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 Rabies is an acute viral infection of the central nervous system caused by the bite of infected animals, commonly dogs or cats.  The saliva of these animals is the reservoir of infection. Virology  The rabies virus is an enveloped, single-stranded, RNA virus belonging to the rhabdovirus group.  The glycoproteins on the viral envelop bind to acetylcholine receptors and contribute to neurovirulence.  This also stimulates T-cell immunity and elicits neutralising antibodies. These antibodies and interferon released from the virus appear to be protective to the host. Epidemiology  There are two epidemiological types of rabies, namely, urban, propagated chiefly by unimmunised dogs and cats, and sylvatic, propagated by foxes, vampire bats. Pathogenesis  After the entry of live virus through saliva following a bite, viral replication starts in striated muscle cells and neuromuscular spindles.  The virus then ascends the peripheral nerve; it travels by autonomic nerves to the salivary glands, adrenal medulla, s eletal muscle etc  Retransmisson from infected saliva and other organ sources continues to invade the central nervous system.  The incubation period is variable, ranging from !" days to over ! year #mean !-$ months%.  The most important neuropathological lesion is the Negri body, an eosinophilic mass of fibrillar matrix and viral particles. Clinical features  The clinical stages are essentially three& #a% prodromal phase, #b% acute encephalitic phase and #c% brainstem dysfunction phase.  't is extremely rare to have recovery. (rodromal phase&  This is characterised by fever, headache, myalgia, nausea, vomiting, sore throat and cough which persists for $-) days.  The local symptom of intense paraesthesia at the site of inoculation is characteristic and is due to involvement of the dorsal root ganglion in a ma*ority of cases. +ncephalitic phase&  (eriods of excessive motor activity, excitation, hallucination, confusion, muscle spasms, meningismus and sei,ures are fairly characteristic.  -yperaesthesia, with excessive irritation to bright light, noise and touch, are often seen,

 +ven an attempt to swallow li0uids leads to painful spasm of the diaphragm. respiratory distress syndrome and gastrointestinal bleeding are the terminal events.  At this stage. this is characteristic of hydrophobia. Post e$posure Immuni%ation .  -ypotension. and dysphagia with excessive salivation.arr2 syndrome  3ea ness in affected extremity that spreads to involve all extremities  4phincter involvement  'nitially. =ocal Treatment of Animal . cardiac arrhythmias.rainstem dysfunction phase  /iplopia. salivation and postural hypotension. !iagnosis  -istory of exposure and chronology of clinical features will distinguish rabies from other viral encephalitis.  (ostmortem. Paralytic or dumb rabies (rare)  Ascending paralysis resembling 1uillain-.  The principles of post exposure treatment include & #a% minimisation of viral load at the site of inoculation by local wound cleansing. consciousness and sensory function are spared.ites and 4cratches  . facial paralysis.<=% with lymphocytosis  (rotein level sometimes mildly elevated  1lucose level generally normal  Rabies virus6specific antibodies develop late in the clinical course. as in the encephalitic form of disease. increased lacrimation.histological demonstration of Negri bodies in brain. Pre"ention and #reatment  There is no cure for rabies. #b% ensuring early and sustained neutralising antibody titre to the virus in the host. pharyngeal and laryngeal muscles and accessory respiratory muscles. (atient will have diaphoresis.  This is soon followed by a rapid downhill course with coma and respiratory paralysis. aboratory features  Routine blood tests are nonspecific.  Rabies virus6specific antibodies in serum and 547 or s in biopsy  547  8ild pleocytosis #9: cells. .  5ardiorespiratory failure occurs. pyramidal tract signs with extensor plantar and dysphonia due to vocal cord involvement are very common. thoroughly washing the wound with soap and water and then applying iodine or >"? ethanol. The first step in management is to administer prompt local wound care.  3ounds caused by animal bites should not be sutured.

animal handlers and laboratory wor ers.  4upportive measures for control of muscular spasm. in three doses of ". the animal should be captured and humanely illed for demonstration of Negri bodies in the brain. gastrointestinal bleeding and thrombocytopenia are essential.  -/5@ is the preferred vaccine. :"? of which is for local infiltration and the rest for intramuscular in*ection into the region. the human victim needs rabies prophylaxis. Acti"e immunisation  -uman diploid cell vaccine #-/5@% is recommended as soon as possible after exposure. respiratory distress syndrome. >. !) and $B.! ml intradermal in*ections on days ".Indications (&) 'f there is human exposure with a bite by any ill. 7ive #! ml% doses are given intramuscularly on days ". Animals which remain healthy for !" days after a bite will not have transmitted rabies at the time of bite.  The first dose should be combined with passive immunisation to ensure high titre of neutralising antibodies. Passi"e immunisation  -uman rabies immune globulin #-R'1% is recommended in a total dose of $" units per g body weight. (') (ersons having a bite by a presumed healthy dog or cat which shows abnormal behaviour within !" days of observation re0uire rabies prophylaxis. 'f confirmed. > and $B.  The 3-C recommends additional doses on days $! and D". Pree$posure prophyla$is  (reexposure prophylaxis with rabies vaccine is indicated in high-ris individuals li e veterinarians. unvaccinated or stray domestic animals having infected saliva. A. .