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Ebola Threatens Sierra Leone

24 March 2014 at 23:16 | 5944 views

By Our Correspondent in Freetown, Sierra Leone.

There has been an outbreak of the deadly disease called Ebola in neighbouring Guinea-Conakry and experts say it’s likely to spread in Sierra Leone, Guinea, Liberia, Guinea Bissau and Mali, five countries that share borders with Guinea-Conkary. But of the five, Sierra Leone is more threatened because the outbreak occurred in South-Western Guinea which is in close proximity to Sierra Leone’s Kambia district in the northern province.

Sierra Leone, like Guinea, does not have the infrastructure and resources to combat any outbreak and relies heavily on international support even for its basic health needs. About 70 people have already died in Guinea from the outbreak and more are in critical condition, according to reports.

It is not known whether the Sierra Leone government has already taken precautionary measures to stop the disease from entering Sierra Leone like screening travellers from Guinea. Hundreds of traders travel to and from Guinea from Sierra Leone on a daily basis.

Many people here think Sierra Leone health officials should immediately travel to Guinea to observe how their Guinean counterparts are handling the situation and learn from them in case Sierra Leone is hit by the disease, which is not a remote possibility. The Health Ministry, they say, should also immediately launch a massive public awareness and education campaign in Kambia and Port Loko districts, two districts closest to South-Western Guinea where the outbreak occurred.

Here are some facts on Ebola from the Wikipedia website:

Ebola virus disease (EVD) or Ebola hemorrhagic fever (EHF) is the human disease that may be caused by any of four of the five known ebola viruses. These four viruses are: Bundibugyo virus (BDBV), Ebola virus (EBOV), Sudan virus (SUDV), and Taï Forest virus (TAFV, formerly and more commonly Côte d’Ivoire Ebola virus (Ivory Coast Ebolavirus, CIEBOV)). EVD is a viral hemorrhagic fever (VHF), and is clinically nearly indistinguishable from Marburg virus disease (MVD).


The genera Ebolavirus and Marburgvirus were originally classified as the species of the now-obsolete Filovirus genus. In March 1998, the Vertebrate Virus Subcommittee proposed in the International Committee on Taxonomy of Viruses (ICTV) to change the Filovirus genus to the Filoviridae family with two specific 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, DC, to change the "-like viruses" to "-virus" resulting in today’s Ebolavirus and Marburgvirus.[1]
Phylogenetic tree comparing the Ebolavirus and Marburgvirus. Numbers indicate percent confidence of branches.

Rates of genetic change are 100 times slower than influenza A in humans, but on the same magnitude as those of hepatitis B. Extrapolating backwards using these rates indicates that Ebolavirus and Marburgvirus diverged several thousand years ago.[2] However, paleoviruses (genomic fossils) of filoviruses (Filoviridae) found in mammals indicate that the family itself is at least tens of millions of years old.[3] Fossilized viruses that are closely related to ebolaviruses have been found in the genome of the Chinese hamster.[4]

The five characterised Ebola species are:

Zaire ebolavirus (ZEBOV)

Also known simply as the Zaire virus, ZEBOV has the highest case-fatality rate of the ebolaviruses, up to 90% in some epidemics, with an average case fatality rate of approximately 83% over 27 years. There have been more outbreaks of Zaire ebolavirus than of any other species. The first outbreak occurred on 26 August 1976 in Yambuku. The first recorded case was Mabalo Lokela, a 44‑year-old schoolteacher. The symptoms resembled malaria, and subsequent patients received quinine. Transmission has been attributed to reuse of unsterilized needles and close personal contact.

Sudan ebolavirus (SEBOV)

Like the Zaire virus, SEBOV emerged in 1976; it was at first assumed to be identical with the Zaire species. SEBOV is believed to have broken out first among cotton factory workers in Nzara, Sudan, with the first case reported as a worker exposed to a potential natural reservoir. The virus was not found in any of the local animals and insects that were tested in response. The carrier is still unknown. The lack of barrier nursing (or "bedside isolation") facilitated the spread of the disease. The most recent outbreak occurred in May, 2004. Twenty confirmed cases were reported in Yambio County, Sudan, with five deaths resulting. The average fatality rates for SEBOV were 54% in 1976, 68% in 1979, and 53% in 2000 and 2001.

Reston ebolavirus (REBOV)

Discovered during an outbreak of simian hemorrhagic fever virus (SHFV) in crab-eating macaques from Hazleton Laboratories (now Covance) in 1989. Since the initial outbreak in Reston, Virginia, it has since been found in non-human primates in Pennsylvania, Texas and Siena, Italy. In each case, the affected animals had been imported from a facility in the Philippines,[7] where the virus has also infected pigs.[8] Despite its status as a Level‑4 organism and its apparent pathogenicity in monkeys, REBOV did not cause disease in exposed human laboratory workers.[9]

Côte d’Ivoire ebolavirus (CIEBOV)

Also referred to as Taï Forest ebolavirus and by the English place name, "Ivory Coast", it was first discovered among chimpanzees from the Taï Forest in Côte d’Ivoire, Africa, in 1994. Necropsies showed blood within the heart to be brown; no obvious marks were seen on the organs; and one necropsy showed lungs filled with blood. Studies of tissues taken from the chimpanzees showed results similar to human cases during the 1976 Ebola outbreaks in Zaire and Sudan. As more dead chimpanzees were discovered, many tested positive for Ebola using molecular techniques. The source of the virus was believed to be the meat of infected Western Red Colobus monkeys, upon which the chimpanzees preyed. One of the scientists performing the necropsies on the infected chimpanzees contracted Ebola. She developed symptoms similar to those of dengue fever approximately a week after the necropsy, and was transported to Switzerland for treatment. She was discharged from the hospital after two weeks and had fully recovered six weeks after the infection.

Bundibugyo ebolavirus (BEBOV)

On 24 November 2007, the Uganda Ministry of Health confirmed an outbreak of Ebolavirus in the Bundibugyo District. After confirmation of samples tested by the United States National Reference Laboratories and the CDC, the World Health Organization confirmed the presence of the new species. On 20 February 2008, the Uganda Ministry officially announced the end of the epidemic in Bundibugyo, with the last infected person discharged on 8 January 2008. An epidemiological study conducted by WHO and Uganda Ministry of Health scientists determined there were 116 confirmed and probable cases of the new Ebola species, and that the outbreak had a mortality rate of 34% (39 deaths). In 2012, there was an outbreak of Bundibugyo ebolavirus in a northeastern province of the Democratic Republic of the Congo. There were 15 confirmed cases and 10 fatalities.

Signs and symptoms

Manifestation of Ebola begins with a sudden onset of an influenza-like stage characterized by general malaise, fever with chills, arthralgia, myalgia, and chest pain. Nausea is accompanied by abdominal pain, diarrhea, and vomiting. Respiratory tract involvement is characterized by pharyngitis with sore throat, cough, dyspnea, and hiccups. The central nervous system is affected as judged by the development of severe headaches, agitation, confusion, fatigue, depression, seizures, and sometimes coma.

Cutaneous presentation may include: maculopapular rash, petechiae, purpura, ecchymoses, and hematomas (especially around needle injection sites). In general, development of hemorrhagic symptoms is indicative of a negative prognosis. However, contrary to popular belief, hemorrhage does not lead to hypovolemia and is not the cause of death (total blood loss is low except during labor). Instead, death occurs due to multiple organ dysfunction syndrome (MODS) due to fluid redistribution, hypotension, disseminated intravascular coagulation, and focal tissue necroses.

The mean incubation period, best calculated currently for EVD outbreaks due to EBOV infection, is 12.7 days (standard deviation = 4.3 days), but can be as long as 25 days.


All patients show some extent of coagulopathy and impaired circulatory system symptomology. Bleeding from mucous membranes and puncture sites is reported in 40–50% of cases, while maculopapular rashes are evident in approximately 50% of cases. Sources of bleeds include hematemesis, hemoptysis, melena, and aforementioned bleeding from mucous membranes (gastroinestinal tract, nose, vagina and gingiva). Diffuse bleeding, however, is rare, and is usually exclusive to the gastrointestinal tract.


EVD is caused by four of five viruses classified in the genus Ebolavirus, family Filoviridae, order Mononegavirales: Bundibugyo virus (BDBV), Ebola virus (EBOV), Sudan virus (SUDV), and Taï Forest virus (TAFV). The fifth virus, Reston virus (RESTV), is thought to be apathogenic for humans and therefore not discussed here.

Risk factors

Between 1976 and 1998, from 30,000 mammals, birds, reptiles, amphibians, and arthropods sampled from outbreak 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. 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.

Plants, arthropods, and birds have also been considered as possible reservoirs; however, bats are considered the most likely candidate. Bats were known to reside in the cotton factory in which the index cases for the 1976 and 1979 outbreaks were employed, and they have also been implicated in Marburg virus infections in 1975 and 1980. Of 24 plant species and 19 vertebrate species experimentally inoculated with EBOV, only bats became infected. The absence of clinical signs in these bats is characteristic of a reservoir species. 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 fragments. As of 2005, three types of fruit bats (Hypsignathus monstrosus, Epomops franqueti, and Myonycteris torquata) have been identified as being in contact with EBOV. They are now suspected to represent the EBOV reservoir hosts.

The existence of integrated genes of filoviruses in some genomes of small rodents, insectivorous bats, shrews, tenrecs, and marsupials indicates a history of infection with filoviruses in these groups as well. However, it has to be stressed that infectious ebolaviruses have not yet been isolated from any nonhuman animal.

Bats drop partially eaten fruits and pulp, then terrestrial mammals 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 have led to research towards viral shedding in the saliva of bats. Fruit production, animal behavior, and other factors vary at different times and places that may trigger outbreaks among animal populations. Transmission between natural reservoirs and humans are rare, and outbreaks are usually traceable to a single index case where an individual has handled the carcass of gorilla, chimpanzee, or duiker. The virus then spreads person-to-person, especially within families, hospitals, and during some mortuary rituals where contact among individuals becomes more likely.

The virus has been confirmed to be transmitted through body fluids. Transmission through oral exposure and through conjunctiva exposure is likely and has been confirmed in non-human primates. Filoviruses are not naturally transmitted by aerosol. They are, however, highly infectious as breathable 0.8–1.2 micrometre droplets in laboratory conditions; because of this potential route of infection, these viruses have been classified as Category A biological weapons.

All epidemics of Ebola have occurred in sub-optimal hospital conditions, where practices of basic hygiene and sanitation are often either luxuries or unknown to caretakers and where disposable needles and autoclaves are unavailable or too expensive. In modern hospitals with disposable needles and knowledge of basic hygiene and barrier nursing techniques, Ebola has never spread on a large scale. In isolated settings such as a quarantined hospital or a remote village, most victims are infected shortly after the first case of infection is present. The quick onset of symptoms from the time the disease becomes contagious in an individual makes it easy to identify sick individuals and limits an individual’s ability to spread the disease by traveling. Because bodies of the deceased are still infectious, some doctors had to take measures to properly dispose of dead bodies in a safe manner despite local traditional burial rituals.


Like all mononegaviruses, ebolavirions contain linear 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.[32] Ebolavirus genomes are approximately 19 kilobase pairs long and contain seven genes in the order 3’-UTR-NP-VP35-VP40-GP-VP30-VP24-L-5’-UTR.[33] The genomes of the five different ebolaviruses (BDBV, EBOV, RESTV, SUDV, and TAFV) differ in sequence and the number and location of gene overlaps.


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. In general, Ebolavirions are 80 nm in width, but vary somewhat in length. In general, the median particle length of ebolaviruses ranges from 974–1,086 nm (in contrast to marburgvirions, whose median particle length was measured to be 795–828 nm), but particles as long as 14,000 nm have been detected in tissue culture. Ebolavirions consist of seven structural proteins. At the center is the helical ribonucleocapsid, which consists of the genomic RNA wrapped around a polymer of nucleoproteins (NP). Associated with the ribonucleoprotein is the RNA-dependent RNA polymerase (L) with the polymerase cofactor (VP35) and a transcription activator (VP30). The ribonucleoprotein is embedded in a matrix, formed by the major (VP40) and minor (VP24) matrix proteins. These particles are surrounded by a lipid membrane derived from the host cell membrane. The membrane anchors a glycoprotein (GP1,2) that projects 7 to 10 nm spikes away from its surface. While nearly identical to marburgvirions in structure, ebolavirions are antigenically distinct.


Niemann–Pick C1 (NPC1) appears to be essential for Ebola infection. Two independent studies reported in the same issue of Nature showed that Ebola virus cell entry and replication requires the cholesterol transporter protein NPC1. When cells from Niemann Pick Type C1 patients (who have a mutated form of NPC1) were exposed to Ebola virus in the laboratory, the cells survived and appeared immune to the virus, further indicating that Ebola relies on NPC1 to enter cells. This might imply that genetic mutations in the NPC1 gene in humans could make some people resistant to one of the deadliest known viruses affecting humans. The same studies described similar results with Ebola’s cousin in the filovirus group, Marburg virus, showing that it too needs NPC1 to enter cells. Furthermore, NPC1 was shown to be critical to filovirus entry because it mediates infection by binding directly to the viral envelope glycoprotein. A later study confirmed the findings that NPC1 is a critical filovirus receptor that mediates infection by binding directly to the viral envelope glycoprotein and that the second lysosomal domain of NPC1 mediates this binding.

In one of the original studies, a small molecule was shown to inhibit Ebola virus infection by preventing the virus glycoprotein from binding to NPC1.[36][38] In the other study, mice that were heterozygous for NPC1 were shown to be protected from lethal challenge with mouse adapted Ebola virus. Together, these studies suggest NPC1 may be potential therapeutic target for an Ebola anti-viral drug.


The ebolavirus life cycle begins with virion attachment to specific 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 proteins. Ebolavirus RNA polymerase (L) binds to a single promoter located at the 3’ end of the genome. Transcription 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 greatest abundance, whereas those toward the 5’ end are least likely to be transcribed. The gene order is, therefore, a simple but effective form of transcriptional regulation. The most abundant protein produced is the nucleoprotein, whose concentration in the cell determines when L switches from gene transcription to genome replication. 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 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.

Endothelial cells, mononuclear phagocytes, and hepatocytes are the main 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 and host immune defenses. The GP forms a trimeric complex, which binds the virus to the endothelial cells lining the interior 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 system by 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. The presence of viral particles and cell damage resulting from budding causes 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 in a loss of vascular integrity. This loss in vascular integrity is furthered with synthesis of GP, which reduces specific integrins responsible for cell adhesion to the inter-cellular structure, and damage to the liver, which leads to coagulopathy.


EVD is clinically indistinguishable from Marburg virus disease (MVD) and can also easily be confused with many other diseases prevalent 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 diseases that should be included in the differential diagnosis include the following: leptospirosis, scrub typhus, plague, Q fever, candidiasis, histoplasmosis, trypanosomiasis, visceral leishmaniasis, hemorrhagic smallpox, measles, and fulminant viral hepatitis.[citation needed] Non-infectious diseases that can be confused with EVD are acute promyelocytic leukemia, hemolytic uremic syndrome, snake envenomation, clotting factor deficiencies/platelet disorders, thrombotic thrombocytopenic purpura, hereditary hemorrhagic telangiectasia, Kawasaki disease, and even warfarin intoxication.

EVD’s most important clinical indicator is the patient’s medical history, especially travel and occupational history and the patient’s exposure to wildlife. EVD can be confirmed by isolating ebolaviruses from or by detection of ebolavirus antigen or genomic or subgenomic RNAs in patient blood or serum samples during the acute phase of EVD. Ebolavirus isolation is usually performed by inoculation of grivet kidney epithelial Vero E6 or MA-104 cell cultures or by inoculation of human adrenal carcinoma SW-13 cells, all of which reacting to infection with characteristic cytopathic effects. Filovirions can easily be visualized and identified in cell culture by electron microscopy due to their unique filamentous shapes, but electron microscopy cannot differentiate the various filoviruses alone despite some overall length differences. Immunofluorescence assays are used to confirm ebolavirus presence in cell cultures. During an outbreak, virus isolation and electron microscopy are most often not feasible options. The most common diagnostic methods are therefore RT-PCR in conjunction with antigen-capture ELISA which can be performed in field or mobile hospitals and laboratories. Indirect immunofluorescence assays (IFAs) are not used for diagnosis of EVD in the field anymore.


As an outbreak of ebola progresses, bodily fluids from diarrhea, vomiting, and bleeding represent a hazard. Due to lack of proper equipment and hygienic practices, large-scale epidemics occur mostly in poor, isolated areas without modern hospitals or well-educated medical staff. Many areas where the infectious reservoir exists have just these characteristics. In such environments, all that can be done is to immediately cease all needle-sharing or use without adequate sterilization procedures, isolate patients, and observe strict barrier nursing procedures with the use of a medical-rated disposable face mask, gloves, goggles, and a gown at all times, strictly enforced for all medical personnel and visitors. The aim of all of these techniques is to avoid any person’s contact with the blood or secretions of any patient, including those who are deceased.

Vaccines have protected nonhuman primates. The six months needed for immunization impede counter-epidemic uses. In 2003, a vaccine using an adenoviral (ADV) vector carrying the Ebola spike protein therefore was tested on crab-eating macaques. The monkeys twenty-eight days later were challenged with the virus and remained resistant.[62] A vaccine based on attenuated recombinant vesicular stomatitis virus (VSV) vector carrying either the Ebola glycoprotein or the Marburg glycoprotein in 2005 protected nonhuman primates, opening clinical trials in humans. The study by October completed the first human trial, over three months giving three vaccinations safely inducing 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. Trying the vaccine on a strain of Ebola that more resembles the one that infects humans is the next step.[citation needed]

The Food and Drug Administration has approved no candidate vaccines, the most promising whereof are DNA vaccines or derive from adenoviruses, vesicular stomatitis Indiana virus (VSIV) or filovirus-like particles (VLPs) because these candidates could protect nonhuman primates from ebolavirus-induced disease. DNA vaccines, adenovirus-based vaccines, and VSIV-based vaccines have entered clinical trials.

Ebolaviruses are not transmitted by aerosol during natural EVD outbreaks. Without an approved vaccine, EVD prevention predominantly involves behavior modification, proper personal protective equipment, and sterilization/disinfection.

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. The research is reported in Proceedings of National Academy of Sciences.

The natural maintenance hosts of ebolaviruses are unidentified: primary infection cannot necessarily be prevented in nature. Avoiding EVD such risk factors as contact with bats or nonhuman primates therefore is highly recommended and may be impossible for inhabitants of tropical forests or people dependent on nonhuman primates as a food source.

The most straightforward prevention method during EVD outbreaks is not touching patients, their excretions, and body fluids, or possibly contaminated materials and utensils. Patients should be isolated, and medical staff should be trained and apply strict barrier nursing techniques (disposable face mask, gloves, goggles, and a gown at all times). Traditional burial rituals, especially those requiring embalming of bodies, should be discouraged or modified, ideally with the help of local traditional healers.

Ebolaviruses are World Health Organization Risk Group 4 Pathogens, requiring Biosafety Level 4-equivalent containment. Laboratory researchers have to be properly trained in BSL-4 practices and wear proper personal protective equipment.

No FDA-approved ebolavirus-specific therapy for EVD exists. Treatment is primarily supportive in nature and includes minimizing invasive procedures, balancing fluids and electrolytes to counter dehydration, administration of anticoagulants early in infection to prevent or control disseminated intravascular coagulation, administration of procoagulants late in infection to control hemorrhaging, maintaining oxygen levels, pain management, and administration of antibiotics or antimycotics to treat secondary infections. Hyperimmune equine immunoglobulin raised against EBOV has been used in Russia to treat a laboratory worker who accidentally infected herself with EBOV—but the patient died anyway. Experimentally, 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. Such a recombinant post-exposure vaccine was also used to treat a German researcher who accidentally pricked herself with a possibly EBOV-contaminated needle. Treatment might have been successful as she survived. However, actual EBOV infection could never be demonstrated without a doubt. Novel, very promising, experimental therapeutic regimens rely on antisense technology. Both small interfering RNAs (siRNAs) and phosphorodiamidate morpholino oligomers (PMOs) targeting the EBOV genome could prevent disease in nonhuman primates.

During an outbreak in the Democratic Republic of the Congo in 1995, seven of eight patients having received blood transfusions from convalescent individuals survived.[86] However, this potential treatment is considered controversial.

In general, prognosis is poor (average case-fatality rate of all EVD outbreaks to date = 68%). If a patient survives, recovery may be prompt and complete, or protracted with sequelae, such as orchitis, arthralgia, myalgia, desquamation, or alopecia. Ocular manifestations, such as photophobia, hyperlacrimation, iritis, iridocyclitis, choroiditis and blindness have also been described. It is important to note that EBOV and SUDV are known to be able to persist in the sperm of some survivors, which could give rise to secondary infections and disease via sexual intercourse.


Distribution of Ebola and Marburg virus in Africa (note that integrated genes from filoviruses have been detected in mammals from the New World as well. (A) Known points of filovirus disease. Projected distribution of ecological niche of: (B) all filoviruses, (C) ebolaviruses, (D) marburgviruses.

Outbreaks of EVD have mainly been restricted to Africa. The virus often consumes the population. Governments and individuals quickly respond to quarantine the area while the lack of roads and transportation helps to contain the outbreak. EVD was first described after almost simultaneous viral hemorrhagic fever outbreaks occurred in Zaire and Sudan in 1976. EVD is believed to occur after an ebolavirus is transmitted to a human index case via contact with an infected animal host. Human-to-human transmission occurs via direct contact with blood or bodily fluids from an infected person (including embalming of a deceased victim) or by contact with contaminated medical equipment such as needles. In the past, explosive nosocomial transmission has occurred in underequipped African hospitals due to the reuse of needles and lack of implementation of universal precautions. Aerosol transmission has not been observed during natural EVD outbreaks. The potential for widespread EVD epidemics is considered low due to the high case-fatality rate, the rapidity of demise of patients, and the often remote areas where infections occur.