Human Rabies

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Human Rabies

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

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