PET
CLASSIFIED'S
                RABIES
NATIONAL ASSOCIATION OF STATE PUBLIC HEALTH VETERINARIANS
NATURAL HISTORY OF RABIES

RABIES VIRUS CAUSES AN ACUTE ENCEPHALITIS IN ALL WARM-BLOODED
HOSTS, INCLUDING HUMANS, AND THE OUTCOME IS ALMOST ALWAYS FATAL.
ALTHOUGH ALL SPECIES OF MAMMALS ALTHOUGH ALL SPECIES OF
MAMMALS ARE SUSCEPTIBLE TO RABIES VIRUS INFECTION, ONLY  A FEW
SPECIES ARE IMPORTANT AS RESERVOIRS FOR THE DISEASE.  IN THE
UNITED STATES, SEVERAL DISTINCT RABIES VIRUS VARIANTS HAVE BEEN
IDENTIFIED IN TERRESTRIAL MAMMALS, INCLUDING RACCOONS,
SKUNKS,FOXES, AND COYOTES. IN ADDITION TO THESE TERRESTRIAL
RESERVOIRS, SEVERAL SPECIES OF INSECTIVOROUS BATS ARE ALSO
RESERVOIRS FOR RABIES.

TRANSMISSION
TRANSMISSION OF RABIES VIRUS USUALLY BEGINS WHEN INFECTED SALIVA
OF A HOST IS PASSED TO AN UNINFECTED ANIMAL. VARIOUS ROUTES OF
TRANSMISSION  HAVE BEEN DOCUMENTED AND INCLUDE CONTAMINATION OF
MUCOUS MEMBRANES(I.E, EYES, NOSE, ,MOUTH), AEROSOL TRANSMISSION,
AND CORNEAL TRANSPLANTATIONS. THE MOST COMMON MODE OF RABIES
VIRUS TRANSMISSION IS THROUGH THE BITE AND VIRUS- CONTAINING SALIVA
OF AN INFECTED HOST.

















FOLLOWING PRIMARY INFECTION ( SEE FIGURE, NUMBERS 1 & 2), THE VIRUS
ENTERS AND ECLIPSE PHASE IN WHICH IT CANNOT BE EASILY DETECTED
WITHIN THE HOST. THIS PHASE MAY LAST FOR SEVERAL DAYS OR MONTHS.
INVESTIGATIONS HAVE SHOWN BOTH DIRECT ENTRY OF VIRUS INTO
PERIPHERAL NERVES AT THE SITE OF INFECTION AND INDIRECT ENTRY
AFTER VIRAL REPLICATION IN NON-NERVOUS TISSUE (I.E., MUSCLE CELLS).
DURING THE ECLIPSE PHASE, THE HOST IMMUNE DEFENSES MAY CONFER IS
A GOOD ANTIGEN. THE UPTAKE OF THE VIRUS INTO PERIPHERAL NERVES IS
IMPORTANT FOR PROGRESSIVE INFECTION TO OCCUR(SEE FIGURE,
NUMBER 3)

AFTER UPTAKE INTO PERIPHERAL NERVES, RABIES VIRUS IS TRANSPORTED
TO THE CENTRAL NERVOUS SYSTEM (CNS) VIA RETROGRADE AXOPLASMIC
FLOW. TYPICALLY THIS OF INFECTION. THE INCUBATION PERIOD (SEE
FIGURE, NUMBER 4) IS THE TIME FROM EXPOSURE TO ONSET. OF CLINICAL
SIGNS OF DISEASE. THE INCUBATION PERIOD AMY VARY FROM A FEW DAYS
TO SEVERAL YEARS, BUT IS TYPICALLY 1 TO 3 MONTHS. DISSEMINATION OF
VIRUS WITHIN THE (CNS) IS RAPID AND INCLUDES EARLY INVOLVEMENT OF
LIMBIC SYSTEM NEURONS ( SEE FIGURE, NUMBER 5). ACTIVE CEREBRAL
INFECTION IS FOLLOWED BY PASSIVE CENTRIFUGAL SPREAD OF VIRUS TO
PERIPHERAL NERVES. THE AMPLIFICATION OF INFECTION WITHIN THE CNS
OCCURS THROUGH CYCLES OF VIRAL REPLICATION AND CELL- TO -CELL
TRANSFER OF PROGENY VIRUS. CENTRIFUGAL SPREAD OF VIRUS MAY LEAD
TO THE INVASION OF HIGHLY INNERVATED SITES OF VARIOUS
TISSUES,INCLUDING THE SALIVARY GLANDS. DURING THIS PERIOD CEREBRAL
INFECTION, THE CLASSIC BEHAVIORAL CHANGES ASSOCIATED WITH RABIES
DEVELOP.

SIGN AND SYMPTOMS

THE FIRST SYMPTOMS OF RABIES MAY BE NONSPECIFIC FLU- LIKE SIGNS--
MALAISE, FEVER, OR HEADACHE, WHICH MAY LAST FOR DAYS. THERE MAY
BE DISCOMFORT OR PARESTHESIA AT THE SITE OF EXPOSURE ( BITE),
PROGRESSING WITHIN DAYS TO SYMPTOMS OF CEREBRAL DYSFUNCTION,
ANXIETY. CONFUSION, AGITATION, PROGRESSING TO DELIRIUM, ABNORMAL
BEHAVIOR, HALLUCINATIONS, AND INSOMNIA. THE ACUTE PERIOD OF
DISEASE TYPICALLY ENDS AFTER 2 TO 10 DAYS (6). ONCE CLINICAL SIGNS
OF RABIES APPEAR , THE DISEASE IS NEARLY ALWAYS FATAL, AND
TREATMENT IS TYPICALLY SUPPORTIVE. DISEASE PREVENTION IS ENTIRELY
PROPHYLACTIC AND INCLUDES BOTH PASSIVE ANTIBODY ( IMMUNE
GLOBULIN) AND VACCINE. NON-LETHAL EXCEPTIONS ARE EXTREMELY RARE.
TO DATE ONLY SIX DOCUMENTED CASES OF HUMAN SURVIVAL FROM
CLINICAL RABIES HAVE BEEN REPORTED AN EACH INCLUDED A HISTORY OF
EITHER PRE- OR POST-EXPOSURE PROPHYLAXIS.

PATHOLOGY
PATHOLOGY OF RABIES INFECTION IS TYPICALLY DEFINED BY ENCEPHALITIS
AND MYELITIS. PERIVASCULAR INFILTRATION WITH LYMPHOCYTES,
POLYMORPHONUCLEAR LEUKOCYTES, AND PLASMA CELLS CAN OCCUR
THROUGHOUT THE ENTIRE CNS. RABIES INFECTION FREQUENTLY CAUSES
CYTOPLASMIC EOSINOPHILIC INCLUSION BODIES ( NEGRI BODIES) IN
NEURONAL CELLS, ESPECIALLY PYRAMIDAL CELLS OF THE HIPPOCAMPUS
AND PURKINJE CELLS OF THE CEREBELLUM. THESE INCLUSIONS HAVE BEEN
IDENTIFIED AS AREAS OF ACTIVE VIRAL REPLICATION BY THE
IDENTIFICATION OF RABIES VIRAL ANTIGEN.

SEVERAL FACTORS MAY AFFECT THE OUTCOME OF RABIES EXPOSURE.
THESE INCLUDE THE VIRUS VARIANT, THE DOSE OF VIRUS INOCULUM, THE
ROUTE AND LOCATION OF EXPOSURE, AS WELL AS INDIVIDUAL HOST
FACTORS, SUCH AS AGE AND HOST.
1.RACCOON IS BITTEN
    BY A RABID ANIMAL
2. RABIES VIRUS      
     ENTERS THE       
       RACCOON          
       THROUGH          
 INFECTED SALIVA.
3.RABIES VIRUS       
SPREADS THROUGH
   THE NERVES TO     
  THE SPINAL CORD   
       AND BRAIN.
4.THE VIRUS INCUBATES IN           
    RACCOON'S BODY FOR            
APPROXIMATELY 3-12 WEEKS.
THE RACCOON HAS NO SIGNS OF
   ILLNESS DURING THIS TIME.
5. WHEN IT REACHES  
   THE BRAIN, THE       
  VIRUS MULTIPLIES
RAPIDLY, PASSES TO
      THE SALIVARY      
   GLANDS AND THE    
   RACCOON BEGINS   
     TO SHOW SIGNS    
          DISEASE.
6. THE INFECTED          
ANIMAL USUALLY        
DIES WITHIN 7 DAYS   
OF BECOMING SICK.