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Ebola virus main
Ebola – A growing threat
• First identified in 1976.
• Ebola river valley ; where the first
reported outbreak occurred.
• Currently , this is the 7th
outbreak
since 1976.
• Cultural practices in Africa : Diet
to Death rites.
• Associated with CFR ~ 30-90%,
depending on various virus
species.
Outbreaks of filoviridae infection
Ebola virus main
Ebola virus
• Family : filoviridae
• Group of enveloped , non-segmented, negative strand
RNA viruses with characteristic filamentous shape
• Ebola virus species :
– EBOV
– Sudan ebolavirus
– Bundibugyo ebolavirus
– Reston ebolavirus
– Tai forest ebolavirus
• Prototype pathogen of viral hemorrhagic fever ; EHF
DRC , Sudan , Republic of
Congo & Uganda
Structure of ebolavirus
Ebola virus main
Ebola virus main
Route of infection
• Ebola virus seems to enter the host through
mucosal surfaces, breaks, and abrasions in the
skin, or by parenteral introduction.
• Most human infections in outbreaks seem to
occur by direct contact with infected patients or
cadavers.
• Infectious virus particles or viral RNA have been
detected in semen, genital secretions,and in skin of
infected patients;they have also been isolated from
skin, body fluids, and nasal secretions of
experimentally infected non-human primates.
• Reuse of contaminated needles played an important
part in the 1976 outbreaks of Ebola virus in Sudan and
Zaire.
• Butchering of a chimpanzee for food was linked to
outbreaks of Zaire Ebola virus in Gabon,and contact
exposure was the probable route of transmission.
• Handling and consumption of freshly killed bats was
associated with an outbreak of Zaire Ebola virus in DRC.
Clinical manifestations
• Incubation period of 2 – 21 days
• Abrupt onset ; fever , chills , malaise & myalgia
• Multisystem involvement
– Anorexia, nausea, vomiting, abdominal pain, diarrhoea
– Chest pain, shortness of breath, cough, nasal discharge
– Conjunctival infection, postural hypotension, oedema
– Headache, confusion, coma
– Petechiae, ecchymoses, uncontrolled oozing from
venepuncture sites, mucosal haemorrhages, and post-
mortem evidence of visceral haemorrhagic effusions
• A macropapular rash with varying severity of erythema
and desquamate ; Day 5—7 of the illness
• Abdominal pain
– Hyperamylasaemia
– Pancreatitis.
• In later stages
– Shock
– Convulsions
– Severe metabolic disturbances
– Diffuse coagulopathy
• Patients with fatal disease develop clinical signs early
during infection and die typically between day 6 and 16
with hypovolaemic shock and multiorgan failure.
• Severe Haemorrhages ; present in fewer than half of
patients.
• In non-fatal cases, patients have fever for several days
and improve typically around day 6—11, about the time
that the humoral antibody response is noted.
• Convalescence is extended and often associated with
sequelae such as myelitis, recurrent hepatitis,
psychosis, or uveitis.
• Pregnant women have an increased risk of miscarriage,
and clinical findings suggest a high death rate for
children of infected mothers.
Case definition for Ebola Virus Disease
Person Under Investigation (PUI)
A person who has both consistent signs or symptoms and risk factors
as follows:
• Elevated body temperature or subjective fever or symptoms,
including severe headache, fatigue, muscle pain, vomiting,
diarrhea, abdominal pain, or unexplained hemorrhage ; AND
• An epidemiological risk factor within the 21 days before the onset
of symptoms.
Confirmed Case
• Laboratory-confirmed diagnostic evidence of Ebola virus
infection.
Laboratory findings
• Early leucopenia (as low as 1000 cells/μL)
– Lymphopenia and subsequent neutrophilia
– Left shift with atypical lymphocytes
– Thrombocytopenia (50 000—100 000 cells per μL)
– Increased serum aminotransferase concentrations (AST >
ALT)
– Hyperproteinaemia, and proteinuria.
– PT & PTT are prolonged
– Fibrin split products are detectable
• In a later stage, secondary bacterial infection might lead to
raised counts of white blood cells.
Target cells & tissues
• Broad cell tropism.
• Preferential replication sites ; Monocytes, macrophages,
dendritic cells, endothelial cells, fibroblasts,
hepatocytes, adrenal cortical cells, and several types of
epithelial cells.
• Virus glycoprotein is the primary determinant of
vascular-cell injury
• Ebola virus infection of endothelial cells induces
structural damage
Ebola virus main
Immune system evasion
• Upon viral infection, the IFN
response can be triggered by
sensors such as retinoic acid-
inducible gene I (RIG-I)
protein and the melanoma
differentiation-associated
gene 5 (MDA-5) protein that
recognize dsRNA or
ribonucleoprotein complexes.
• Fatal Ebola infections are
marked by unchecked viral
replication combined with an
inadequate antiviral
response.
• VP35 is able to disrupt the pathway by competing with RIG-1
for the binding of dsRNA.
• VP24 suppresses interferon production ; VP24 competes with
STAT1 to bind karyopherin α1, blocking nuclear accumulation
and leading to inhibition of IFN signaling.
• In addition, infected macrophages release increased amounts
of nitric oxide (NO); High concentrations of NO depresses the
mitochondrial membrane potential, causing apoptosis.
• In dendritic cells , VP35 suppresses upregulation of co-
stimulatory molecules & pro-inflammatory cytokines ;
attenuates their ability to activate CD4+ T-cells.
• Large numbers of lymphocytes undergo apoptosis ;
progressive lymphopenia and lymphoid depletion at
death.
– TNF-related apoptosis-inducing ligand (TRAIL) and
Fas death receptor pathways
– Impairment of dendritic cell function induced by
Ebola virus infection
– Abnormal production of soluble mediators such as
nitric oxide that have proapoptotic properties
– Direct interactions between lymphocytes and Ebola
virus proteins
Hemorrhagic manifestations in non human primates
Petechiae on arm & axillary region Haemorrhages in the ileum
Gastroduodenal lesion
Connecting the cellular mechanism to hemorrhagic fever
Destabilization of vascular
endothelium
Facilitates entry of viruses
Massive hemorrhage
Hypovolemic shock
Activation of coagulation cascade
Catastrophic thrombosis
Ebola haemorrhagic fever presents as a viral
prodrome with a high potential for differential
diagnosis
 Malaria
 Typhoid fever
 Shigellosis
 Menigococcal septicaemia
 Plague
 Leptospirosis
 Relapsing fever
 Typhus
 Chikungunya fever
 Fulminant viral hepatitis
Laboratory diagnosis
• Laboratory diagnosis of Ebola virus is achieved in two ways:
– Measurement of host-specific immune responses to infection
– Detection of viral particles, or particle components in infected
individuals.
• RT-PCR and antigen detection ELISA are the primary assays to
diagnose an acute infection.
• Viral antigen and nucleic acid can be detected in blood from day
3 up to 7—16 days after onset of symptoms.
• For antibody detection ; Direct IgG and IgM ELISAs and IgM
capture ELISA.
• IgM antibodies
– Appear : 2 days post onset of symptoms
– Disappear : 30 and 168 days after infection.
• IgG-specific antibodies develop between day 6 and 18 after
onset and persist for many years.
• A IgM or rising IgG titre constitutes a strong presumptive
diagnosis.
• Decreasing IgM, or increasing IgG titres (four-fold), or both,
in successive paired serum samples are highly suggestive of
a recent infection
Management
• Isolation of patients .
• Strict barrier nursing procedures ; Protective clothing and
respirators.
• Cadavers are residual risks and should be handled
accordingly.
• Traditional funeral and caretaking methods contribute to the
spread of the virus and potentiate outbreaks.
• Symptomatic and supportive treatment.
• Strategies should include isolation, malaria treatment, broad
spectrum antibiotics, and antipyretics before diagnosis.
• Fluid substitution, preferentially intravenous administration,
and analgesics
• Shock, cerebral oedema, renal failure, coagulation
disorders, and secondary bacterial infection have to be
managed and can be life-saving.
• Organ failure should be addressed appropriately
– Dialysis for kidney failure
– Extracorporeal membrane oxygenation for lung
failure.
• At present, no strategy has proved successful in specific
pre-exposure and postexposure treatment of Ebola virus
infections in man
Treatment
Ebola virus main
Prevention
• There is no FDA-approved
vaccine available for Ebola.
• Healthcare workers who may
be exposed to people with
Ebola should follow these steps:
– Wear appropriate PPE
(Gloves,masks,caps,safety
glasses,medical coats /
surgical gowns,surgical
drapes)
– Practice proper infection
control and sterilization
measures.
– Isolate patients with Ebola from other patients.
– Avoid direct contact with the bodies of people who
have died from Ebola.
– Notify health officials in case of direct contact with
the blood or body fluids, feces, saliva, urine, vomit,
and semen of a person who is sick with Ebola.
Thankyou ... !!

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Ebola virus main

  • 2. Ebola – A growing threat • First identified in 1976. • Ebola river valley ; where the first reported outbreak occurred. • Currently , this is the 7th outbreak since 1976. • Cultural practices in Africa : Diet to Death rites. • Associated with CFR ~ 30-90%, depending on various virus species.
  • 5. Ebola virus • Family : filoviridae • Group of enveloped , non-segmented, negative strand RNA viruses with characteristic filamentous shape • Ebola virus species : – EBOV – Sudan ebolavirus – Bundibugyo ebolavirus – Reston ebolavirus – Tai forest ebolavirus • Prototype pathogen of viral hemorrhagic fever ; EHF DRC , Sudan , Republic of Congo & Uganda
  • 9. Route of infection • Ebola virus seems to enter the host through mucosal surfaces, breaks, and abrasions in the skin, or by parenteral introduction. • Most human infections in outbreaks seem to occur by direct contact with infected patients or cadavers.
  • 10. • Infectious virus particles or viral RNA have been detected in semen, genital secretions,and in skin of infected patients;they have also been isolated from skin, body fluids, and nasal secretions of experimentally infected non-human primates.
  • 11. • Reuse of contaminated needles played an important part in the 1976 outbreaks of Ebola virus in Sudan and Zaire. • Butchering of a chimpanzee for food was linked to outbreaks of Zaire Ebola virus in Gabon,and contact exposure was the probable route of transmission. • Handling and consumption of freshly killed bats was associated with an outbreak of Zaire Ebola virus in DRC.
  • 12. Clinical manifestations • Incubation period of 2 – 21 days • Abrupt onset ; fever , chills , malaise & myalgia • Multisystem involvement – Anorexia, nausea, vomiting, abdominal pain, diarrhoea – Chest pain, shortness of breath, cough, nasal discharge – Conjunctival infection, postural hypotension, oedema – Headache, confusion, coma – Petechiae, ecchymoses, uncontrolled oozing from venepuncture sites, mucosal haemorrhages, and post- mortem evidence of visceral haemorrhagic effusions
  • 13. • A macropapular rash with varying severity of erythema and desquamate ; Day 5—7 of the illness • Abdominal pain – Hyperamylasaemia – Pancreatitis. • In later stages – Shock – Convulsions – Severe metabolic disturbances – Diffuse coagulopathy
  • 14. • Patients with fatal disease develop clinical signs early during infection and die typically between day 6 and 16 with hypovolaemic shock and multiorgan failure. • Severe Haemorrhages ; present in fewer than half of patients. • In non-fatal cases, patients have fever for several days and improve typically around day 6—11, about the time that the humoral antibody response is noted.
  • 15. • Convalescence is extended and often associated with sequelae such as myelitis, recurrent hepatitis, psychosis, or uveitis. • Pregnant women have an increased risk of miscarriage, and clinical findings suggest a high death rate for children of infected mothers.
  • 16. Case definition for Ebola Virus Disease Person Under Investigation (PUI) A person who has both consistent signs or symptoms and risk factors as follows: • Elevated body temperature or subjective fever or symptoms, including severe headache, fatigue, muscle pain, vomiting, diarrhea, abdominal pain, or unexplained hemorrhage ; AND • An epidemiological risk factor within the 21 days before the onset of symptoms. Confirmed Case • Laboratory-confirmed diagnostic evidence of Ebola virus infection.
  • 17. Laboratory findings • Early leucopenia (as low as 1000 cells/μL) – Lymphopenia and subsequent neutrophilia – Left shift with atypical lymphocytes – Thrombocytopenia (50 000—100 000 cells per μL) – Increased serum aminotransferase concentrations (AST > ALT) – Hyperproteinaemia, and proteinuria. – PT & PTT are prolonged – Fibrin split products are detectable • In a later stage, secondary bacterial infection might lead to raised counts of white blood cells.
  • 18. Target cells & tissues • Broad cell tropism. • Preferential replication sites ; Monocytes, macrophages, dendritic cells, endothelial cells, fibroblasts, hepatocytes, adrenal cortical cells, and several types of epithelial cells. • Virus glycoprotein is the primary determinant of vascular-cell injury • Ebola virus infection of endothelial cells induces structural damage
  • 20. Immune system evasion • Upon viral infection, the IFN response can be triggered by sensors such as retinoic acid- inducible gene I (RIG-I) protein and the melanoma differentiation-associated gene 5 (MDA-5) protein that recognize dsRNA or ribonucleoprotein complexes. • Fatal Ebola infections are marked by unchecked viral replication combined with an inadequate antiviral response.
  • 21. • VP35 is able to disrupt the pathway by competing with RIG-1 for the binding of dsRNA. • VP24 suppresses interferon production ; VP24 competes with STAT1 to bind karyopherin α1, blocking nuclear accumulation and leading to inhibition of IFN signaling. • In addition, infected macrophages release increased amounts of nitric oxide (NO); High concentrations of NO depresses the mitochondrial membrane potential, causing apoptosis. • In dendritic cells , VP35 suppresses upregulation of co- stimulatory molecules & pro-inflammatory cytokines ; attenuates their ability to activate CD4+ T-cells.
  • 22. • Large numbers of lymphocytes undergo apoptosis ; progressive lymphopenia and lymphoid depletion at death. – TNF-related apoptosis-inducing ligand (TRAIL) and Fas death receptor pathways – Impairment of dendritic cell function induced by Ebola virus infection – Abnormal production of soluble mediators such as nitric oxide that have proapoptotic properties – Direct interactions between lymphocytes and Ebola virus proteins
  • 23. Hemorrhagic manifestations in non human primates Petechiae on arm & axillary region Haemorrhages in the ileum Gastroduodenal lesion
  • 24. Connecting the cellular mechanism to hemorrhagic fever Destabilization of vascular endothelium Facilitates entry of viruses Massive hemorrhage Hypovolemic shock Activation of coagulation cascade Catastrophic thrombosis
  • 25. Ebola haemorrhagic fever presents as a viral prodrome with a high potential for differential diagnosis  Malaria  Typhoid fever  Shigellosis  Menigococcal septicaemia  Plague  Leptospirosis  Relapsing fever  Typhus  Chikungunya fever  Fulminant viral hepatitis
  • 26. Laboratory diagnosis • Laboratory diagnosis of Ebola virus is achieved in two ways: – Measurement of host-specific immune responses to infection – Detection of viral particles, or particle components in infected individuals. • RT-PCR and antigen detection ELISA are the primary assays to diagnose an acute infection. • Viral antigen and nucleic acid can be detected in blood from day 3 up to 7—16 days after onset of symptoms. • For antibody detection ; Direct IgG and IgM ELISAs and IgM capture ELISA.
  • 27. • IgM antibodies – Appear : 2 days post onset of symptoms – Disappear : 30 and 168 days after infection. • IgG-specific antibodies develop between day 6 and 18 after onset and persist for many years. • A IgM or rising IgG titre constitutes a strong presumptive diagnosis. • Decreasing IgM, or increasing IgG titres (four-fold), or both, in successive paired serum samples are highly suggestive of a recent infection
  • 28. Management • Isolation of patients . • Strict barrier nursing procedures ; Protective clothing and respirators. • Cadavers are residual risks and should be handled accordingly. • Traditional funeral and caretaking methods contribute to the spread of the virus and potentiate outbreaks. • Symptomatic and supportive treatment. • Strategies should include isolation, malaria treatment, broad spectrum antibiotics, and antipyretics before diagnosis. • Fluid substitution, preferentially intravenous administration, and analgesics
  • 29. • Shock, cerebral oedema, renal failure, coagulation disorders, and secondary bacterial infection have to be managed and can be life-saving. • Organ failure should be addressed appropriately – Dialysis for kidney failure – Extracorporeal membrane oxygenation for lung failure. • At present, no strategy has proved successful in specific pre-exposure and postexposure treatment of Ebola virus infections in man
  • 32. Prevention • There is no FDA-approved vaccine available for Ebola. • Healthcare workers who may be exposed to people with Ebola should follow these steps: – Wear appropriate PPE (Gloves,masks,caps,safety glasses,medical coats / surgical gowns,surgical drapes) – Practice proper infection control and sterilization measures.
  • 33. – Isolate patients with Ebola from other patients. – Avoid direct contact with the bodies of people who have died from Ebola. – Notify health officials in case of direct contact with the blood or body fluids, feces, saliva, urine, vomit, and semen of a person who is sick with Ebola.

Notas do Editor

  1. Shown is an ebolavirus particle and its characteristic filamentous shape. The negative-strand RNA genome is found in the center of particles in an encapsidated form as the nucleocapsid, together with the polymerase complex. Embedded in the virus membrane are trimeric glycoprotein spikes. Beneath the membrane is the matrix protein, which facilitates morphogenesis and budding of virus particles. The image is based on Protein Data Bank identifiers 3CSY and 1ES6 (www.rcsb.org) and Electron Microscopy Data Bank identifier EMD-2043 (www.emdatabank.org). The abbreviation ssRNA denotes single-stranded RNA. ; Ebola virus particles have a uniform diameter of 80 nm but can greatly vary in length, with lengths up to 14 000 nm.1, 3 The genome consists of seven genes in the order 3′ leader, nucleoprotein, virion protein (VP) 35, VP40, glycoprotein, VP30, VP24, RNA-dependent RNA polymerase . The inner ribonucleoprotein complex of virion particles consists of the RNA genome encapsulated by the nucleoprotein, which associates with VP35, VP30, and RNA-dependent RNA polymerase to the functional transcriptase—replicase complex.5 The proteins of the ribonucleoprotein complex have additional functions such as the role of VP35, which is an interferon antagonist.6 VP40 serves as the matrix protein and mediates particle formation.7 VP24, another structural protein associated with the membrane, interferes with interferon signalling.8 The glycoprotein is the only transmembrane surface protein of the virus and forms trimeric spikes consisting of glycoprotein 1 and glycoprotein 2—two disulphide-linked furin-cleavage fragments.1 An important distinction of Ebola virus from other Mononegavirales is the production of a soluble glycoprotein, which is the primary product of the GP gene, and gets secreted to large quantities from infected cells.9, 10