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Human Rabies
 

Human Rabies

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    Human Rabies Human Rabies Presentation Transcript

    • Human Rabies By Dr. Osman Sadig
      • Rabies virus Neurotropic virus with high affinity to the nervous system & salivary glands
      • - RNA virus belongs to Rabdoviruses – bullet shaped wz surface spikes.
      • - Incidence: All over za world except ? Australia and New-Zealand. WHO= 35000 annual death , more than 99% in developing countries where canine rabies is still endemic.
      • - Rabies is maintained as endemic disease through animal to animal bite transmission .
      • Epidemiology:
      • - Rabies is principally zoonosis , sp in dogs which cause 90% of reported human rabies. Other domestic animals that transmit the diseas include cats, cattle, sheep, horses & pigs .
      • Wild animals include foxes, wolfs, jackals,vampire bats & cave dwelling bats in Latin Am.
      • - Two epidemiological forms exist:
      • a- Urban : transmitted mainly by dogs & cats
      • b- Sylvian or Wild : transmitted by foxes and
      • bats.
      • Transmission
      • Transmission is:
      • a- usually from a rabid dog through bite or non bite exposure by contamination of skin scratches & mucous membranes with infected saliva.
      • b- Rarely air borne droplet infection in labs and
      • from cave dwelling bats.
      • c- Human to human spread is not confirmed
      • (through biting, kissing or sexual intercourse) except wz corneal grafts.
      • Pathogenesis
      • - After inoculation the virus multiplies in muscle before it enters the peripheral nerves & ascend centripetally to the CNS .
      • - IP varies wz the strain , severity of the bite and proximity of the bite to CNS . It is 1-2/12 on the average ( 9/7-19 years). < 1year in 95%
      • - The virus multiplies in the spinal cord & brain before being carried to za salivary glands, lungs
      • kid & other organs via the autonomic NS.
      • - The Pathology in the CNS is rapidly progressive
      • meningo encehalomyelitis with perivascular
      • inflam of za grey matter, degen of nervous tissue and Negri bodies (ovoid eosinophilic cytoplasmic bodies) in 70-90% of cases.
      • - During IP the dis can be prevented by immunization, but once the virus spreads to CNS it can no longer be prevented.
      • Clinical features
      • - During the IP the patient is well except for symptoms related to bite wound .
      • - Patient may experience pain & parathesiae at the bite site when the virus multiplies in the dorsal root ganglia.
      • 1/ Prodromal period 2/ acute neurological period 3/ coma
      • 1- Prodromal period (1-7 days)
      • - Symptoms begin when the virus enters the
      • CNS.
      • - Early symptoms are non specific wz fever,
      • sore throat, malaise, HA, anorexia, nausea
      • and vomiting. In 50% the 1 st specific
      • symptoms may be pain & parathesiae
      • at za site of bite. Anxiety, apprehension, irritability, agitation, nervousness, insomnia and
      • psychosis suggest neurological involvement
      • 2- Acute neurologic period
      • The prodrome usually merges with acute neurologic period which presents either as furious (classical) in 80% or paralytic (dumb)
      • in 20%which dominates the entire clinical picture
      • in infection from rabid bats.
      • a/ Furious rabies :
      • This presents with:
      • 1- Hyperactivity with agitation, running about
      • and biting. This can occur spontaneously or
      • precipit by tactile, auditory or visual stimuli.
      • In betw attacks za pt is co-operative & orient
      • 2- Autonomic instability : hyperthermia, tachycard
      • HT, hypersalivation, dilated pupils.
      • 3- Hydrophobia in 50% of cases: due to spasm of pharynx, larynx & resp muscles leading to
      • chocking & panic on drinking or sight of water
      • or by blowing of air on the face – Aerophagia
      • 4- Fever with prostration , hypervent, focal or
      • generalized seizures (and rarely priapism)
      • may occur.
      • 5- There may be hyper reflexia & spasticity
      • 6- Patient may die from convulsions or cardio respiratory arrest in 1-2/52.
      • b/ Paralytic rabies :
      • 1- There is symmetrical ascending paralysis
      • resembling GB without mental symptoms.
      • Paralysis may be diffuse & symmetrical or
      • ascending. It may be max. in the bitten
      • extremity. Neck is stiff.
      • 2- Features of furious rabies are absent .
      • 3- Fever & headache are frequent.
      • 4- The duration of acute neurologic period is
      • longer in paralytic rabies
      • 3- Coma
      • Mental state deteriorates from confusion to
      • disorientation to stupor & finally coma.
      • 1- Coma begins within 2/52 of the onset of symp
      • and may last for hours or months.
      • 2- Fatal or potentially fatal Complications may
      • occur during coma phase.
      • - CNS : ICP, seizures, hypothalamic syndr (e.g
      • D. insipidus, inappropriate ADH secret)
      • and autonomic manifestations e.g HT,
      • hypoten, hypotherm, cardiac arrhythm
      • - Resp : Hypervent, hypovent & resp depressio
      • progressive hypoxia, decr lung compli
      • pneumonia, pneumothorax & R. arrest
      • - CVS: cardiac arrhythmias & arrest,
      • myocarditis, CCF & hypotension,
      • SVC thrombosis
      • - ARF, UTI, GIT bleeding.
      • Recovery :
      • Only 3 cases recovered from presumed Rabies
      • since 1970s. All of them received either post or
      • pre exposure TR and were resuscitated in the ICU.
      • Diagnosis
      • 1- Clinical during life in most
      • 2- IFA of cervical skin biopsy, cornel impression
      • and salivary gland secretions detects Rabies
      • Ags.
      • 3- Ser & CSF anti-rabies Abs .
      • 5- Viral isolation from saliva, brain tissue, CSF,
      • corneal impressions, urine or tracheal secretio
      • 3- Findings in CSF are those of encephalitis.
      • 6- Negri bodies pos mortum .
      • 7- The diagn should be made pathologically in
      • in brain of the biting animal.
      • Diff diagnosis
      • 1- Other viral encephalitis
      • 2- Tetanus
      • 3- Rabies hysteria
      • 4- G. Barrie.
      • TR of human Rabies
      • 1- No specific chemotherapy . It is only palliative.
      • Interferon & C/S are not effective
      • 2- Nursing in a quiet dark room
      • 3- Supportive TR with fluid & nutrition (parental
      • or through gastrostomy)
      • 4- TR in ICU with facilities for cardio-resp support
      • 5- TR complications e.g. sedation wz phenothiaz
      • and diazepam, seizures wz anti-convulsants,
      • anti- arrhythmics, BT for bleeding, vasopressin
      • for inappropriate ADH secretion
      • Prevention of Rabies
      • As Rabies is almost fatal disease prevention is
      • essential through:
      • 1- Control of Rabies in domestic animals is the cornerstone of prevention.
      • 2- Post exposure TR
      • Post exposure TR :
      • Did za pt has actually been exposed to za virus?
      • whether or not to offer TR at all ?
      • - Rabid dog almost exhibit signs of Rabies at the time of bite or few days later & if the dog remained healthy during the 5 days observation period it is unlikely to be infected at za time of
      • exposure.
      • - Post exposure prophylaxis include:
      • 1- Local wound toilet
      • 2- Immune ser admins (passive immunizat)
      • 3- Vaccine admins (active immunization )
      • - TR should be started immediately & rarely delayed beyond 48 hours.
      • - For max benefit the 3 components should be
      • undertaken together.
      • 1- Local TR include cleansing to za depth of the
      • wound wz 20% soap solution, local infiltr of
      • HRIG & excision of damaged tissues leaving
      • the wound unsutured. ( 90% protection)
      • 2- Passive HRIG admin provides protection in
      • the 1 st 1-2/52 before the vaccine exerts its
      • response & should only be omitted if pre or
      • post exposure prophylaxis had previously
      • been given. It should be given regardless of
      • the age, sp of animal, severity of bite & time
      • since exposure.
      • Dose 20 IU/kg HRIG: 50% locally & 50% in
      • the buttocks at diff site from the vaccine.
      • For animal RIG the dose is 40 IU/kg.
      • HRIG should not be delayed beyond a week
      • if the vaccine is administered 1 st .
      • 3- Vaccine admin : HDCV in the deltoid muscle at
      • days 0,3,7,14,28 & 90. If the victim had been
      • previously immunized wz pre or post exposur
      • prophylaxis include wound cleansing and
      • HDCV at days 0,3.
      • - Begin vaccination & observe the animal for
      • 5 days and stop vacc if it remained healthy
      • during observation period. Continue vacc if it
      • becomes sick. If the animal dies or killed the brain is examined by IFA for Negri bodies.
      • - In countries where human products of vaccine
      • are not available & when the risk of Rabies is
      • slight (licks on the skin & bite of covered areas)
      • vacc can be delayed during observation period
      • or local products re administered e.g Semple
      • vacc 2.5 ml S/C for 14 days (nervous tissue vac
      • - To minimize za cost 0.1 ml is given at 8 sites
      • ID in day 0 and booster doses at day 7,28.
      • Control of Rabies in animals
      • 1- License of dog acquisition
      • 2- Dogs vaccination
      • 3- Killing stray dogs
      • 4- Monitor reservoir host
      • 5- Quarantine imported dogs to non endemic area
      • Thank you
      • Pre exposure prophylaxis
      • - Dose is HDCV 1ml IM or 0.1 ml I/D repeated
      • 4/52 later & then booster yearly depending on
      • Ab response.
      • - It is given to:
      • 1/ Those who handle potentially infected
      • animals e.g. vitr surgeons & students, staff
      • working wz za virus in za labs. & people
      • visiting endemic areas for > 1/12.