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Ebola (1)DR. GIULIANO RIZZARDINI AND DR. MARIA V IT TORIA COSSU
ASST FATEBENEFRATELL I L .SACCO HOSPITAL
GIULIANO.RIZZARDINI@ASST -FBF-SACCO. IT & MARIA .COSSU@ASST -FBF-SACCO. IT
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OutlineINTRODUCTION
VIRUS
RESERVOIRS
TRANSMISSION
PREVIOUS OUTBREAKS
EBOLA 2013-2016 IN WEST AFRICA
SIGNS AND SYMPTOMS
DIAGNOSIS
TREATMENT
ITALIAN EXPERIENCE
PREVENTION
TtT: BACK UP SLIDES
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INTRODUCTION
VIRUS
RESERVOIRS
TRANSMISSION
PREVIOUS OUTBREAKS
EBOLA 2013-2016 IN WEST AFRICA
SIGNS AND SYMPTOMS
DIAGNOSIS
TREATMENT
ITALIAN EXPERIENCE
PREVENTION
TtT: BACK UP SLIDES
Outline
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Epidemics and Pandemics have shaped our history…
Middle Ages
20th Century
1st Millenium
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…and they continue to threaten us…and place sudden intense demands on national and international health systems
…on some occasions have brought health and social systems to the point of collapse
…the diseases of most concern are those that may have international significance –either as a possible global epidemic or pandemic, or because they pose a risk for travellers with high case fatality rates or have trade implications. Most of these diseases tend to be emerging diseases.
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So, in the context of emerging/epidemic disease at the beginning of the 21st. century:
We have seen the emergence of new or newly recognizedpathogens (e.g. Highly Pathogenic Avian Influenza [H5N1], SARS, Nipah, pandemic influenza [H1N1], novel coronavirus ……)
The resurgence of well characterized outbreak-prone diseases (e.g. dengue, measles, yellow fever, chickungunya, Ebola - also cholera, TB, meningitis, shigellosis)
Human-made "bio-risk" also increasing: accidental and deliberate release of infectious agents as smallpox, SARS, Ebola, anthrax, tularaemia, etc.
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61% of all Emerging Infectious Diseases are Zoonosesaffecting Humans
Frequency of all EID events has significantly increased since 1940, reaching a peak in 1980-1990
61% of EID events are caused by the transmission from animals (zoonoses)
74% of these from wildlife
Zoonotic EIDs from wildlife reach highest proportion in recent decade
Wildlife
Domestic
Animal Human
Translocation
Human
encroachment
Ex situ contact
Ecological
manipulation
Global travel
Urbanization
Biomedical
manipulation
Technology
And Industry
Agricultural
Intensification
Encroachment
Introduction
“Spill over” &
“Spill back”
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SARS; the First Pandemic of 21st Century Changed the World...
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H5N1 avian influenza: A New Global Concern…
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Factors Contributing to the Emergence or Re-Emergence of Infectious Diseases (1)
Human demographic change by which persons begin to live in previously uninhabited remote areas of the world and are exposed to new environmental sources of infectious agents, insects and animals.
Unsustainable urbanization causes breakdowns of sanitary and other public health measures in overcrowded cities (e.g., slums).
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Factors Contributing to the Emergence or Re-Emergence of Infectious Diseases (2)
Economic development and changes in the use of land, including deforestation, reforestation, and urbanization.
Global warming , climate changes cause changes in geographical distribution of agents and vectors.
Changing human behaviours, such as increased use of child-care facilities, sexual and drug use behaviours, and patterns of outdoor recreation.
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International travel and commerce that quickly transport people and goods vast distances.
Changes in food processing and handling, including foods prepared from many different individual animals and countries, and transported great distances.
Factors Contributing to the Emergence or Re-Emergence of Infectious Diseases (3)
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Evolution of pathogenic infectious agents by which they may infect new hosts, produce toxins, or adapt by responding to changes in the host immunity (e.g. influenza, HIV).
Development of resistance by infectious agents such as Mycobacterium tuberculosis and Neisseria gonorrhoeae to chemoprophylactic or chemotherapeutic medicines.
Factors Contributing to the Emergence or Re-Emergence of Infectious Diseases (4)
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Resistance of the vectors of vector-borne infectious diseases to pesticides.
Immunosuppression of persons due to medical treatments or new diseases that result in infectious diseases caused by agents not usually pathogenic in healthy hosts (e.g. leukemia patients).
Factors Contributing to the Emergence or Re-Emergence of Infectious Diseases (5)
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Deterioration in surveillance systems for infectious diseases, including laboratory support, to detect new or emerging disease problems at an early stage (e.g. Indonesian resistance to “scientific colonialism”).
Illiteracy limits knowledge and implementation of prevention strategies.
Lack of political will – corruption, other priorities.
Factors Contributing to the Emergence or Re-Emergence of Infectious Diseases (6)
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Biowarfare/bioterrorism – an unfortunate potential source of new or emerging disease threats (e.g. anthrax and letters).
War, civil unrest – creates refugees, food and housing shortages, increased density of living, etc.
Famine causing reduced immune capacity, etc.
Manufacturing strategies; e.g., pooling of plasma, etc.
Factors Contributing to the Emergence or Re-Emergence of Infectious Diseases (7)
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Public Health Emergency of International Concern (PHEIC)
Defined in IHR 2005 as
‘an extraordinary public health event which constitutes a public health risk to other States through the international spread of disease and may require a coordinated international response’.
Such events are required to be assessed for notification to WHO using a decision instrument
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(PHEIC)4 decision criteria used in assessment of a public health event are :
(a) The seriousness of the event’s public health impact.
(b) The unusual or unexpected nature of the event.
(c) The risk of international spread.
(d) The risk that travel or trade restrictions will be imposed by other countries.
Any 2 criteria Notify WHO
A single case of smallpox, poliomyelitis (WPV), human influenza caused by a new subtype and SARS must be immediately notified to WHO, irrespective of the context in which it occurs.
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The magic word: PREPAREDNESS
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Outbreak Detection and Response without PreparednessDelayed Response
Day
CasesOpportunity
for control
Late Detection
First Case
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Early Detection
Cases
Rapid Response
Outbreak Detection and Response with Preparedness
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WHO RESPONSE
-International Health Regulations
-Global Outbreak Alert and Response Network (GOARN)◦ 120 technical institutions participating
◦ 2000-02 -- Responded to 34 events in 26 countries
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Purpose and scope of the IHR
From three diseases to all public health hazards, irrespective of origin or source
From control of borders to containment at source
From preset measures to adapted response
“to prevent, protect against, control and provide a public health response to the international spread of disease in ways that are commensurate with and restricted to public health risks, and which avoid unnecessary interference with international traffic and trade“ (Article 2)
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No single institution has all the capacity!
Coordinate and support rapid international team deployment to countries for outbreak response
To focus and coordinate global resources - local > regional > global
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WHO global alert and response systems
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PHEIC
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PAHO
AFROWPRO
EMROSEARO
EURO
OperationsStatesWHO Portal
Event Management
System
Information Sharing at WHO
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Strategy for Preventing and Control Ebola Outbreaks
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Fundamental Role of the Public Health Professional
Establish surveillance for: ◦ Unusual diseases
Assure laboratory capacity to investigate new agents (e.g., high-throughput labs)
Develop plans for handling outbreaks of unknown agents
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INTRODUCTION
VIRUS
RESERVOIRS
TRANSMISSION
PREVIOUS OUTBREAKS
EBOLA 2013-2016 IN WEST AFRICA
SIGNS AND SYMPTOMS
DIAGNOSIS
TREATMENT
ITALIAN EXPERIENCE
PREVENTION
TtT: BACK UP SLIDES
Outline
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What is Ebola virus disease (EDV)?Ebola virus disease (EVD), formerly known as Ebola haemorrhagic
fever, is a severe, often fatal illness in humans.
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Viral hemorragic fever
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Hemorrhagic Fevers◦ Definition: a severe multi-system syndrome.
◦ Vascular System Damaged
◦ Body regulation Impaired
◦ Accompanied by hemorrhage
◦ MOF
◦ Four families of viruses
◦ Arenaviruses (Junin Virus)
◦ Bunyaviruses (Nariovirus )
◦ Flaviviruses (ie. Yellow Fever)
◦ Filoviruses (Marburg & Ebola)
◦ RNA viruses covered in a lipid coating
◦ Viruses are geographically restricted to areas where host species (reservoir) live
◦ Humans are not natural reservoirs for these viruses
◦ CDC Classification: BSL-4 Agent
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Viral Hemorrhagic Fevers (VHFs)
The severity and clinical presentation of VHFs maysignificantly change according to several differentfactors related to the type of the causative agent, and the host epidemiological and clinical features. In general, patients with VHFs show fever and coagulation abnormalities that may progress towardsdisseminated intravascular coagulation, multiorganfailure, shock and, eventually, death
The VHFs are a diverse group of animal and human illnesses that are caused by fourdistinct families of RNA viruses: Filoviridae, Arenaviridae, Bunyaviridae, and Flaviviridae.
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Filoviridae
Marburgvirus was the first ever filovirus recognized, discovered in 1967 when laboratory workers in
Marburg, Germany developed hemorrhagic feverafter handling tissue of African green monkeys from
Uganda.
The 1967 outbreak proved fatal in seven of the 37 cases.
Filoviridae are a family of enveloped, non-segmented, negative-strand RNA viruses that share a similar filamentous structure.
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Structure
Filovirus: like other members of this family, Ebola is thread-like in structure
◦ Variable shapes
◦ “U” shaped
◦ Coiled
◦ Circular
◦ Branched
http://bepast.org/docs/photos/Ebola/em_ebola.jpg
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Genus Ebolavirus is 1 of 3 members of the Filoviridae family (filovirus), along with genus Marburgvirus and genus Cuevavirus.
Genus Ebolavirus comprises 5 distinct species:
- Bundibugyo ebolavirus (BDBV)
- Zaire ebolavirus (EBOV)
- Sudan ebolavirus (SUDV)
- Taï Forest ebolavirus (TAFV)
- Reston ebolavirus (RESTV)*
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*Reston Ebolavirus (RESTV) The Good Cousin
Found in Philippines and China
Causes respiratory disease in pigs
Infects humans, but no disease
Pig farmers, abattoir workers, others have antibodies
Some cross-reaction with Zaire EBOV
Are people with RESTV antibodies immune?
Can RESTV antibodies be used for therapy?
Will RESTV antibodies from natural infections confuse diagnosis of Ebola virus disease?
39
*Miranda & Miranda 2011; Pan et al 2014
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Infectious disease terminology
Inoculating dose = the number of viral particles that enter the host; minimum inoculating dose of Ebolavirus is very low (1-10 viruses)
Incubation period = days from when the person was exposed and symptoms first develop; aver. EBOV = 11 days (2 – 21 days)
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Survival outside hostDried – 24 hr at 25°C; 14 days at 4°C
In fluids – up to 46 days at 25°C
Ebolavirus is killed by:
◦ Heat 60ºC for 1 hr
◦ Hypochlorite (Chlorine solution)
◦ Alcohols
◦ 3% acetic acid
◦ 1% glutaraldehyde
Piercy et al J Appl Microbiol 2010;109:1531; Sagripanti et al Arch Virol 2010; 155:2035; Health Canada –PDSS - http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/ebola-eng.php
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Environmental contamination in isolation ward
Sudan Ebolavirus outbreak – Uganda 2000
2 positives from 33 environmental specimens
Ebolavirus was detected on a bloody glove and a bloody IV insertion site
Not isolated on bedframes, chairs, stethoscopes, clean gloves, food bowl, spit bowl, body bag cleaned with bleach, body louse.
Bausch et al. J Inf Dis 2007
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Natural history
Virus enters the cell – any cell, but particularly uses macrophages, dendritic cells and monocytes
Spreads to lymph nodes via lymphatics and then to liver and spleen via blood
Secondary spread to all organs
Exits the body in faeces, saliva, sweat, tears, sputum, skin cells, breast milk, semen, urine, vomitus
The WHO states that only people who are very sick are able to spread Ebola disease in saliva, and whole virus has not been reported to be transmitted through sweat. Most people spread the virus through blood, feces and vomit.Entry points for the virus include the nose, mouth, eyes, open wounds, cuts and abrasions
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EVD: a short history
Ebola first appeared in 1976 in 2 simultaneous outbreaks, in Nzara, Sudan, and in Yambuku, Democratic Republic of Congo a village situated near the Ebola River, from which the disease takes its name.
The first known case of EVD was a 44-year old school teacher who presented himself, on 26 August 1976, with a febrile illness at the Yambuku Mission Hospital and died after 13 days the onset of the symptoms.
He started an epidemic that killed 280 of the 313 infected persons (88%).
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Ebola
River
EBOLA: the origin
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Mar 12, 1977 Volume 309 Number 8011p555-614Originally published as Volume 1, Issue 8011
ISOLATION AND PARTIAL CHARACTERISATION OF A NEW VIRUS CAUSING ACUTE HÆMORRHAGIC FEVER IN ZAIRE: K.M Johnson, J.V Lange, P.A Webb, F.A Murphy
VIRAL HÆMORRHAGIC FEVER IN SOUTHERN SUDAN AND NORTHERN ZAIRE: Preliminary Studies on the Aetiological AgentE.T.W. Bowen, G. Lloyd, W.J. Harris, G.S. Platt, A. Baskerville, E.E. Vella
ISOLATION OF MARBURG-LIKE VIRUS FROM A CASE OF HÆMORRHAGIC FEVER IN ZAIRES: Pattyn, G.vanderGroen, W. Jacob, P. Piot, G. Courteille
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571
TABLE !!—COMPARISON OF I.F.A. TITRES OF GUINEAPIGS
IMMUNISED (SINGLE INJECTION) AGAINST MARBURG (’67) ANDMARBURG-LIKE (’76) VIRUSES
they have diagnostic significance. Plastic-embedded formalin-fixed necropsy specimens were examined with the electron
microscope. Although preservation of liver tissue was poor,large numbers of filamentous virus particles and inclusionbodies (masses of tubules) were found (fig. 5) which were indis-
tinguishable from those in Marburg virus-infected human and
guineapig livers studied in 1967 and 1975.6-8
ANTIGENIC COMPARISON WITH MARBURG
An antigenic difference between this isolate and Marburg’67 was demonstrated by indirect immunofluorescence (I.F.A.).An infected Vero-cell suspension was placed in drops on slides,air dried, and then acetone-fixed for 10 min at room tempera-ture. Slides were stored at -T0°C until tested. Marburg ’67
antigen slides, prepared in like manner, were used for compari-son. Reciprocal titres obtained with convalescent human seradrawn during the 1967, 1975, and 1976 outbreaks are listedin table I. With the exception of a weak reaction to Marburgantigen at a 1/4 dilution of the Zaire convalescent serum, thenew isolate was distinct from Marburg virus. The homologous
Marburg titres of 128 and 64 obtained with ’67 and ’75
antigens and antisera were comparable to those reported byWulff and Conrad.9 9
A single-injection immune serum to the new agent was pre-pared in guineapigs, and reciprocal I.F.A. tests were performedwith available similar reagents for Marburg virus. Reciprocaltitres (table n) further confirmed the distinctness of the twoviruses. Although one of two early convalescent sera fromSudan gave a positive reaction with the Zaire antigen (table I)further work is needed to determine whether the haemorrhagic-disease agents from the two countries are identical.
EBOLA VIRUS
With the concurrence of Prof. S. R. Pattyn, Institute of
Tropical Medicine, Antwerp, and Mr E. T. W. Bowen, Micro-
biological Research Establishment, Porton Down, the nameEbola virus is proposed for this new agent. Ebola is a smallriver in Zaire which flows westward, north of Yambuku, the
village of origin of the patient from whom the first isolate wasobtained. In deference to the countries involved and to the lack
of specific knowledge of the original natural source of the
virus, it is also suggested that no names of countries or specifictowns be used.
REFERENCES
1. Wld Hlth Org. wkly epidem. Rec. 1976, 51, (42), p. 325.2. Center for Disease Control. Morbidity and Mortality Weekly Report, 1976,
vol. 25, p. 378.3. Pattyn, S. R., Jacob, W., Van der Groen, G., Piot, P., Courteille, Lancet,
1977, i, 573.4. Bowen, E. T. W., Platt, G. S., Lloyd, G., Baskerville, A., Harris, W. J.,
Vella, E. E. ibid. p. 571.5. Kissling, R. E., Robinson, R. Q., Murphy, F. A., Whitfield, S. G. Science,
1968, 160, 888.6. Center for Disease Control. Morbidity and Mortality Weekly Report, 1975,
vol. 24, p. 89.7. Gear, J. S. S., Cassell, G. A., Gear, A. J., Trappler, B., Clansen, L., Meyers,
A. M., Kew, M. C., Bothwell, T. H., Sher, R., Miller, G. B., Schneider,J., Koormhof, H. J., Gomperts, E. D., Isaacson, M., Gear, J. H. S. Br.med. J. 1975, iv, 489.
8. Murphy, F. A., Simpson, D. I. H., Whitfield, S. G., Zlotnik, I., Carter, G. B.Lab. Invest. 1971, 24, 279.
9. Wulff, H., Conrad, L. J. in Comparative Diagnosis of Viral Diseases. NewYork (in the press).
VIRAL HÆMORRHAGIC FEVER IN SOUTHERN
SUDAN AND NORTHERN ZAIRE
Preliminary Studies on the Aetiological Agent
E. T. W. BOWEN
G. LLOYD
W. J. HARRIS
G. S. PLATT
A. BASKERVILLE
E. E. VELLA
Microbiological Research Establishment, Porton, Salisbury,Wiltshire, England
BETWEEN July and September, 1976, sporadic cases offever with haemorrhagic manifestations were reported inthe areas of Nzara, Maridi, and Lirangu in the southernSudan. The first cases are believed to have been in agri-cultural settlements. An outbreak of a similar disease
was also reported from the zone of Bumba in northernZaire.1 As the epidemic increased in intensity, the dis-
turbingly high percentage of cases reported among hos-
pital personnel suggested direct person-to-person spreadof infection. The illness began with an acute fever,malaise, sore throat, muscular pains, vomiting, and
diarrhoea. Those severely affected had epistaxis, subcon-
junctival haemorrhages, haemoptysis, hsematemeses, andmelaena. Some patients also had a body rash, tremors,and convulsions.
SOURCES OF SPECIMENS
Specimens from the northern Zaire outbreak were referredto the Microbiological Research Establishment, Porton, byProf. S. R. Pattyn of the Institute of Tropical Medicine,
Antwerp. They were an acute-phase serum (no. 718), cell-culturematerials and brains from suckling mice which had alreadybeen inoculated with the serum. We later received a specimenof liver from the same patient and also 5 acute-phase blood
specimens from Zaire via Professor Pattyn. Specimens fromthe southern Sudan were mainly collected at Maridi Hospitaland sent to us directly by Dr Babiker el Tahir, Dr D. H.
Smith, Dr K. Jones, and Dr M. Cornet, who were there to in-
vestigate. They consisted of 3 throat swabs, 3 urine specimens,6 acute-phase blood specimens, and convalescent serum speci-mens. These specimens were sent on dry ice or in liquidnitrogen. Three laboratories engaged in preliminary studies onthe xtiological agent reported the isolation of a virus whichwas morphologically similar to Marburg virus.2
RESULTS OF ATTEMPTS AT VIRUS ISOLATION
Virus isolation from the original human material was
attempted in : (1) culture preparations of Vero cells; (2)suckling mice inoculated intraperitoneally (i.p.) and in-
tracerebrally (i.c.); and (3) young guineapigs (200-250g) inoculated i.p.
Isolation in Guineapigs
So far 5 isolations of the aetiological agent have been
obtained in guineapigs: 4 from specimens from northern Zaireand 1 from a specimen from southern Sudan. Guineapigs in-oculated with these specimens became febrile 105°F (40-5°C)after an incubation period of 4-7 days. The febrile illnesslasted 4-5 days during which the guineapigs failed to thriveand looked ill. 1 of the 12 guineapigs inoculated with originalmaterial died on the 12th day after inoculation. The other 11
guineapigs slowly recovered and were subsequently shown tohave antibodies detectable by fluorescent antibody tests at
titres ranging from 1/64 to 1/128. When whole heparinisedblood from febrile guineapigs was inoculated !.p. into other
guineapigs it produced a similar febrile illness.
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Piot, now 67, was the youngestmember of the original Ebola investigative team and is still
active professionally; some of the others have retired and some
have died.
Health officials go over data collected during the Ebola
outbreak of 1976 in Zaire, nowknown as the Democratic
Republic of Congo.
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Since the first case, over the course of 28 years, 30 outbreaks have been enumerated before the last one
in 2014 in West Africa
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INTRODUCTION
VIRUS
RESERVOIRS
TRANSMISSION
PREVIOUS OUTBREAKS
EBOLA 2013-2016 IN WEST AFRICA
SIGNS AND SYMPTOMS
DIAGNOSIS
TREATMENT
ITALIAN EXPERIENCE
PREVENTION
TtT: BACK UP SLIDES
Outline
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How do people become infected with the virus?
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Gretchen Vogel
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Fruit bats and Ebola virus
Several bat species can host EBOV
Differences in the prevalence of the infection in different bat species and in different
geographical areas are probable.
It has been hypothesized that EBOV infection is a seasonal relatively mild infection in
bats, and climatic factors may influence the size of seasonal epidemics.
EBOV infection would be more prevalent in young animals and in pregnant females
Food shortages in the dry season may promote contacts between bats and humans
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Fruit bats
Hypsignathus
monstrosus
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.
Many bat species live in large colonies
They have the ability to move quickly and spread viruses over considerable distances.
They enjoy great longevity
Increasing human activity leads to interactionsbetween bats, humans, and livestock, thus
increasing the zoonotic potential.
For all these reasons, bats are a potentialsource of emerging diseases.
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INTRODUCTION
VIRUS
RESERVOIRS
TRANSMISSION
PREVIOUS OUTBREAKS
EBOLA 2013-2016 IN WEST AFRICA
SIGNS AND SYMPTOMS
DIAGNOSIS
TREATMENT
ITALIAN EXPERIENCE
PREVENTION
TtT: BACK UP SLIDES
Outline
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Transmission
There is no conclusive evidence for how wild animals contract an EBOV infection.
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Filovirus Cycle of Transmission
P Formenty, World Health Organization, April 2014
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The spillover theory
•The sequences of the virus strains responsible of the different outbreaks in humans differ significantly, suggesting multiple emergences of the infection from the primary animal reservoir.
•The comparison of sequences of different geographical origin and the data of the last epidemic further support the spillover theory.
Wittmann et al PNAS 2007, 104: 17123-27
Baize et al. NEJM 2104
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EBOV transmission
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Monkeys infected with the Ebola virus: the presence of the virus
In the pharynx after 2-4 days after the appearance of the fever
In conjunctions after 5-6 days
In rectal swabs after 5-6 days
In the nasal mucosa after 5-10 days
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Transmission (1): from the animal reservoires
Ebola is introduced into the human population through close contact with the blood, secretions, organs or other bodily fluids of infected animals.
In Africa, infection has been documented through the handling of infected chimpanzees, gorillas, fruit bats, monkeys, warthogs, forest antelope and porcupines found ill or dead or in the rainforest.
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Ebola and bushmeat
Brazzaville market
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Bat soup
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Transmission (2): human-to-human transmission
Ebola then spreads in the community through human-to-human transmission, with infection resulting from direct contact (through broken skin or mucous membranes) with the blood, secretions, organs or other bodily fluids of infected people, and indirect contact with environments contaminated with such fluids.
Burial ceremonies in which mourners have direct contact with the body of the deceased person can also play a role in the transmission of Ebola.
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Airborne transmission has not been documented during EVD outbreaks. Spread by water or food other than
bushmeat has also not been observed, nor has spread by mosquitos or other insects.
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Human-to-Human transmission
Direct contact (through broken skin or mucous membranes) with the blood, secretions, organs or other bodily fluids of infected people
Indirect contact with environments contaminated with fluids.
Burial ceremonies (mourners direct contact with corps)
The patients become contagious once symptoms begin. They are not contagious during incubation period.
Virus transmitted through the semen for up to 7 weeks after recovery from illness.
Health-care workers have frequently been infected .
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Body fluids that may contain ebolaviruses include saliva, mucus, vomit, feces, sweat, tears, breast milk, urine, and semen. The WHO states that only people who are very sick are able to spread Ebola in saliva, and whole virus has not been transmitted through sweat. Most people spread the virus through blood, feces, and vomit. Entry points include the nose, mouth, eyes, or open wounds, cuts and abrasions. Contact with objects contaminated by the virus, particularly needles and syringes, may also transmit the infection. The virus is able to survive on objects for a few hours in a dried state and can survive for a few days within body fluids. Ebola virus may be able to persist in the semen of survivors for up to seven weeks after recovery, which could give rise to infections via sexual intercourse. Otherwise, people who have recovered are not infectious. The potential for widespread infections in countries with medical systems capable of observing correct medical isolation procedures is considered low. Usually when someone has symptoms, they are sufficiently unwell that they are unable to travel without assistance.
Dead bodies remain infectious, thus people who engage in practices ranging from traditional burial rituals to more modern processes such as embalming are at risk. Nearly two thirds of the cases of Ebola infections in Guinea during the 2014 outbreak are believed to have been contracted via unprotected (or unsuitably protected) contact with infected corpses during certain Guinean burial rituals.
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Timeline for how a person with Ebola becomes more infectious over time:
Source: Public Health England
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EVD in health-care workers
Health-care workers have frequently been infected while treating patients with suspected or confirmed EVD. This has occurred through close contact with patients when infection control precautions are not strictly practiced.
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Is sexual transmission possible ?
Men who have recovered from the disease can still transmit the virus through their semen for up to 7 weeks after recovery from illness.
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Infectious disease terminology
Attack rate = Percent of people in an exposed group who develop the disease; EBOV = 16-40%
Case fatality rate = Percent of infected people who die; EBOV West Africa = 40% (11310/28616)
Reproduction number = Average number of new cases that occur from a single case; EBOV = 1.3
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The basic reproduction number
R0 = Average number of new cases that occur from a single case
C = the number of susceptible people in the population that the affected patients are in contact with
= the infectiousness of the organism
D = duration of infectivity of affected patients
R0 = C x x D
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Values of R0 of well-known infectious diseases
Disease Transmission R0
Measles Airborne 12–18
Pertussis Airborne droplet 12–17
Diphtheria Saliva 6–7
Smallpox Airborne droplet 5–7
Polio Fecal-oral route 5–7
Rubella Airborne droplet 5–7
Mumps Airborne droplet 4–7
HIV/AIDS Sexual contact 2–5
SARS Airborne droplet 2–5[2]
Influenzae
(1918 Pandemic Strain)Airborne droplet 2–3[
2014 Ebola Outbreak Bodily fluid1-2
Unless noted R0 values are from: History and Epidemiology of Global Smallpox Eradication From the training course titled "Smallpox: Disease, Prevention, and Intervention". The CDC and the World Health Organization. Slide 16-17.
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The importance of Effective Reproduction Number (Rt)
If one case of EVD (on average) infects greater than one other person, Rt is >1 and the epidemic grows; e.g., as in West Africa where Rt was initially 3 decreasing to 1.3
If one case of EVD (on average) infects less than one other person, Rt is <1 and the epidemic slows and stops; e.g., as in DRC where Rt is 0.84
The aim of outbreak control is to reduce Rt to less than 1
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Looking at past outbreaks, estimates of R0 for:
Ebola Zaire ranged from 1.4-4.7 and for
Ebola Sudan ranged from 1.3-2.7
R0 has not been estimated for Ebola Bundibugyo
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What about serosurveys?
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Niche modelling suggests that Ebola virus should be widely distributed over equatorial Africa, including countries from which Ebola virus infections have
not been reported.
The most confusing results, however, stem from a myriad of serosurveys, which revealed anti-Ebola virus antibodies in human beings from all over
Africa.
Many of these studies were done during the 1980s and 1990s and varied in quality: different assays were used to detect antibodies (eg,
immunofluorescence assay, ELISA, western blot); seemingly arbitrary cutoffswere sometimes used to differentiate negative from positive results; differentEbola virus antigens were used for assay development (eg, whole inactivatedvirions vs individual viral proteins); sample cohort sizes diverged; and proper
controls were or could often not be included.
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Asymptomatic EbolaIt is not known how frequently asymptomatic Ebola virus infection occurs, yetit could affect the course of epidemics. High rates of asymptomatic infection
would reduce incidence through herd immunity, radically altering model predictions of epidemic spread.
If those with asymptomatic infection are infectious, perhaps with persistentviral shedding, it would help explain some failures in control and the
emergence of new chains of transmission.
The extent of asymptomatic infection is unclearbecause previous findings have varied widely (eg, from 1% to 46% of household contacts), with positive results
reported in some populations unlikely to have beenexposed to filoviruses.
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Plausible explanations for these discrepant serosurvey results are:
The serosurveys are artifacts due to cross- reaction of Ebola virus antigenswith non-anti- Ebola virus antibodies;
the detected antibodies stem from contact with undiscovered, non-pathogenic filoviruses that are endemic in Africa and that are closely relatedto Ebola virus;
or Ebola virus causes widespread subclinical infection in human beings
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Lancet Infect Dis 2017 Published Online February 27, 2017 http://dx.doi.org/10.1016/ S1473-3099(17)30111-1
This new highly specific and sensitive assay showed asymptomaticinfection with Ebola virus was uncommon despite high exposure. The low prevalence suggests asymptomatic infection contributes little to herd immunity in Ebola, and even if infectious, would account for few
transmissions.
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Thank you for your attention
DR. GIULIANO RIZZARDINI AND DR. MARIA V IT TORIA COSSU
ASST FATEBENEFRATELL I L .SACCO HOSPITAL
GIULIANO.RIZZARDINI@ASST -FBF-SACCO. IT & MARIA .COSSU@ASST -FBF-SACCO. IT