever (RVF) is a viral zoonosis (affects primarily domestic livestock, but can be passed to humans) causing fever. It is spread by the bite of infected mosquitoes, typically the Aedes or Culex genera.

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The disease is caused by the RVF virus, a member of the genus Phlebovirus (family Bunyaviridae). The disease was first reported among livestock in Kenya around 1915, but the virus was not isolated until 1931. RVF outbreaks occur across sub-Saharan Africa, with outbreaks occurring elsewhere infrequently (but sometimes severely – in Egypt in 1977-78, several million people were infected and thousands died during a violent epidemic. In Kenya in 1998, the virus claimed the lives of over 400 Kenyans. In September 2000 an outbreak was confirmed in Saudi Arabia and Yemen).

In humans the virus can cause several different syndromes. Usually sufferers have either no symptoms or only a mild illness with fever, headache, myalgia and liver abnormalities. In a small percentage of cases (< 2%) the illness can progress to hemorrhagic fever syndrome, meningoencephalitis (inflammation of the brain), or affecting the eye. Patients who become ill usually experience fever, generalized weakness, back pain, dizziness, and weight loss at the onset of the illness. Typically, patients recover within 2-7 days after onset.

RVF virus is a member of the Phlebovirus genus, one of the five genera in the family Bunyaviridae. The virus was first identified in 1931 during an investigation into an epidemic among sheep on a farm in the Rift Valley of Kenya. Since then, outbreaks have been reported in sub-Saharan and North Africa. In 1997-98, a major outbreak occurred in Kenya, Somalia and Tanzania and in September 2000, RVF cases were confirmed in Saudi Arabia and Yemen, marking the first reported occurrence of the disease outside the African continent and raising concerns that it could extend to other parts of Asia and Europe.

Approximately 1% of human sufferers die of the disease. Amongst livestock the fatality level is significantly higher. In pregnant livestock infected with RVF there is the abortion of virtually 100% of fetuses. An epizootic (animal disease epidemic) of RVF is usually first indicated by a wave of unexplained abortions.

TRANSMISSION TO HUMANS:
*The vast majority of human infections result from direct or indirect contact with the blood or organs of infected animals. The virus can be transmitted to humans through the handling of animal tissue during slaughtering or butchering, assisting with animal births, conducting veterinary procedures, or from the disposal of carcasses or fetuses. Certain occupational groups such as herders, farmers, slaughterhouse workers and veterinarians are therefore at higher risk of infection. The virus infects humans through inoculation, for example via a wound from an infected knife or through contact with broken skin, or through inhalation of aerosols produced during the slaughter of infected animals. The aerosol mode of transmission has also led to infection in laboratory workers.

*There is some evidence that humans may also become infected with RVF by ingesting the unpasteurized or uncooked milk of infected animals.

*Human infections have also resulted from the bites of infected mosquitoes, most commonly the Aedes mosquito.

*Transmission of RVF virus by hematophagous (blood-feeding) flies is also possible.

*To date, no human-to-human transmission of RVF has been documented, and no transmission of RVF to health care workers has been reported when standard infection control precautions have been put in place.

*There has been no evidence of outbreaks of RVF in urban areas.

CLINICAL FEATURES IN HUMANS
Mild form of RVF in humans

*The incubation period (interval from infection to onset of symptoms) for RVF varies from two to six days.

*Those infected either experience no detectable symptoms or develop a mild form of the disease characterized by a feverish syndrome with sudden onset of flu-like fever, muscle pain, joint pain and headache.

*Some patients develop neck stiffness, sensitivity to light, loss of appetite and vomiting; in these patients the disease, in its early stages, may be mistaken for meningitis.

*The symptoms of RVF usually last from four to seven days, after which time the immune response becomes detectable with the appearance of antibodies and the virus gradually disappears from the blood.

Severe form of RVF in humans:

*While most human cases are relatively mild, a small percentage of patients develop a much more severe form of the disease. This usually appears as one or more of three distinct syndromes: ocular (eye) disease (0.5-2% of patients), meningoencephalitis (less than 1%) or haemorrhagic fever (less than 1%).

*Ocular form: In this form of the disease, the usual symptoms associated with the mild form of the disease are accompanied by retinal lesions. The onset of the lesions in the eyes is usually one to three weeks after appearance of the first symptoms. Patients usually report blurred or decreased vision. The disease may resolve itself with no lasting effects within 10 to 12 weeks. However, when the lesions occur in the macula, 50% of patients will experience a permanent loss of vision. Death in patients with only the ocular form of the disease is uncommon.

*Meningoencephalitis form: The onset of the meningoencephalitis form of the disease usually occurs one to four weeks after the first symptoms of RVF appear. Clinical features include intense headache, loss of memory, hallucinations, confusion, disorientation, vertigo, convulsions, lethargy and coma. Neurological complications can appear later (> 60 days). The death rate in patients who experience only this form of the disease is low, although residual neurological deficit, which may be severe, is common.

*Haemorrhagic fever form: The symptoms of this form of the disease appear two to four days after the onset of illness, and begin with evidence of severe liver impairment, such as jaundice. Subsequently signs of haemorrhage then appear such as vomiting blood, passing blood in the faeces, a purpuric rash or ecchymoses (caused by bleeding in the skin), bleeding from the nose or gums, menorrhagia and bleeding from venepuncture sites. The case-fatality ratio for patients developing the haemorrhagic form of the disease is high at approximately 50%. Death usually occurs three to six days after the onset of symptoms. The virus may be detectable in the blood for up to 10 days, in patients with the hemorrhagic icterus form of RVF.

The total case fatality rate has varied widely between different epidemics but, overall, has been less than 1% in those documented. Most fatalities occur in patients who develop the haemorrhagic icterus form.

DIAGNOSIS
Acute RVF can be diagnosed using several different methods. Serological tests such as enzyme-linked immunoassay (the “ELISA” or “EIA” methods) may confirm the presence of specific IgM antibodies to the virus. The virus itself may be detected in blood during the early phase of illness or in post-mortem tissue using a variety of techniques including virus propagation (in cell cultures or inoculated animals), antigen detection tests and RT-PCR.

TREATMENT AND VACCINE
*As most human cases of RVF are relatively mild and of short duration, no specific treatment is required for these patients. For the more severe cases, the predominant treatment is general supportive therapy.

*An inactivated vaccine has been developed for human use. However, this vaccine is not licensed and is not commercially available. It has been used experimentally to protect veterinary and laboratory personnel at high risk of exposure to RVF. Other candidate vaccines are under investigation.

RVF VIRUS IN ANIMAL HOSTS
*RVF is able to infect many species of animals causing severe disease in domesticated animals including cattle, sheep, camels and goats. Sheep appear to be more susceptible than cattle or camels.

*Age has also been shown to be a significant factor in the animal’s susceptibility to the severe form of the disease: over 90% of lambs infected with RVF die, whereas mortality among adult sheep can be as low as 10%.

*The rate of abortion among pregnant infected ewes is almost 100%. An outbreak of RVF in animals frequently manifests itself as a wave of unexplained abortions among livestock and may signal the start of an epidemic.

RVF VECTORS
*Several different species of mosquito are able to act as vectors for transmission of the RVF virus. The dominant vector species varies between different regions and different species can play different roles in sustaining the transmission of the virus.

*Among animals, the RVF virus is spread primarily by the bite of infected mosquitoes, mainly the Aedes species, which can acquire the virus from feeding on infected animals. The female mosquito is also capable of transmitting the virus directly to her offspring via eggs leading to new generations of infected mosquitoes hatching from eggs. This accounts for the continued presence of the RVF virus in enzootic foci and provides the virus with a sustainable mechanism of existence as the eggs of these mosquitoes can survive for several years in dry conditions. During periods of heavy rainfall, larval habitats frequently become flooded enabling the eggs to hatch and the mosquito population to rapidly increase, spreading the virus to the animals on which they feed.

*There is also a potential for epizootics and associated human epidemics to spread to areas that were previously unaffected. This has occurred when infected animals have introduced the virus into areas where vectors were present and is a particular concern. When uninfected Aedes and other species of mosquitoes feed on infected animals, a small outbreak can quickly be amplified through the transmission of the virus to other animals on which they subsequently feed.

PREVENTION AND CONTROL
Controlling RVF in animals

*Outbreaks of RVF in animals can be prevented by a sustained programme of animal vaccination. Both modified live attenuated virus and inactivated virus vaccines have been developed for veterinary use. Only one dose of the live vaccine is required to provide long-term immunity but the vaccine that is currently in use may result in spontaneous abortion if given to pregnant animals. The inactivated virus vaccine does not have this side effect, but multiple doses are required in order to provide protection which may prove problematic in endemic areas.

*Animal immunization must be implemented prior to an outbreak if an epizootic is to be prevented. Once an outbreak has occurred animal vaccination should NOT be implemented because there is a high risk of intensifying the outbreak. During mass animal vaccination campaigns, animal health workers may, inadvertently, transmit the virus through the use of multi-dose vials and the re-use of needles and syringes. If some of the animals in the herd are already infected and viraemic (although not yet displaying obvious signs of illness), the virus will be transmitted among the herd, and the outbreak will be amplified.

*Restricting or banning the movement of livestock may be effective in slowing the expansion of the virus from infected to uninfected areas.

*As outbreaks of RVF in animals precede human cases, the establishment of an active animal health surveillance system to detect new cases is essential in providing early warning for veterinary and human public health authorities.

Public health education and risk reduction:

*During an outbreak of RVF, close contact with animals, particularly with their body fluids, either directly or via aerosols, has been identified as the most significant risk factor for RVF virus infection. In the absence of specific treatment and an effective human vaccine, raising awareness of the risk factors of RVF infection as well as the protective measures individuals can take to prevent mosquito bites, is the only way to reduce human infection and deaths.

Public health messages for risk reduction should focus on:
*reducing the risk of animal-to-human transmission as a result of unsafe animal husbandry and slaughtering practices. Gloves and other appropriate protective clothing should be worn and care taken when handling sick animals or their tissues or when slaughtering animals.
*reducing the risk of animal-to-human transmission arising from the unsafe consumption of fresh blood, raw milk or animal tissue. In the epizootic regions, all animal products (blood, meat and milk) should be thoroughly cooked before eating.

*the importance of personal and community protection against mosquito bites through the use of impregnated mosquito nets, personal insect repellent if available, by wearing light coloured clothing (long-sleeved shirts and trousers) and by avoiding outdoor activity at peak biting times of the vector species.
Infection control in health care settings
*Although no human-to-human transmission of RVF has been demonstrated, there is still a theoretical risk of transmission of the virus from infected patients to healthcare workers through contact with infected blood or tissues. Healthcare workers caring for patients with suspected or confirmed RVF should implement Standard Precautions when handling specimens from patients.

*Standard Precautions define the work practices that are required to ensure a basic level of infection control. Standard Precautions are recommended in the care and treatment of all patients regardless of their perceived or confirmed infectious status. They cover the handling of blood (including dried blood), all other body fluids, secretions and excretions (excluding sweat), regardless of whether they contain visible blood, and contact with non-intact skin and mucous membranes. A WHO Aide–memoire on Standard Precautions in health care is available at: http://www.who.int/csr/resources/publications/standardprecautions/en/index.html

*As noted above, laboratory workers are also at risk. Samples taken from suspected human and animal cases of RVF for diagnosis should be handled by trained staff and processed in suitably equipped laboratories.

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Vector control
*Other ways in which to control the spread of RVF involve control of the vector and protection against their bites.
*Larviciding measures at mosquito breeding sites are the most effective form of vector control if breeding sites can be clearly identified and are limited in size and extent. During periods of flooding, however, the number and extent of breeding sites is usually too high for larviciding measures to be feasible.

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RVF FORESCASTING AND CLIMATIC MODELS
Forecasting can predict climatic conditions that are frequently associated with an increased risk of outbreaks, and may improve disease control. In Africa, Saudi Arabia and Yemen RVF outbreaks are closely associated with periods of above-average rainfall. The response of vegetation to increased levels of rainfall can be easily measured and monitored by Remote Sensing Satellite Imagery. In addition RVF outbreaks in East Africa are closely associated with the heavy rainfall that occurs during the warm phase of the El Niño/Southern Oscillation (ENSO) phenomenon.

These findings have enabled the successful development of forecasting models and early warning systems for RVF using satellite images and weather/climate forecasting data. Early warning systems, such as these, could be used to detect animal cases at an early stage of an outbreak enabling authorities to implement measures to avert impending epidemics.

Within the framework of the new International Health Regulations (2005), the forecasting and early detection of RVF outbreaks, together with a comprehensive assessment of the risk of diffusion to new areas, are essential to enable effective and timely control measures to be implemented.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://en.wikipedia.org/wiki/Rift_Valley_fever
http://www.who.int/mediacentre/factsheets/fs207/en/

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