AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

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*

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

Section 3 of 10  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

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.

DIFFERENTIALS

Section 4 of 10  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Other Problems to be Considered

Acute surgical abdomen versus abdominal signs of Ebola hemorrhagic fever
Crimean-Congo hemorrhagic fever
Note: A main concern in dealing with Ebola viral infections is the potential for human-to-human spread of virus before the correct diagnosis is made. This risk includes all medical personnel in direct contact with the patient, the patient's blood, or other body fluids or tissues.

WORKUP

Section 5 of 10  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Lab Studies

• The early phase of infection is characterized by thrombocytopenia, leukopenia, and a pronounced lymphopenia. Neutrophilia develops after several days, as do elevations in aspartate aminotransferase and alanine aminotransferase. Bilirubin may be normal or slightly elevated. With the onset of anuria, blood urea nitrogen and serum creatinine increase. Terminally ill patients may develop a metabolic acidosis that may contribute to the observation that these patients often have tachypnea, which may be an attempt at compensatory hyperventilation.
• The most commonly used test to identify infection has been the indirect immunofluorescence test. Concern over the sensitivity and utility of this test has resulted in the development of confirmatory tests. Definitive diagnosis currently rests on isolation of the virus in tissue culture and serologic testing. However, isolation of Ebola virus in tissue culture is a high-risk procedure and can be performed safely only in a few high-containment laboratories throughout the world.
• The risks in viral isolation have led to the development of other modalities that better lend themselves to laboratories with limited containment systems. Tests used to confirm the diagnosis of Ebola include a recently developed immunohistochemical test performed on formalin-fixed postmortem skin taken from patients who have died of Ebola hemorrhagic fever. This test is safe, sensitive, and specific, and it can be used for diagnosis and surveillance.  
• • Serologic testing includes an antigen detection enzyme-linked immunosorbent assay (ELISA), an immunoglobulin M–capture ELISA using EBO-Z viral antigens harvested from infected Vero E6 cells, and an immunoglobulin G (IgG) ELISA using detergent-extracted Ebola antigens.
  • Electron microscopy has been used to identify filoviruses in tissue but has obvious limitations as a diagnostic modality in the areas where human outbreaks have occurred.⁸
• Ebola hemorrhagic fever should be considered in patients with recent travel to areas where Ebola has been reported or in patients with exposure to known cases and who exhibit signs and symptoms consistent with Ebola.
• Diagnosis usually is confirmed by serologic testing. The most commonly used test in the past has been the indirect fluorescent antibody test (IFAT). However, concern over the specificity of the IFAT has led to the development and use of other tests, including ELISA, radioimmunoassay, radioimmunoprecipitation assay, and Western blot assay.
• Presently, an immunoglobulin M (IgM) ELISA and an IgG ELISA have been demonstrated to be both sensitive and specific.  
• • The IgM ELISA becomes positive in experimental primates within 6 days of infection but does not remain positive for extended periods. These qualities indicate the IgM test may be used to document acute Ebola infection.
  • The IgG ELISA is more specific than the IFAT, and it remains positive for long periods. Thus, the IgG ELISA for Ebola appears to be a superior test for seroprevalence investigations.

Procedures

• Antigen-detection ELISA - Identifies Ebola antigens
• IgM-capture ELISA - Uses EBO-Z viral antigens grown in Vero E6 cells to detect anti-EBO-Z IgM antibodies
• IgG-capture ELISA - Uses detergent-extracted viral antigens to detect IgG anti-Ebola antibodies

Histologic Findings

Although capable of involving many tissues, the virus has a predilection for endothelial cells, hepatocytes, and mononuclear phagocytes. Viral replication is associated with extensive focal necrosis and is most severe in the liver, spleen, lymph nodes, kidney, lung, and gonads. In the liver, councilmanlike bodies of focal necrosis similar to those seen in yellow fever are prevalent. However, the focal necrosis associated with Ebola replication results in a minimal effective inflammatory response. Late in the disease, the intestinal mucosa may separate from the lamina propria and slough.

TREATMENT

Section 6 of 10  

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• Follow-up
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• References

Medical Care

• Presently, no specific therapy is available that has demonstrated efficacy in the treatment of Ebola hemorrhagic fever.
• • Ribavirin, an antiviral drug previously used in other types of viral hemorrhagic fever, has no demonstrable anti-Ebola activity in vitro and has failed to protect Ebola-infected primates.
  • During the 1995 outbreak in Kikwit, DRC, human convalescent plasma was used to treat 8 patients with proven Ebola disease. Only 1 of these patients died.
  • Human recombinant interferon alpha-2b used in conjunction with hyperimmune equine IgG delayed but did not prevent death in Ebola-infected cynomolgus macaques.
  • Four laboratory workers in Russia who had possible Ebola exposure were treated with a combination of a goat-derived anti-Ebola immunoglobulin plus recombinant human alpha-2 interferon. One of these patients had a high-risk exposure and developed clinical evidence of Ebola infection. All 4 patients recovered. Equine IgG containing high-titer neutralizing antibodies to Ebola protected guinea pigs and baboons but was not effective in protecting infected rhesus monkeys.
• Supportive therapy with attention to intravascular volume, electrolytes, nutrition, and comfort care is of benefit to the patient.
• • Such care must be administered with strict attention to barrier isolation.
  • All body fluids (blood, saliva, urine, stool) contain infectious virions and should be handled with great care.
  • Patients who have died of Ebola should be buried promptly and with as little contact as possible.
• Experimental therapies are being investigated.
• • DNA vaccines expressing either envelope GP or nucleocapsid protein (NP) genes of Ebola virus have been demonstrated to induce protection in adult mice exposed to Ebola virus. These vaccines were administered by coating gold beads with DNA expressing the genes for either GP or NP, and they were delivered by skin particle bombardment using a PowderJect-XR gene gun. Both vaccines induced measurable antibody responses detected by ELISA and induced cytotoxic T-cell immunity.
  • Another approach has been to raise neutralizing antibodies in goats or horses that are specific for the GP of Ebola. These may be useful in both vaccine design and prophylactic use.

Surgical Care

• Surgical intervention generally follows a mistaken diagnosis in which Ebola-associated abdominal signs are mistaken for a surgical abdominal emergency. Such a mistake often is fatal for the patient and for any surgical team members who become contaminated with the patient's blood.

Consultations

• Whenever the diagnosis of Ebola or any other viral hemorrhagic fever is considered, the US Centers for Disease Control and Prevention, along with local and state health officials, should be contacted.
• Prompt consultation with an infectious diseases physician should be made, and strict barrier isolation should be instituted.
• No attempt should be made to culture the virus, except when performed in a maximum-containment biosafety level 4 laboratory with laboratory personnel wearing positive-pressure suits equipped with high-efficiency particulate air filters and an umbilical-fed air supply.

Diet

• Nutrition is complicated by the patient's nausea, vomiting, and diarrhea.
• Intravascular volume repletion is one of the most important supportive measures.

Activity

• Recovery often requires months. Weight gain and return of strength are slow.
• Ebola virus continues to be present for many weeks after resolution of the clinical illness.
• Semen from men recovering from Ebola infection has been shown to contain infectious virus, and Ebola has been transmitted by sexual intercourse involving recovering men and their sex partners.

MEDICATION

Section 7 of 10  

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• References

Presently, no specific anti-Ebola viral agents are available. Recent work has demonstrated that nucleoside analogue inhibitors of S-adenosylhomocysteine hydrolase (SAH) inhibited EBO-Z viral replication. SAH is a cell-encoded enzyme that, when inhibited, indirectly inhibits transmethylation reactions required for viral replication.

Passive immunity has been attempted using equine-derived hyperimmune globulins and human-derived convalescent immune globulin preparations. Although these preparations are not proven in preventing or modifying human Ebola hemorrhagic fever, some patients have survived clinical Ebola disease following their use. The survival of these patients suggests that passive immunity may be of benefit in some patients.

No commercially available Ebola vaccines are available. However, a recombinant human monoclonal antibody directed against the envelope GP of Ebola has been demonstrated to possess neutralizing activity. This Ebola neutralizing antibody may be useful in vaccine development or as a passive prophylactic agent.

Another approach has been evaluated in the rhesus macaque model of Ebola hemorrhagic fever, which carries a mortality rate that approaches 100%. Geisbert et al administered recombinant nematode anticoagulant protein, a potent inhibitor of tissue factor-initiated coagulation.⁹ One third of the monkeys given the nematode anticoagulant protein survived a lethal dose of Ebola virus, whereas 16 of the 17 (94%) control animals died. This approach targeted the hemorrhagic disease component of the infection rather than the virus itself.

FOLLOW-UP

Section 8 of 10  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Further Inpatient Care

• Survivors can produce infectious virions for prolonged periods. Therefore, strict barrier isolation in a private room away from traffic patterns must be maintained throughout the illness.
• Patient's urine, stool, sputum, and blood, along with any objects that have come in contact with the patient or the patient's body fluids (such as laboratory equipment), should be disinfected with a 0.5% sodium hypochlorite solution.

Further Outpatient Care

• Patients who survive continue to shed virus for weeks to months. Because Ebola virus has been isolated from seminal fluid 61 days after the onset of clinical disease, patients should abstain from sexual intercourse for 3 months.
• Recovery often requires months. Weight gain and return of strength are slow.
• The incubation period is 2-21 days. Individuals who were exposed to infected patients should be watched closely for signs of early Ebola disease.

Deterrence/Prevention

• Work continues on a vaccine for Ebola virus infection in primates. Sullivan et al from the Vaccine Research Center at the US National Institutes of Health and the Special Pathogens Branch at the US Centers for Disease Control and Prevention have reported on the combination of naked DNA vaccine capable of encoding Ebola proteins followed by a booster vaccination with a recombinant adenoviral vector expressing Ebola GP(Z).¹⁰  
• • In this study, cynomolgus macaques were injected with 3 doses of the DNA vaccine, 1 dose every 4 weeks. Twelve weeks later, the macaques were vaccinated with the recombinant adenoviral vector. After another 12 weeks, unvaccinated macaques and vaccinated macaques were injected with a lethal dose of Ebola virus. All unvaccinated macaques died, while none of the vaccinated macaques died.
  • This work indicates that primates can be vaccinated against Ebola and can develop both a cell-mediated response (thought to be a result of the DNA vaccine) and a humoral antibody response (thought to result from the recombinant adenoviral vaccine).
• Other attempts at designing vaccines that work in primates used vaccine strategies that were successful in mice and guinea pigs. Geisbert and colleagues at the US Army Medical Research Institute of Infectious Diseases in Fort Detrick, Md studied a series of vaccines that included RNA replicon particles from an attenuated strain of Venezuelan equine encephalitis virus that expressed Ebola virus glycoprotein and nucleoprotein, a recombinant vaccina virus that expressed Ebola glycoprotein, liposomes containing lipid A and inactivated Ebola virus, and a concentrated, inactivated whole-virion Ebola preparation.¹¹ Although these vaccines protected rodents against an Ebola challenge, the vaccines did not protect Cynomolgus macaques (M fascicularis) or rhesus macaques (Macaca mulatta) against exposure to Ebola.
• Ebola is transmissible person to person by direct contact with an infected patient's blood or other body fluids. Airborne transmission of the Reston strain occurred among primates, and, although most cases in humans occur following direct contact with a patient or their blood or body fluids, transmission of Ebola via the airborne route cannot be dismissed.
• Infection control inside and outside of medical facilities relies on barrier protection using double gloves, fluid-impermeable gowns, face shields with eye protection, and coverings for legs and shoes.

Complications

• Ocular complications have been reported in 3 of 20 survivors (15%) of the 1995 Ebola outbreak in the DRC. Patients reported ocular pain, photophobia, increased lacrimation, and decreased visual acuity. All had documented uveitis, and all improved with topical application of 1% atropine and steroids.
• Survivors have developed the following late manifestations:
• • Myalgias
  • Asymmetric and migratory arthralgias
  • Headache
  • Fatigue
  • Bulimia
  • Amenorrhea
  • Hearing loss
  • Tinnitus
  • Unilateral orchitis
  • Suppurative parotitis

Prognosis

• Prognosis is poor. Patients surviving for 2 weeks often make a slow recovery.

Patient Education

• Because the source of Ebola is unknown, education and prevention of primary cases is problematic.
• Education of communities at risk, especially health care workers, can greatly reduce the number of secondary person-to-person transmissions.

MULTIMEDIA

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Media file 1:  Ebola virus. Courtesy of the US Centers for Disease Control and Prevention.
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REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

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16. Feldmann H, Slenczka W, Klenk HD. Emerging and reemerging of filoviruses. Arch Virol Suppl. 1996;11:77-100. [Medline].
17. Formenty P, Leroy EM, Epelboin A, Libama F, Lenzi M, Sudeck H, et al. Detection of Ebola virus in oral fluid specimens during outbreaks of Ebola virus hemorrhagic fever in the Republic of Congo. Clin Infect Dis. Jun 1 2006;42(11):1521-6. [Medline].
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Article Last Updated: Apr 2, 2008