3. INTRODUCTION
Ebola virus disease (EVD), formerly Ebola
hemorrhagic fever(EHF) is a Zoonotic dx, caused by
Ebola virus.
Ebola is single stranded monosagmented RNA virus.
It causes severe hemorrhagic fever that resembles
fulminant septic shock.
Acquired upon contact with blood or body fluid of
an infected person or animal.
4. Epidemiology
1st discovered in 1976, near River Ebola in DRC.
Outbreaks; Several outbreaks mainly in Africa (DRC,
Sudan, Uganda, Gabon, Liberia , Sierra Leone, Nig.)
2014 Outbreak in West Africa;
Started from Guinea in 2013, spread to Liberia,
Sierra Leone, Nigeria, and Senegal.
As of Sept 2014, 4390 laboratory-confirmed
including 2226 deaths (case-fatality rate 51%).
5. Epidemiology Continuation
Johannesburg 1996; Med Doc from Gabon,
infected a Nurse- she died.
Few infections in Italy, USA, UK, Russia,
Philippines; Laboratory contamination.
7. Classification
Belongs to ORDER MONONEGAVIRALES.
FAMILY; FILOVIRIDAE. Filum in Latin=Thread like.
Members= Ebola + Marburg virus.
GENUS; EBOLAVIRUS- named after River Ebola in DR
Congo(where 1st case was recorded in 1976)
Has 5 species;
• Zaire Virus; Most virulent, fatality rate upto 90%.
8. Classification Continue
• Sudan Virus; Fatality rate of upto 50%
•Cote d’ivoire Virus, formerly Tai River Virus.
• Bundibugyo Virus; Least virulent,30% fatality rate.
Uganda.
• Reston Virus; Not pathogenic in human, seen in
animal reservoir, mostly in Philippines/USA.
Classified as "hemorrhagic fever viruses" due to
clinical presentation; Coagulation defects
capillary leak syndrome, and shock.
9. Transmission
Bats drop partially eaten fruits, which
Monkeys, Antelopes, Man, etc feed on and
contact the disease.
Contact with Blood or body fluid of infected
animals/person.
Burial ceremonies- Direct contact with the corpse
of infected person. Embalming
Formites; Utensils used by infected person, can
spread the disease.
10. Transmission Continue
Sexually; Men who have recovered from the
disease, can transmit the virus, through their semen
for up to 8/52 after recovery from illness.
Aerosol; Its documented in Laboratories, not in real
life. Reston Virus.
Accidental Laboratories infections- USA, UK,
Russia, Italy, Philippines.
Biological warfare; Speculation.
Asymptomatic person in incubation period,
likely non infectious.
12. Pathogenesis
Body entry; The Virus Enters the body through
mucous membranes, breaks in the skin, or
parenterally.
Glycoprotein synthesis(GP); After infection, the
Virus synthesize GP called Ebola virus GP, that binds
the virus to Macrophages/ neutrophils, Dendritic
cells, and Endothelial cells of blood vessels.
13. Pathogenesis Continue
Macrophage/ Nuetrophils inactivation; EV uses EV
GP to invade Macrophage/ Neutrophil, then inhibit
early steps of their activation.
This inactivation allows the virus to evade immune
system, colonize the host cells, and begin to
replicate in large number.
Systemic Spread; spread to LN, Liver, spleen,
fibroblasts, and many other cell types, resulting in
extensive tissue damage.
14. Pathogenesis Continue
Systemic Inflammatory response;
The presence of viral particles,
extensive tissue/cell damage, and break down
product of necrotic cells, causes the release of
cytokines, chemokines, and other proinflammatory
mediators, like;
TNF-α, IL-6, IL-8, macrophage chemotactic
protein (MCP)-1, and nitric oxide (NO) from
infected macrophages and other cells.
This chemicals result in fever, inflammation,
malaise, vasodilatation, increased vascular
permeability, hypotension, and shock.
15. Pathogenesis Continue
Coagulation defects ;
• Viral invasion of hepatocytes and vascular
endothelial cells, results in vascular and Liver damage.
•Infected macrophages synthesize tissue factor
(TF), triggering the extrinsic coagulation pathway.
•Proinflammatory cytokines also induce
macrophages to produce Tissue Factor. These
processes lead to coagulopathy seen in EVD
16. Pathogenesis Continue
Impairment of adaptive immunity;
•EV disable antigen-specific immune responses, by
damaging Dendritic cells, which are responsibility for
the initiation of adaptive immune responses.
•Infected Dendritic cells fail to undergo maturation,
thus unable to present antigens to lymphocytes, as
such Ebola pt, fail to develop antibodies to the virus.
•Failure of adaptive immunity and lymphocyte
apoptosis, explain how EV cause severe/fatal illness.
17. Pathogenesis Continuation
•Lymphocytes remain uninfected, but undergo
reactionary apoptosis, most likely due to
inflammatory mediators and/or the loss of support
signals from dendritic cells.
•Virus-specific lymphocyte proliferation still occurs,
despite massive apoptosis, but it arrives too late to
prevent a fatal outcome.
19. LATE SYMPTOM/SIGN;
•Ecchymosis /bruising,
•Oozing from venipuncture site.
•Bleeding nose, ear.
•Eye inflammation(conjunctivitis).
•Bleeding from mouth/rectum.
•Genital swelling(labia/scrotum).
•Roof of mouth looks red.
•Spontaneous miscarriages.
•Confusion, Seizures, coma.
•Death mostly due to Shock.
20. SING/SYMPTOMS CONT.
•The disease could progress to multi organ failure and
septic shock, with eventual death( averagely 6-10).
•In fatal disease, patients fail to mount adequate
immune response for unknown reasons.
•.
•In non-fatal cases, patients improve 6-11 days after
the onset of symptoms.
•The formation of antigen-antibody complexes during
recovery may cause acute arthralgias and other
symptoms.
21. DIAGONOSIS
Clinical Diagnosis;
• Difficult, early symptoms are none specific.
• Its takes high index of suspicion.
Laboratory Diagnosis;
•(ELISA) testing;
•Polymerase chain reaction(PCR)- DNA test.
•Virus isolation.
•Immunohistochemistry/ Immunoflorescence test
22. Diagnosis Continuation
Laboratory findings;
•Leucophenia; Is start with Lymphopenia, followed
Neutrophilia (WCC 1000/microL ).
•Thrombocytopenia; Platelet counts 50,000-
100,000/microL).
•Transaminitis; Elevated serum AST/ALT and Amylase
•Decrease in total plasma protein; Hepatocytes
damage/capillary leak syndrome.
23. L A B ORATORY FINDING CONTINUATION
•Renal abnormality; Proteinuria and renal
insufficiency.
•Coagulation abnormalities; Prolonged Prothrombin
(PT) and partial thromboplastin times (PTT). Fibrin
degradation products are elevated, consistent with
disseminated intravascular coagulation (DIC).
Differential Diagnosis;
•Other Heamorrhagic fevers; Marburg/Dangue/Yellow
•Typhoid Fever
•Malaria
24. PREVENTION AND CONTROL
•Avoid bush-meat.
•Regular washing of hands.
•Early detection/Contact tracing/Isolation.
•Screening travelers from affected countries
•Quarantine of suspected case(21/7)
•Barrier nursing techniques
•Use personal protective equip.(PPE)
•Proper sterilization of equipments
•No washing of carcass
•Proper burials of died.
•Public awareness.
25. PROGNOSIS
•EVD is the most lethal disease known to mankind
•Has poor prognosis, with fatality rate upto 90%.
•Effected people die from Shock.
•Ebola Virus Zaire is most deadly, fatality of 90%.
•Ebola virus Bundibugyo and Sudan has the
Fatality upto 50%.
26. TREATMENT
Ebola has no cure.
Supportive treatment only;
• Oxygen; Help breathing
•Antibiotics; Prevent 2’ bacterial infection.
•Analgesic; Fever and body ache.
•IVF; Maintain fluid and electrolyte balance.
•Transfusion; Bleeding
27. EXPERIMENTAL DRUGS
Zmapp
•Is a combination of 3 different monoclonal
antibodies that bind to the protein of the Ebola
virus. Mapp Biopharmaceutical Inc, USA.
•Has not yet been tested in humans for safety or
effectiveness.
Nano Silver; A Nigerian drug. Little is know
about it.
28. VACCINE
•None Available at present.
Virus like particles: VSV-EBOV, is Canadian made
Vaccine. At trial level
Non-replicating vectors: alpha virus, DNA vaccines,
recombinant adenovirus based vectors (rAD)
29. References;
CDC website http://www.cdc.gov/vhf/ebola/about.html
WHO website http://www.who.int/csr/disease/ebola/en/
The Lancet Ebola Resource Centre http://ebola.thelancet.com/
Journals - Bulletin of the WHO, NEJM and BMJ, August and
September 2014 issues
Wikipedia
Daily trust newspaper
Image courtesy – bbc.co.uk, Google images, CDC and WHO