The virus spreads by direct contact with blood or other body fluids of an infected human or other animal. Infection with the virus may also occur by direct contact with a recently contaminated item or surface. Spread of the disease through the air between primates, including humans, has not been documented in either laboratory or natural conditions. The virus may be spread by semen or breast milk for several weeks to months after recovery. Fruit bats are believed to be the normal carrier in nature, able to spread the virus without being affected by it. Humans become infected by contact with the bats or with a living or dead animal that has been infected by bats. After human infection occurs, the disease may also spread between people. Other diseases such as malaria, cholera, typhoid fever, meningitis and other viral hemorrhagic fevers may resemble EVD. Blood samples are tested for viral RNA, viral antibodies or for the virus itself to confirm the diagnosis.
Control of outbreaks requires coordinated medical services, along with a certain level of community engagement. The medical services include: rapid detection of cases of disease, contact tracing of those who have come into contact with infected individuals, quick access to laboratory services, proper care and management of those who are infected and proper disposal of the dead through cremation or burial. Prevention includes limiting the spread of disease from infected animals to humans. This may be done by handling potentially infected bush meat only while wearing protective clothing and by thoroughly cooking it before consumption. It also includes wearing proper protective clothing and washing hands when around a person with the disease. Samples of body fluids and tissues from people with the disease should be handled with special caution.
No specific treatment or vaccine for the virus is commercially available, although a number of potential treatments are being studied. Efforts to help those who are infected are supportive; they include either oral rehydration therapy (drinking slightly sweetened and salty water) or giving intravenous fluids as well as treating symptoms. This supportive care improves outcomes. EVD was first identified in 1976 in an area of Sudan (now part of South Sudan), and in Zaire (now the Democratic Republic of the Congo). The disease typically occurs in outbreaks in tropical regions of sub-Saharan Africa. Through 2013, the World Health Organization reported a total of 1,716 cases in 24 outbreaks. The largest outbreak to date is the ongoing epidemic in West Africa, which is centered in Guinea, Sierra Leone and Liberia. As of 10 December 2014, this outbreak has 18,232 reported cases resulting in 6,990 deaths.
Signs & Symptoms
The length of time between exposure to the virus and the development of symptoms (incubation period) is between 2 to 21 days. Most often this is between 4 to 10 days.[14] However, recent estimates based on mathematical models predict that around 5% of cases may take greater than 21 days to develop.
Symptoms usually begin with a sudden influenza-like stage characterized by feeling tired, fever, weakness, decreased appetite, muscle pain, joint pain, headache, and sore throat. The fever is usually higher than 38.3 °C (100.9 °F). This is often followed by vomiting, diarrhea and abdominal pain.Next, shortness of breath and chest pain may occur, along with swelling, headaches and confusion. In about half of the cases, the skin may develop a maculopapular rash (a flat red area covered with small bumps), which may be seen 5 to 7 days after symptoms begin.
In some cases, internal and external bleeding may occur. This typically begins five to seven days after the first symptoms. All infected people show some decreased blood clotting. Bleeding from mucous membranes or from sites of needle punctures has been reported in 40–50 percent of cases.This may result in the vomiting of blood, coughing up of blood or blood in stool. Bleeding into the skin may create petechiae, purpura, ecchymoses or hematomas (especially around needle injection sites). Bleeding into the whites of the eyes may also occur. Heavy bleeding is uncommon, and if it occurs, it is usually located within the gastrointestinal tract.
Recovery may begin between 7 and 14 days after the start of symptoms. Death, if it occurs, follows typically 6 to 16 days from the start of symptoms and is often due to low blood pressure from fluid loss. In general, bleeding often indicates a worse outcome, and this blood loss may result in death.People are often in a coma near the end of life. Those who survive often have ongoing muscle and joint pain, liver inflammation, and decreased hearing among other difficulties.Additionally they develop antibodies against Ebola that last at least 10 years but it is unclear if they are immune to repeated infections. If someone survives Ebola, they can no longer transmit the disease.
Cause
EVD in humans is caused by four of five viruses of the genus Ebolavirus. The four are Bundibugyo virus (BDBV), Sudan virus (SUDV), Taï Forest virus (TAFV) and one simply called Ebola virus (EBOV, formerly Zaire Ebola virus). EBOV, species Zaire ebolavirus, is the most dangerous of the known EVD-causing viruses, and is responsible for the largest number of outbreaks. The fifth virus, Reston virus (RESTV), is not thought to cause disease in humans, but has caused disease in other primates.[27][28] All five viruses are closely related to marburg viruses.
Transmission - Life cycles of the Ebola virus
Between people, Ebola disease spreads only by direct contact with the blood or body fluids of a person who has developed symptoms of the disease. Body fluids that may contain ebola viruses include saliva, mucus, vomit, feces, sweat, tears, breast milk, urine and semen. The WHO states that only people who are very sick are able to spread Ebola disease in saliva, and whole virus has not been reported to be transmitted through sweat. Most people spread the virus through blood, feces and vomit. Entry points for the virus include the nose, mouth, eyes, open wounds, cuts and abrasions. Ebola may be spread through large droplets; however, this is believed to occur only when a person is very sick. This can happen if a person is splashed with droplets. Contact with surfaces or objects contaminated by the virus, particularly needles and syringes, may also transmit the infection. The virus is able to survive on objects for a few hours in a dried state and can survive for a few days within body fluids.
Reservoir
The natural reservoir for Ebola has yet to be confirmed; however, bats are considered to be the most likely candidate species. Three types of fruit bats (Hypsignathus monstrosus, Epomops franqueti and Myonycteris torquata) were found to possibly carry the virus without getting sick.[54] As of 2013, whether other animals are involved in its spread is not known. Plants, arthropods and birds have also been considered possible viral reservoirs.
Bats were known to roost in the cotton factory in which the first cases of the 1976 and 1979 outbreaks were observed, and they have also been implicated in Marburg virus infections in 1975 and 1980. Of 24 plant and 19 vertebrate species experimentally inoculated with EBOV, only bats became infected. The bats displayed no clinical signs of disease, which is considered evidence that these bats are a reservoir species of EBOV. In a 2002–2003 survey of 1,030 animals including 679 bats from Gabon and the Republic of the Congo, 13 fruit bats were found to contain EBOV RNA.Antibodies against Zaire and Reston viruses have been found in fruit bats in Bangladesh, suggesting that these bats are also potential hosts of the virus and that the filoviruses are present in Asia.
Between 1976 and 1998, in 30,000 mammals, birds, reptiles, amphibians and arthropods sampled from regions of EBOV outbreaks, no Ebola virus was detected apart from some genetic traces found in six rodents (belonging to the species Mus setulosus and Praomys) and one shrew (Sylvisorex ollula) collected from the Central African Republic. However, further research efforts have not confirmed rodents as a reservoir. Traces of EBOV were detected in the carcasses of gorillas and chimpanzees during outbreaks in 2001 and 2003, which later became the source of human infections. However, the high rates of death in these species resulting from EBOV infection make it unlikely that these species represent a natural reservoir for the virus.
Electron micrograph of an Ebola virus virion
Ebola viruses contain single-stranded, non-infectious RNA genomes. Ebola virus genomes contain seven genes including 3'-UTR-NP-VP35-VP40-GP-VP30-VP24-L-5'-UTR. The genomes of the five different ebola viruses (BDBV, EBOV, RESTV, SUDV and TAFV) differ in sequence and the number and location of gene overlaps. As all filoviruses, ebola virions are filamentous particles that may appear in the shape of a shepherd's crook, of a "U" or of a "6," and they may be coiled, toroid or branched. In general, ebola virions are 80 nanometers (nm) in width and may be as long as 14,000 nm.
Their life cycle is thought to begin with a virion attaching to specific cell-surface receptors such as C-type lectins, DC-SIGN, or integrins, which is followed by fusion of the viral envelope with cellular membranes. The virions taken up by the cell then travel to acidic endosomes and lysosomes where the viral envelope glycoprotein GP is cleaved. This processing appears to allow the virus to bind to cellular proteins enabling it to fuse with internal cellular membranes and release the viral nucleocapsid. The Ebola virus structural glycoprotein (known as GP1,2) is responsible for the virus' ability to bind to and infect targeted cells. The viral RNA polymerase, encoded by the L gene, partially uncoats the nucleocapsid and transcribes the genes into positive-strand mRNAs, which are then translated into structural and nonstructural proteins. The most abundant protein produced is the nucleoprotein, whose concentration in the host cell determines when L switches from gene transcription to genome replication. Replication of the viral genome results in full-length, positive-strand anti genomes that are, in turn, transcribed into genome copies of negative-strand virus progeny. Newly synthesized structural proteins and genomes self-assemble and accumulate near the inside of the cell membrane. Virions bud off from the cell, gaining their envelopes from the cellular membrane from which they bud from. The mature progeny particles then infect other cells to repeat the cycle. The genetics of the Ebola virus are difficult to study because of EBOV virulent characteristics.
Source : Wikipedia
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