Epidemiology: The current outbreak ofEbola hemorrhagic fever in Ugandamarks the 16th recognized time the virushas erupted since its discovery in 1976(Table 1).1,2 Each outbreak nudges uscloser to understanding the savage natureof this virus and its effect on primates.From the first devastating epidemics inZaire and Sudan we learned that acutelyill patients are intensely viremic,2 that pa-tient-isolation supplies and barrier-nurs-ing techniques save lives3 and that thedisease’s name is misleading because he-morrhage occurs in less than 50% ofcases.4 However, 25 years later we stilldon’t know the identity of the naturalreservoir of the virus, the significance ofelevated IgG antibodies after infection orthe function of circulating glycoproteinseen during the acute phase of infection.5

The Ebola virus has 4 subtypes: Zaire,Sudan, Ivory Coast and Reston.2 Reston,the strain that caused the outbreaksamong monkeys imported from thePhilippines to the United States in theearly 1990s, is distinguished by its appar-ent non-African origin and by its lesserpathogenicity in humans.2 Monkeys ap-pear susceptible hosts for all 4 subtypes

but are not likely the primary reservoir,because they become ill and die rapidlywhen infected, much like humans.2 Theexperimental inoculation of an arbitrarylist of animals demonstrated that certainspecies of bats are able to support replica-tion and circulation of high levels of thevirus without contracting the disease.6

The search continues for a hypothesis toexplain this observation.

Transmission is through contact withblood or body fluids from infected pa-tients or monkeys.1,2,5 Large quantities ofthe virus are present in the dermal tissueof infected people; the virus most likelyenters the body through contact of con-taminated fingers with oral mucosa orconjunctiva. The virus has been isolatedin semen and vaginal secretions, sotransmission may also occur throughsexual activity and during pregnancy.5

Close contacts, family members andcaregivers are at high risk; 30% of physi-cians who provided care during the 1995outbreak in Kikwit, Democratic Repub-lic of the Congo, contracted the disease.5

The virus targets endothelial cells,macrophages, monocytes and hepato-cytes. It causes focal necrosis of theliver, lymphoid organs, kidneys, testesand ovaries. During the acute phase thevirus activates multiple cytokines impli-cated in the pathogenesis of vascularpermeability and shock, and it producesa circulating, soluble glycoprotein thathas been speculated to interfere withimmune response.2,5

Clinical management: After an incuba-tion period of 4–20 days, patients presentwith nonspecific symptoms (fever, con-junctivitis, muscle pain, headache, bloodydiarrhea, sore throat) that are easily mis-taken for shigellosis, typhoid fever ormalaria.2,7 This initial phase is quickly fol-lowed by vomiting, rash, decreased kid-ney and liver function and possibly bleed-ing (epistaxis, hematemesis, melena,petechiae, oozing from puncture sites).

Excellent tests for rapidly identifyingviral nucleic acids, proteins and anti-bodies have been developed.8 In the epi-demics to date, however, these testshave mostly been unavailable on site,

since few African laboratories are capa-ble of accessing and utilizing them.8

There is no specific treatment forEbola hemorrhagic fever, although ef-forts are under way to develop drugssuch as mRNA cap methyltransferaseinhibitors, which might help to halttransmission.8 Treatment is supportive.In general, patients die 6 to 9 weeks afterthe onset of symptoms.2 In the past, case-fatality rates have exceeded 50% andhave reached 90%.1 The current out-break in Uganda is remarkable for itsrelatively low case-fatality rate of 40%.

Prevention: We don’t know whereEbola comes from or how the first hu-man case in any outbreak occurs. Thismakes primary prevention difficult. Sec-ondary prevention depends on early de-tection and control. Strategies to facili-tate this include continued support forthe improvement of basic public healthstandards in developing countries, inter-national preparedness for a coordinatedresponse when Ebola infection erupts,improved rapidity of diagnosis by theprovision of effective, rapid tests on siteand continued research on the reservoir,virology and treatment of Ebola hemor-rhagic fever.8 — Erica Weir, CMAJ

References1. Health Canada. Disease information: Ebola haemor-

rhagic fever. Available: www.hc-sc.gc.ca/hpb/lcdc/osh/info/ebola_e.html (accessed 2001 Jan 31).

2. Colebunders R, Borchert M. Ebola haemor-rhagic fever – a review. J Infect 2000;40:16-20.

3. Heymann DL, Barakamfitiye D, Szczeniowski M,Muyembe-Tamfum JJ, Bele O, Rodier G. Ebolahemorrhagic fever: lessons from Kikwit, Demo-cratic Republic of the Congo. J Infect Dis 1999;179(Suppl 1):S283-6.

4. Bwaka MA, Bonnet MJ, Calain P, ColebundersR, De Roo A, Guimard Y, et al. Ebola hemor-rhagic fever in Kikwit, Democratic Republic ofthe Congo: clinical observation in 103 patients. JInfect Dis 1999:179(Suppl 1):S1-7.

5. Peters CJ, LeDuc JW. An introduction to Ebola:the virus and the disease [review]. J Infect Dis1999;179(Suppl 1):ix-xvi.

6. Swanepoel R, Leman P, Burt F. Experimentalinoculation of plants and animals with Ebolavirus. Emerg Infect Dis 1996:2:321-5.

7. Muyembe-Tamfum J, Kipasa M, Kiyungu C,Colebunders R. Ebola outbreak in Kikwit, De-mocratic Republic of the Congo: discovery andcontrol measures. J Infect Dis 1999;179(Suppl 1):S259-62.

8. Johnson K. Gleanings from the harvest: sugges-tions for priority actions against Ebola virus epi-demics. J Infect Dis 1999;179(Suppl 1):S287-8.

Ebola erupts again

❙❙❙Public Health

Table 1: Outbreaks of Ebola hemor-rhagic fever

Year Country

No. of human cases

1976 Zaire*SudanEngland

318284

11977 Zaire 11979 Sudan 341989 Philippines

United States00

1992 Italy 01994 Gabon

Ivory Coast441

1995 Zaire 3151996 Gabon

South AfricaUnited StatesPhilippines

37200

2000 Uganda 428†

*Currently the Democratic Republic of the Congo.†As of Jan. 16, 2001. Source: Health Canada.1

CMAJ • MAR. 6, 2001; 164 (5) 685

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