Ebola

This burden continues to build up as the list of new pathogens and diseases extends into the 21st century with an outbreak of SARS due to a newly identified coronavirus; an outbreak of human monkeypox in the Western hemisphere; human cases of avian influenza in Asia; the identification of bovine spongiform encephalopathy-infected cattle in the United States; outbreaks of Marburg hemorrhagic fever in Angola and Ebola hemorrhagic fever in the Democratic Republic of the Congo; and the establishment of West Nile virus as endemic in North America.

This article will focus on Ebola, one of the seven agents that have made a significant appearance in this century. It was first recognized during a human outbreak in 1976 with almost simultaneous outbreaks in both the Sudan and the Democratic Republic of Congo (DRC). It was named after a river in the DRC. Recently, in 2012, an outbreak was reported in Uganda and panic gripped its east African neighbours due to its highly lethal nature. It is one of at least 30 known viruses capable of causing viral hemorrhagic fever syndrome. Such outbreaks are initiated by virus introduction to humans from a still-unknown source and are perpetuated by human-to-human transmission. It is a member of the Filoviridae family and in the present nomenclature it’s classified into 5 separate species.

They include:

• Sudanebolavirus ,

• Zaire ebolavirus,

• Ivory Coast ebolavirus/ Côte d'Ivoire Ebola virus,

• Restonebolavirus,

• Bundibugyo ebolavirus.

Route of Infection

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 Sudan ebolavirus and Zaire ebolavirus may be transmitted by contact with mucous membranes, conjunctiva, pharynx and gastrointestinal surfaces, small breaks in the skin, and, at least experimentally, by aerosol.

Pathophysiology

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 Councilman-like bodies. In fatal infections, the host's tissues and blood contain large numbers of Ebola virions, and their tissues and body fluids are highly infectious. 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. A soluble, nonstructural secretory glycoprotein is produced in large quantities early in Ebola infection.

The nonstructural secretory glycoprotein binds to neutrophil CD16b, a neutrophil-specific Fc g receptor III, and inhibits early neutrophil activation. The nonstructural secretory glycoprotein also may be responsible for the profound lymphopenia that characterizes Ebola infection. Thus, nonstructural secretory glycoprotein is believed to play pivotal roles in the ability of Ebola to prevent an early and effective host immune response.

Symptoms

The incubation period for Ebola ranges from 2 to 21 days. The onset of illness is abrupt and is characterized by fever, headache, joint and muscle aches, sore throat, and weakness, followed by diarrhea, vomiting, and stomach pain. A rash, red eyes, hiccups and internal and external bleeding may be seen in some patients. Diagnosis Antigen-capture enzyme-linked immunosorbent assay (ELISA) testing, IgM ELISA, polymerase chain reaction (PCR), and virus isolation can be used to diagnose a case of Ebola within a few days of the onset of symptoms. Persons tested later in the course of the disease or after recovery can be tested for IgM and IgG antibodies.

Treatment

The predominant treatment is general supportive therapy. It 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. Prognosis Prognosis is generally poor. If a patient survives, recovery may be prompt and complete, or protracted with sequelae, such as orchitis, arthralgia, myalgia, desquamation, alopecia and ocular manifestations. Researchers do not understand why some people are able to recover from Ebola HF and others are not.

Prevention and prophylaxis

The prevention of Ebola presents many challenges. Because the identity and location of the natural reservoir of Ebola virus are unknown, there are few established primary prevention measures. 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. Prevention of ebola therefore relies predominantly on behavior modification, proper personal protective equipment, and sterilization/disinfection.