By:Nur Sumaiyyah Lawson Binti Abdullah..

1. EBOLA VIRUS DISEASE
NUR SUMAIYYAH LAWSON
BIOMEDICAL DIAGNOSTIC 11
(BBD 4024)
CLINICAL MICROBIOLOGY

3. INTRODUCTION
DISASTER
• A total of 2,615 Ebola infections and 1,427 deaths
• highest case fatality rates of any human virus, 88%
ETYMOLOGY
• First recorded outbreak at, Yambuku in democratic republic of
congo (EBOLA RIVER)
VIRUS ( Latin virulentus)
• Viruses do not contain enzymes for energy production or
protein synthesis.
• small infectous agent that replicates only inside the
living cells of other organisms

4. STROKES YEAR REGIONS
AFFECTED
DESCRIPTION
FIRST 1976 Democratic republic
of congo (ZAIRE) &
sudan
First outbreak of
Ebola. Hemorrhagic
fever
SECOND 1989 Reston ,Virginia mysterious
outbreak. (initially
diagnosed as Simian
hemorrhagic fever
virus (SHFV)) among a
shipment of crab-
eating macaque
monkeys imported
from the Philippines.
named Reston
ebolavirus (REBOV)
THIRD 2014 WEST AFRICA
-affecting Guinea,
Sierra Leone, Liberia
and Nigeria.
largest outbreak to
the date

5. Ebola Taxonomy
• Group : Group V (-)sense RNA
• Order : Mononegavirales
• Family : Filoviridae
• Genus : Ebolavirus

6. Sudan
(SUDV)
Bundibugyo
(BDBV)
Tai forest
(TAFV)
Formerly
Cote d-Ivoire
Species
Zaire ebola
(EBOV)
The most
dangerous
Reston
(RESTV)
Non-humans
Ebola Species

8. Virological Aspects
• Family Filoviridae in the
order Mononegavirales
• Five species
• Zaire, Sudan, Taï,
Reston, Bundibugyo
• Enveloped, non-
segmented, negative-
strand RNA virus,
filamentous
• Genes arranged linearly
coding for seven structural
proteins - NP, VP35, VP40,
GP, VP30, VP24 and L with
NP
• GP, transmembrane
protein and responsible
for receptor binding and
membrane fusion
Rizwan SA, VMCHRI

9. STRUCTURE

10. • Viral cores
–stack up in cell
–migrate to the cell surface
–Produce trans-membrane proteins
–Push through cell surface
–Become enveloped by cell
membrane
• ssRNA- Genome Mutations
–Capable of rapid mutation
–very adaptable to evade host
defenses and environmental change
Ebola
Virus
Attach to
walls
Leakage of
blood and
serum into
surrounding
tissue
Wbcs’
attack
Wbcs’
dissolve
Chemical
released
Pro-
inflammatory
cytokines
Pro coagulants
Also released
Blood
vessels
more
damaged
Permanent
bleeding
Entire
body leaks
and
dissolves
Ebola Pathophysiology

11. Ebola Pathophysiology

12. Modes of Transmission
• Direct contact (through broken skin or mucous
membranes) with
– a sick person's blood or body fluids (urine, saliva,
faeces, vomit, semen)
– objects (such as needles) that have been
contaminated with infected body fluids
– infected animals
• High risk groups – bush meat hunters, relatives of
patients, funeral attendees, corpse handlers, lab
personnel
I

13. Transmission

14. CAUSES
• Ebola Virus Disease in humans is caused by 4
of the 5 viruses of the genus Ebolavirus. The
four are Bundibugyo virus , Sudan virus, Taï
Forest virus and one called Ebola
virus (EBOV).
• EBOV, species Zaire ebolavirus, is the most
dangerous of the viruses causing the largest
number of outbreaks.

15. Zaire Ebolavirus

16. SIGNS AND SYMPTOMS (1)
Early symptoms :
Influenza(fever,headache,joint & abdominal
pain)
Vomiting,diarrhoea
Loss of appetite
Chest pain,shortness of breath
Weakness
Maculopapular rash(50% cases)

17. Maculopapular Rash

18. SIGNS AND SYMPTOMS (2)
Acute symptoms :
Bleeding from mucous membrane(eg.nose)
Bleeding of the skin
Subconjunctival haemorrhages
Decreased blood clotting
Multiple organ dysfunction syndrome which
leads to death

19. Bleeding of the Skin

20. Subconjunctival Haemorrhages
in GI tract

22. COMPLICATIONS
• Recovery may begin between 7 and 14 days after
first symptom.
• Death is often due to low blood pressure from
fluid loss. In general, bleeding often indicates a
worse outcome, and blood loss may result in
coma and death.
• Those who survive often have ongoing muscular
and joint pain, liver inflammation, and may have
continued feelings of tiredness and weakness,
decreased appetite.

23. DIAGNOSIS (1)
• Laboratory indicators include a low platelet
count; an initially decreased WBC count followed
by an increased WBC count; elevated levels of the
liver enzymes alanine aminotransferase (ALT) and
aspartate aminotransferase (AST); and
abnormalities in blood clotting often consistent
with disseminated intravascular coagulation
(DIVC) such as a prolonged prothrombin time,
partial thromboplastin time, and bleeding time.

24. TEST NORMAL VALUE
Platelet count 150000-300000mcL
WBC count 4500-10000mcL
Alanine aminotransferase(ALT) 10-40U/L (males)
7-35U/L(females)
Aspartate aminotransferase(AST) 14-20U/L (males)
10-36U/L (females)
Prothrombin time (PT) 10-12 sec
Partial thromboplastin time (aPTT) 25-38 sec
Bleeding time (BT) 3-7 min

25. DIAGNOSIS (2)
• In early phase - ELISA,PCR, Virus isolation
• In later phase - IgM and IgG antibodies
• In deceased patients – immunohistochemistry,
PCR, virus isolation
• Strict precautions during transportation of
samples.

26. PCR Test

27. ELISA test

28. TREATMENT
• No proven antiviral drug
• Providing intravenous fluids and balancing
electrolytes (body salts)
• Treating other infections if they occur
• Personal Protective Equipment
• Isolation of Ebola patients from contact
• No licensed vaccine for EVD is available. Several
vaccines are being tested, but none are available
for clinical use.

29. Experimental Treatments
• ZMapp – a combo of 3 monoclonal antibodies
• TKM-Ebola – targets RNA of the virus
• MB-2003 - prevents infection when
administered within one to two days
• BCX-4430 – RNA polymerase
• Whole blood and serum transfusion from
recovered patients

30. PREVENTION (1)
• Public health measures -
early detection and
isolation, contact tracing
and rigorous infection
control measures
• Screening of travellers
from affected countries in
airports, seaports and land
borders
• Quarantine and
observation of suspected
cases for 21 days from
exposure

31. PREVENTION (2)
• All suspected or confirmed
cases, single closed patient
room
• Avoiding contact
• A log book containing details
of persons entering
• Personalprotective equipment
for caretakers
• Minimum use of sharps.
In this 2014 photo provided by the Samaritan's Purse aid organization, Dr. Kent Brantly, left, treats an Ebola patient at the Samaritan's Purse Ebola Case Management
Center in Monrovia, Liberia. On Saturday, July 26, 2014, the North Carolina-based aid organization said Brantly tested positive for the disease and was being treated at a
hospital in Monrovia.
View of an isolation center for people infected with Ebola at Donka Hospital in Conakry.

32. CASE STUDY (1)
• On the 5 November 1976 one investigator at the
Microbiological Research Establishment accidentally
pricked his thumb through a protective rubber glove
while transferring homogenized liver from a guinea-pig
infected with a new virus. According to standard safety
protocol he immediately removed the glove and
immersed his thumb in hypochlorite solution then
squeezed it vigorously. There was no bleeding and
careful examination with a hand lens failed to reveal a
puncture wound. He was kept under surveillance, and
on the sixth day became ill.

33. CASE STUDY
• Shortly after midnight on 11 November his temperature
rose to 37 4°C. During the early morning he complained of
central abdominal pain and nausea. He developed an
erythematous rash. He did not vomit or have the headache
or myalgia. He was transferred to the high-security
infectious diseases unit . When he was admitted he felt
physically exhausted and complained of anorexia, nausea,
and central abdominal pain.His temperature was 38°C . He
was alert and did not seem to be particularly ill.
• Apart from slight abdominal tenderness there were no
other abnormal findings. Treatment was started with
human interferon given by intramuscular injection in a
dose of 3 million units every 12 hours for 14 days.

34. CASE STUDY
• The next morning his temperature was normal
and he was free from symptoms, but later in the
evening his temperature rose again to 39°C.
Apart from loss of appetite there were no other
symptoms. By this time direct electron
microscopy had shown virus particles in the
patient's blood. In view of this finding it was
thought advisable to give the patient
convalescent serum from people convalescing
after the recent African outbreak. The serum was
given by slow intravenous infusion over a period
of four hours.

35. CASE STUDY
• On the fourth day of illness his temperature fell
to normal. About midday he had a sudden
violent bout of shivering followed by a sharp
rise in temperature to 40°C. This was
accompanied by nausea and a single episode of
vomiting. His mental state began to change and
over the next 24 hours there was striking
deterioration in concentration and memory.
Protein was detected in his urine for the first
time and persisted thereafter until the fever
subsided

36. CASE STUDY
• Over the next 72 hours, there was severe malaise
and extreme weakness. Profuse watery diarrhea
developed and continued for two days
accompanied by persistent vomiting.
• On the sixth day of illness, a further 330 ml of
convalescent serum was infused and followed by
Hartmann's solution to correct the dehydration.
His general condition started to improve and he
made an uneventful and slow recovery over 10
weeks.

37. DISCUSSION (1)
• The nature of the accident and the absence-of a
visible puncture mark indicate the invasiveness
of Ebola virus and the high susceptibility of man.
The course and duration of the illness were
similar to patients infected with Ebola with the
characteristic clinical syndrome of the rash,
excessive fatigue, and considerable
gastrointestinal disturbance.
• The oliguria and proteinuria present at the height
of the illness could have been attributed to
deposition of immune complexes in the kidney

38. DISCUSSION (2)
• The relatively mild course of the illness and
the absence of haemorrhage might have been
due to early treatment with interferon and
convalescent serum. At present, apart from
the use of convalescent serum, there is no
definitive cure for Ebola infection making this
a potentially fatal disease.

39. CONCLUSION
• Ebola virus disease also known as Ebola
hemorrhagic fever is a disease of humans and
other primates caused by ebolaviruses. It has
a high risk of death, with patients developing
internal and external bleeding. There is no
definitive cure and management is mainly
supportive ensuring adequate hydration and
symptomatic treatment. Prevention through
isolation, barrier nursing and contact tracing is
essential.

40. QUESTIONS
1. When is the first outbreak of Ebola occur?
2. What are the five types of species in Ebola
species chart?
3. What are the name of the seven genes arranged
linearly coding for structural proteins ?
4. Explain briefly about the Ebola pathophysiology
5. What are the symptoms that were developed
over the next 72 hours in the case study?

41. ANSWERS
1. 1976
2. Bundibugyo species , Sudan species, Taï Forest
species , Zaire ebola species and Reston species
3. NP, VP35, VP40, GP, VP30, VP24 and L with NP
4. Ebola virus attach to the walls causing leakage of blood
and serum into the surrounding tissue. WBC attack and
dissolved.Chemical,proinflammatory,cytokines,procoagula
nts are releases causing the blood vessel to be damaged.
This causes permenant bleeding and as a result,entire
body leaks and dissolves.
5. Severe malaise and extreme weakness. Profuse watery
diarrhea developed

42. REFERENCES
• Emond R T D, Evans B., Bowen E T W , Lloyd G, A
case of Ebola virus infection British Medical
Journal, 1977, 2, 541-544
• Martini, G A, Postgraduate Medical Journal, 1973,
49, 542. 2
• Gear, J S S, et al, British Medical,Journal, 1975, 4,
489.
• H Nishiura, G Chowell, Early transmission
dynamics of Ebola virus disease (EVD), West
Africa, - Euro Surveill March to August 2014
researchgate.net

43. REFERENCES
• Watt A, Moukambi F ,Banadyga L , Groseth A,
Callison J ,Herwig A ,Ebihara H, Feldmann H ,a
Hoenen T, A Novel Life Cycle Modeling System
for Ebola Virus Shows a Genome Length-
Dependent Role of VP24 in Virus Infectivity
Journal of Virology September 2014 Volume
88 Number 18 p. 10511–10524

44. REFERENCES
• Kikwit, Dowell S.F., Mukunu R, Ksiazek T.G ,
Khan S, Rollin P.E., and C. J. Peters
Transmission of Ebola Hemorrhagic Fever: A
Study of Risk Factors in Family Members, The
Journal of Infectious Diseases 1999;179(Suppl
1):S87–91
• Peters C.J. and LeDuc J.W. An Introduction to
Ebola: The Virus and the Disease. The Journal
of Infectious Diseases 1999;179(Suppl 1):ix–xvi