Ebola Virus Disease (EVD): What You Need to Know

Edita Buinauskaitė
LSMU MA, Clinic of Infectious Diseases

West Africa may seem like a distant region, but as international travel becomes increasingly common, it is important to understand diseases such as Ebola virus disease (EVD), which is frequently discussed in the media. According to the World Health Organization (WHO), the most recent outbreak began at the end of 2013 and was confirmed on April 3, 2014, in Guinea. It subsequently spread to Sierra Leone, Liberia, and Nigeria, becoming the largest recorded outbreak of Ebola virus disease.

On August 12, the WHO reported the first confirmed case of Ebola virus infection in Europe: a missionary who returned from Liberia died in a hospital in Madrid after five days of treatment for Ebola virus disease.

Etiology

The Ebola virus, one of the most virulent pathogens affecting humans, is named after the Ebola River in the Democratic Republic of the Congo, where the first outbreak was identified in 1976. The virus belongs to the Filoviridae family, named after the Latin word filum (“thread”), reflecting the filamentous structure of the virus.

Ebola virus is a single-stranded RNA virus with genome organization and replication mechanisms similar to those of rhabdoviruses and paramyxoviruses [2, 3]. Clinically, it causes hemorrhagic fever characterized by coagulation disorders, increased capillary permeability, and shock [4, 5].

Genetically, the Ebola virus is classified into five strains (Zaire, Sudan, Côte d’Ivoire, Bundibugyo, and Reston), which differ in virulence and mortality rates [6]. Since 1976, the Zaire strain has caused multiple outbreaks (ranging from 30 to 300 cases), with mortality rates of 57–88% [7–12]. The Sudan strain has been associated with approximately 50% mortality in several outbreaks in Sudan and Uganda [13–17]. The Côte d’Ivoire strain has been documented in a single human case involving a scientist studying primates [18].

In 2007, the Bundibugyo strain caused outbreaks with a lower mortality rate (approximately 30%) compared to Zaire and Sudan strains [19]. The Reston strain differs significantly, as it primarily affects animals in the Philippines and has not been associated with severe disease in humans [20, 21]. It was first identified in the United States in 1989 in imported macaques, causing fatal outbreaks among animals. Later studies showed co-infection in pigs with both the Reston virus and PRRSV (Arteriviridae) [22].

Epidemiology

The spread of the Ebola virus among wild primates is believed to result from contact with infected reservoir species [23–26]. Bats are considered the most likely natural hosts due to their ability to carry various RNA viruses.

Human infection occurs through direct contact with blood or bodily fluids (vomit, urine, feces, and possibly sweat) from infected individuals. Family members are at high risk when caring for patients or preparing bodies for burial [28]. Healthcare workers are also at risk, particularly when protective measures are not used; for example, during the 2014 outbreak, 170 healthcare workers were infected [8].

Transmission may also occur through contact with contaminated surfaces or ingestion of infected material [29]. Although airborne transmission is not considered a primary route, laboratory exposure through aerosols has been reported. Historical outbreaks, such as the 1976 Yambuku incident, demonstrated how unsafe medical practices (reuse of contaminated syringes) led to rapid spread and high mortality [30, 31].

There is no evidence that Ebola virus is transmitted by mosquitoes or other arthropods. WHO data indicate that mortality rates may reach up to 52% (or 54% according to ULAC data from August 28, 2014), with 3069 cases and 1552 deaths reported during the outbreak in West Africa [1].

Pathogenesis

Due to the difficulty of conducting clinical studies during outbreaks, most data on Ebola virus pathogenesis come from animal experiments. Regardless of the route of infection, the virus initially targets macrophages and dendritic cells [5, 32].

After entering host cells, the virus replicates rapidly, causing cell death and releasing large amounts of viral particles. It spreads through lymphatic tissue and infects multiple organs, including the liver, spleen, and endocrine tissues. Viral spread is facilitated by suppression of type I interferon responses [33].

As the disease progresses, widespread tissue necrosis occurs. Filoviruses also induce a systemic inflammatory response through the release of cytokines and chemokines [32]. Infected macrophages produce TNF-α, IL-1β, IL-6, MCP-1, and nitric oxide [34], all of which have been detected in infected patients [36, 37].

Coagulation disorders arise indirectly through activation of the extrinsic coagulation pathway, with tissue factor production playing a key role [39]. Elevated D-dimer levels are detected early in infection [39, 40]. Immune dysfunction, including impaired dendritic cell function and lymphocyte apoptosis, contributes to severe disease outcomes [4].

Clinical Features

The incubation period ranges from 2 to 21 days. Transmission occurs only in symptomatic individuals. The disease begins with sudden fever, chills, and malaise, followed by symptoms such as headache, muscle pain, nausea, vomiting, diarrhea, and abdominal pain.

As the disease progresses, patients may develop hypotension, shock, and coagulation disorders. Bleeding is typically mild (petechiae, bruising, bleeding at injection sites), while severe hemorrhage occurs mainly in advanced stages [43–45].

A characteristic maculopapular rash may appear during the first week of illness. In severe cases, kidney failure, delirium, coma, and irreversible shock may develop [47]. Survivors often experience prolonged recovery, including fatigue, weight loss, skin desquamation, and hair loss [48].

Diagnosis

Early diagnosis is critical. Laboratory findings include leukopenia, thrombocytopenia, elevated liver enzymes, and proteinuria. Viral detection is performed using ELISA or PCR methods [51].

Definitive diagnosis requires virus isolation or electron microscopy and is conducted only in high-level biosafety laboratories.

Treatment

There is no confirmed specific treatment for Ebola virus disease. Management is primarily supportive, including fluid replacement, blood pressure stabilization, and correction of coagulation disorders [53, 54].

Experimental therapies, including interferons, monoclonal antibodies, and antiviral agents, have shown varying levels of success in animal studies but remain under investigation [52–60].

Infection Control

WHO and CDC guidelines emphasize strict infection control measures, including isolation, protective equipment, and proper handling of contaminated materials. Ebola virus is transmitted through bodily fluids, and standard precautions for bloodborne pathogens are effective in limiting its spread [65].

Role of the Community

Effective outbreak control depends not only on medical interventions but also on community engagement. Public education, cultural understanding, and cooperation with local populations are essential for monitoring, isolation, and prevention efforts [66–68].