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Rabies in Raccoons

Raccoons act as a reservoir for rabies in the United States.  In fact, the majority of rabies cases in the U.S. are in wildlife, with raccoon cases predominating.  In the U.S., 90% of all rabies cases occur in wildlife.  During 2000, raccoon rabies made up 41% of wildlife cases diagnosed with skunks, bats and foxes making up the balance.  To limit the exposure of humans and domestic animals to rabies, it is important for veterinarians to know the current geographic distribution of rabies, the procedure if a human or animal is bitten by a wild animal, and be familiar with rabies diagnostic testing.

Geographic distribution: Raccoon rabies was much less prevalent in the U.S. prior to 1950.   From 1950-1970, the incidence of raccoon rabies began to rise, especially in Florida and Georgia.  In 1977, a variant of raccoon rabies distinct from the southern variant was detected in Virginia and West Virginia.  This variant has since spread north along the eastern seaboard to Ontario, Canada, and was reported in northwest Ohio in 1996.  Eventually this rabies variant converged with the southern variant in North Carolina.

In most states with raccoon rabies, there has been an increased number of cases; however, Ohio has reported fewer cases.  In 2000, 10 of 19 states which have reported raccoon variant rabies reported an increase in the number of cases.  However, Ohio reported no cases in 2000.  This was a decrease from the 6 cases reported in 1999.  This may be because Ohio has used extensive wildlife rabies control programs, including rabies vaccine baiting.

Human or Domestic Animal Exposure:

Veterinarians should discourage ownership of raccoons or any wildlife.  No parenteral vaccines are approved for use in raccoons and prior vaccination does not contraindicate euthanasia and testing.  Captive raccoons in exhibits may have been incubating rabies when caught and, therefore, should be quarantined for a minimum of 180 days before exhibition.

If a human is bitten by a raccoon (or any wildlife) the animal should be regarded as rabid.  The raccoon should be humanely euthanized and the brain tested for rabies.  If  human exposure occurs, it should always be reported to the local or state health department.  Bites or scratches should be thoroughly washed immediately.  A bite to a human requires the initiation of post-exposure prophylaxis.

Animals potentially exposed to rabies by a raccoon or other wild animal not availablefor testing should be handled as an exposure.  Unvaccinated domestic animals which are exposed should be euthanized immediately.  If the owner is unwilling to do this, the animal should be placed in strict isolation for six months.  The animal should be vaccinated one month before release.  Animals that are current on rabies vaccinations should be revaccinated immediately and observed for 45 days.

  It is important to remember that the guidelines for bites from wildlife are different from those for bites to humans from healthy domestic animals.  If a dog, cat, or ferret bites a human, the animal should be quarantined and observed for ten days.  The animal should not be given a rabies vaccination during this time.  At the first sign of illness, the animal should be evaluated by a veterinarian and reported to the local health department.  If signs of rabies develop, the animal should be euthanized, appropriate brain tissue removed and shipped refrigerated to the State Board of Health.  Any unwanted animal that bites a human may be euthanized immediately and submitted for testing.

Diagnostics:  No antemortem tests are sensitive enough to be considered reliable for diagnosis.  Handling live suspect animals should be done cautiously using safety equipment such as rabies poles, cages, and heavy gloves.  The animal should be euthanized humanely in a way that does not damage the animal’s brain.  The head can be removed and the whole animal or head should be chilled until examined.  The head should not be frozen as freezing causes tissue damage and may delay diagnosis.

  The standard diagnostic test for rabies is the direct fluorescent antibody test (FAT).  This test can be performed quickly and has a sensitivity and specificity approaching 100%.  In this test, microscope slides of brain from the affected animal are fixed in acetone.  The slides are then exposed to rabies specific nucleocapsid fluorescent antibody.  They are evaluated on a microscope with an energy source which allows visualization of fluorescent marker fixed to the antibodies.  It is not necessary that the animal be showing neurologic signs at the time of examination.  If there is virus in the saliva, there will be detectable virus in the CNS by FAT.

  Rabies can also be diagnosed histopathologically through the identification of intracytoplasmic inclusions in large neurons called Negri bodies.  Negri bodies can be found in the thalamus, hypothalamus, pons, cerebral cortex, and dorsal horn of the spinal cord.  In carnivores, they are most common in the neurons of the hippocampus.  In herbivores, they are often found in the Purkinje cells.  The bodies are best seen with Seller’s or van Gieson’s stain; they stain magenta.  Negri bodies are not seen during all stages of infection and this test is no longer used for routine diagnosis.

  In Indiana, animals or brain tissue is sent directly to the Board of Health as soon as possible for official examination at:

Rabies Laboratory
Indiana State Board of Health
P.O. Box 7203
635 N. Barnhill Dr.
Indianapolis, IN  46207
(317) 233-8036

Conclusion:  There have been no confirmed human deaths associated with rabid raccoons; however, there has been an increased number of rabies cases in domestic animals in the northeast due to raccoon rabies.  Therefore, rabid raccoons could potentially lead to human exposure through rabid domestic animals.

-by Paul Rennekamp, Class of 2003

-edited by Dr. Christine Hanika, ADDL Pathologist


1. ADDL User’s Guide.  Purdue University 1998.
2. Anonymous :2000.  Update Raccoon Rabies: Epizootic – United States and Canada, 1999,  Morbidity and Mortality Weekly Report.  Abstract 49: 31-35.
3. Chomel BB: 1999.  Rabies Exposure and Clinical Disease in Animals.  Rabies: Guidelines for Medical Professionals. p.24
4. Green CE, Dreesen DW: 1998.  Rabies. Infectious Diseases of the Dog and Cat. 2nd ed.  121-122.
5. Jenkins SR: 1999.  Compendium of Animal Rabies Control, 1999 National Association of State Public Health     Veterinarians, Inc. Rabies:  Guidelines For Medical Professionals.  81-83.
6. Krebs JW et al: 2001.  Rabies Surveillance in the United States during 2000.  JAVMA. Abstract 219 (12):     1687-1699.
7. Rupprecht CE: 2002.  Rabies: Reemergence of the Disease. Supplement to Compendium on Continuing Education for the Practicing Veterinarian 24 :57-60.
8. Trimarchi CV: 1999.  The Diagnosis of Rabies.  Rabies:  Guidelines for Medical Professionals.  p 58-60.




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