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Rubella + rabies

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Rubella + rabies

  1. 1. RUBELLARABIES Dr Kamran Afzal Asst Prof Microbiology
  2. 2. Rubella virus• Family – Togaviridae• Genus – Rubivirus• Enveloped• Spherical virus carrying hemagglutinin• Virus multiply in the cytoplasm of infected cell• Rapidly inactivated by chemical agents, ultraviolet light, low pH and heat
  3. 3. Transmission• Adults and children – Acquired, (i.e. not congenital) – Transmitted via airborne droplet emission – May also be present in the urine, feces – The reservoir exists entirely in active human cases – Replication in nasopharynx and regional lymph nodes – 5-7 days Viremia, with spread to tissues• Fetus – Placenta and fetus infected during viremia, in a pregnant female
  4. 4. Systemic Events
  5. 5. Clinical Features• Malaise• Low grade fever• Morbilliform rash – Rash starts on face and extremities – Rarely lasts more than 5 days – No features of the rash give clues to definitive diagnosis of Rubella First described as distinct clinical entity in German literature – ‘German measles’
  6. 6. Clinical Features• Incubation period 14 days• Maculopapular rash and lymphadenopathy occur 14 days after exposure• The clinical events occurring in the neonatal age are more important and divided into two major groups 1. Post Natal Rubella (Acquired) 2. Congenital Rubella
  7. 7. ComplicationsArthralgia or arthritis adult female up to 70% children rareThrombocytopenic purpura 1/3,000 casesEncephalitis 1/6,000 casesNeuritis rareOrchitis rare
  8. 8. Congenital Rubella Syndrome (CRS)• Maternal viremia with Rubella infection during pregnancy may result in infection of placenta and fetus• Infection may lead to fetal death or premature delivery• Severity of damage to fetus depends on gestational age• Up to 85% of infants affected if infected during first trimester• >20 weeks of pregnancy, fetal defects are uncommon• The growth rate of fetal cells is reduced – Leads to deranged and hypoplastic organ development – Results in structural damage and abnormalities
  9. 9. • Microcephaly – Deafness – Mental retardation• Cataracts• Heart defects• Bone alterations• Liver and spleen damage
  10. 10. Classical Triad in CRSClassical Triad• Microcephaly / Deafness• Cardiac abnormalities• Cataract
  11. 11. Laboratory Diagnosis• Positive serologic test for Rubella IgM antibody• 4 x rise in Rubella IgG by any standard serologic assay - - Agglutination, ICT, ELISA, HAI• Isolation of Rubella virus from clinical specimen – nasopharyngeal swab, urine
  12. 12. Serology
  13. 13. Interpretation of Serology
  14. 14. Isolation and Identification of virus• Nasopharyngeal or throat swabs taken 6 days prior or after appearance of rash are a good source of Rubella virus• The virus can be cultured on continuous cell lines Rabbit kidney cells (RK 13) and Vero cells• Cell cultured antigens can be detected by IF methods
  15. 15. Treatment and Prevention• Rubella is a mild self limited illness• No specific treatment or Antiviral treatment is indicated• Clinically missed Rubella in the 1st 3-4 months of pregnancy is associated with fetal infections• CRS can be prevented by effective immunization of the young children and teenage girls
  16. 16. Rubella Vaccine• Composition Live virus (RA 27/3 strain)• Duration of Immunity Lifelong• Schedule At least 1 dose• Should be administered as MMR or MMRV• INDICATIONS – All infants 12 months of age and older – Susceptible adolescents and adults without documented evidence of Rubella immunity – Emphasis on non-pregnant women of childbearing age
  17. 17. RABIES
  18. 18. RabiesIt is an acute infectious disease of warm-bloodedanimals and humans characterized by an involvementof the nervous system resulting in death
  19. 19. Rabies Virus Genus: Lyssavirus(lyssa: the Greek goddess of madness, rage, and frenzy) Include members of the Rhabdoviridiae family Rabies, Makola, Duvenhage Morphology:  Enveloped bullet-shaped virus  5 structural proteins  SS RNA, negative sense, non-segmented, non-polar
  20. 20. Transmission of Rabies virus The dog is the most common cause of Rabies transmission worldwide, cats second In developed countries: dogs are immunized, other species of wild animals are reservoirs Bats: always considered rabid
  21. 21. Transmission of Rabies virus Infected saliva enters bite wounds  Virus migrates up peripheral nerves to the spinal cord and reaches the brain  Virus shed in the saliva during, before or after clinical symptoms Aerosol transmission: documented from caves with large populations of infected bats Organ donations: documented from early corneal transplantation (2004)
  22. 22. Rabies virus attacks the Central Nervous System Watch as the rabies virus from an exposure on the leg spreads up the spinal cord to the brain and throughout the rest of the body Rabies virus entering the body
  23. 23. Incubation Period Averages 3-8 weeks  Can be as short as 1 week or up to 1 year Bite location and viral load are the two most important factors in incubation of the virus
  24. 24. Pathogenesis Budding from the plasma membrane of muscle cells into unmyelinated nerve endings Retrograde axoplasmic flow to the CNS Virus replication in dorsal root ganglia (DRG) and anterior horn cells  Prophylaxis at this stage cannot prevent death
  25. 25.  Eventually, the virus spreads centrifugally from the CNS to the heart, skin, salivary and serous glands in the tongue All major organs may contain the virus (except blood) Organs from patients with unexplained neurologic disease may transmit rabies by transplantation
  26. 26. Clinical features in Humans General weakness, discomfort, fever or headache Prickling or itching sensation at the site of bite Cerebral dysfunction Anxiety, confusion, agitation, delirium Abnormal behavior Hallucinations, and insomnia Hydrophobia The acute period of disease ends after 2 to 10 days Once clinical signs of rabies appear, the disease is nearly always fatal
  27. 27. Laboratory Diagnosis Serology Virus cultivation The Direct Fluorescent Antibody test (DFA) Histopathology
  28. 28.  Serology  Circulating antibodies appear slowly but they are usually present by the time of onset of clinical symptoms Virus cultivation  The most definitive means of diagnosis is by virus cultivation from saliva and infected tissue  Virus cultivation can be done using cell cultures or the specimen is inoculated intra-cerebrally into mice
  29. 29.  Direct Fluorescent AntibodyThe Direct Fluorescent Antibody test (DFA) is done oncorneal impressions or neck skin biopsy
  30. 30.  Histopathology of Brain  Negri bodies are diagnostic of Rabies
  31. 31. SPECIFIC GUIDELINES AND PROCEDURESManagement of Potential Rabies Exposure
  32. 32. Management and PreventionPre-exposure prophylaxis Inactivated rabies vaccine is given to persons at increased risk of rabies e.g. vets, animal handlers, laboratory workers etcPost-exposure prophylaxis In cases of bites, suspected dogs and cats should be held for 10 days for observation If signs develop, they should be killed and their tissues examined
  33. 33. Post-exposure Prophylaxis Wound treatment - surgical debridement Passive immunization - human rabies immunoglobulin is given around the area of the wound and an I/M dose Active immunization - The human diploid cell vaccine (HDCV) is administered I/M, 5 doses are given on days 1,3,7,14 and 28 Combined treatment with passive and active immunization is much more effective than active immunization alone
  34. 34. Recommended Post-exposure ProphylaxisCategory of exposure to suspect rabid Post-exposure measuresanimalCategory I – touching or feeding Noneanimals, licks on intact skin (i.e. noexposure)Category II – nibbling of uncovered skin, Immediate vaccination and localminor scratches or abrasions without treatment of the woundbleedingCategory III – single or multiple Immediate vaccination andtransdermal bites or scratches, licks on administration of rabiesbroken skin; contamination of mucous immunoglobulin; local treatment of themembrane with saliva from licks, woundexposures to bats.
  35. 35. Rabies VaccinesThe vaccines which are available for humans areinactivated whole virus vaccines  Nervous Tissue Preparation  Duck Embryo Vaccine  Human Diploid Cell Vaccine (HDCV) - this is currently the best vaccine available with an efficacy rate of nearly 100% and rarely any severe reactions, however it is very expensive
  36. 36. TreatmentPOST-EXPOSURE TREATMENT (PET) LOCAL WOUND TREATMENT- Wash with soap/detergent and water preferably for 10 min- Apply alcohol or povidone iodine antiseptic- Anti-Tetanus toxoid I/M- Avoid suturing and wound dressing
  37. 37. Antimicrobials- Co-amoxiclav- Cloxacillin- Cefuroxime
  38. 38. Special Conditions Babies born of rabid mothers should be given ARV as early after birth as possible Pregnancy and infancy are not C/I to treatment Bites of rodents, rabbits, guinea pig- NO PET Dogs, cats, livestock, wild animals- Give PET
  39. 39. Prevention and Control Canine rabies accounts for more than 99% of all human rabies Control measures include  Stray dog control  Vaccination of dogs  Quarantine of imported animals
  40. 40. Oral Rabies Vaccination for animals
  41. 41. A raccoon consuming a bait laden with ORV
  42. 42. What kind of animals get rabies? The rabies virus can infect all mammals
  43. 43.  Animals less likely to get rabies
  44. 44. Animals that don’t carry rabies Frogs, turtles, birds, bees and snakes