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Ebola virus disease

Classification and external resources

1976 photograph of two nurses standing in front of Mayinga N., a person with

Ebola virus disease; she died only a few days later due to severe internal

hemorrhaging.

ICD-10 A98.4

(http://apps.who.int/classifications/icd10/browse/2010/en#/A98.4)

ICD-9 065.8 (http://www.icd9data.com/getICD9Code.ashx?icd9=065.8)

DiseasesDB 18043 (http://www.diseasesdatabase.com/ddb18043.htm)

MedlinePlus 001339

(http://www.nlm.nih.gov/medlineplus/ency/article/001339.htm)

eMedicine med/626 (http://www.emedicine.com/med/topic626.htm)

MeSH D019142 (http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?

field=uid&term=D019142)

Ebola virus diseaseFrom Wikipedia, the free encyclopedia

Ebola virus disease (EVD)or Ebola hemorrhagic fever(EHF) is a disease of humansand other primates caused byan ebolavirus. Symptoms starttwo days to three weeks aftercontracting the virus, with afever, sore throat, muscle pain,and headaches. Typicallynausea, vomiting, and diarrheafollow, along with decreasedfunctioning of the liver andkidneys. Around this time,affected people may begin tobleed both within the body and

externally. [1]

The virus may be acquiredupon contact with blood orbodily fluids of an infectedanimal (commonly monkeys or

fruit bats).[1] Spread throughthe air has not beendocumented in the natural

environment.[2] Fruit bats arebelieved to carry and spreadthe virus without being affected.Once human infection occurs,the disease may spreadbetween people as well. Malesurvivors may be able totransmit the disease via semenfor nearly two months. In orderto make the diagnosis, typicallyother diseases with similarsymptoms such as malaria,cholera, and other viralhemorrhagic fevers are first excluded. To confirm the diagnosis, blood samples are tested for viral antibodies,

viral RNA, or the virus itself.[1]

Prevention includes decreasing the spread of disease from other infected animals to humans. This may be doneby checking such animals for infection and killing and properly disposing of the bodies if the disease isdiscovered. Properly cooking meat and wearing protective clothing when handling meat may also be helpful, asare wearing protective clothing and washing hands when around a person with the disease. Samples of bodily

fluids and tissues from people with the disease should be handled with special caution.[1]

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There is no specific treatment for the disease.[1] Efforts to help those who are infected are supportive and

include giving either oral rehydration therapy (slightly sweet and salty water to drink) or intravenous fluids.[1] The

disease has a high mortality rate, often killing between 50% and 90% of those infected with the virus.[1][3] EVDwas first identified in Sudan and the Democratic Republic of the Congo. The disease typically occurs in

outbreaks in tropical regions of Sub-Saharan Africa.[1] From 1976 (when it was first identified) through 2013,

fewer than 1,000 people per year have been infected.[1][4] The largest outbreak to date is the ongoing 2014

West Africa Ebola outbreak, which is affecting Guinea, Sierra Leone, Liberia, and Nigeria.[5][6] As of August

2014, more than 1,750 suspected cases have been reported.[7] Efforts are ongoing to develop a vaccine;

however, none yet exists.[1]

Contents

1 Signs and symptoms

2 Causes

2.1 Transmission

2.2 Reservoir

2.3 Virology

3 Pathophysiology

4 Diagnosis

4.1 Classification

4.2 Differential diagnosis

5 Prevention

5.1 Behavioral changes

5.2 Quarantine

5.3 Vaccine

5.4 Laboratory

6 Treatment

7 Prognosis

8 Epidemiology

8.1 1976

8.2 1995 to 2013

8.3 2014 outbreak

9 History

10 Society and culture

11 Other animals

11.1 Domestic animals

12 Research

12.1 Medications

12.2 Antibodies

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Symptoms of Ebola.[8]

Life cycles of the Ebolavirus

12.3 Use of untested experimental drugs

12.4 Other treatments

13 References

14 External links

Signs and symptoms

Signs and symptoms of Ebola usually begin suddenly with a flu-likestage characterized by fatigue, fever, headaches, and joint, muscle,

and abdominal pain.[9][10] Vomiting, diarrhea and loss of appetite are

also common.[10] Less common symptoms include the following: sorethroat, chest pain, hiccups, shortness of breath and trouble

swallowing.[10] The average time between contracting the infectionand the start of symptoms is 8 to 10 days, but it can vary between 2

and 21 days.[10] Skin manifestations may include a maculopapular

rash (in about 50% of cases).[11] Early symptoms of EVD may besimilar to those of malaria, dengue fever, or other tropical fevers,

before the disease progresses to the bleeding phase.[9]

In 40–50% of cases, bleeding from puncture sites and mucousmembranes (e.g. gastrointestinal tract, nose, vagina, and gums) has

been reported.[12] In the bleeding phase, which typically starts 5 to 7 days after first symptoms[13] internal and

subcutaneous bleeding may present itself through reddening of the eyes and bloody vomit.[9] Bleeding into theskin may create petechiae, purpura, ecchymoses, and hematomas (especially around needle injection sites).Types of bleeding known to occur with Ebola virus disease include vomiting blood, coughing it up or blood in

the stool. Heavy bleeding is rare and is usually confined to the gastrointestinal tract.[11][14] In general, the

development of bleeding symptoms often indicates a worse prognosis and this blood loss can result in death.[9]

All people infected show some symptoms of circulatory system involvement, including impaired blood

clotting.[11] If the infected person does not recover, death due to multiple organ dysfunction syndrome occurs

within 7 to 16 days (usually between days 8 and 9) after first symptoms.[13]

Causes

EVD is caused by four of five viruses classified in the genusEbolavirus, family Filoviridae, order Mononegavirales. The fourdisease-causing viruses are Bundibugyo virus (BDBV), Sudan virus(SUDV), Taï Forest virus (TAFV), and one called simply, Ebola virus(EBOV, formerly Zaire Ebola virus)). Ebola virus is the sole memberof the Zaire ebolavirus species, and the most dangerous of theknown Ebola disease causing viruses, as well as being responsible for

the largest number of outbreaks.[15] The fifth virus, Reston virus(RESTV), is not thought to be disease-causing in humans. The fiveEbola viruses are closely related to the Marburg viruses.

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Bushmeat being prepared for cooking

in Ghana, 2013. Human consumption

of equatorial animals in Africa in the

form of bushmeat has been linked to

the transmission of diseases to

people, including Ebola.[28]

Transmission

It is not entirely clear how Ebola is spread.[16] EVD is believed to occur after an ebola virus is transmitted to aninitial human by contact with an infected animal's body fluids. Human-to-human transmission can occur via directcontact with blood or bodily fluids from an infected person (including embalming of an infected dead person) or

by contact with contaminated medical equipment, particularly needles and syringes.[17] Semen is infectious in

survivors for up to 50 days. Transmission through oral exposure and through conjunctiva exposure is likely[18]

and has been confirmed in non-human primates.[19] The potential for widespread EVD infections is consideredlow as the disease is only spread by direct contact with the secretions from someone who is showing signs of

infection.[17] The quick onset of symptoms makes it easier to identify sick individuals and limits a person's abilityto spread the disease by traveling. Because dead bodies are still infectious, some doctors disposed of them in a

safe manner, despite local traditional burial rituals.[20]

Medical workers who do not wear appropriate protective clothing may also contract the disease.[21] In the past,hospital-acquired transmission has occurred in African hospitals due to the reuse of needles and lack of universal

precautions.[22][23]

Airborne transmission has not been documented during previous EVD outbreaks.[2] They are, however,

infectious as breathable 0.8–1.2 micrometre laboratory generated droplets;[24] because of this potential route of

infection, these viruses have been classified as Category A biological weapons.[25] Recently the virus has beenshown to travel without contact from pigs to non-human primates, although the same study failed to achieve

transmission in that manner between primates.[26]

Bats drop partially eaten fruits and pulp, then land mammals such as gorillas and duikers feed on these fallenfruits. This chain of events forms a possible indirect means of transmission from the natural host to animalpopulations, which has led to research towards viral shedding in the saliva of bats. Fruit production, animalbehavior, and other factors vary at different times and places that may trigger outbreaks among animal

populations.[27]

Reservoir

Bats are considered the most likely natural reservoir of the Ebola virus

(EBOV); plants, arthropods, and birds have also been considered.[29]

Bats were known to reside in the cotton factory in which the firstcases for the 1976 and 1979 outbreaks were employed, and theyhave also been implicated in Marburg virus infections in 1975 and

1980.[30] Of 24 plant species and 19 vertebrate species

experimentally inoculated with EBOV, only bats became infected.[31]

The absence of clinical signs in these bats is characteristic of areservoir species. In a 2002–2003 survey of 1,030 animals including679 bats from Gabon and the Republic of the Congo, 13 fruit bats

were found to contain EBOV RNA fragments.[32] As of 2005, threetypes of fruit bats (Hypsignathus monstrosus, Epomops franqueti,and Myonycteris torquata) have been identified as being in contactwith EBOV. They are now suspected to represent the EBOV

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Electron micrograph of an Ebola virus

virion

reservoir hosts.[33][34] Antibodies against Ebola Zaire and Reston viruses have been found in fruit bats in

Bangladesh, thus identifying potential virus hosts and signs of the filoviruses in Asia.[35]

Between 1976 and 1998, in 30,000 mammals, birds, reptiles, amphibians, and arthropods sampled fromoutbreak regions, no ebolavirus was detected apart from some genetic traces found in six rodents (Mus

setulosus and Praomys) and one shrew (Sylvisorex ollula) collected from the Central African Republic.[30][36]

Traces of EBOV were detected in the carcasses of gorillas and chimpanzees during outbreaks in 2001 and2003, which later became the source of human infections. However, the high lethality from infection in these

species makes them unlikely as a natural reservoir.[30]

Transmission between natural reservoir and humans is rare, and outbreaks are usually traceable to a single case

where an individual has handled the carcass of gorilla, chimpanzee, or duiker.[37] Fruit bats are also eaten by

people in parts of West Africa where they are smoked, grilled, or made into a spicy soup.[34][38]

Virology

Genome

Like all mononegaviruses, ebolavirions contain linear nonsegmented,single-strand, non-infectious RNA genomes of negative polarity thatpossesses inverse-complementary 3' and 5' termini, do not possess a5' cap, are not polyadenylated, and are not covalently linked to a

protein.[39] Ebolavirus genomes are approximately 19 kilobase pairslong and contain seven genes in the order 3'-UTR-NP-VP35-VP40-

GP-VP30-VP24-L-5'-UTR.[40] The genomes of the five differentebolaviruses (BDBV, EBOV, RESTV, SUDV, and TAFV) differ insequence and the number and location of gene overlaps.

Structure

Like all filoviruses, ebolavirions are filamentous particles that may appear in the shape of a shepherd's crook or

in the shape of a "U" or a "6", and they may be coiled, toroid, or branched.[40] In general, ebolavirions are80 nm in width, but vary somewhat in length. In general, the median particle length of ebolaviruses ranges from974 to 1,086 nm (in contrast to marburgvirions, whose median particle length was measured at 795–828 nm),

but particles as long as 14,000 nm have been detected in tissue culture.[41]

Replication

The ebolavirus life cycle begins with virion attachment to specific cell-surface receptors, followed by fusion ofthe virion envelope with cellular membranes and the concomitant release of the virus nucleocapsid into thecytosol. The viral RNA polymerase, encoded by the L gene, partially uncoats the nucleocapsid and transcribesthe genes into positive-strand mRNAs, which are then translated into structural and nonstructural proteins.Ebolavirus RNA polymerase (L) binds to a single promoter located at the 3' end of the genome. Transcriptioneither terminates after a gene or continues to the next gene downstream. This means that genes close to the 3'end of the genome are transcribed in the greatest abundance, whereas those toward the 5' end are least likely tobe transcribed. The gene order is, therefore, a simple but effective form of transcriptional regulation. The mostabundant protein produced is the nucleoprotein, whose concentration in the cell determines when L switchesfrom gene transcription to genome replication. Replication results in full-length, positive-strand antigenomes that

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Pathogenesis schematic

are, in turn, transcribed into negative-strand virus progeny genome copy. Newly synthesized structural proteinsand 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 they bud from. The mature progeny particles then infect other

cells to repeat the cycle.The Ebola Virus genetics are difficult to study due to its virulent nature[42]

Pathophysiology

Endothelial cells, mononuclear phagocytes, and hepatocytes are themain targets of infection. After infection, a secreted glycoprotein(sGP) known as the Ebola virus glycoprotein (GP) is synthesized.Ebola replication overwhelms protein synthesis of infected cells andhost immune defenses. The GP forms a trimeric complex, which bindsthe virus to the endothelial cells lining the interior surface of bloodvessels. The sGP forms a dimeric protein that interferes with thesignaling of neutrophils, a type of white blood cell, which allows thevirus to evade the immune system by inhibiting early steps ofneutrophil activation. These white blood cells also serve as carriers totransport the virus throughout the entire body to places such as the

lymph nodes, liver, lungs, and spleen.[43]

The presence of viral particles and cell damage resulting from buddingcauses the release of cytokines (to be specific, TNF-α, IL-6, IL-8,etc.), which are the signaling molecules for fever and inflammation.The cytopathic effect, from infection in the endothelial cells, results ina loss of vascular integrity. This loss in vascular integrity is furtheredwith synthesis of GP, which reduces specific integrins responsible forcell adhesion to the inter-cellular structure, and damage to the liver,

which leads to coagulopathy.[44]

Diagnosis

The medical history, especially travel and work history along with exposure to wildlife are important to suspectthe diagnosis of EVD. The diagnosis is confirmed by isolating the virus, detecting its RNA or proteins, ordetecting antibodies against the virus in a person's blood. Isolating the virus by cell culture, detecting the viralRNA by polymerase chain reaction (PCR) and detecting proteins by enzyme-linked immunosorbent assay(ELISA) is effective early and in those who have died from the disease. Detecting antibodies against the virus is

effective late in the disease and in those who recover.[45]

During an outbreak, virus isolation is often not feasible. The most common diagnostic methods are therefore real

time PCR and ELISA detection of proteins, which can be performed in field or mobile hospitals.[46] Filovirionscan be seen and identified in cell culture by electron microscopy due to their unique filamentous shapes, butelectron microscopy cannot tell the difference between the various filoviruses despite there being some length

differences.[41]

Classification

The genera Ebolavirus and Marburgvirus wereoriginally classified as the species of the now-obsoleteFilovirus genus. In March 1998, the Vertebrate Virus

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Phylogenetic tree comparing the Ebolavirus and

Marburgvirus. Numbers indicate percent confidence

of branches.

A researcher working with the Ebola

virus while wearing a BSL-4 positive

pressure suit to avoid infection

Subcommittee proposed in the International Committeeon Taxonomy of Viruses (ICTV) to change theFilovirus genus to the Filoviridae family with twospecific genera: Ebola-like viruses and Marburg-likeviruses. This proposal was implemented in Washington,DC, on April 2001 and in Paris on July 2002. In 2000,another proposal was made in Washington, D.C., tochange the "-like viruses" to "-virus" resulting in today's

Ebolavirus and Marburgvirus.[47]

Rates of genetic change are 100 times slower thaninfluenza A in humans, but on the same magnitude asthose of hepatitis B. Extrapolating backwards usingthese rates indicates that Ebolavirus and Marburgvirus

diverged several thousand years ago.[48] However,paleoviruses (genomic fossils) of filoviruses (Filoviridae)found in mammals indicate that the family itself is at least

tens of millions of years old.[49] Fossilized viruses thatare closely related to ebolaviruses have been found in

the genome of the Chinese hamster.[50]

Differential diagnosis

The symptoms of EVD are similar to those of Marburg virus disease.[51] It can also easily be confused withmany other diseases common in Equatorial Africa such as other viral hemorrhagic fevers, falciparum malaria,typhoid fever, shigellosis, rickettsial diseases such as typhus, cholera, gram-negative septicemia, borreliosis suchas relapsing fever or EHEC enteritis. Other infectious diseases that should be included in the differentialdiagnosis include the following: leptospirosis, scrub typhus, plague, Q fever, candidiasis, histoplasmosis,trypanosomiasis, visceral leishmaniasis, hemorrhagic smallpox, measles, and fulminant viral hepatitis. Non-infectious diseases that can be confused with EVD are acute promyelocytic leukemia, hemolytic uremicsyndrome, snake envenomation, clotting factor deficiencies/platelet disorders, thrombotic thrombocytopenic

purpura, hereditary hemorrhagic telangiectasia, Kawasaki disease, and even warfarin poisoning.[52][53][54][55]

Prevention

Behavioral changes

Ebola viruses are contagious, with prevention predominantly involvingbehavior changes, proper full-body personal protective equipment,and disinfection. Techniques to avoid infection involve not contacting

infected blood or secretions, including from those who are dead.[16]

This involves suspecting and diagnosing the disease early and using

standard precautions for all patients in the healthcare setting.[56]

Recommended measures when caring for those who are infectedinclude isolating them, sterilizing equipment, and wearing protective

clothing including masks, gloves, gowns, and goggles.[16] Handwashing is important but can be difficult in areas where there is not

even enough water for drinking.[9]

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Due to lack of proper equipment and hygienic practices, large-scale epidemics have occurred mostly in poor,isolated areas without modern hospitals or well-educated medical staff. Traditional burial rituals, especially those

requiring embalming of bodies, should be discouraged or modified.[56] Airline crews, who fly to these areas of

the world, are taught to identify Ebola and isolate anyone who has symptoms.[57]

Quarantine

Quarantine, also known as enforced isolation, is usually effective in decreasing spread.[58][59] Governments

often quarantine areas where the disease is occurring or individuals who may be infected.[60] In the United

States, the law allows quarantine of those infected with Ebola.[61] The lack of roads and transportation may help

slow the disease in Africa. During the 2014 outbreak, Liberia closed schools.[62]

Vaccine

No vaccine is currently available for humans.[1][63][64] The most promising candidates are DNA vaccines[65] or

vaccines derived from adenoviruses,[66] vesicular stomatitis Indiana virus (VSIV)[67][68][69] or filovirus-like

particles (VLPs)[70] because these candidates could protect nonhuman primates from ebolavirus-induceddisease. DNA vaccines, adenovirus-based vaccines, and VSIV-based vaccines have entered clinical

trials.[71][72][73][74]

Vaccines have protected nonhuman primates. Immunization takes six months, which impedes the counter-epidemic use of the vaccines. Searching for a quicker onset of effectiveness, in 2003, a vaccine using anadenoviral (ADV) vector carrying the Ebola spike protein was tested on crab-eating macaques. Twenty-eight

days later, they were challenged with the virus and remained resistant.[66] A vaccine based on attenuatedrecombinant vesicular stomatitis virus (VSV) vector carrying either the Ebola glycoprotein or the Marburg

glycoprotein in 2005 protected nonhuman primates,[75] opening clinical trials in humans.[71] The study byOctober completed the first human trial, over three months giving three vaccinations safely inducing an immuneresponse. Individuals for a year were followed, and, in 2006, a study testing a faster-acting, single-shot vaccine

began; this new study was completed in 2008.[72] Trying the vaccine on a strain of Ebola that more resemblesone that infects humans is the next step.

On 6 December 2011, the development of a successful vaccine against Ebola for mice was reported. Unlike the

predecessors, it can be freeze-dried and thus stored for long periods in wait for an outbreak.[76] Anexperimental vaccine made by researchers at Canada's national laboratory in Winnipeg was used, in 2009, to

pre-emptively treat a German scientist who might have been infected during a lab accident.[77] However, actual

EBOV infection could never be demonstrated without a doubt.[78] Experimentally, recombinant vesicularstomatitis Indiana virus (VSIV) expressing the glycoprotein of EBOV or SUDV has been used successfully in

nonhuman primate models as post-exposure prophylaxis.[79][80]

Laboratory

Ebola viruses are World Health Organization Risk Group 4 pathogens, requiring biosafety level 4-equivalentcontainment. Laboratory researchers must be properly trained in BSL-4 practices and wear proper personalprotective equipment.

Treatment

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A hospital isolation ward in Gulu,

Uganda, during the October 2000

outbreak

No ebolavirus-specific treatment exists.[64] Treatment is primarilysupportive in nature and includes minimizing invasive procedures,balancing fluids and electrolytes to counter dehydration, administration ofanticoagulants early in infection to prevent or control disseminatedintravascular coagulation, administration of procoagulants late in infectionto control bleeding, maintaining oxygen levels, pain management, and theuse of medications to treat bacterial or fungal secondary

infections.[81][82][83] Early treatment may increase the chance of

survival.[84] A number of experimental treatments are being studied.[85]

In the United States, the FDA's animal efficacy rule can be used incombination with a phase I clinical trial to demonstrate reasonable safetyfor an experimental, unapproved drug, to obtain permission to treatpeople who are infected with Ebola with the drug under the Expanded access program. The Animal EfficacyRule exists, because the normal path for testing the safety and efficacy of drugs is not possible for diseases

caused by dangerous pathogens or toxins.[86] The FDA allowed two drugs, ZMapp and an RNA interferencedrug called "TKM-Ebola", to be used in people infected with Ebola under these programs during the 2014

outbreak.[87]

The unavailability of experimental treatments in the most affected regions during the 2014 outbreak spurredcontroversy, with some calling for experimental drugs to be made more widely available in Africa on ahumanitarian basis, and others warning that making unproven experimental drugs widely available would beunethical, especially in light of past experimentation conducted in developing countries by Western drug

companies.[88][89] As a result of the controversy, the World Health Organization convened an expert meeting ofbioethicists on 11 August 2014 to consider the implications of making the experimental treatment more widely

available.[90] The panel reached consensus that the circumstances warrant the use of unproven interventions withas yet unknown efficacy and adverse effects both for treatment and for prevention, and also said that decidingwhich treatments should be used and how to distribute them equitably were matters that needed further

discussion.[91]

Prognosis

The disease has a high mortality rate: often between 50 percent and 90 percent.[1][3] As of April 2014,

information from WHO across all occurrences to date puts the overall fatality rate at 60%-65%.[1] There areindications based on variations in death rate between countries that early and effective treatment of symptoms

(e.g., supportive care to prevent dehydration) may reduce the fatality rate significantly.[92] If an infected personsurvives, recovery may be quick and complete. Prolonged cases are often complicated by the occurrence oflong-term problems, such as inflammation of the testicles, joint pains, muscle pains, skin peeling, or hair loss.Eye symptoms, such as light sensitivity, excess tearing, iritis, iridocyclitis, choroiditis, and blindness have alsobeen described. EBOV and SUDV may be able to persist in the semen of some survivors for up to seven

weeks, which could give rise to infections and disease via sexual intercourse.[1]

Epidemiology

The disease typically occurs in outbreaks in tropical regions of Sub-Saharan Africa.[1] From 1976 (when it was

first identified) through 2013, fewer than 1,000 people per year have been infected.[1][4] The largest outbreak todate is the ongoing 2014 West Africa Ebola virus outbreak, which is affecting Guinea, Sierra Leone,Liberia and

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CDC worker incinerates medical

waste from Ebola patients in Zaire in

1976

Nigeria[5][6] As of the end of July 2014, more than 1320 cases have been identified.[5]

1976

The first identified case of Ebola was on 26 August 1976, inYambuku, a small rural village in Mongala District in northern

Democratic Republic of the Congo (DRC, then known as Zaire).[93]

The first victim, and the index case for the disease, was village schoolheadmaster Mabalo Lokela, who had toured an area near the CentralAfrican Republic border along the Ebola river between 12-22August. On 8 September he died of what would become known as

the Ebola virus species of the ebolavirus.[94] Subsequently a numberof other cases were reported, almost all centered on the Yambuku

mission hospital or having close contact with another case.[95] 318cases and 280 deaths occurred in the DRC. The Ebola outbreak wascontained with the help of the World Health Organization andtransport from the Congolese air force, by quarantining villagers,sterilizing medical equipment, and providing protective clothing. Thevirus responsible for the initial outbreak, first thought to be Marburgvirus was later identified as a new type of virus related to Marburg,and named after the nearby Ebola river. Another ebolavirus, theSudan virus species, was also identified that same year when an

outbreak occurred in Sudan, affecting 284 people and killing 151.[96]

1995 to 2013

The second major outbreak occurred in 1995 in the Democratic Republic of Congo, affecting 315 and killing254. The next major outbreak occurred in Uganda in 2000, affecting 425 and killing 224; in this case the Sudan

virus was found to be the ebolavirus species responsible for the outbreak. .[97]

In August 2007, 103 people were infected by a suspected hemorrhagic fever outbreak in the village ofKampungu, Democratic Republic of the Congo. The outbreak started after the funerals of two village chiefs, and217 people in four villages fell ill. The World Health Organization sent a team to take blood samples for analysis

and confirmed that many of the cases were the result of Ebolavirus.[98][99] [100] The 2007 outbreak eventuallyaffected 264 individuals and resulted in the deaths of 187.

On 30 November 2007, the Uganda Ministry of Health confirmed an outbreak of Ebola in the BundibugyoDistrict. After confirmation of samples tested by the United States National Reference Laboratories and theCenters for Disease Control, the World Health Organization confirmed the presence of a new species of

Ebolavirus, which was tentatively named Bundibugyo.[101] The epidemic came to an official end on 20February 2008. While it lasted, 149 cases of this new strain were reported, and 37 of those led to deaths.

On 25 December 2008, it was reported that the Ebola virus had killed 9 and infected 21 people in the Western

Kasai province of the Democratic Republic of Congo.[102] On 29 December, Doctors Without Bordersreported 11 deaths in the same area, stating that a further 24 cases were being treated. In January 2009, Angolaclosed down part of its border with the Democratic Republic of Congo to prevent the spread of the

outbreak.[103]

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Increase over time in the cases and

deaths during the 2014 outbreak.

The Who confirmed two small outbreaks in Uganda in 2012. The first outbreak affected 7 people and resultedin the death of 4 and the second affected 24, resulting in the death of 17. The Sudan variant was responsible forboth outbreaks.

On 17 August 2012, the Ministry of Health of the Democratic Republic of the Congo reported an outbreak of

the Ebola-Bundibugyo variant[104] in the eastern region.[105] By 21 August, the WHO reported a total of 15

cases and 10 fatalities.[106] No evidence suggested that this outbreak was connected to the Ugandan

outbreak.[107] By 13 September 2012, the WHO revealed that the virus had claimed 32 lives and that theprobable cause of the outbreak was tainted bush meat hunted by local villagers around the towns of Isiro and

Viadana.[108]

2014 outbreak

In March 2014, the World Health Organization (WHO) reported amajor Ebola outbreak in Guinea, a western African nation; it is the

largest ever documented, and the first recorded in the region.[109]

Researchers traced the outbreak to a two-year old child who died on

6 December.[110] As of 10 April 2014, WHO reported 157suspected and confirmed cases in Guinea, 22 suspected cases inLiberia, 8 suspected cases in Sierra Leone, and 1 suspected case in

Mali.[111][112] By 31 July 2014, they reported that the death toll had

reached 826 people from 1440 cases.[113] On 8 August, the WHOdeclared the epidemic to be an international public health emergency.Urging the world to offer aid to the affected regions, the Director-General said, "Countries affected to datesimply do not have the capacity to manage an outbreak of this size and complexity on their own. I urge the

international community to provide this support on the most urgent basis possible."[114][115] Further attempts tocontain the outbreak were enacted by placing troops on roads to cordon off the infected areas and stop those

who may be infected from leaving and further spreading the virus.[116]

Emory University Hospital was the first US hospital to care for people exposed to Ebola.[117] In July 2014, twoAmerican medical providers were exposed while treating infected patients in Liberia. In August, arrangementswere made for them to be transported to Emory via speciality aircraft. Emory Hospital has a specially builtisolation unit set up in collaboration with the CDC to treat people exposed to certain serious infectious

diseases.[118][119][120][121]

History

Ebola virus was first isolated in 1976 during outbreaks of Ebola hemorrhagic fever in Zaire[122] and Sudan.[123]

The strain of Ebola that broke out in Zaire has one of the highest case fatality rates of any human virus, roughly

90%.[124]

The name of the disease originates from one of those first recorded outbreaks in 1976 in Yambuku, Democratic

Republic of the Congo (then Zaire), which lies on the Ebola River.[122]

In late 1989, Hazelton Research Products' Reston Quarantine Unit in Reston, Virginia, suffered a mysteriousoutbreak of fatal illness (initially diagnosed as Simian hemorrhagic fever virus (SHFV)) among a shipment ofcrab-eating macaque monkeys imported from the Philippines. Hazelton's veterinary pathologist sent tissue

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Cases of ebola fever in Africa from 1979 to 2008.

samples from dead animals to the United States Army Medical Research Institute of Infectious Diseases(USAMRIID) at Fort Detrick, Maryland, where a laboratory test known as an ELISA assay showed antibodies

to Ebola virus.[125] An electron microscopist from USAMRIID discovered filoviruses similar in appearance toEbola in tissue samples taken from crab-eating macaque imported from the Philippines to Hazleton Laboratories

Reston, Virginia.[126]

Shortly afterward, a US Army team headquartered at USAMRIID went into action to euthanize the monkeyswhich had not yet died, bringing those monkeys and those which had already died of the disease to Ft. Detrick

for study by the Army's veterinary pathologists and virologists, and eventual disposal under safe conditions.[125]

Blood samples were taken from 178 animal

handlers during the incident.[127] Of those, sixanimal handlers eventually seroconverted. Whenthe handlers did not become ill, the CDCconcluded that the virus had a very low

pathogenicity to humans.[128]

The Philippines and the United States had noprevious cases of Ebola infection, and uponfurther isolation, researchers concluded it wasanother strain of Ebola, or a new filovirus ofAsian origin, which they named Restonebolavirus (REBOV) after the location of the

incident.[125]

Some scientists also believe that the Plague ofAthens, which wiped out about a third of itsinhabitants during the Peloponnesian War, may have been caused by Ebola. However, these studies are

conflicting, and point to other possible diseases such as typhoid.[129]

Society and culture

Given the lethal nature of Ebola, and since no approved vaccine or treatment is available, it is classified as abiosafety level 4 agent, as well as a Category A bioterrorism agent by the Centers for Disease Control and

Prevention. It has the potential to be weaponized for use in biological warfare.[130][131]

Other animals

In general, outbreaks of EVD among human populations result from handling infected wild animal carcasses. Ingeneral, declines in animal populations precede outbreaks among human populations. Since 2003, such declineshave been monitored through surveillance of animal populations with the aim of predicting and preventing EVD

outbreaks in humans.[132] Recovered carcasses from gorillas contain multiple Ebola virus strains, which suggestmultiple introductions of the virus. Bodies decompose quickly and carcasses are not infectious after three to fourdays. Contact between gorilla groups is rare, suggesting transmission among gorilla groups is unlikely, and that

outbreaks result from transmission between viral reservoir and animal populations.[133]

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Researchers looking at slides of

cultures of cells that make

monoclonal antibodies. These are

grown in a lab and the researchers

are analyzing the products to

select the most promising of

them.

Ebola has a high mortality among primates.[134] Frequent outbreaks of Ebola may have resulted in the deaths of

5,000 gorillas.[135] Outbreaks of EVD may have been responsible for an 88% decline in tracking indices of

observed chimpanzee populations in 420 square kilometer Lossi Sanctuary between 2002 and 2003.[133]

Transmission among chimpanzees through meat consumption constitutes a significant risk factor, while contact

between individuals, such as touching dead bodies and grooming, is not.[136]

Domestic animals

Ebola virus can be transmitted to dogs and pigs.[137] While dogs may be asymptomatic, pigs tend to developsymptomatic disease.

Research

Medications

Favipiravir looks like it may be useful in a mouse model of the disease.[9] Estrogen receptor drugs used to treat

infertility and breast cancer (clomiphene and toremifene) inhibit the progress of Ebola virus in infected mice.[138]

Ninety percent of the mice treated with clomiphene and fifty percent of those treated with toremifene survived

the tests.[138] Given their oral availability and history of human use, these drugs would be candidates for treatingEbola virus infection in remote geographical locations, either on their own or together with other antiviral drugs.

Antibodies

During an outbreak 1999 in the Democratic Republic of the Congo,seven of eight people who received blood transfusions from individuals

who had previously survived the infection survived themselves.[139]

However, this potential treatment is considered controversial.[140]

Intravenous antibodies appear to be protective in non-human primates

who have been exposed to large doses of Ebola.[141]

Use of untested experimental drugs

On 31 July 2014, an experimental drug, ZMapp, was first tested onhumans. It was administered to two Americans who had been infected

with Ebola. Both people appeared to have had positive results.[142][143]

Soon thereafter ZMapp was administered to a third Ebola patient, a 75

year old priest, who nonetheless died.[144]

On 12 August the WHO released an advisory statement regarding the ongoing Ebola outbreak, recommendingspecifically for the more widespread use of the compassionate use exemption for experimental drugs, in effortsto contain the ongoing Ebola outbreak, with the aim of more quickly halting and eliminating the current Ebola

outbreak.[145]

Other treatments

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Other promising treatments rely on antisense technology. Both small interfering RNAs (siRNAs) andphosphorodiamidate morpholino oligomers (PMOs) targeting the Zaire Ebola virus (ZEBOV) RNA polymerase

L protein could prevent disease in nonhuman primates.[146][147] TKM-Ebola is a small-interfering RNA

compound, currently tested in a phase I clinical trial in people.[148][87]

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the Swiss Institute of Bioinformatics

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Special Pathogens Branch

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Global Alert and Response

Virus Pathogen Database and Analysis Resource (ViPR): Filoviridae (http://www.viprbrc.org/brc/home.do?

decorator=filo)

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postexposure protection against lethal filovirus infections". Nature Medicine 16 (9): 991–994.

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1.2726740). The Canadian Press.

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3D macromolecular structures of the Ebola virus archived in the EM Data Bank(EMDB)

(http://www.ebi.ac.uk/pdbe/emdb/searchResults.html/?q=ebola)

Google Map of Ebola Outbreaks (https://maps.google.com/maps/ms?

msa=0&msid=202977755949863934429.0004c658eb30f9c4fb1c0&ie=UTF8&t=h&ll=27.371767,5.273438&s

pn=110.017392,184.21875&z=2&source=embed&dg=feature)

WHO recommended infection control measures

(http://www.who.int/csr/bioriskreduction/filovirus_infection_control/en/)

Retrieved from "http://en.wikipedia.org/w/index.php?title=Ebola_virus_disease&oldid=621381246"

Categories: Ebola Health in Africa

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