11. Ebola, Rubella AndRabies

7/29/2019 11. Ebola, Rubella AndRabies

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Ebola Virus & MarburgFiloviridae family

The Marburg virus was isolated for the first time in 1967

As a result of three simultaneous outbreaks among laboratory staff inMarburg, Frankfurt, and Belgrade

Ebola: Four strainsEbola-Zaire, Ebola-Sudan, Ebola-

Cote dIvoire, Ebola-Reston

The subtypes of Ebola virus Zaire and Sudan are highly virulent.

Probable reservoir rodent or bat

Common name: Ebola

Both Ebola and Marburg Causes hemorrhagic fever


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General features

Filoviruses are pleomorphic,

long filamentous thread likeforms with RNA

Coiled RNA in spike-covered

envelope from host cell

Long rods (800-1000 nm) Replication = 8 hours

Therefore, spreads rapidly


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History

First identified in Sudan

Ebola virus after a

river in Zaire Outbreaks occurred all

over Sudan, Zaire,Congo, Gabon, and theIvory Coast.

Between 1976 and1996, over 1000 deathshave been recorded.


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Modes of Transmission

There are 3 modes of

infection:

1. Unsterilized needles

2. Suboptimal Hospital

conditions

3. Personal contact


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Clinical features contd..

Symptoms are abrupt and unexpected.

Incubation between 2 and 21 days

Starts with red eyes, then leads to fever, headache

Flu-like symptoms, fatigue, internal/externalbleeding, massive hemorrhage (uncontrollable

bleeding)

Severe vomiting, Abdominal pain , Diarrhea,Pharyngitis, Conjunctivitis


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Clinical features contd..

Extremely high body temperature

Impaired liver function

The infected body is also corroding away from theinside.

A cadaver's internal organs have been compared to

black and red tapioca pudding


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Diagnosis

Viral antigens can be detected by ELISA

Patients

sera may contain virulent virus

Vero, MA-104 cell lines can bee used forcultivation.

PCR can be used for diagnosis.


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Treatment and Prevention

There is no cure for Ebola

Maintaining renal functionand electrolyte balance and

combating hemorrhage andshock

No vaccine

Due to the extreme biohazard,

doctors must wear Level 4containment suits.

They are the equivalence of aspacesuit.


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RUBELLA (GERMAN MEASLES)


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Rubella

From Latin meaning "little red"

Discovered in 18th century - thought to be variant of

measles

First described as distinct clinical entity in Germanliterature

Congenital rubella syndrome (CRS) described byGregg in 1941


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Rubella Virus

Togavirus

Rubrivirus genus RNA virus

One antigenic type

Rapidly inactivated by chemical agentsultraviolet light, low pH, and heat


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Rubella Pathogenesis

Respiratory transmission of virus

Replication in nasopharynx and regional lymphnodes

Viremia 5-7 days after exposure with spread totissues

Placenta and fetus infected during viremia


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Rubella Clinical Features

Incubation period 14 days

(range 12-23 days)

Prodrome of low-grade fever

Maculopapular rash 14-17 days afterexposure

Lymphadenopathy in second week


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Rash of Rubella


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Congenital Rubella Syndrome

Infection may affect all organs

May lead to fetal death or premature delivery

Severity of damage to fetus depends ongestational age

Up to 85% of infants affected if infected during

first trimester


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Congenital Rubella Syndrome

Deafness

Cataracts

Heart defects

Microcephaly

Mental retardation

Bone alterations

Liver and spleen damage


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Rubella Laboratory Diagnosis

Isolation of rubella virus from clinicalspecimen (e.g., nasopharynx, urine)

Positive serologic test for rubella IgM antibody

Significant rise in rubella IgG by any standard

serologic assay (e.g., enzyme immunoassay)


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Prevention

Since 1968, a highly effective live attenuatedvaccine has been available with 95%efficacy

Universal vaccination is now offered to allinfants as part of the MMR regimen.


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Rabies Virus Member of the Lyassavirus of the Rhabdoviridae.

ssRNA enveloped virus, characteristic bullet-shapedappearance with 6-7 nm spike projections.

Virion 130-240nm

-ve stranded RNA codes for 5 proteins

Nucleocapsid (N), polymerase proteins (L, P), matrix (M),

and glycoprotein (G)

Exceedingly wide range of hosts. There are 5 other members of Lyassavirus : Mokola,

Lagosbat, Duvenhage, EBL-1, and EBL-2.

Duvenhage and EBL-2 have been associated with human

rabies.


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Rabies Virus

Structure of rabies virus

Rabies virus particles


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Epidemiology

Rabies is a zoonosis which is prevalent in wildlife. The mainanimals involved differs from continent to continent.

Europe fox, bats

Middle East wolf, dog

Asia dog

Africa dog, mongoose, antelope

N America foxes, skunks, raccoons,bats

S America dog, vampire bats


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Pathogenesis

The commonest mode of transmission in man is by the biteof a rabid animal, usually a dog.

Rabies is an acute infection of the CNS which is almostinvariably fatal

Following inoculation, the virus replicates in the striated orconnective tissue at the site of inoculation

Enters the peripheral nerves through the neuromuscularjunction.


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Pathogenesis contd

It then spreads to the CNS in the endoneurium ofthe Schwann cells.

Terminally, there is widespread CNS involvement

But few neurons infected with the virus show structural

abnormalities.

The nature of the profound disorder is still notunderstood

Site of bite determine the speed of progression of

clinical manifestation


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Clinical Findings

An acute, fulminant, fatal encephalitis The incubation period in humans is typically 12

months

May be as short as 1 week or as long as many years (up to

19 years)

Usually shorter in children than in adults

The clinical spectrum can be divided into three

phases A short prodromal phase

An acute neurologic phase

Coma.

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Clinical Findings contd..

The prodrome

lasting 210 days

May show any of the following nonspecificsymptoms

Malaise

Anorexia

Headache, photophobia, nausea and vomiting, sorethroat, and fever

Usually there is an abnormal sensation around the

wound site.

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Acute neurologic phase

lasts 27 days

Patients show signs of nervous system dysfunction

Nervousness, apprehension, hallucinations, and bizarrebehavior

General sympathetic over activity is observed, including

lacrimation, pupillary dilatation, and increased salivation

and perspiration A large fraction of patients will exhibit hydrophobia (fear

of water)

The act of swallowing precipitates a painful spasm of the

throat muscles. 26


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Coma

Convulsive seizures or coma and death

The major cause of death is respiratory paralysis

Paralytic rabies occurs in about 20% of patients, most

frequently in those infected with bat rabies virus

The disease course is slower, with some patients surviving

30 days

Recovery and survival are extremely rare. 27


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Laboratory Diagnosis

Histopathology - Negri bodies are pathognomonic of rabies.However, Negri bodies are only present in 71% of cases

Rapid virus antigen detection - in recent years, virus antigen

detection by IF had become widely used

Corneal impressions or neck skin biopsy are taken

The Direct Fluorescent Antibody test (DFA) is commonly

used


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Laboratory Diagnosis

Virus cultivation - The most definitive means ofdiagnosis

From saliva and infected tissue

Cell cultures may be used or more commonly, the specimen is

inoculated intracerebrally into infant mice.

Serology - circulating antibodies appear slowly inthe course of infection

But they are usually present by the time of onset of clinical

symptoms.


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Negri Body in neuron cell Positive DFA test

Diagnosis of Rabies contd.


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Pre-exposure prophylaxis - Inactivated rabies vaccine may beadministered to persons at increased risk

E.g. vets, animal handlers, laboratory workers etc.

Post-exposure prophylaxis - In cases of animal bites, dogs andcats in a rabies endemic area should be held for 10 days forobservation.

If signs develop in the dog or cat, they should be killed and theirtissue examined for diagnosis


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Wild animals are not observed but if captured, theanimal should be killed and examined

The essential components of postexposureprophylaxis

The local treatment of wounds and active and passiveimmunization.

Once rabies is established, there is nothing much thatcould be done except intensive supportive care.


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Postexposure Prophylaxis

Wound treatment - surgical debridement should be carried out

Experimentally, the incidence of rabies in animals can bereduced by local treatment alone.

Passive immunization - human rabies immunoglobulin aroundthe area of the wound; to be supplemented with an I.m. dose toconfer short term protection.

Active immunization - the human diploid cell vaccine (HDCV)is the best preparation available.

The vaccine is usually administered into the deltoid region, and5 doses are usually given.


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Postexposure Prophylaxis

Combined treatment with rabies immunoglobulin and activeimmunization is much more effective than active immunizationalone

Equine rabies immunoglobulin (ERIG) is available in many

countries and is considerably cheaper than HRIG


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Rabies VaccinesThe vaccines which are available for humans are presentare inactivated whole virus vaccines.

Nervous Tissue Preparation e.g. Simple Vaccine -

associated with the rare complication ofdemyelinating allergic encephalitis.

Duck Embryo Vaccine - this vaccine strain is grown

in embryonated duck eggs

This vaccine has a lower risk of allergic encephalitis but

is considerably less immunogenic.


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Rabies Vaccines

Human Diploid Cell Vaccine (HDCV) - this iscurrently the best vaccine available with anefficacy rate of nearly 100%

Rarely any severe reactions. However it is veryexpensive.

Other Cell culture Vaccines - because of the expense ofHDCV, other cell culture vaccines are being developed for

developing countries

However recent data suggests that a much reduced dose ofHDCV given intradermally may be just be effective.


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Control of Rabies

Urban - canine rabies accounts for more than99% of all human rabies. Control measures

against canine rabies include; stray dog control.

Vaccination of dogs

Quarantine of imported animals

Wildlife - this is much more difficult to controlthan canine rabies.

11. Ebola, Rubella AndRabies

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