Introduction
Background
Ebola virus is one of at least 18 known viruses capable of causing the viral hemorrhagic fever syndrome. Although agents of the viral hemorrhagic fever syndrome constitute a geographically diverse group of viruses, to date, all are RNA viruses, all are considered zoonoses, all damage the microvasculature resulting in increased vascular permeability, and all are members of 1 of 4 families: Arenaviridae, Bunyaviridae, Flaviviridae, and Filoviridae.
The family Filoviridae resides in the order Mononegavirales and contains the largest genome within the order. Originally considered members of the family Rhabdoviridae, Ebola virus and the antigenically distinct Marburg virus now comprise the family Filoviridae.
For additional information on Ebola virus and other emerging and re-emerging infectious diseases, see Medscape's Emerging and Reemerging Infectious Diseases Resource Center.
Pathophysiology
Epidemiology
Ebola and Marburg viruses are responsible for well-documented outbreaks of severe human hemorrhagic fever with resultant case mortality rates ranging from 23% for Marburg virus (Marburg, Germany; 1967) to 88% for Ebola virus (Yambuku, Democratic Republic of the Congo [DRC]; formerly Zaire; 1976). Ebola virus (Reston, Va; 1989) also has caused a highly lethal disease in cynomolgus macaques (Macaca fascicularis) imported into Reston, Va from the Philippines, but it caused no deaths in 4 infected employees who worked at the primate facility that housed these animals.
Ultrastructure and pathogenesis
The 4 distinguishable subtypes of Ebola and the single subtype of Marburg virus comprise the known members of the family Filoviridae. Controversy remains regarding the question of whether the 4 distinguishable Ebola viruses are subtypes or separate species.
Filoviruses share a characteristic filamentous form with a uniform diameter of approximately 80 nm but display a great variation in length. Filaments may be straight, but they are often folded on themselves. Ebola virus has a nonsegmented, negative-stranded, RNA genome containing 7 structural and regulatory genes. The Ebola genome codes for 4 virion structural proteins (VP30, VP35, nucleoprotein, and a polymerase protein [L]) and 3 membrane-associated proteins (VP40, glycoprotein [GP], and VP24). The GP gene is positioned fourth from the 3' end of the 7 linearly arranged genes.
Following infection, human and nonhuman primates experience an early period of rapid viral multiplication that, in lethal cases, is associated with an ineffective immunological response. Although a full understanding of Ebola must await further investigations, part of the pathogenesis has been elucidated. Most Filovirus proteins are encoded in single reading frames; the surface GP is encoded in 2 frames (open reading frame [ORF] I and ORF II). The ORF I (amino-terminal) of the gene encodes for a small (50-70 kd), soluble, nonstructural secretory glycoprotein (sGP) that is produced in large quantities early in Ebola infection.1
The sGP binds to neutrophil CD16b, a neutrophil-specific Fc g receptor III, and inhibits early neutrophil activation. The sGP also may be responsible for the profound lymphopenia that characterizes Ebola infection. Thus, sGP is believed to play pivotal roles in the ability of Ebola to prevent an early and effective host immune response. One hypothesis is that the lack of sGP production by Marburg virus may explain the reduced virulence with this agent as compared to that of African-derived Ebola.
Leroy et al reported their observations of 24 close contacts of symptomatic patients actively infected with Ebola.2 Eleven of the 24 contacts developed evidence of asymptomatic infection associated with viral replication. Viral replication was proven by the authors' ability to amplify positive-stranded Ebola RNA from the blood of the asymptomatic contacts. A detailed study of these infected but asymptomatic individuals revealed that they had an early (4-6 d after infection) and vigorous immunologic response with production of interleukin-1beta, interleukin-6, and tumor necrosis factor, resulting in enhanced cell-mediated and humoral-mediated immunity. In patients who eventually died, proinflammatory cytokines were not detected even after 2-3 days of symptomatic infection.
A second glycoprotein of 120-150 kd, transmembrane glycoprotein, is incorporated into the Ebola virion and binds to endothelial cells but not to neutrophils. Ebola virus is known to invade, replicate in, and destroy endothelial cells. Destruction of endothelial surfaces is associated with disseminated intravascular coagulation, and this may contribute to the hemorrhagic manifestations that characterize many, but not all, Ebola infections.
Clinical infection in human and nonhuman primates is associated with rapid and extensive viral replication in all tissues. Viral replication is accompanied by widespread and severe focal necrosis. The most severe necrosis occurs in the liver, and this is associated with the formation of councilmanlike bodies similar to those seen in yellow fever. In fatal infections, the host's tissues and blood contain large numbers of Ebola virions, and their tissues and body fluids are highly infectious.
Presently, 4 distinct subtypes have been identified, each named for the location where it caused documented human or animal disease. Two Africa subtypes, Ebola virus Zaire (EBO-Z) and Ebola virus Sudan (EBO-S), have been responsible for most of the reported deaths caused by filoviruses. Clinical disease due to African-derived Ebola virus is severe and, with the exception of 2 patients infected with the Ebola virus Côte-d'Ivoire (EBO-C) subtype who survived, is associated with a mortality rate of 65% (Sudan, 1979) to 89% (DRC, Dec 2002 to Apr 2003). The fourth subtype is Ebola virus Reston (EBO-R), which was first isolated in 1989 in monkeys imported from a single Philippine exporter. A virtually identical isolate imported from the same Philippine exporter was detected in 1992 in Siena, Italy.
Between 1994 and 1997, a stable strain of Ebola caused 3 successive outbreaks of hemorrhagic fever in Gabon (mortality rates ranged from 60-74%).3 Because the Gabon strain has a greater than 99% homology of the nucleoprotein and GP gene regions with EBO-Z, it has not been considered a distinct subtype.
To date, no reservoir has been identified for any Filovirus. However, in 1996, members of the National Institute for Virology of South Africa went to Kikwit, Zaire (now the DRC) and evaluated the infectivity of Ebola for 24 species of plants and 19 species of vertebrates and invertebrates.4 Insectivorous bats, Tadarida pumila, and fruit bats, Epomophorus wahlbergi, were found to support Ebola virus replication without dying. Furthermore, serum Ebola titers in infected fruit bats reached as high as 10 million fluorescent focus-forming units per milliliter, and feces contained viable Ebola virus.
Mechanisms of dispersion
African-derived Filovirus infections are characterized by transmission from an unknown host (possibly bats) to humans or nonhuman primates, presumably via direct contact with body fluids such as saliva or blood or other infected tissues. Evidence in nonhuman primates indicates that EBO-Z and EBO-S may be transmitted by contact with mucous membranes, conjunctiva, pharynx and gastrointestinal surfaces, small breaks in the skin, and, at least experimentally, by aerosol.5 Dogs have been shown to acquire asymptomatic Ebola infections, possibly by contact with virus-laden droplets of urine, feces, or blood of unknown hosts.6 Of epidemiologic significance was the observation that seroprevalence rates in dogs rose in a linear fashion as sampling approached areas of human cases and reached as high as 31.8%. Thus, an increase in canine seroprevalence may serve as an indicator of increasing Ebola circulation in primary vectors within specific geographical areas.
Human infection with African-derived strains has often occurred in caregivers, either family or medical, or in family members who have prepared dead relatives for burial. Late stages of Ebola are associated with the presence of large numbers of virions in body fluids, tissues, and, especially, skin. Individuals who come into contact with patients infected with Ebola without proper barrier protection are at high risk of becoming infected. A recent report from the DRC identified Ebola virus RNA in 100% of oral secretions in patients with Ebola virus RNA in their serum. Both serum and oral secretions were tested with reverse-transcriptase polymerase chain reaction (RT-PCR). Thus, oral secretions may be capable of transmitting Ebola virus.
The first recorded outbreak occurred in Yambuku, DRC in 1976, where 316 patients were infected. In the largest recorded urban outbreak to date (DRC, 1995; 318 cases), admission to a hospital acted to greatly amplify the frequency of transmission. The lack of proper barrier protection (gloves, fluid-resistant gowns, and proper sanitation) and the use and reuse of contaminated medical equipment, especially needles and syringes, resulted in rapid nosocomial spread of infection. Only after adequate barrier protection and alteration in burial rituals were implemented was the outbreak contained.
Unlike Asian-derived Ebola (ie, the Reston strain traced to a Philippine supplier of primates), African-derived strains appear to be spread more often by direct contact than by the respiratory route. However, the Reston strain has repeatedly been demonstrated to spread among nonhuman primates and possibly from primates to humans via the respiratory route. Fortunately, although the Reston subtype has been documented to cause infection in humans, it does not appear to be pathogenic to humans.
Frequency
United States
Ebola is not endemic in the United States. However, several human infections with the Reston strain of Ebola have been acquired by animal care workers at primate holding facilities within the United States. Fortunately, the Reston strain has not demonstrated pathogenic effects in humans. Others at potential risk are laboratory workers who work with infected animals or with the virus in tissue culture.
International
Individuals considered at risk for Ebola hemorrhagic fever include persons with a travel history to sub-Saharan Africa, persons who have recently cared for infected patients, and animal workers who have worked with primates infected with African-derived Ebola subtypes.
Table 1. History of Ebola Virus Sudan Outbreaks*
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Table
| Year | Location | Reported Cases, No. | Deaths, No. (%) |
|---|---|---|---|
| 1976 | Sudan | 284 | 151 (53) |
| 1979 | Sudan | 34 | 22 (65) |
| 2000-2001 | Uganda | 425 | 224 (53) |
| 2004 | Sudan | 17 | 17 (41) |
| Total | 760 | 414 (54.5) |
| Year | Location | Reported Cases, No. | Deaths, No. (%) |
|---|---|---|---|
| 1976 | Sudan | 284 | 151 (53) |
| 1979 | Sudan | 34 | 22 (65) |
| 2000-2001 | Uganda | 425 | 224 (53) |
| 2004 | Sudan | 17 | 17 (41) |
| Total | 760 | 414 (54.5) |
*Data taken from the Centers for Disease Control and Prevention and The World Health Organization.
Table 2. History of Ebola Virus Zaire Outbreaks*
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Table
| Year | Location | Reported Cases, No. | Deaths, No. (%) |
|---|---|---|---|
| 1976 | Zaire | 318 | 280 (88) |
| 1977 | Zaire | 1 | 1 (100) |
| 1994 | Gabon | 52 | 31 (60) |
| 1995 | DRC | 315 | 250 (81) |
| Jan 1996 to Apr 1996 | Gabon | 37 | 21 (57) |
| Jul 1996 to Jan 1997 | Gabon | 60 | 45 (74) |
| 1996 | South Africa (acquired in Gabon) | 1 | 1 (100) |
| Oct 2001 to Mar 2002 | Gabon | 65 | 53 (82) |
| Oct 2001 to Mar 2002 | DRC | 59 | 44 (75) |
| Dec 2002 to Apr 2003 | DRC | 143 | 128 (89) |
| Nov 2003 to Dec 2004 | DRC | 35 | 29 (83) |
| Total | 1,086 | 883 (81.3) |
| Year | Location | Reported Cases, No. | Deaths, No. (%) |
|---|---|---|---|
| 1976 | Zaire | 318 | 280 (88) |
| 1977 | Zaire | 1 | 1 (100) |
| 1994 | Gabon | 52 | 31 (60) |
| 1995 | DRC | 315 | 250 (81) |
| Jan 1996 to Apr 1996 | Gabon | 37 | 21 (57) |
| Jul 1996 to Jan 1997 | Gabon | 60 | 45 (74) |
| 1996 | South Africa (acquired in Gabon) | 1 | 1 (100) |
| Oct 2001 to Mar 2002 | Gabon | 65 | 53 (82) |
| Oct 2001 to Mar 2002 | DRC | 59 | 44 (75) |
| Dec 2002 to Apr 2003 | DRC | 143 | 128 (89) |
| Nov 2003 to Dec 2004 | DRC | 35 | 29 (83) |
| Total | 1,086 | 883 (81.3) |
*Data taken from the Centers for Disease Control and Prevention and The World Health Organization.
Table 3. History of Ebola Virus Côte-d’Ivoire Outbreaks (No Deaths Reported)*
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| Year | Location | Reported Cases, No. |
|---|---|---|
| 1994 | Côte-d’Ivoire | 1 |
| 1995 | Liberia | 1 |
| Total | 2 |
*Data taken from the Centers for Disease Control and Prevention and The World Health Organization.
Table 4. History of Ebola Virus Reston Outbreaks (No Deaths Reported)*
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Table
| Year | Location | Proven† Cases Reported, No. |
|---|---|---|
| Oct 1989 | Reston, Va | 4 |
| Nov 1989 | Philadelphia, Pa | Unknown |
| 1990 | Reston, Va | Unknown |
| 1990 | Alice, Tex | Unknown |
| Total | 4 |
| Year | Location | Proven† Cases Reported, No. |
|---|---|---|
| Oct 1989 | Reston, Va | 4 |
| Nov 1989 | Philadelphia, Pa | Unknown |
| 1990 | Reston, Va | Unknown |
| 1990 | Alice, Tex | Unknown |
| Total | 4 |
*Data taken from the Centers for Disease Control and Prevention and The World Health Organization.
†Humans infected based on serologic evidence, but without clinical disease.
In January 2008, the CDC reported an update on an Ebola virus outbreak in the District of Bundibugyo, Uganda. This outbreak is thought to have begun in August 2007. As of December 16, 2007, 124 people had contracted the disease, and at least 35 patients had died. Of special interest is that the Ebola strain involved in this outbreak appears to be a new strain that is distinct from the previously known 4 strains. However, further investigation is necessary before this virus can be confirmed as a fifth strain of Ebola.7
Mortality/Morbidity
Morbidity and mortality rates are very high, and they vary with the strain of Ebola.
- The most highly lethal Ebola subtype is EBO-Z, which has been reported to have a mortality rate as high as 89%.
- The EBO-S subtype has a reported mortality rate, ranging from 41-65%.
Race
- No evidence exists for a racial predilection in Ebola infection. Because most cases have occurred in sub-Saharan Africa, most patients have been black.
Sex
- No sex predilection exists.
- Men, by the nature of their work exposure in forest and savanna regions, may be at increased risk of acquiring a primary infection from an as yet unknown vector.
- Because women provide much of the direct care for ill family members and are involved in the preparation of the bodies of deceased family, they may be at increased risk of acquiring a secondary infection. However, men and women who are medical health care providers seem to share a high and equal risk of infection.
Age
- In the 1995 outbreak in Kikwit, DRC, infection rates in children were significantly less than in adults. During this outbreak, only 27 (8.6%) of the 315 patients diagnosed with Ebola were aged 17 years or younger. This apparent sparing of children occurs even though 50% of the population of the DRC is younger than 16 years.
- Although definitive evidence is lacking, epidemiologic evidence suggests that children are less likely to come into direct contact with ill patients than adults.
- Other viral hemorrhagic syndromes, such as Crimean-Congo hemorrhagic fever and Hantavirus infections, also show a predominance of adult patients and a relative sparing of young children.
Clinical
History
In patients who have Ebola infection, 2 types of exposure history are recognized, primary and secondary.
- Primary exposure
- These histories usually involve travel to or work in an Ebola-endemic area such as sub-Saharan Africa, especially the DRC (formerly Zaire), Sudan, Gabon, and Côte d'Ivoire.
- Because the natural reservoir of Ebola has not been identified, the relationship between specific exposure to potential arthropod, animal, or plant vectors and disease remains unknown. However, a history of exposure to tropical African forests is more frequent in patients with Ebola than is a history of working within cities in the same region.
- Secondary exposure
- This refers to human-to-human or primate-to-human exposures.
- In each major outbreak, medical personnel or family members who cared for patients or those who prepared deceased patients for burial were at very high risk.
- Another group at risk for infection are animal care workers who provide care for primates. This latter group includes patients who developed infection with the Reston strain of Ebola but did not develop Ebola disease.
Physical
The findings upon physical examination depend on the stage of disease in which patients present. Early in the disease, patients may present with fever, pharyngitis, and severe constitutional signs and symptoms. A maculopapular rash, more easily seen on white skin than on dark skin, is often present, as is bilateral conjunctival injection. Late in the disease, patients often develop an expressionless hippocratic facies. At this point in the disease, bleeding from intravenous puncture sites and mucous membranes is common. Of interest is that, in the 1976 Ebola outbreak, bleeding was seen in most cases, whereas, in the 1995 Ebola outbreak, bleeding occurred in only half the patients. Myocarditis and pulmonary edema also are seen in the later stages of the disease. Terminally ill patients often die tachypneic, hypotensive, anuric, and in a coma.
- Clinical course
- Human infections with African-derived strains are characterized by an incubation period of 3-8 days in primary cases and slightly longer in secondary cases. However, cases with incubation periods of 19 and 21 days have been observed.
- The onset of clinical symptoms is sudden. Severe headache (50-74%), arthralgias or myalgias (50-79%), fever with or without chills (95%), anorexia (45%), and asthenia (85-95%) occur early in the disease.
- Gastrointestinal symptoms, including abdominal pain (65%), nausea and vomiting (68-73%), and diarrhea (85%), soon follow. Evidence of mucous membrane involvement includes conjunctivitis (45%), odynophagia or dysphagia (57%), and bleeding from multiple sites in the gastrointestinal tract. Bleeding from mucous membranes and puncture sites is reported in 40-50% of patients.
- A cutaneous rash, which in survivors desquamates during convalescence, is seen in approximately 15% of patients. Terminally ill patients often are obtunded, anuric, tachypneic, normothermic, and in shock.
- Although the mechanism is unclear, hiccups have been noted in fatal cases of Ebola in both the 1976 and the 1995 outbreaks in the DRC. In the 1995 Ebola outbreak in Kikwit, DRC, tachypnea was the single-most discriminating sign that separated survivors (0%) from patients who died (37%) (P = 0.027).
Causes
- Human Ebola hemorrhagic fever is caused by infection with 3 of the 4 presently known subtypes of Ebola: EBO-Z, EBO-S, and EBO-C. The fourth species, EBO-R, has caused human infection but, to date, has not been documented to cause human disease.
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Further Reading
Keywords
Ebola virus, viral hemorrhagic fever syndrome, Arenaviridae, Bunyaviridae, Flaviviridae, Filoviridae, EBO-Z, Marburg virus, Ebola infection, Ebola virus Zaire, Ebola virus Sudan, EBO-S, African-derived Ebola virus, Ebola virus Côte-d'Ivoire, EBO-C, Ebola virus Reston, EBO-R
