The Ebola virus has 4 subtypes: Zaire, Sudan, Ivory Coast and Reston.² Reston, the strain that caused the outbreaks among monkeys imported from the Philippines to the United States in the early 1990s, is distinguished by its apparent non-African origin and by its lesser pathogenicity in humans.² Monkeys appear susceptible hosts for all 4 subtypes but are not likely the primary reservoir, because they become ill and die rapidly when infected, much like humans.² The experimental inoculation of an arbitrary list of animals demonstrated that certain species of bats are able to support replication and circulation of high levels of the virus without contracting the disease.⁶ The search continues for a hypothesis to explain this observation.

Transmission is through contact with blood or body fluids from infected patients or monkeys.^1,2,5 Large quantities of the virus are present in the dermal tissue of infected people; the virus most likely enters the body through contact of contaminated fingers with oral mucosa or conjunctiva. The virus has been isolated in semen and vaginal secretions, so transmission may also occur through sexual activity and during pregnancy.⁵ Close contacts, family members and caregivers are at high risk; 30% of physicians who provided care during the 1995 outbreak in Kikwit, Democratic Republic of the Congo, contracted the disease.⁵

The virus targets endothelial cells, macrophages, monocytes and hepatocytes. It causes focal necrosis of the liver, lymphoid organs, kidneys, testes and ovaries. During the acute phase the virus activates multiple cytokines implicated in the pathogenesis of vascular permeability and shock, and it produces a circulating, soluble glycoprotein that has been speculated to interfere with immune response.^2,5

Clinical management: After an incubation period of 4–20 days, patients present with nonspecific symptoms (fever, conjunctivitis, muscle pain, headache, bloody diarrhea, sore throat) that are easily mistaken for shigellosis, typhoid fever or malaria.^2,7 This initial phase is quickly followed by vomiting, rash, decreased kidney and liver function and possibly bleeding (epistaxis, hematemesis, melena, petechiae, oozing from puncture sites).

Excellent tests for rapidly identifying viral nucleic acids, proteins and antibodies have been developed.⁸ In the epidemics to date, however, these tests have mostly been unavailable on site, since few African laboratories are capable of accessing and utilizing them.⁸

There is no specific treatment for Ebola hemorrhagic fever, although efforts are under way to develop drugs such as mRNA cap methyltransferase inhibitors, which might help to halt transmission.⁸ Treatment is supportive. In general, patients die 6 to 9 weeks after the onset of symptoms.² In the past, case-fatality rates have exceeded 50% and have reached 90%.¹ The current outbreak in Uganda is remarkable for its relatively low case-fatality rate of 40%.