RABIES

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,

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

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