Basic Information Rabies

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BASIC INFORMATION

ABOUT RABIES

DR.MOHAMMAD KHALID

MBBS,FCPS(Medicine)


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History of Rabies

Rabies is known to be one of the oldest and most dreaded

disease reported since ancient times

Rabies has been reported in early Babylonian, Greek,

Roman Record

The virus was not seen under the E/M until 1960s

People/settlers from Europe Brought rabies to America

through their animals who were carriers of the virus Louis Pasteur experimented his rabies vaccine on a 6

years old boy Joseph Meister in 1885


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What is Rabies

Rabies comes from a Latin wordmeaning To Rage

It is a deadly but preventable viraldisease

It is transmitted through bite of Rabid

animals It affects mammals (warm blooded

animals)


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Wild: Dog, Fox, Jackal, Raccoon, Wolf, Cat, Bat etc.

Domestic/pets

Dog, cat, livestock

Rabies in Rodents not found PEP usually not required, treatment can be

given on individual assessment.

What is Rabies(Contd)


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Classification and structure

Most rabies viruses belong to genusLyssavirus and family Rhabdoviridae:

- Bullet shaped RNA viruses- Approx180 nm long 75 nm wide

- The negative stranded RNA genomecontain five genes

- The genes encodes five proteins Nucleoprotein, phosphoprotein, Matrix

protein, glycoprotein, polymerase


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Transmission

Rabies passes from animal to animal

animal to human.

Most common route is bite from infectedanimal

Non bite exposures

Infectious material from rabid animal i.e. virusladen saliva, infected brain tissue accidentallycoming in contact with mucous membrane, orwound


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Transmission(Contd)

Aerosol

Lab workers working with virus

Few documented cases of rabies beingcontracted in caves where vampire bat reside

Human to human transmission usually does not occur (risk if patient bites)

eight documented cases - recipients of cornealtransplantswhere donors had symptoms

resembling rabies

Thailand (2), India (2), Iran (2), USA (1),

France (1)


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Incubation period(time from exposure to the onset of clinical

sign of disease)

Typically 1-3 months (20 90 days)

but varies from few days to several years


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Viral entry and spread

Following primary infection, there is eclipse

phase i.e. virus is not detected in the host

tissue - varies from days to several months

Presence of viral antigen in host tissue

stimulates Cell Mediated Immune responseand it can stop viral entry in nerve


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Viral entry and spread (contd)

Once virus enters the nerve, the process

is progressive infection

Entry may be direct or indirect

Myocytes unmyelinated fibers

motor/sensory neurons

Move at rate 8-20 mm/day

Retrograde axoplasmic flow


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Stages of entry and spread

Attachment to nerve cell

Penetration in nerve cell (adsorption)

Replication in nerve cell

Budding attack new cells

Centrifugal spread from CNS to nervesof skin, intestine, salivary gland


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Dissemination

Once inside the CNS the process becomerapid

Active CNS infection is followed bypassive centrifugal spread

Invasion of highly innervated sites i.e.

salivary gland, skin and intestine Period of cerebral infection is followed bybehavioral changes


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Symptoms/signs

Clinical history

History of bite, suspicion of rabies

No history of bite problematic

especially prodromal stage

Rabies progression takes 7-14 days

Mean time between initial presentation

and death is about 16 days


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Symptoms/signs (contd)

Prodromal stage (2 10 days)

Flu-like symptoms nonspecificpharyngitis fever, malaise, headache,

anorexia and vomiting

Paresthesias at site of bite or scratchbegins during prodromal stage


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Symptoms/signs (contd)Neurologic Stage (2 7 Days)

Patient present with:

Aphasia, incoordination, paresis, paralysis,behavioral changes, unusual anxiety, agitation,

hyperactivity, hyper salivation, hyper-

lacrimation, myoclonus

Difficulty in swallowing (foaming at mouth,

inability to swallow), hydrophobia

&aerophobia


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Complications

Hypotension, Cardiac arrhythmias, Cardiac arrest,

Coma, DIC and respiratory failure

Differential Diagnosis

Bacterial Meningitis

Viral Encephalitis herpes simplex encephalitis

Gullien barrie syndrome

Cerebral Malaria

Symptoms/signs (contd)Neurologic Stage (2 7 Days)


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Pathology

Encephalitis/Myelitis

Brain tissue infiltrated by lymphocytes,

neutrophils and plasma cells Eosinophilic inclusions (Negri-bodies) in

neuronal cells

Pyramidal cells of hippocampusPurkinjee cells of cerebellum

cortex

Spinal ganglia.


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Thank you


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Situation Analysis(Contd)

The majority of Rabies cases reported to CDCoccur in wild animals.

Domestic animal account for less than 10%.

In Pakistan data about Rabies is an adequate. Data at HMIS is about animal bite cases.

During 1994-1997 47,059 animal bite cases and1998-2000 1,70,508 cases were registered

A 5% mortality rate would lead to the death ofapproximately 1800-2000 rabies cases everyyear.


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Situation Analysis

More than 60,000 deaths occur per annum

globally.

Human Rabies cases have been documented onall continents except Australia and Antarctic.

In USA Rabies is reported in wild animals

In 1997 4 people died of human Rabies in USA.

Hawaii has been declared free of Rabies.


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Post Exposure Prophylaxis

All unprovoked animal attacks are consideredhigh risk for rabies

If bite or m.m contact is inflicted by domesticanimal already vaccinated and ownerquarantine it for 10 days PEP can be with held

If animal shows signs of rabies, euthenize and

send for lab testing Treatment is started and if result is negative

then treatment is with held


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Immediate treatment for bites scratches fromhigh risk animal.

Although no human to human transmissiondocumented but exposure to CSF, saliva orm.m of a person suspected of having rabies.

The handler should receive complete

prophylaxis. Human/Equine Immune globulin and vaccine

recommended for treatment.

Post Exposure Prophylaxis(contd)


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Five shots of vaccine given on day 0, 3, 7,

14, 28 on deltoid region

Vaccine take 7-30 days to induce activeresponse lasting 2 year.

For children dose same as for adults

anterolateral thigh.



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Gluteral area not preferred - poor absorption.

Passive Immunization HRIG/ERIG.

Immediate protection with serum half life 21days.

I.G. half infiltrated in and around the woundlocally and rest injected in gluteal area.

In Immune-compromised person measuresserum antibodies to detect adequate Immuneresponse.



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I.G. safe during pregnancy

I.G may cause hypersensitivity. Do not

administer IG in repeated doses oncetreatment started with vaccine.

Administer live vaccines 14 30 days

before or 6-12 weeks after I.G.



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Ab response to vaccine may be delayed if I.G.administered simultaneously with rabies I.G

Hypersensitivity reaction may occur withvaccine also.

Corticosteroids, anti malarial radiationstherapy and Immune suppressive drugs may

reduce protective efficacy of vaccine. Persons receiving Immune suppressive therapy

should receive RIG.



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Treatment schedule

Wash wound with soap water copiously

Administer T.T

Do not stitch the wound. If need be then

stitch after infiltrating it with I.G

If wound is cat-I reassurance


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Treatment schedule (contd)

If wound is cat-II 5 shots Rabies vaccine.

If wound is cat-III, HRIG/ERIG+Rabies

vaccine.

Blood test done after 1month of the last

shot.

If titer 0.5 IU/ml and above it is safe.

If less than 0.5 IU/ml inject boosters.


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Prophylaxis Before Exposure

Pet handlers, vet, lab workers.

Traveling to area where medical care

difficult to find/or rabies endemic area.

Inject 3 shots 0, 7, 21 or 28 doses.

Pre-exposure prophylaxis obviates the need

for post exposure RI but not R.V.


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Signs

Changes in animal behaviour

General sickness, fever, loss of appetite.

Problem in swallowing

Excessive irritability Increase drooling

Unusual vocalization.

Aggression

Restlessness

Paralysis and death


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Prevention

Get your pet registered and vaccinated.

Leashed wear vaccination tag.

Stray dog elimination campaign

launched.

Community should also participate.

Date post:	04-Apr-2018
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Basic Information Rabies

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