Ebola virus disease

Ebola redirects here. For other uses, see Ebola

(disambiguation).
Ebola virus disease (EVD), Ebola hemorrhagic fever
(EHF) or simply Ebola is a disease of humans and other
primates caused by an ebolavirus. Symptoms start two
days to three weeks after contracting the virus, with a
fever, sore throat, muscle pain and headaches. Typically,
vomiting, diarrhea and rash follow, along with decreased
function of the liver and kidneys. Around this time, af-
fected people may begin to bleed both within the body
and externally.
[1]
The virus may be acquired upon contact with blood
or other bodily uids of an infected human or other
animal.
[1]
Spreading through the air has not been docu-
mented in the natural environment.
[2]
Fruit bats are be-
lieved to be a carrier and may spread the virus without
being aected. Once human infection occurs, the dis-
ease may spread between people as well. Male survivors
may be able to transmit the disease via semen for nearly
two months. To diagnose EVD, other diseases with sim-
ilar symptoms such as malaria, cholera and other viral
hemorrhagic fevers are rst excluded. Blood samples are
tested for viral antibodies, viral RNA, or the virus itself
to conrm the diagnosis.
[1]
Outbreak control requires community engagement, case
management, surveillance and contact tracing, appropri-
ate laboratory service, and proper disposal of remains
through cremation or burial.
[1][3]
Prevention includes de-
creasing the spread of disease from infected animals to
humans. This may be done by checking such animals for
infection and killing and properly disposing of the bodies
if the disease is discovered. Properly cooking meat and
wearing protective clothing when handling meat may also
be helpful, as are wearing protective clothing and washing
hands when around a person with the disease. Samples
of bodily uids and tissues from people with the disease
should be handled with special caution.
[1]
No specic treatment for the disease is yet available.
[1]
Eorts to help those who are infected are supportive and
include giving either oral rehydration therapy (slightly
sweet and salty water to drink) or intravenous uids.
[1]
This supportive care improves outcomes.
[1]
The disease
has a high risk of death, killing between 25% and 90%
of those infected with the virus (average is 50%).
[1]
EVD
was rst identied in an area of Sudan that is now part of
South Sudan, as well as in Zaire (now 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 rst identied) through 2013,
the World Health Organization reported a total of 1,716
cases.
[1][4]
The largest outbreak to date is the ongoing
2014 West African Ebola outbreak, which is aecting
Guinea, Sierra Leone, Liberia, and Nigeria.
[5][6]
As of
3 October 2014, 7,497 suspected cases resulting in the
deaths of 3,439 have been reported.
[7]
Eorts are under
way to develop a vaccine; however, none yet exists.
[1]
1 Signs and symptoms
Signs and symptoms of Ebola.
[8]
Signs and symptoms of Ebola virus disease (EVD) usually
begin suddenly with an inuenza-like stage characterized
by fatigue, fever, headaches, and pain in the joints, mus-
cles, and abdomen.
[9][10]
Vomiting, diarrhea, and loss of
appetite are also common.
[10]
Less common symptoms
include the following: sore throat, chest pain, hiccups,
shortness of breath, and trouble swallowing.
[10]
The aver-
age time between contracting the infection and the start
of symptoms (incubation period) is 8 to 10 days, but it
can vary between 2 and 21 days.
[10][11]
Skin manifesta-
tions may include a maculopapular rash (in about 50%
of cases).
[12]
Early symptoms of EVD may be similar to
those of malaria, dengue fever, or other tropical fevers,
before the disease progresses to the bleeding phase.
[9]
In 4050% of cases, bleeding from puncture sites and
1
2 2 CAUSES
mucous membranes (e.g., gastrointestinal tract, nose,
vagina, and gums) has been reported.
[13]
In the bleeding
phase, which typically begins ve to seven days after rst
symptoms,
[14]
internal and subcutaneous bleeding may
present itself in the form of reddened eyes and bloody
vomit.
[9]
Bleeding into the skin may create petechiae,
purpura, ecchymoses, and hematomas (especially around
needle injection sites).
[15]
Suerers may cough up blood,
vomit it, or excrete it in their stool.
[16]
Heavy bleeding is rare and is usually conned to the gas-
trointestinal tract.
[12][17]
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 signs of circulatory system involvement, in-
cluding impaired blood clotting.
[12]
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 rst symptoms.
[14]
2 Causes
Main articles: Ebolavirus (taxonomic group) and Ebola
virus (specic virus)
EVD is caused by four of ve viruses classied
Life cycles of the Ebolavirus
in the genus Ebolavirus, family Filoviridae, order
Mononegavirales. The four disease-causing viruses are
Bundibugyo virus (BDBV), Sudan virus (SUDV), Ta
Forest virus (TAFV), and one called, simply, Ebola virus
(EBOV, formerly Zaire Ebola virus). Ebola virus is the
sole member of the Zaire ebolavirus species and the most
dangerous of the known EVD-causing viruses, as well as
being responsible for the largest number of outbreaks.
[18]
The fth virus, Reston virus (RESTV), is not thought
to be disease-causing in humans. These ve viruses are
closely related to marburgviruses.
2.1 Transmission
Human-to-human transmission can occur via direct con-
tact with blood or body uid from an infected person
(including embalming of an infected dead person) or by
contact with objects contaminated by the virus, particu-
larly needles and syringes.
[19]
Other body uids that may
transmit ebolaviruses include saliva, mucus, vomit, fe-
ces, sweat, tears, breast milk, urine, and semen. Entry
points include the nose, mouth, eyes, or open wounds,
cuts and abrasions.
[20]
The potential for widespread EVD
infections is considered low as the disease is only spread
by direct contact with the secretions from someone who
is showing signs of infection.
[19]
The symptoms limit a
persons ability to spread the disease as they are often
too sick to travel.
[21]
Because dead bodies are still in-
fectious, traditional burial rituals may spread the disease.
Nearly two thirds of the cases of Ebola in Guinea dur-
ing the 2014 outbreak are believed to be due to burial
practices.
[22][23]
Semen may be infectious in survivors for
up to 7 weeks.
[1]
It is not entirely clear how an outbreak
is initially started.
[24]
The initial infection is believed to
occur after an ebolavirus is transmitted to a human by
contact with an infected animals body uids.
One of the primary reasons for spread is that the health
systems in the part of Africa where the disease occurs
function poorly.
[25]
Medical workers who do not wear ap-
propriate protective clothing may contract the disease.
[26]
Hospital-acquired transmission has occurred in African
countries due to the reuse of needles and lack of universal
precautions.
[27][28]
Some healthcare centers caring for
people with the disease do not have running water.
[29]
Airborne transmission has not been documented dur-
ing EVD outbreaks.
[2]
They are, however, infectious as
breathable 0.81.2 m laboratory-generated droplets.
[30]
The virus has been shown to travel, without contact,
from pigs to primates, although the same study failed
to demonstrate similar transmission between non-human
primates.
[31]
Bats drop partially eaten fruits and pulp, then land mam-
mals such as gorillas and duikers feed on these fallen
fruits. This chain of events forms a possible indirect
means of transmission from the natural host to animal
populations, which has led to research towards viral shed-
ding in the saliva of bats. Fruit production, animal behav-
ior, and other factors vary at dierent times and places
that may trigger outbreaks among animal populations.
[32]
2.2 Reservoir
Bats are considered the most likely natural reservoir
of EBOV. Plants, arthropods, and birds were also
considered.
[1][34]
Bats were known to reside in the cotton
factory in which the rst cases for the 1976 and 1979 out-
breaks were observed, and they have also been implicated
in Marburg virus infections in 1975 and 1980.
[35]
Of 24
plant species and 19 vertebrate species experimentally
inoculated with EBOV, only bats became infected.
[36]
The absence of clinical signs in these bats is character-
istic of a reservoir species. In a 20022003 survey of
2.3 Virology 3
Bushmeat being prepared for cooking in Ghana, 2013. Human
consumption of equatorial animals in Africa in the formof bush-
meat has been linked to the transmission of diseases to people,
including Ebola.
[33]
1,030 animals including 679 bats from Gabon and the
Republic of the Congo, 13 fruit bats were found to contain
EBOV RNA fragments.
[37]
As of 2005, three types of
fruit bats (Hypsignathus monstrosus, Epomops franqueti,
and Myonycteris torquata) have been identied as being
in contact with EBOV. They are now suspected to repre-
sent the EBOV reservoir hosts.
[38][39]
Antibodies against
Zaire and Reston viruses have been found in fruit bats
in Bangladesh, thus identifying potential virus hosts and
signs of the loviruses in Asia.
[40]
Between 1976 and 1998, in 30,000 mammals, birds,
reptiles, amphibians and arthropods sampled from out-
break regions, no Ebola virus was detected apart from
some genetic traces found in six rodents (Mus setulo-
sus and Praomys) and one shrew (Sylvisorex ollula) col-
lected from the Central African Republic.
[35][41]
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 lethality from infection in these species makes
them unlikely as a natural reservoir.
[35]
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.
[42]
Fruit bats are also eaten by peo-
ple in parts of West Africa where they are smoked, grilled
or made into a spicy soup.
[39][43]
2.3 Virology
Main articles: Ebolavirus (taxonomic group) and Ebola
virus (specic virus)
Electron micrograph of an Ebola virus virion
2.3.1 Genome
Like all mononegaviruses, ebolavirions contain lin-
ear nonsegmented, single-strand, non-infectious RNA
genomes of negative polarity that possesses inverse-
complementary 3' and 5' termini, do not possess a
5' cap, are not polyadenylated, and are not covalently
linked to a protein.
[44]
Ebolavirus genomes are ap-
proximately 19 kilobase pairs long and contain seven
genes in the order 3'-UTR-NP-VP35-VP40-GP-VP30-
VP24-L-5'-UTR.
[45]
The genomes of the ve dier-
ent ebolaviruses (BDBV, EBOV, RESTV, SUDV, and
TAFV) dier in sequence and the number and location
of gene overlaps.
2.3.2 Structure
Like all loviruses, ebolavirions are lamentous particles
that may appear in the shape of a shepherds crook or
in the shape of a U or a 6, and they may be coiled,
toroid, or branched.
[45]
In general, ebolavirions are 80 nm
in width, but vary somewhat in length. In general, the me-
dian particle length of ebolaviruses ranges from 974 to
1,086 nm (in contrast to marburgvirions, whose median
particle length was measured at 795828 nm), but par-
ticles as long as 14,000 nm have been detected in tissue
culture.
[46]
2.3.3 Replication
The ebolavirus life cycle begins with virion attachment
to specic cell-surface receptors, followed by fusion
of the virion envelope with cellular membranes and
the concomitant release of the virus nucleocapsid into
the cytosol. 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 pro-
teins. Ebolavirus RNA polymerase (L) binds to a sin-
gle promoter located at the 3' end of the genome. Tran-
scription either 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 great-
est abundance, whereas those toward the 5' end are least
likely to be transcribed. The gene order is, therefore, a
4 4 DIAGNOSIS
simple but eective form of transcriptional regulation.
The most abundant protein produced is the nucleopro-
tein, whose concentration in the cell determines when
L switches from gene transcription to genome replica-
tion. Replication results in full-length, positive-strand
antigenomes that are, in turn, transcribed into negative-
strand virus progeny genome copy. Newly synthesized
structural proteins and genomes self-assemble and accu-
mulate near the inside of the cell membrane. Virions bud
o fromthe cell, gaining their envelopes fromthe cellular
membrane they bud from. The mature progeny particles
then infect other cells to repeat the cycle. The Ebola virus
genetics are dicult to study due to its virulent nature.
[47]
3 Pathophysiology
Pathogenesis schematic
Endothelial cells, macrophages, monocytes, and liver
cells are the main targets of infection. After infection,
a secreted glycoprotein (sGP) known as the Ebola virus
glycoprotein (GP) is synthesized. Ebolavirus replication
overwhelms protein synthesis of infected cells and host
immune defenses. The GP forms a trimeric complex,
which binds the virus to the endothelial cells lining the in-
terior surface of blood vessels. The sGP forms a dimeric
protein that interferes with the signaling of neutrophils, a
type of white blood cell, which allows the virus to evade
the immune systemby inhibiting early steps of neutrophil
activation. These white blood cells also serve as carriers
to transport the virus throughout the entire body to places
such as the lymph nodes, liver, lungs, and spleen.
[48]
The presence of viral particles and cell damage result-
ing from budding causes the release of chemical sig-
nals (TNF-, IL-6, IL-8, etc.), which are the signaling
molecules for fever and inammation. The cytopathic ef-
fect, from infection in the endothelial cells, results in a
loss of vascular integrity. This loss in vascular integrity
is furthered with synthesis of GP, which reduces spe-
cic integrins responsible for cell adhesion to the inter-
cellular structure, and damage to the liver, which leads to
improper clotting.
[49]
4 Diagnosis
The travel and work history along with exposure to
wildlife are important to consider when the diagnosis of
EVD is suspected. The diagnosis is conrmed by isolat-
ing the virus, detecting its RNA or proteins, or detecting
antibodies against the virus in a persons blood. Isolat-
ing the virus by cell culture, detecting the viral RNA by
polymerase chain reaction (PCR) and detecting proteins
by enzyme-linked immunosorbent assay (ELISA) works
best early and in those who have died from the disease.
Detecting antibodies against the virus works best late in
the disease and in those who recover.
[50]
During an outbreak, virus isolation is often not feasi-
ble. The most common diagnostic methods are therefore
real-time PCR and ELISA detection of proteins, which
can be performed in eld or mobile hospitals.
[51]
Filoviri-
ons can be seen and identied in cell culture by electron
microscopy due to their unique lamentous shapes, but
electron microscopy cannot tell the dierence between
the various loviruses despite there being some length
dierences.
[46]
Marburg
Ebola
.5 subst/site
100
94
99/94
94
98
99/58
90
96
100
100
100
100
09 DRC 1999
Ravn , Kenya 1987
Ozonlins, Zimbabwe 1975
Popp, Uganda/Germany 1967
Musoke, Kenya 1980
Zaire, Yambuku 1976
Zaire, Kikwit 1995
Cote dIvoire, 1994
Bundibugyo, Uganda 2007
Reston, USA 1989
Sudan, Gulu Uganda 2000
07 DRC 1999
05 DRC 1999
1379c Angola 2005
Phylogenetic tree comparing the Ebolavirus and Marburgvirus.
Numbers indicate percent condence of branches.
5.2 Quarantine 5
4.1 Classication
The genera Ebolavirus and Marburgvirus were originally
classied as the species of the now-obsolete Filovirus
genus. In March 1998, the Vertebrate Virus Subcom-
mittee proposed in the International Committee on Tax-
onomy of Viruses (ICTV) to change the Filovirus genus
to the Filoviridae family with two specic genera: Ebola-
like viruses and Marburg-like viruses. 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., to change the extquotedbl-
like viruses to extquotedbl-virus resulting in todays
Ebolavirus and Marburgvirus.
[52]
Rates of genetic change are 100 times slower than
inuenza A in humans, but on the same magnitude
as those of hepatitis B. Extrapolating backwards us-
ing these rates indicates that ebolaviruses and mar-
burgviruses diverged several thousand years ago.
[53]
However, paleoviruses (genomic fossils) of loviruses
(Filoviridae) found in mammals indicate that the family
itself is at least tens of millions of years old.
[54]
Fossilized
viruses that are closely related to ebolaviruses have been
found in the genome of the Chinese hamster.
[55]
4.2 Dierential diagnosis
The symptoms of EVD are similar to those of Marburg
virus disease.
[56]
It can also easily be confused with many
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 such as
relapsing fever or EHEC enteritis. Other infectious dis-
eases that should be included in the dierential diagnosis
include the following: leptospirosis, scrub typhus, plague,
Q fever, candidiasis, histoplasmosis, trypanosomiasis,
visceral leishmaniasis, hemorrhagic smallpox, measles,
and fulminant viral hepatitis.
[57]
Non-infectious diseases
that can be confused with EVD are acute promye-
locytic leukemia, hemolytic uremic syndrome, snake
envenomation, clotting factor deciencies/platelet disor-
ders, thrombotic thrombocytopenic purpura, hereditary
hemorrhagic telangiectasia, Kawasaki disease, and even
warfarin poisoning.
[58][59][60][61]
5 Prevention
5.1 Infection control and containment
The risk of transmission is increased among those car-
ing for people infected. Recommended measures when
caring for those who are infected include isolating them,
sterilizing equipment and surfaces, and wearing pro-
tective clothing including masks, gloves, gowns, and
A researcher working with the Ebola virus while wearing a BSL-
4 positive pressure suit to avoid infection
goggles.
[24]
If a person with Ebola dies, direct con-
tact with the body of the deceased patient should be
avoided.
[24]
In order to reduce the spread, the World Health Organi-
zation recommends raising community awareness of the
risk factors for Ebola infection and the protective mea-
sures individuals can take.
[62]
These include avoiding con-
tact with infected people and regular hand washing us-
ing soap and water.
[63]
Traditional burial rituals, espe-
cially those requiring washing or embalming of bodies,
should be discouraged or modied.
[64][65]
Social anthro-
pologists may help nd alternatives to traditional rules for
burials.
[66]
Airline crews are instructed to isolate anyone
who has symptoms resembling Ebola virus disease.
[67]
Ebolaviruses can be eliminated with heat (heating for
30 to 60 minutes at 60 C or boiling for 5 minutes).
On surfaces, some lipid solvents such as some alcohol-
based products, detergents, sodium hypochlorite (bleach)
or calcium hypochlorite (bleaching powder), and other
suitable disinfectants at appropriate concentrations can be
used as disinfectants.
[68][69]
In laboratories where diagnostic testing is carried out,
biosafety level 4-equivalent containment is required,
since ebolaviruses are World Health Organization Risk
Group 4 pathogens. Laboratory researchers must be
properly trained in BSL-4 practices and wear proper per-
sonal protective equipment.
5.2 Quarantine
Quarantine, also known as enforced isolation, is usu-
ally eective in decreasing spread.
[70][71]
Governments
often quarantine areas where the disease is occurring
or individuals who may be infected.
[72]
In the United
States, the law allows quarantine of those infected
with ebolaviruses.
[73]
During the 2014 outbreak, Liberia
closed schools.
[74]
6 8 EPIDEMIOLOGY
5.3 Contact tracing
Contact tracing is regarded as important to contain an
outbreak. It involves nding everyone who had close
contact with infected individuals and watching for signs
of illness for 21 days. If any of these contacts comes
down with the disease, they should be isolated, tested, and
treated. Then repeat the process by tracing the contacts
contacts.
[75][76]
6 Treatment
6.1 Standard support
A hospital isolation ward in Gulu, Uganda, during the October
2000 outbreak
No ebolavirus-specic treatment is currently
approved.
[77]
However, survival is improved by early
supportive care with rehydration and symptomatic
treatment.
[1]
Treatment is primarily supportive in
nature.
[78]
These measures may include management of
pain, nausea, fever and anxiety, as well as rehydration via
the oral or by intravenous route.
[78]
Blood products such
as packed red blood cells, platelets or fresh frozen plasma
may also be used.
[78]
Other regulators of coagulation
have also been tried including heparin in an eort to
prevent disseminated intravascular coagulation and
clotting factors to decrease bleeding.
[78]
Antimalarial
medications and antibiotics are often used before the
diagnosis is conrmed,
[78]
though there is no evidence to
suggest such treatment is in any way helpful.
6.2 Intensive care
Intensive care is often used in the developed world.
[15]
This may include maintaining blood volume and elec-
trolytes (salts) balance as well as treating any bacterial
infections that may develop.
[15]
Dialysis may be needed
for kidney failure while extracorporeal membrane oxy-
genation may be used for lung dysfunction.
[15]
6.3 Alternative medicine
The Food and Drug Administration (FDA) advises peo-
ple to watch out for fraudulent products to treat Ebola.
[79]
They have send out a warning letter to a seller of colloidal
silver who makes claims of benet.
[80]
7 Prognosis
The disease has a high mortality rate which varies be-
tween 25 percent and 90 percent of those infected.
[1][81]
As of September 2014, information from WHO puts the
average mortality among those infected at 50%.
[1]
The
90% rate was just reported in a single outbreak.
[82]
There
are indications based on variations in death rate between
countries that early and eective treatment of symptoms
(e.g., supportive care to prevent dehydration) may re-
duce the fatality rate signicantly.
[83]
If an infected per-
son survives, recovery may be quick and complete. Pro-
longed cases are often complicated by the occurrence of
long-termproblems, such as inammation 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 also been de-
scribed. 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 inter-
course.
[1]
8 Epidemiology
For more about specic outbreaks and their descriptions,
see List of Ebola outbreaks.
The disease typically occurs in outbreaks in tropical re-
gions of Sub-Saharan Africa.
[1]
From 1976 (when it was
rst identied) through 2013, the World Health Organi-
zation reported 1,716 conrmed cases.
[1][4]
The largest
outbreak to date is the ongoing 2014 West Africa Ebola
virus outbreak, which is aecting Guinea, Sierra Leone,
Liberia and Nigeria.
[5][6]
As of 8 October, 8,033 sus-
pected cases have been identied, with 3,865 deaths.
[7]
8.1 1976
An outbreak of Ebola virus disease (EVD) occurred
between June and November 1976 in southern Sudan
and was caused by Sudan virus (SUDV), one of the
ebolaviruses. The Sudan outbreak infected 284 people
and killed 151. The rst identiable case in Sudan oc-
curred on 27 June in a storekeeper in a cotton factory in
Nzara, who was hospitalized on 30 June and died on 6
July.
[84]
In August 1976, an outbreak of EVD caused by Ebola
virus (formerly called Zaire ebolavirus) began in Yam-
8.3 2014 outbreak 7
CDC worker incinerates medical waste from Ebola patients in
Zaire in 1976
buku, a small rural village in Mongala District in north-
ern Democratic Republic of the Congo (then known as
Zaire), with the rst case identied on 26 August.
[85]
The
rst victim, and the index case for the disease, was vil-
lage school headmaster Mabalo Lokela, who had toured
an area near the Central African Republic border along
the Ebola River between 1222 August. On 8 September
he died of what would become known as the Ebola virus
(EBOV) member of the ebolaviruses.
[86]
Subsequently a
number of other cases were reported, almost all centered
on the Yambuku mission hospital or having close contact
with another case.
[86]
318 cases and 280 deaths (a 88%fa-
tality rate) occurred in the DRC.
[87]
The Zaire outbreak
was contained with the help of the World Health Orga-
nization and transport from the Congolese air force, by
quarantining villagers, sterilizing medical equipment, and
providing protective clothing. The virus responsible for
the initial outbreak, rst thought to be Marburg virus, was
later identied as a new type of virus related to Marburg,
and named after the nearby Ebola river.
8.2 1995 to 2013
The second major outbreak occurred in 1995 in the
Democratic Republic of Congo, aecting 315 and killing
254. The next major outbreak occurred in Uganda in
2000, aecting 425 and killing 224; in this case the Su-
dan virus was found to be the ebolavirus species responsi-
ble for the outbreak.
[88]
In 2003 there was an outbreak in
the Republic of Congo that aected 143 and killed 128,
a death rate of 90%, the highest to date.
[89]
In 2004 a Russian scientist died from Ebola after sticking
herself with an infected needle.
[90]
In August 2007, 103 people were infected by a suspected
hemorrhagic fever outbreak in the village of Kampungu,
Democratic Republic of the Congo. The outbreak started
after the funerals of two village chiefs, and 217 people in
four villages fell ill.
[88][91][92]
The 2007 outbreak eventu-
ally aected 264 individuals and resulted in the deaths of
187.
[1]
On 30 November 2007, the Uganda Ministry of Health
conrmed an outbreak of Ebola in the Bundibugyo Dis-
trict in Western Uganda. After conrmation of sam-
ples tested by the United States National Reference
Laboratories and the Centers for Disease Control, the
World Health Organization conrmed the presence of a
new species of Ebolavirus, which was tentatively named
Bundibugyo.
[93]
The WHO reported 149 cases of this
new strain and 37 of those led to deaths.
[1]
The WHO conrmed two small outbreaks in Uganda in
2012. The rst outbreak aected 7 people and resulted in
the death of 4 and the second aected 24, resulting in the
death of 17. The Sudan variant was responsible for both
outbreaks.
[1]
On 17 August 2012, the Ministry of Health of the Demo-
cratic Republic of the Congo reported an outbreak of the
Ebola-Bundibugyo variant
[94]
in the eastern region.
[95][96]
Other than its discovery in 2007, this was the only time
that this variant has been identied as the ebolavirus re-
sponsible for an outbreak. The WHO revealed that the
virus had sickened 57 people and claimed 29 lives. The
probable cause of the outbreak was tainted bush meat
hunted by local villagers around the towns of Isiro and
Viadana.
[1][97]
8.3 2014 outbreak
Main article: 2014 West Africa Ebola virus outbreak
In March 2014, the World Health Organization (WHO)
reported a major Ebola outbreak in Guinea, a west-
ern African nation.
[98]
Researchers traced the outbreak
to a two-year old child who died on 28 December
2013.
[99][100]
The disease then rapidly spread to the neigh-
boring countries of Liberia and Sierra Leone. It is the
largest Ebola outbreak ever documented, and the rst
recorded in the region.
[98]
On 8 August 2014, the WHO declared the epidemic
to be an international public health emergency. Urg-
ing the world to oer aid to the aected regions, the
Director-General said, Countries aected to date sim-
ply do not have the capacity to manage an outbreak of
this size and complexity on their own. I urge the inter-
national community to provide this support on the most
8 9 HISTORY
Increase over time in the cases and deaths during the 2014 out-
break
urgent basis possible.
[101]
By mid-August 2014, Doc-
tors Without Borders reported the situation in Liberias
capital Monrovia as catastrophic and deteriorating
daily. They reported that fears of Ebola among sta
members and patients had shut down much of the citys
health system, leaving many people without treatment
for other conditions.
[102]
By late August 2014, the dis-
ease had spread to Nigeria, and one case was reported
in Senegal.
[103][104] [105][106]
On 30 September 2014, the
rst conrmed case of Ebola in the United States was
diagnosed.
[107]
The patient died eight days later.
[108]
Aside from the human cost, the outbreak has severely
eroded the economies of the aected countries. A
Financial Times report suggested the economic impact of
the outbreak could kill more people than the virus itself.
As of 23 September, in the three hardest hit countries,
Liberia, Sierra Leone, and Guinea, there were only 893
treatment beds available while the current need was 2122.
In a 26 September statement, the WHO said, The Ebola
epidemic ravaging parts of West Africa is the most se-
vere acute public health emergency seen in modern times.
Never before in recorded history has a biosafety level four
pathogen infected so many people so quickly, over such a
broad geographical area, for so long.
[109]
By 8 October, 8,033 suspected cases and 3,865 deaths
had been reported;
[7]
however, the World Health Or-
ganization has said that these numbers may be vastly
underestimated.
[110]
The WHO reports that more than
216 healthcare workers are among the dead, partly due
to the lack of equipment and long hours.
[111][112]
9 History
For more about the outbreak in Virginia, US, see Reston
virus.
The rst recorded outbreak of EVD occurred in
Southern Sudan in June 1976. A second outbreak
soon followed in the Democratic Republic of the Congo
(then Zaire).
[113]
Virus isolated from both outbreaks was
Cases of ebola fever in Africa from 1979 to 2008.
named Ebola virus after the Ebola River, located near
the Zaire outbreak.
[114]
Reports conict about who ini-
tially coined the name: either Karl Johnson of the Amer-
ican CDC team
[115]
or Belgian researchers.
[116]
Although
it was assumed that the two outbreaks were connected,
scientists later realized that they were caused by distinct
species of loviruses, Sudan virus and Ebola virus.
[113]
In late 1989, Hazelton Research Products Reston Quar-
antine Unit in Reston, Virginia, suered a mysterious
outbreak of fatal illness (initially diagnosed as Simian
hemorrhagic fever virus (SHFV)) among a shipment of
crab-eating macaque monkeys imported from the Philip-
pines. Hazeltons veterinary pathologist sent tissue sam-
ples from dead animals to the United States Army Med-
ical Research Institute of Infectious Diseases (USAM-
RIID) at Fort Detrick, Maryland, where a laboratory test
known as an ELISA assay showed antibodies to Ebola
virus.
[117]
An electron microscopist from USAMRIID
discovered loviruses similar in appearance to Ebola in
the tissue samples sent fromHazelton Research Products
Reston Quarantine Unit.
[118]
Shortly afterward, a US Army team headquartered at
USAMRIID went into action to euthanize the monkeys
which had not yet died, bringing those monkeys and those
which had already died of the disease to Ft. Detrick for
study by the Armys veterinary pathologists and virolo-
gists, and eventual disposal under safe conditions.
[117]
Blood samples were taken from 178 animal handlers dur-
ing the incident.
[119]
Of those, six animal handlers even-
tually seroconverted, including one who had cut himself
with a bloody scalpel.
[48][120]
When the handlers did not
become ill, the CDC concluded that the virus had a very
low pathogenicity to humans.
[120]
The Philippines and the United States had no previous
cases of Ebola infection, and upon further isolation, re-
searchers concluded it was another strain of Ebola, or a
new lovirus of Asian origin, which they named Reston
ebolavirus (RESTV) after the location of the incident.
[117]
11.2 Domesticated animals 9
10 Society and culture
Ebolavirus is classied as a biosafety 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,
[121][122]
and was investigated by the Biopreparat for such use, but
might be dicult to prepare as a weapon of mass de-
struction because the virus becomes ineective quickly
in open air.
[123]
10.1 Literature
Richard Preston's 1995 best-selling book, The Hot Zone,
dramatized the Ebola outbreak in Reston, Virginia.
[124]
William Close's 1995 Ebola: A Documentary Novel of
Its First Explosion and 2002 Ebola: Through the Eyes of
the People focused on individuals reactions to the 1976
Ebola outbreak in Zaire.
[125]
Tom Clancy's 1996 novel, Executive Orders, involves a
Middle Eastern terrorist attack on the United States using
an airborne form of a deadly Ebola virus strain named
Ebola Mayinga (see Mayinga N'Seka).
[126]
11 Other animals
11.1 Wild animals
It is widely believed that outbreaks of EVD among hu-
man populations result from handling infected wild ani-
mal carcasses. Some research suggests that an outbreak
in the wild animals used for consumption, bushmeat, may
result in a corresponding human outbreak. Since 2003,
such outbreaks have been monitored through surveillance
of animal populations with the aim of predicting and pre-
venting Ebola outbreaks in humans.
[127]
Recovered carcasses fromgorillas contain multiple Ebola
virus strains, which suggest multiple introductions of
the virus. Bodies decompose quickly and carcasses
are not infectious after three to four days. Contact
between gorilla groups is rare, suggesting transmission
among gorilla groups is unlikely, and that outbreaks re-
sult from transmission between viral reservoir and animal
populations.
[128]
Ebola has a high mortality among primates.
[129]
Frequent
outbreaks of Ebola may have resulted in the deaths of
5,000 gorillas.
[130]
Outbreaks of Ebola may have been
responsible for an 88% decline in tracking indices of ob-
served chimpanzee populations in 420 square kilometer
Lossi Sanctuary between 2002 and 2003.
[128]
Transmis-
sion among chimpanzees through meat consumption con-
stitutes a signicant risk factor, while contact between in-
dividuals, such as touching dead bodies and grooming, is
not.
[131]
11.2 Domesticated animals
Reston virus (RESTV) can be transmitted to pigs.
[132]
This virus was discovered during an outbreak of what
at the time was thought to be simian hemorrhagic fever
virus (SHFV) in crab-eating macaques in Reston, Vir-
ginia (hence the name Reston elabavirus) in 1989. Since
the initial outbreak it has since been found in nonhuman
primates in Pennsylvania, Texas, and Italy. In each case,
the aected animals had been imported from a facility in
the Philippines,
[72]
where the virus had infected pigs.
[133]
Despite its status as a Level4 organism and its apparent
pathogenicity in monkeys, RESTV has not caused dis-
ease in exposed human laboratory workers.
[134]
In 2012 it
was demonstrated that the virus can travel without contact
frompigs to nonhuman primates, although the same study
failed to achieve transmission in that manner between
primates.
[132]
According to the WHO, routine cleaning
and disinfection of pig (or monkey) farms with sodium
hypochlorite or other detergents should be eective in
inactivating the Reston ebolavirus. If an outbreak is sus-
pected, the area must be immediately quarantined.
[135]
While pigs that have been infected with RESTV tend
to show symptoms of the disease, it has been shown
that dogs may become infected with EBOV and remain
asymptomatic. Dogs in some parts of Africa scavenge
for their food and it is known that they sometimes eat
infected animals and the corpses of humans. Although
they remain asymptomatic, a 2005 survey of dogs dur-
ing an EBOV outbreak found that over 31.8% showed a
seroprevalence for EBOV closest to an outbreak versus
9% a farther distance away.
[136]
12 Research
A number of experimental treatments are being
studied.
[137]
In the United States, the Food and Drug Ad-
ministration (FDA)'s animal ecacy rule is being used
to demonstrate reasonable safety to obtain permission to
treat people who are infected with Ebola. It is being used
because the normal path for testing drugs is not possible
for diseases caused by dangerous pathogens or toxins.
Experimental drugs are made available for use with the
approval of regulatory agencies under named patient
programs, known in the US as expanded access.
[138]
On 12 August 2014 the WHO released a statement that
the use of not yet proven treatments is ethical in certain
situations in an eort to treat or prevent the disease.
[139]
12.1 Medications
12.1.1 Antivirals
A number of antiviral medications are being studied.
10 12 RESEARCH
Researchers looking at slides of cultures of cells that make mon-
oclonal antibodies. These are grown in a lab and the researchers
are analyzing the products to select the most promising of them.
Favipiravir, an anti-viral drug approved in Japan for
stockpiling against inuenza pandemics, appears to
be useful in a mouse model of Ebola.
[9][140]
On 4
October 2014, it was reported that a French nun who
contracted Ebola while volunteering in Liberia was
cured with Favipiravir treatment.
[141]
BCX4430 is a broad-spectrum small molecule
antiviral drug developed by BioCryst Pharmaceuti-
cals and undergoing animal testing as a potential hu-
man treatment for Ebola by USAMRIID.
[142]
The
drug has been approved to progress to Phase 1 tri-
als, expected late in 2014.
[143]
Brincidofovir, another broad-spectrum antiviral
drug, has been granted an emergency FDA approval
as an investigational new drug for the treatment of
Ebola, after in vitro tests found it to be eective
against Ebola virus.
[144]
It has subsequently been
used to treat the rst patient diagnosed with Ebola
in the USA, after he had recently returned from
Liberia.
[145][146]
Lamivudine, an antiviral drug which is usually used
to treat HIV / AIDS, was reported in September
2014 to have been used successfully to treat 13 out
of 15 Ebola-infected patients by a doctor in Liberia,
as part of a combination therapy also involving intra-
venous uids and antibiotics to combat opportunis-
tic bacterial infection of Ebola-compromised inter-
nal organs.
[147]
Western virologists have however ex-
pressed caution about the results, due to the small
number of patients treated and confounding factors
present. Researchers at the NIH stated that lamivu-
dine had so far failed to demonstrate anti-Ebola ac-
tivity in preliminary in vitro tests, but that they would
continue to test it under dierent conditions and
would progress it to trials if even slight evidence for
ecacy is found.
[148]
Lack of available treatment options has spurred re-
search into a number of other possible antivirals
targeted against Ebola, including natural products
such as scytovirin and grithsin,
[149][150]
as well
as synthetic drugs including FGI-103, FGI-104,
FGI-106, dUY11 and LJ-001,
[151]
and other newer
agents.
[152][153][154]
12.1.2 Antisense technology
Other promising treatments rely on antisense technol-
ogy. Both small interfering RNAs (siRNAs) and
phosphorodiamidate morpholino oligomers (PMOs) tar-
geting Ebola virus (EBOV) RNA polymerase L pro-
tein could prevent disease in nonhuman primates.
[155][156]
TKM-Ebola is a small interfering RNA compound,
currently being tested in a Phase I clinical trial in
humans.
[157][158]
Sarepta Therapeutics has completed a
Phase I clinical trial with its Morpholino oligo targeting
Ebola virus.
[159]
12.1.3 Other
Two selective estrogen receptor modulators used to treat
infertility and breast cancer (clomiphene and toremifene)
have been found to inhibit the progress of Ebola virus in
vitro as well as in infected mice. Ninety percent of the
mice treated with clomiphene and fty percent of those
treated with toremifene survived the tests.
[160]
The study
authors conclude that given their oral availability and his-
tory of human use, these drugs would be candidates for
treating Ebola virus infection in remote geographical lo-
cations, either on their own or together with other antivi-
ral drugs.
A 2014 study found that three ion channel blockers
used in the treatment of heart arrhythmias, amiodarone,
dronedarone and verapamil, block the entry of Ebola
virus into cells in vitro.
[161]
Melatonin has also been suggested as a potential treat-
ment for Ebola based on promising in vitro results.
[162]
ZMapp is a monoclonal antibody vaccine. The limited
supply of the drug has been used to treat a small num-
ber of individuals infected with the Ebola virus. Al-
though some individuals have recovered, the outcome
is not considered statistically signicant.
[163]
ZMapp has
proved eective in a trial involving Rhesus macaque
monkeys.
[164][157]
12.2 Blood products
The WHO has stated that transfusion of whole blood or
puried serum from Ebola survivors is the therapy with
the greatest potential to be implemented immediately, al-
though there is little information as to its ecacy.
[165]
September 2014, WHO issued an interim guideline for
this therapy.
[166]
The blood serum from those who have
survived an infection is currently being studied to see
11
if it is an eective treatment.
[167]
During a meeting ar-
ranged by WHO this research was deemed to be a top
priority.
[167]
Seven of eight people with Ebola survived
after receiving a transfusion of blood donated by in-
dividuals who had previously survived the infection in
an 1999 outbreak in the Democratic Republic of the
Congo.
[78][168]
This treatment, however, was started late
in the disease meaning they may have already been re-
covering on their own and the rest of their care was bet-
ter than usual.
[78]
Thus this potential treatment remains
controversial.
[15]
Intravenous antibodies appear to be pro-
tective in non-human primates who have been exposed to
large doses of Ebola.
[169]
The World Health Organisation
has approved the use of convalescent serum and whole
blood products to treat people with Ebola.
[170]
12.3 Vaccine
As of September 2014, no vaccine was approved
by the United States Food and Drug Administration
(FDA) for clinical use in humans.
[171][167]
It was hoped
that one would be initially available by November
2014.
[167]
The most promising candidates are DNA vac-
cines
[172]
or vaccines derived from adenoviruses,
[173]
vesicular stomatitis Indiana virus (VSIV)
[174][175][176]
or
lovirus-like particles (VLPs)
[177]
because these candi-
dates could protect nonhuman primates from ebolavirus-
induced disease. DNA vaccines, adenovirus-based vac-
cines, and VSIV-based vaccines have entered clinical
trials.
[178][179][180][181]
Vaccines have protected nonhuman primates. Immu-
nization takes six months, which impedes the counter-
epidemic use of the vaccines. Searching for a quicker
onset of eectiveness, in 2003, a vaccine using an
adenoviral (ADV) vector carrying the Ebola spike pro-
tein was tested on crab-eating macaques. Twenty-eight
days later, they were challenged with the virus and re-
mained resistant.
[173]
A vaccine based on attenuated re-
combinant vesicular stomatitis virus (VSV) vector carry-
ing either the Ebola glycoprotein or the Marburg glyco-
protein in 2005 protected nonhuman primates,
[182]
open-
ing clinical trials in humans.
[178]
Over a three month hu-
man trial, three vaccinations safely induced an immune
response. 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.
[179]
Try-
ing the vaccine on a strain of Ebola that more resembles
one that infects humans is the next step.
[183]
On 6 De-
cember 2011, the development of a successful vaccine
against Ebola for mice was reported. Unlike the prede-
cessors, it can be freeze-dried and thus stored for long
periods in wait for an outbreak.
[184]
An experimental vac-
cine made by researchers at Canadas national labora-
tory in Winnipeg was used, in 2009, to pre-emptively
treat a German scientist who might have been infected
during a lab accident.
[185]
However, actual EBOV infec-
tion was never demonstrated beyond doubt.
[186]
Experi-
mentally, recombinant vesicular stomatitis Indiana virus
(VSIV) expressing the glycoprotein of EBOV or SUDV
has been used successfully in nonhuman primate models
as post-exposure prophylaxis.
[187][188]
The CDCs recom-
mendations are currently under review.
Simultaneous phase 1 trials of an experimental vac-
cine known as the NIAID/GSK vaccine commenced
in September 2014.
[189]
GlaxoSmithKline and the NIH
jointly developed the vaccine,
[189]
based on a modied
chimpanzee adenovirus, and contains parts of the Zaire
and Sudan ebola strains.
[189]
If this phase is completed
successfully, the vaccine will be fast tracked for use in
West Africa. In preparation for this, GSK is preparing a
stockpile of 10,000 doses.
[190][191]
13 See also
List of human disease case fatality rates
14 References
Notes
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15 External links
Ebola virus disease at DMOZ
CDC: Ebola hemorrhagic fever Centers for Dis-
ease Control and Prevention, Special Pathogens
Branch
WHO: Ebola haemorrhagic fever World Health
Organization, Global Alert and Response
Google Map of Ebola Outbreaks
WHO recommended infection control measures
20 16 TEXT AND IMAGE SOURCES, CONTRIBUTORS, AND LICENSES
16 Text and image sources, contributors, and licenses
16.1 Text
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