Rabies



Rabies


Abdel Kareem Abu-Malouh

Jonathan P. Moorman



INTRODUCTION



  • Rabies is an acute CNS disease caused by rabies virus infection.


  • Rabies virus is a bullet-shaped virus with a single-stranded RNA, a member of the genus Lassa virus and the family rhabdoviridae.


  • The virus is highly neurotropic and replicates slowly within muscle cells.


  • It causes more than 50,000 deaths each year worldwide, mostly in developing countries.


  • The infection is invariably fatal if prophylactic measures are not applied.


EPIDEMIOLOGY



  • All mammals can transmit rabies virus.



    • Infection is usually caused by dog bites in Asia and Africa and by bat bites in North America.


    • Transmission from cats, cattle, raccoons, skunks, and foxes have been reported.


  • Infection can be transmitted by salivary contact with nonintact skin or mucus membranes.


  • Transmission can occur without awareness of the bite or exposure (sleeping adult or child).


  • Transmission by transplanted cornea and other solid organs has been reported.


  • No known person-to-person transmission



    • Infected patients still need to be in contact and respiratory isolation.


  • Forty percent of cases occur in children under 15 years of age.


  • >Fifteen million people worldwide receive rabies postexposure prophylaxis (PEP) yearly (Table 43-1).


PATHOGENESIS



  • Incubation period is 1 to 3 months in human but can be up to more than 1 year.


  • After inoculation into muscle cells, the virus is transmitted from the peripheral nerves to dorsal root ganglia and then to the brain.


  • PEP is ineffective once the virus enters into the peripheral nerve.


  • The virus spreads rapidly throughout the CNS, undergoing massive replication.



    • Induces neuronal dysfunction rather than neuronal death


    • Causes Negri bodies, the most characteristic pathologic change in the CNS


    • Mainly in Purkinje cells of the cerebellum and pyramidal cells of the hippocampus


  • The virus then spreads from the CNS through peripheral nerves to salivary glands, liver, muscle, skin, adrenals, and heart.



    • Excreted abundantly in saliva









      Table 43-1 Postexposure Prophylaxis of Rabies

































      Vaccination Status


      Intervention


      Regimen


      Not previously vaccinated


      Wound cleansing


      All PEP should begin with immediate thorough cleansing of all wounds with soap and water. If available, a virucidal agent (e.g., povidineiodine solution) should be used to irrigate the wounds.



      Human rabies immune globulin (HRIG)


      Administer 20 IU/kg body weight. If anatomically feasible, the full dose should be infiltrated around and into the wound(s), and any remaining volume should be administered at an anatomical site (intramuscular) distant from vaccine administration. Also, HRIG should not be administered in the same syringe as vaccine. Because RIG might partially suppress active production of rabies virus antibody, no more than the recommended dose should be administered.



      Vaccine


      Human diploid cell vaccine (HDCV) or purified chick embryo cell vaccine (PCECV) 1.0 mL, IM (deltoid area), one each on days 0, 3, 7, and 14.


      Previously vaccinated


      Wound cleansing


      All PEP should begin with immediate thorough cleansing of all wounds with soap and water. If available, a virucidal agent such as povidine-iodine solution should be used to irrigate the wounds.



      HRIG


      HRIG should not be administered.



      Vaccine


      HDCV or PCECV 1.0 mL, IM (deltoid area), one each on days 0 and 3.


      Adapted from Rupprecht CE, et al; CDC. Use of a reduced (4 dose) vaccine schedule for postexposure prophylaxis to prevent human rabies. MMWR Morb Mortal Wkly Rep 2010;59(RR-2):1-9.

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Jun 22, 2016 | Posted by in INFECTIOUS DISEASE | Comments Off on Rabies

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