FLOWCHART FLOWCHART

Diseases / List of Viral Diseases / Disease description:

Rabies (with special reference to Raccoons and to Rabies in Europe)

Click here for full page view with caption Click here for full page view with caption Click here for full page view with caption Click here for full page view with caption Click here for full-screen view with caption Click here for full-screen view with caption Click here for full-screen view with caption

 

INDEX - INFORMATION AVAILABLE

GENERAL INFORMATION

SUSCEPTIBILITY, DISEASE CHARACTERISTICS & DIAGNOSIS

TREATMENT & CONTROL

Scroll down OR use INDEX
to navigate in this page

THE FOLLOWING INFORMATION IS HELD ON THE INFECTIOUS AGENT INFORMATION PAGE
Rhabdoviridae: Rhabdoviridae- Rabies virus (with special reference to raccoon rabies variant and to the virus in European wildlife)

  • Virus Structure and Identification
  • Associated Host Species of Virus (Animal Types Affected) and Hazard / Risk
  • Virus Life Cycle, Transmission and Effects of Chemicals
  • Transmission and Biogeographical / Climatic Range for Virus

CLICK THIS LINK FOR Rhabdoviridae: Rhabdoviridae- Rabies virus (with special reference to raccoon rabies variant and to the virus in European wildlife)

Return to top of page

General and References

Disease Summary

  • Acute viral central nervous system disease. (B58.1.w1)
  • Normally a disease of bats and carnivores. (B47)
  • Acute fatal viral encephalomyelitis. (B209.1.w1)
  • Rarely recorded in birds: not considered natural reservoirs. Infection has been produced experimentally in geese and ducks and virus has been isolated from ducks.

Return to top of page

Alternative Names (Synonyms)

  • Al kalebe
  • Beshenstvo
  • Derriengue (bovine paralytic rabies)
  • Hari
  • Hydrophobia (humans)
  • Kalevet
  • Kuang cheng
  • Le rage
  • La rabia
  • Lyssa
  • Mal de calderas
  • Oulo fato
  • Polar madness
  • Rabbia
  • Rabhas
  • Rabia
  • Rage
  • Raiva
  • Thao
  • Tollwut

Return to top of page

Disease Type

 Viral

Return to top of page

Infectious/Non-Infectious Agent (directly associated with the Disease)

  • Rabies virus - Rhabdoviridae, an RNA virus (B58.1.w1)

Species/Taxa

Chemical

  • --

Physical

  • --

Return to top of page

References

Disease Author

Debra Bourne MA VetMB PhD MRCVS (V.w5)

Referee

Suzanne I. Boardman BVMS MRCVS (V.w6), Dr Robert G. McLean (V.w42), Rick Rossatte (V.w95), Dr Claude T Sabeta PhD (V.w167)

References

Detailed references are provided attached to specific sections.

ORGANISATIONS

ELECTRONIC LIBRARY
(Further Reading)
Click image for full contents list of ELECTRONIC LIBRARY

Return to top of page

Epidemiology and Host Susceptibility Factors

Incubation Period, Time Course and Persistence of Disease

General Editorial Description

The following editorial comment summarises detailed information given within the LITERATURE REPORTS for RABIES IN RACCOONS. Links to the LITERATURE REPORTS are provided at the bottom of this box. Limited data on rabies in general is provided in the literature reports but is not intended to be comprehensive.

1) INCUBATION PERIOD

General:

  • The incubation period for rabies is very variable, generally several weeks but varying from a week to a year or longer, depending on the virus strain, host species and the site of inoculation. In humans, periods from less than 10 days to as long as six years have been recorded, but more than half of cases show an incubation period of one to three months. Bites to the head or neck are generally associated with shorter incubation while bites to the extremities produce longer incubation periods.

In Procyon lotor - Common Raccoon

  • The incubation period for rabies in raccoons has been recorded to be as short as 10 days and as long as 107 days (based on laboratory studies). From a study of naturally occurring raccoon rabies in raccoons in Ontario, Canada it was suggested that the most usual incubation period might be about five weeks, but with the possibility of both shorter and longer periods.
  • For detailed, referenced information on rabies in raccoons see: Rabies - Incubation Period (Disease Reports)

2) DISEASE DURATION (TO DEATH) IN INDIVIDUAL ANIMALS

  • The clinical course for rabies is generally a matter of days - one to 10 days is usual, longer courses are seen occasionally. The prodrome may last one to three days, the furious stage one to seven days (in dogs) and the paralytic stage two to four days. 

In Procyon lotor - Common Raccoon

  • While raccoons inoculated with a street rabies virus originating from a dog have sometimes been found dead without prior clinical signs, more usually raccoons with natural or experimental rabies infection have shown clinical signs for periods of less than one day up to 17 days.
  • Note: there is little data from recent experiments, since, as part of humane experimental protocols, animals are usually euthanised as soon as definite clinical signs are noticed.
  • For detailed, referenced information on rabies in raccoons see: Rabies - Disease Duration (to Recovery) in Individual Animals (Disease Reports)

3) TIME COURSE / PERSISTENCE OF DISEASE IN A SUSCEPTIBLE POPULATION

  • Endemic levels of rabies may be maintained in a population for decades. (J128.9.w1)

In Procyon lotor - Common Raccoon

  • In endemic areas, raccoon rabies may be maintained in the population for decades, as has been seen in the south-eastern states and in the mid-Atlantic and north-eastern states. However, in a smaller population, the disease is not necessarily maintained indefinitely.
  • In general, there appears to be a seasonal pattern to reports of rabid raccoons, with peaks in spring; peaks at other times of year have been less consistent. It has been suggested that the spring peak is associated with the raccoon breeding season. 
  • For detailed, referenced information on rabies in raccoons see: Rabies - Time Course-Persistence of Disease in a Susceptible Population (Disease Reports)
CLICK THE LINKS FOR Literature Reports
CLICK THE LINKS FOR Editorial Overviews Available
  • --

Return to top of page

Mortality / Morbidity / Susceptibility / Life stage affected

General Editorial Description The following editorial comment summarises detailed information given within the LITERATURE REPORTS for RABIES IN RACCOONS. Links to the LITERATURE REPORTS are provided at the bottom of this box. Limited data on rabies in general is provided in the literature reports but is not intended to be comprehensive.
1) NUMBER OF DEATHS
  • There is a very high fatality rate for individuals showing clinical signs of rabies. However, not all individuals die after either natural or artificial exposure to the virus. The outcome of exposure may be affected by factors such as the virus strain, dose, route and site of exposure (e.g. greater mortality following inoculation into the head or neck), and species exposed.
  • For Procyon lotor - Common Raccoon:
    • Raccoons may be infected by both raccoon rabies and other strains of rabies virus, and this infection can be fatal. However, it is also apparent, both from  experimental studies and from the prevalence of seropositive raccoons in wild populations, that rabies infection in raccoons is not always fatal and that raccoons may encounter rabies virus, seroconvert, but not develop fatal illness. Experimental evidence suggests that raccoons have intermediate susceptibility, with higher resistance than foxes or skunks but lower resistance than Didelphis virginiana - Virginian opossum.
    • Rabies is acknowledged as one of the two diseases which may affect raccoons on a population level, the other being canine distemper (Canine Distemper).
    • Detailed information, referenced is provided in the literature reports linked below.
2) NUMBER OF ANIMALS AFFECTED
  • The occurrence of rabies is variable. Worldwide in humans it is estimated that there may be 35,000 to 50,000 or even 100,000 cases annually. In the developing world, rabies in dogs is often a serious problem, while in the developed world, rabies in dogs is controlled and rabies is seen mainly in wild carnivore reservoirs and bats. For example, in the USA in 2004 there were 6,836 confirmed cases in nonhuman animals and eight cases in humans.
  • Procyon lotor - Common Raccoon
    • Raccoons may be infected by both raccoon rabies and other strains of rabies virus, and this infection can be fatal. However, it is also apparent, both from experimental studies and from the prevalence of seropositive raccoons in wild populations, that rabies infection in raccoons is not always fatal and that raccoons may encounter rabies virus, seroconvert, and not show illness (or death).
    • Detailed information, referenced is provided in the literature reports linked below.
3) EFFECTS OF AGE, SEX AND PHYSIOLOGICAL STATUS
  • Susceptibility to rabies infection may be affected by the age, sex and physiological status of the exposed animal. Young animals may be more susceptible than adults. Antibody titres do not directly correlate with protection against infection, since other immunological factors also play a role in preventing rabies. 
  • In Procyon lotor - Common Raccoon
    • It is not known whether male or female, adult or juvenile raccoons are more susceptible to rabies. Percentage of different classes of raccoons positive for rabies in different epidemiological studies have varied.
    • In general, raccoons with high levels of serum neutralising antibodies appear more able to survive challenge with lethal street rabies (either raccoon rabies or other rabies strains) than raccoons with only low levels of antibodies, or without antibodies. However, the relationship between serum neutralising antibody titre and resistance to rabies virus is not exact: in some vaccination experiments, some raccoons with relatively low titres have survived challenge while other individuals with relatively high titres have succumbed to challenge.
    • Detailed information, referenced is provided in the literature reports linked below.
4) EFFECTS OF BODY CONDITION AND OTHER DISEASES
  • Genetic factors are recognised as affecting susceptibility to rabies.
  • Reactivation of rabies virus infection may occur due to stress.
  • In Procyon lotor - Common Raccoon
    • It is possible that raccoon susceptibility to rabies may be increased by stress and by concurrent disease.
CLICK THE LINKS FOR Literature Reports
CLICK THE LINKS FOR Editorial Overviews Available
  • --

Return to top of page

Clinical & Pathological Characteristics, and Diagnosis
Clinical Signs (by physiological system)
Overall Clinical Presentation

The following editorial comment summarises detailed information given within the LITERATURE REPORTS for RABIES IN RACCOONS. Links to the LITERATURE REPORTS are provided at the bottom of this box. Limited data on rabies in general is provided in the literature reports but is not intended to be comprehensive.

  • Most signs of rabies are neurological. "Most of the clinical signs of rabies are expressions of impaired neuronal function (altered neurotransmission) in the CNS. the mechanisms involved are largely unknown." (J214.187.w1)
  • Prodromal stage
    • This stage is not usually observed in wild animals but is well recognised in humans and may be seen in closely observed pets. It involves vague changes in temperament (e.g. restlessness, increased nervousness or loss of fear, hyperactivity), and other nonspecific signs such as inappetance, dysphagia, vomiting, diarrhoea and pyrexia.
  • Furious form
    • The furious form involves general excitative signs with hyperaesthesia to stimuli (auditory, visual and tactile), ataxia/incoordination, "staring" eyes, sudden and apparently unprovoked agitation and aggression to either other individuals or inanimate objects. Often there is abnormal vocalisation. In some species increased sexual activity is seen. Convulsive seizures during this stage may be fatal but generally animals progress from this stage to the paralytic form before death.
  • Local signs
    • Some individuals chew at the site of inoculation or at their extremities.
  • Paralytic form 
    • The paralytic form of rabies, involving paresis or paralysis, usually follows the furious form but sometimes is seen directly following the prodromal stage. It generally lasts one to two days. This form involves ascending flaccid paralysis and there may be frequent urination or incontinence, tenesmus, constipation, tail flaccidity, jaw paralysis causing inability to eat, but with profuse salivation, and respiratory muscle paralysis causing respiratory distress. Signs may end in convulsions, coma and death
  • Rarely, death from rabies occurs without any clinical signs. 
  • Rare survivors of clinical rabies may have severe neurological sequelae.
In Procyon lotor - Common Raccoon
  • Prodromal signs of reduction or cessation of eating and drinking have been seen in experimental infection.
  • Raccoons with rabies often show altered behaviour, such as appearing around human dwellings during daylight or wandering aimlessly, and may appear obviously sick, incoordinated or paralysed. Raccoons with rabies are often reported to be unaggressive but to lose their fear of humans and dogs. Frankly aggressive behaviour is also reported. "Sick" animals may bite when handled.
  • In one experiment with a raccoon rabies variant, sudden onset neurological signs were seen including combinations of circling, head-pressing, head-tilt, excess licking, mainly of the genital area and tail tip, and occasional self-mutilation of the limbs or genital area occurred.
  • In experimental infections with strains other than raccoon rabies variant, vague signs of depression, anorexia and lethargy, increased alertness or apprehension, aggression, increased vocalisation, excessive friendliness, incoordination and paralysis have all been noted.
  • It is possible that more severe clinical neurological signs may be seen in raccoons infected with raccoon rabies variant than in raccoons infected with other rabies variants.
  • Note: Individual raccoons without any behavioural signs have also tested positive for rabies.
  • The presence of porcupine quills in a raccoon should raise the suspicion of rabies (although not all raccoons with embedded quills are rabid).
  • Detailed information, referenced is provided in the literature reports linked below.
CLICK THE LINKS FOR Literature Reports on Specific Clinical Characteristic Descriptions available
CLICK THE LINKS FOR Editorial Overviews Available

Return to top of page

Clinical Pathology (Testing Samples incl. Serology)
Overall Clinical Pathology findings The following editorial comment summarises detailed information given within the LITERATURE REPORTS for RABIES IN RACCOONS. Links to the LITERATURE REPORTS are provided at the bottom of this box. Limited data on rabies in general is provided in the literature reports but is not intended to be comprehensive.
  • Antibodies may be detected using tests such as ELISAs or the rapid fluorescent focus inhibition test. Demonstration of the presence of virus neutralizing antibodies indicates that the individual has been exposed to viral antigen, but does not necessarily indicate disease: an individual may be seropositive following vaccination or having developed immunity following natural exposure. In clinical rabies, antibodies usually develop late in the clinical course. 
  • For further information on serological tests see: Rabies virus (with special reference to raccoon rabies variant) - Detection and Identification Techniques (Viral Reports)
  • Glycosuria may be present in rabid animals.
  • Prominent lymphocytic pleocytosis may be detected in CSF.
  • Demonstration of rabies virus neutralizing antibodies in the CSF in association with suggestive clinical signs supports a diagnosis of rabies. 
  • Rabies may be found in the saliva, including during the days before onset of clinical signs, but may be detected only intermittently.
In Procyon lotor - Common Raccoon
  • Antibodies may be detected in the blood of raccoons. Antibodies have been detected in raccoons following survival of experimental rabies infection, prior to death from experimental infection, and in wild raccoons, particularly those captured during or shortly after a rabies epizootic. Repeated sampling has shown the presence of antibodies to be maintained, sometimes for many months.
  • It is not known whether raccoons with antibodies to rabies transmit these antibodies to their offspring and whether this is protective. In one experiment with a vaccinia-rabies glycoprotein recombinant vaccine, cubs of females which were vaccinated during pregnancy were born with virus neutralising antibodies. However, it was not known whether this reflected passive transfer of antibodies or transmission of the vaccine virus in utero
  • Mononuclear pleocytosis of the CSF has been noted in raccoons with rabies. Mild lymphocytic pleocytosis has been seen in raccoons following vaccination and challenge with street rabies virus.
  • Rabies virus may be found in the saliva of raccoons both during the period of clinical rabies and shortly before clinical signs develop.
  • Infrared thermography can detect rabies infected raccoons (in an experimental setting), even with only mild clinical signs, by the increased temperature of the nose and rostrum.
  • Detailed information, referenced is provided in the literature reports linked below.
CLICK THE LINKS FOR Literature Reports
  • --
CLICK THE LINKS FOR Editorial Overviews Available
  • --

Return to top of page

Pathological Findings (by anatomical system)
Overview

The following editorial comment summarises detailed information given within the LITERATURE REPORTS for RABIES IN RACCOONS. Links to the LITERATURE REPORTS are provided at the bottom of this box. Limited data on rabies in general is provided in the literature reports but is not intended to be comprehensive.

GROSS PATHOLOGY
  • There are no pathognomic gross findings
  • Externally, there may be fresh or healed bite wounds, and sometimes gross trauma due to self-mutilation. In areas with porcupines, quills may be found in the muzzle of affected animals. There may be an unusual odour, probably related to reduced hygiene in terminal disease.
  • In the CNS there may be congestion of meningeal vessels, the brain tissue may appear pinker than usual an there may be mild cerebral oedema.
In Procyon lotor - Common Raccoon
  • Normally, there are no gross lesions in raccoons with rabies. Areas of alopecia and skin reddening have been seen in association with excess licking/self mutilation in raccoons in one experiment.
  • Detailed information, referenced is provided in the literature reports linked below.
HISTOPATHOLOGY
  • Histopathological changes do not reflect the severity of the clinical disease.
  • The general CNS findings are those of viral encephalitis, including Perivascular cuffing, vascular congestion, neuronophagia, neuronal degeneration and focal to diffuse gliosis. Lesions may be most severe in the brain stem.
  • The presence of Negri bodies is considered pathognomic for rabies, but these are only seen in about 50 - 75% of cases. These are found most commonly in ganglionic cells of the hippocampus and in Purkinje cells of the cerebellum.
  • Spongiform lesions may be found in the grey matter, in the neuropil and in neuronal cell bodies of the thalamus and cerebral cortex.
  • Spinal and cranial nerve ganglia, particularly the Gasserian ganglia, may show an inflammatory response. 
  • Note: There is no visible inflammatory response in the brain of some rabid individuals. (J214.187.w1)
In Procyon lotor - Common Raccoon
  • The main affected area is the CNS. The usual finding is of multifocal nonsuppurative encephalitis, bilateral but not necessarily symmetrical, affecting the brain stem, cerebrum and spinal cord, with perivascular mononuclar cell cuffing of blood vessels, multifocal gliosis and, in severely affected areas, neuronal degeneration.
  • Outside the CNS, lesions may be found in the Gasserian ganglia, with inflammatory infiltration, mainly mononuclear. 
  • Negri bodies are usually visible in the CNS; these may be larger and more numerous in raccoons infected with raccoon rabies variant than in raccoons infected with other rabies variants. Negri bodies may also be found in the Gasserian ganglia and in cells of other ganglia.
  • Atypical findings have included:
    • Absence of lesions of rabies encephalitis, in a naturally infected raccoon with concurrent canine distemper virus (CDV) infection (lesions typical of canine distemper virus infection were present);
    • Eosinophilic encephalitis in a raccoon experimentally infected with the canine MD5951 rabies strain; the raccoons had at least three different parasitic infections, which may be relevant in these findings.
  • Detailed information, referenced is provided in the literature reports linked below.
ELECTRON MICROSCOPY
  • Rod shaped or bullet-shaped virus particles, 180-200 by 75-80 nm, are found most commonly in the CNS and the salivary glands. Neurons which contain matrices may also have large numbers of virus particles budding from the rough endoplasmic reticulum membrane and the plasma membrane. 

VIRUS ISOLATION

In Procyon lotor - Common Raccoon

  • In general, rabies virus may be found in the brain and salivary gland of rabid raccoons. However, in two experiments with a virus strain originating in Mexican free-tailed bats Tadrida brasiliensis mexicana, the salivary glands were virus negative. Rabies virus may also be found in other tissues, such as pancreas, adrenal, kidney and spleen, but is found much less consistently in such organs.
  • Detailed information, referenced is provided in the literature reports linked below.
CLICK THE LINKS FOR Literature Reports on Specific Pathological Findings Descriptions available
CLICK THE LINKS FOR Editorial Overviews Available
  • --

Return to top of page

Diagnostic Criteria

General Indicative Signs "Rabies must be considered in the differential diagnosis of any mammal with unexplained neurologic illness." (N7.39.w1)
  • Clinical signs are considered characteristic and may allow suspicion, but are not pathognomonic. (B47, B58.1.w1, B209.1.w1)
    • Signs of rabies are not always characteristic, and may vary greatly between different animals. (B417.2.2.5.w1, D387.2.1.13.w2a13)
  • In countries with endemic urban rabies, clinical signs are important for rabies diagnosis. (J21.73.w3)
    • Since signs can be mistaken for other conditions, rabies should be considered in any human patient with neurological signs, and in any animal which has bitten a human. (J21.73.w3)
  • In a rabies-endemic area, rabies must be considered in any animal with acute or progressive CNS dysfunction. (J15.23.w4)
  • Note: Rabies cannot be discounted as a diagnosis because the animal has been vaccinated: (J15.23.w4)
    • Vaccine failures do occur on occasion, usually in individuals with low antibody titres following vaccination; (J15.23.w4)
    • Vaccination following infection is not always protective. (J15.23.w4)
  • Rabies should be considered in any suspected case of encephalitis in mammals, particularly in taxa at high risk of rabies, such as Carnivora and Chiroptera. (B209.1.w1)
Definitive Diagnosis

Click here for full page view with caption Click here for full-screen view with caption Rabies virus infected neurons, FITC. Click here for full-page view with caption. Click here for full page view with caption

 

"A case definition of rabies is supported by either virus isolation, detection of viral antigen or nucleic acid, or demonstration of rabies-specific antibodies in the CSF in a clinically suspect animal." (B209.1.w1) Definitive diagnoses requires laboratory tests to identify the rabies virus or specific components of the virus. (B417.2.2.5.w1)
  • Antemortem diagnosis may be carried out; virus may be detected by skin biopsy, corneal impressions, saliva or CSF collection and swabs of eye, nasal mucosa or throat. A positive result confirms infection but negative findings do not preclude the possibility of rabies infection. (B209.1.w1, B360.10.w10, B360.11.w11, J21.73.w3, J93.36.w2, J98.358.w3)
  • In experimental infection, infected raccoons can be differentiated from non-infected raccoons by infrared thermography: the nose and rostrum are at significantly higher temperatures in raccoons with clinical signs (changed from black to white on an infrared thermal image). (J2.37.w1)
  • Post mortem examination is required for definitive diagnosis. (B209.1.w1)

The following may be used for rabies diagnosis:

  • Light microscopy/Detection of Negri bodies
    • Histological examination of brain sections or impression smears by light microscopy, in particular detection of characteristic Negri bodies, was the standard method of rabies diagnosis for many years. This has been replaced by the direct fluorescent antibody test, but is still used routinely in some developing countries. It has the advantages of requiring little equipment and giving a rapid result (within a couple of hours) but it is much less sensitive than immunological methods, particularly for partially autolysed samples. Additionally, false positive results may occur if nonspecific inclusion bodies are present. The OIE no longer recommends histopathology for the diagnosis of rabies.
  • Mouse inoculation test
    • For many years, mouse inoculation was considered the most sensitive way to detect rabies virus. However, it has now been superseded by modern methods for routine diagnosis. Several days are required for a diagnosis by this method. It is still used occasionally to confirm a test result, for example following human exposure to a suspect rabid animal which is negative by other tests. 
  • Electron microscopy
    • Examination by electron microscopy can be used to detect viral inclusions (corresponding to Negri bodies) and virus particles. 
  • Virus isolation in cell culture
    • Cell culture is not commonly used for virus isolation but can be useful in cases where immunoflorescence is inconclusive. It can be used for testing saliva and cerebrospinal fluid samples from living individuals as well as for testing brain and salivary gland tissues post mortem. Murine blastoma cells are recommended for cultivation of street rabies strains. Immunofluorescence is used to detect virus antigen in the cultured calls. While a positive cell culture result in a sample from a living animal allows a definite diagnosis of rabies, a negative result in samples from a live animal is not conclusive. A plaque assay has been developed using chicken embryo cells.
  • Fluorescent antibody test
    • The direct fluorescent antibody test (FAT) is presently the standard test for rabies virus detection. It is fast and reliable (sensitive and specific) for use on fresh or frozen tissue, and may be used on tissue which is degraded. It can be carried out on histological sections or on impression smears. In large animals, distribution of virus within the CNS may vary considerably and it is important to examine the cerebellum, brain stem and hippocampus using the FAT. Recently, a procedure has been developed allowing the use of FAT on formalin-fixed tissues.
  • Immunoperoxidase
    • An immunoperoxidase method, using the streptavidin-biotin complex and polyclonal or polyclonal antibodies may be used for detection of rabies in formalin fixed paraffin embedded tissue sections.
    • Raccoon rabies variant:
      • The monoclonal antibody (mAb) 802-2 was shown in a study to detect rabies antigen in paraffin embedded tissue sections from rabid raccoons. (J3.136.w4)
  • Direct rapid immunohistochemical test (dRIT)
    • This test can be used on brain touch impressions and the reaction product is visible under an ordinary light microscope (mangeta inclusions, while the neuronal background is blue). The test allows diagnosis within one hour. It can be used on frozen samples or samples preserved in glycerol, and has a sensitivity similar to that of the direct fluorescent antibody test.
  • RT-PCR
    • RT-PCR to detect lyssavirus nucleic acid is not used in routine rabies diagnosis but is useful for confirmation of IFA test results in formalin-fixed or decomposed material unsuitable for virus isolation, and has been used in antemortem diagnosis. This method may be used on samples of brain tissue, saliva or CSF, and may allow detection of very small amounts of viral material, in tissues which are fresh, degraded or fixed.
  • NASBA
    • NASBA is able to detect very small amounts of rabies virus RNA and has been used to test the saliva and CSF in humans with clinical illness.

Antibody detection in CSF:

  • Demonstration of rabies virus neutralizing antibodies in the CSF, in association with suggestive clinical signs, supports a diagnosis of rabies. (B209.1.w1)
    • Vaccination against rabies does not result in the presence of rabies virus neutralizing antibodies in the CSF. (B209.1.w1)
    • Antibodies are, rarely, found in the CSF of a healthy individual animal; this strongly suggests prior illness with and recovery from rabies. (B209.1.w1)
  • In humans, antibodies may be detected in only about 14% of individuals in the first eight days of infection, but positive in about 58% from day nine onward. (J98.358.w3)

Detailed information, referenced is provided in the literature reports linked below.

CLICK THE LINKS FOR Specific Technique Reports
CLICK THE LINKS FOR Specific Clinical Pathology Findings (Sample Results)
  • --
CLICK THE LINKS FOR Specific Pathological Findings 
  • --
Similar Diseases

The following editorial comment summarises detailed information given within the LITERATURE REPORTS for RABIES IN RACCOONS. Links to the LITERATURE REPORTS are provided at the bottom of this box. Limited data on rabies in general is provided in the literature reports but is not intended to be comprehensive.

General

  • A variety of other diseases including distemper [Canine Distemper], hepatitis, listeriosis, tetanus, botulism [Avian Botulism] and some parasitic infections as well as some plant and chemical toxins may cause signs similar to those seen in rabid animals.

In Procyon lotor - Common Raccoon: 

  • Canine Distemper is the other main disease causing nervous signs in raccoons. 
    • Note: Rabies may occur concurrently with canine distemper (Canine Distemper) therefore diagnosis of distemper does not rule out a diagnosis of rabies without further testing for rabies.
  • Other diseases reported in raccoons and which may cause neurological signs include Sarcocystis neurona protozoan encephalitis, toxoplasmosis, West Nile virus infection (West Nile Virus Disease), environmental toxicoses (e.g. ethylene glycol toxicity, lead poisoning, methyl mercury toxicity) and cerebral neoplasia (astrocytoma).
  • Detailed information, referenced is provided in the literature reports linked below.
CLICK THE LINKS FOR Specific Similar Disease Reports
CLICK THE LINKS FOR OVERVIEWS of management techniques available

Return to top of page

Treatment and Control

Specific Medical Treatment (Antiserum, Antidote, Anti-(viral/bacterial/fungal) etc.)

Specific Medical Treatment In general, animals suspected of having rabies are either euthanased or placed in quarantine; treatment is not applied. (B23.20.w15, B47)

Treatment of humans after suspected exposure to rabies is aggressive prophylactic treatment. (B47) [see below - prophylactic treatment]

ANTISERUM

  • Treatment of humans after suspected exposure includes use of human-origin rabies immune globulin. [see below - prophylactic treatment]

ANTIVIRAL DRUGS

  • In 2004, treatment with the antiviral drug ribavirin was used, together with drug-induced coma and mechanical respiration, in the successful treatment of a 15-year-old girl with clinical rabies. (N7.53.w2)
CLICK THE LINKS FOR Literature Reports
  • --
CLICK THE LINKS FOR OVERVIEWS of management techniques available
  • No specific techniques described

Return to top of page

General Nursing and Surgical Techniques

Nursing and Supportive Care
  • In general, animals suspected of having rabies are either euthanased or placed in quarantine; treatment is not applied. (B23.20.w15, B47)
    • For individual animals bitten or scratched by a known or suspected rabid animal, wound care should be provided prior to the animal being quarantined. (B23.20.w15)
  • In humans: In 2004, drug-induced coma and mechanical respiration was used, together with treatment with the antiviral drug ribavirin, in the successful treatment of a 15-year-old girl with clinical rabies. (N7.53.w2)
CLICK THE LINKS FOR Literature Reports
  • --
Surgical Treatment
  • Not applicable for this disease.

CLICK THE LINKS FOR Literature Reports
  • Not applicable for this disease
CLICK THE LINKS FOR OVERVIEWS of management techniques available

Return to top of page

Vaccination & Prophylactic Treatment

Vaccination

Click here for full-screen view with caption

Animals
  • Vaccines are administered intramuscularly in the thigh at a single site (unless otherwise specified by the manufacturer). (B47)

  • Inactivated vaccines injected intramuscularly appear to be safe and effective in various species. (B58.1.w1)
  • Vaccination of domestic cats and dogs is recommended. (B47)

    • Vaccination is commonly used in domestic pets in endemic areas (B58.1.w1).

    • Vaccination should commence at three months of age. (B47)

    • In dogs either modified live virus vaccines or inactivated virus preparations may be used. (B47)

    • Cats should not be vaccinated with modified live virus vaccines as a small proportion may develop vaccine-induced rabies. (B47)

    • Depending on the vaccine boosters may be required annually or every three years. (B47)

  • Horses and ruminants can be vaccinated; annual boosters are required. (B47)

  • Vaccines can also be used in non-domestic animals. (B101)

  • In zoos, vaccination "may be considered for animals that are particularly rare, are valuable, or may have frequent potential contact with free-ranging reservoirs, especially in epizootic areas." Mammals which are candidates for vaccination may be vaccinated at three months old and revaccinated yearly. Previously vaccinated individuals which are overdue for a booster should be given a single dose of vaccine and returned to an annual schedule of vaccination. (B23.20.w15)

    • Vaccines should be used by licensed veterinarians, and administered in accordance with the information on the product label or package insert. Vaccines given by the intramuscular route should be administered in a muscle mass suitable for the volume to be injected, and avoiding adipose tissue depots. (B23.20.w15)

    • "Use of a rabies vaccine with a 3-year duration of immunity should probably be encouraged because of its potency." (B23.20.w15)

      • Information from manufacturers indicates that three-year vaccines provide 90% to 100% efficacy of protection from rabies challenge following a single dose in cats or dogs and challenge studies have shown effective immunity at three years post vaccination. (J14.40.w2)

  • Requirements for oral vaccines include safety considerations, effectiveness and monitoring of the impact of oral vaccination in the field: (D387.2.1.13.w2a13)
    • "The vaccine should not induce any adverse signs in target and nontarget species. For vaccines used for dog immunisation, saliva should be checked for the absence of vaccinal virus because of possible contact with humans." (D387.2.1.13.w2a13)
    • "The attenuated rabies virus-based vaccines must achieve the lowest residual pathogenicity for target and nontarget species." (D387.2.1.13.w2a13)
      • "This is of utmost importance in the case of oral vaccination of dogs as dogs are often in close contact with humans" (D387.2.1.13.w2a13)
      • "The recombinant vaccines cannot induce any risk of rabies; the safety controls concern only the possible residual pathogenicity of the recombined parental virus." (D387.2.1.13.w2a13)
    • "The protection induced by the vaccine must be tested not only with the virus itself (to determine the minimal vaccinating dose) but also with manufactured baits ready to be used in the field. For foxes for instance, the vaccine should have a minimal titre corresponding to at least ten times the 100% protective dose (obtained with the same vaccine experimentally by direct oral instillation)." (D387.2.1.13.w2a13)
      • "The protection status cannot be then checked by serology only; a virulent challenge with the homologous street rabies virus is necessary because of the important implication of cell-mediated immunity in response to oral vaccination." (D387.2.1.13.w2a13)
    • "The stability of the vaccine in the field is important. The European Commission stresses the importance of checking the 100% protective dose after 7 days of exposure at 25C. "
      • "Each vaccine bait should be tested for stability with a melting point above 40C, and the blister or sachet containing the vaccine should still be covered by the bait casing after 7 days exposure at 40C." (D387.2.1.13.w2a13)
    • Impact of vaccination in the population of the targeted host/vector is monitored directly and indirectly: (D387.2.1.13.w2a13)
      • "Directly by measuring the bait uptake by the wild target species. This supposes that a biomarker (generally tetracycline) is included in the bait casing. The same examination allows the age of animals to be determined." (D387.2.1.13.w2a13)
      • "Directly by measuring the serological response of target animals. This serological control is better done using validated ELISA techniques as they are more robust than seroneutralisation tests when testing poor quality field specimens." (D387.2.1.13.w2a13)
      • "Indirectly by measuring the incidence of rabies in the vaccinated area. Typing of field isolates should be performed either by using MAbs or by sequencing positive samples from areas where the target species have been vaccinated with attenuated vaccines to possibly distinguish vaccine and field virus strains." (D387.2.1.13.w2a13)
      • Note: "The first two controls should be performed on specially killed animals to collect good quality samples. Rabies monitoring is more sensitive when performed in found dead or ill animals." (D387.2.1.13.w2a13)
  • Oral vaccines currently recommended by WHO are the recombinant VRG and the highly attenuated modified live vaccine SAG2. [2008](D387.2.1.13.w2a13)
  • Vaccination of wildlife may be used in the control of rabies where wild species are the major vectors.

    • Oral vaccination has been used to control and even eliminate rabies from wild populations in some areas, for example foxes in parts of Europe, using an attenuated SAD-B19 rabies virus strain. (B360.27.w27, J64.7.w4)

    • Trap-vaccinate-release of raccoons, skunks and feral cats was used, in conjunction with trap-and-shoot in core areas around known rabies cases, to control and eliminate an outbreak of raccoon rabies in New Brunswick, Canada. (P102.16.w2)

  • SAD-BHK (Street-Alabama Dufferin grown in baby hamster kidney cell culture) has been shown to be effective for the oral immunisation of foxes, being safe and resulting in development of high titres of anitibodies, but less effective at inducing an antibody response in several other species. (J270.10S4.w4)
  • SAD, SAD-B19 and SAD Vnukovo 32 appear to be capable of protecting foxes when cell culture fluid, without any concentration, is used as the vaccine. (J64.7.w4)
    • SAD is not completely harmless in all non-target animals, having residual pathogenicity for rodents. (B695.24.w24, J64.7.w4, J270.10S4.w4)
    • SAD has been used extensively in Switzerland, Federal Republic of Germany, France and Italy. It was noted [1988] that: "About one million doses have been distributed within chicken heads, and no accident has been reported, other than the accidental death of a fox cub, a cat and a stone marte. (Wandeler, personal communication." [1988](J64.7.w4)
      • A very few cases of apparent vaccine-induced rabies have been reported in foxes associated with SAD vaccines. However, these appear to be isolated incidents with no indication of further transmission. (J71.154.w)
    • SAD B19 was first used in the Federal Republic of Germany in 1985, and in Austria, Belgium, France, Italy and Luxembourg starting in 1986. After distribution of more than six million Tubingen meat meal and fat meal baits, no accidents had been reported. Rate of uptake of SAD B19 in Tubingen baits, as determined by tetracycline (incorporated as a biomarker) in bones was 70 - 80%, with probably a slightly lower percentage developing serological conversion. (J64.7.w4)
    • SAG-1 is a mutant derived from SAD Bern. It was shown to be effective as an oral vaccine in foxes and to be avirulent in laboratory mice and four species of wild rodents. (J238.23.w1)
      • SAG-1 was first used in Switzerland in 1988, on a wider scale in France in 1990, and again in Switzerland starting in 1991. (B695.24.w24)
    • SAG2 is a double avirulent mutant derived from SAD Berne; it has a glutamate coded by GAA in position 333 instead of an arginine (the first two nucleotides coding at this position have mutated) . This shows excellent genetic stability, and apathogenicity for adult mice, foxes, dogs and cats, while oral administration has been shown to protect foxes and dogs against lethal rabies virus challenge. (J62.60.w5, J70.12.w2)
      • SAG-2 has been used in Austria, France and Switzerland and Lichtenstein. (B695.24.w24)
  • Vaccinia-rabies glycoprotein recombinant virus vaccine was first trialled in Belgium in 1987, using chicken heads as baits.  (J64.7.w4)
  • Note: In the USA, only one oral vaccine, Raboval V-RG vaccinia-rabies glycoprotein recombinant virus vaccine, is licensed for use in wildlife. (J249.111.w2, P21.107.w1, P102.16.w3)
  • For vaccination of wildlife, modified live virus is required in baits for oral immunisation. (B684.6.w6)
  • For field application of oral vaccine, the following are required: (B695.24.w24)
    • A safe and effective vaccine, immunising the target host species under field conditions but posing the lowest possible risk to target species and to non-target species and humans.
    • A successful system which will deliver the vaccine to the oral mucosa.
    • A bait which is attractive to the target species (and not to non-target species) in which the vaccine can be distributed.
    • A strategy (spatial and temporal) for distributing baits containing vaccine, which will result in a sufficiently high proportion of the target species becoming vaccinated.

    (B695.24.w24)

  • Based on comparison of effectiveness of SAD-B19, SAG-1 and V-RG in France, the later was most effective, probably due to better thermostability of the vaccine-bait. (B695.24.w24)
  • Hand-distribution of baits around fox dens in early summer appears to be the most effective method for ensuring that fox cubs become immunised, but this is expensive. It is most likely to be suitable for elimination of residual foci of rabies in limited areas. (B695.24.w24)
In Europe
  • Oral immunisation targeting Vulpes vulpes - Red fox has been effective at nearly completely eliminating sylvatic terrestrial (classical, lyssavirus 1) rabies across western and central Europe. (B684.6.w6, J64.23.w1)
  • Vaccines which have been used in Europe in oral vaccination campaigns include SAD-Bern and SAD-B19 (modified live vaccines used extensively before 1988; SAD-Bern has also been used on a wide-scale in the Czech Republic more recently), SAG-1 (a modified live virus developed from SAD-Bern, an escape mutant selected in the presence of an antiglycoprotein monoclonal antibody), vaccinia-rabies-glycoprotein recombinant (VRG) vaccine, SAD-P5/88 (used widely in Europe), SAD-Vnukovo (modified live vaccine produced and used in the Slovak Republic) (Vnukovo-32 and Vnukovo 32/107) and SAG-2. (B695.24.w24, J3.139.w8)
  • Baits which have been used in European vaccination campaigns include chicken heads, Tubingen bait, Raboral, Rabifox Oral, Rabifox Dessau, Wusterhausen, Lysvulpen, GNK Moscow and (experimental use) Tallow-SFE baits. (B695.24.w24)
  • Re-emergence may occur if vaccination campaigns are stopped or reduced too early, and following reintroduction of the disease across borders. (B695.24.w24)
  • EU guidelines indicate that following any re-emergence of rabies, vaccine baits should be distributed over an area of 20-50 km wide, at a rate of 18-20 baits per km in areas of low fox density and 20-30 baits per km in areas of high fox density. (B684.6.w6)

Vaccination campaigns have been most successful where: (J3.139.w8)

  • Vaccines have been distributed over large, coherent areas (10-15000 km2 or larger) simultaneously;
  • Aerial and manual distribution of baits has been used to include all areas of fox habitat within the treated area;
  • Vaccination zones have been progressively expanded towards the remaining infected area;
  • Bait densities were maintained at at least 13-18 per km2;
  • At least two vaccination campaigns were carried out annually (sometimes three have been deemed necessary);
  • Vaccination continued for at least two baiting campaigns following the last recorded case (and in conjunction with appropriate surveillance schemes);
  • Accurate surveillance schemes were used;
  • Quality assurance schemes were used.

(J3.139.w8)

Oral rabies vaccination (ORV) campaigns have been carried out in Europe as follows: (J68.368.w1)

  • Austria: ORV started 1986. There were 1,387 cases per year before the ORV started. Rabies was eliminated in 2006. Control (reduction below 90%) was achieved after 20 vaccination campaigns. By 2010 there had been 42 vaccination campaigns. The border with endemic areas was 1,822 km long. The area of the territory was 78,527 km and the campaigns covered 78, 626 km2 (whole territory covered). (J68.368.w1)
  • Belgium: ORV started 1986. There were 342 cases per year before the ORV started. Rabies was eliminated in 1999. Control was achieved after 14 campaigns and permanent control after 25 campaigns. By 2010 there had been 29 vaccination campaigns. The border with endemic areas was 471 km. The area of the territory was 28,582 km, the vaccinated area was 12,329 km2 and the campaigns covered 43% of the territory. (J68.368.w1)
    • From autumn 1989 to 1991, vaccination with 150,000 baits containing vaccinia-rabies-glycoprotein recombinant (VRG) vaccine were distributed over the whole of the area of Belgium where rabies occurred; this resulted in elimination of rabies from 80% of the initial infected area; after that time baiting was more restricted, targeted to particular areas along political borders, resulting in further decrease and no cases detected in 1993 despite improved surveillance. Confirmation of cases in 1994 along the border with France demonstrated the need for further, restricted, vaccination campaigns. (J238.46.w1)
  • Bulgaria: ORV started 2009. There were 58 cases per year at the start of the ORV and only six in 2010, by which time there had been four vaccination campaigns. The border with endemic areas was 1,022 km, the area of the territory was 105,510 km and the vaccinated area was 59,186 km; the campaigns covered 56% of the area. (J68.368.w1)
  • Croatia: ORV occurred in 1994 with manual distribution of baits (no data on vaccine or bait type). Later, fixed-wing aircraft were used for distribution of SAD-B19 in Tubingen baits and SAD P5/88 in Rabifox Dessau baits. (B695.24.w24)
  • Czech Republic: ORV started 1989. There were 1,712 cases per year before the ORV started. Rabies was eliminated in 2002. Rabies was controlled after 20 campaigns with permanent control after 24 campaigns; to 2010 there had been 42 campaigns. The border with endemic areas was 1,433 km, the territory was 73,644 km and the campaigns covered the whole area. (J68.368.w1)
  • Estonia: ORV started in 2005. There were 1,712 cases per year before ORV started. Rabies was eliminated in 2009; it was under control after seven campaigns and eliminated after 11 campaigns. The border with endemic areas was 480 km, the territory was 43,693 km and the campaigns covered 41,767 km (96%). (J68.368.w1)
  • Finland: SAD-B19 in Tubingen baits used 1988-1999, initially with manual distribution (1988-1989) then with distribution using fixed-wing aircraft. Since eradication, baits distributed every autumn over 250 km along the border with Russia, to 20-20 km deep from the border, as well as compulsory vaccination of dogs used for hunting or showing. (B695.4.w4, B695.24.w24)
  • France: ORV started in 1986. There were 2465 cases per year before the ORV started. Rabies was eliminated in 1998. It was under control after 17 campaigns and eliminated after 25 campaigns. The border with endemic areas was 1,008 km, the area of the territory was 514,550 km and the campaigns covered 147,484 km2 (29% of the territory). (Rabies-free status was lost in 2008 after importation of a dog resulted in limited secondary transmission; this was controlled and rabies-free status was accepted again starting in 2010. (J68.368.w1)
  • Germany: ORV started in 1983. There were 10848 cases per year before ORV started. Rabies was eliminated in 2006; it was controlled after 32 campaigns and was eliminated after 62 campaigns. The border with endemic areas was 1,495 km, the area of the territory was 333,440 km and the campaigns covered 293,290 km2, 88% of the territory. (J68.368.w1)
  • Hungary: ORV started in 1992. There were 892 cases per year before ORV started. In 2010 there were 11 cases. Rabies was under control after 27 campaigns; to 2010 there were 37 campaigns. The border with endemic areas was 1,495 km, the area of the territory was 87,225 km and the campaigns covered the whole territory. (J68.368.w1)
  • Italy:
    • ORV started in 1984. There were 354 cases per year before ORV started. Rabies was eliminated in 1986 after three campaigns; the length of the border with endemic areas was 591 km and 33,776 of the 285,802 km (12%) territory was covered by the campaigns. (J68.368.w1)
    • ORV restarted in 1993; there were 82 cases per year before it started. Rabies was brought under control and eliminated after six campaigns, by 1995. The campaigns covered 4,544 km2 (0.02% of the territory. (J68.368.w1)
    • ORV restarted in 2009. There were 68 cases per year before ORV started. To 2010 there were four vaccination campaigns  over 11% of the territory; there were 209 cases in 2010. (J68.368.w1)
      • This outbreak started in north-east Italy near the border with Slovenia in 2008, then spreading westwards. Testing showed that 77% of foxes sampled after the December 2009-January 2010 vaccination campaign had developed antibodies with titres of at least 0.5 IU/mL (considered protective). Also, there was a clear distinction following the campaign (but not prior to it) in the altitude at which rabies-positive foxes were found - greater numbers at altitudes above the vaccination limit, after the campaign, compared to lower altitude areas in which vaccination had been carried out. [2010](J486.15.w3)
        • Compulsory vaccination of dogs and of domestic herbivores (cattle, sheep, goats, equids) kept outdoors in the affected area and therefore at risk of infection was also part of the control. [2010](J486.15.w3)
      • Initially, ORV using aerial distribution was carried out only below 1,000 m altitude (freezing point altitude) in December-January 2010 and 1,500 m in April-May 2010 to avoid repeated freeze-thaw cycles on the baits. However, spatial analysis indicated rabies hotspots at higher altitudes therefore the May 02010 campaign was extended up to 2,300 m. [2012](J19.140.w1)
  • Latvia:
    • ORV started in 1999; there were 169 cases per year before ORV started. The campaigns covered 60,978 of 64,635 km of territory (94%); there were 10 campaigns. (J68.368.w1)
    • ORV restarted in 2005; there were 421 cases per year before ORV started. There were 16 cases in 2010. Rabies was brought under control after 11 campaigns; there had been 11 campaigns to 2010. The campaigns covered 60,978 of 64635 km of territory (94%). (J68.368.w1)
  • Lithuania:
    • ORV started in 1995; there were 80 cases per year before ORV started. After 11 campaigns it had not yet been eliminated. The campaigns covered 60,927 km out of the total territory of 61,011 km2 (nearly 100%). (J68.368.w1)
    • ORV restarted in 2006; there were 2232 cases per year at this time and in 2010 there were only 33 cases. Rabies was brought under control after six campaigns; to 2010 there had been 10 campaigns. (J68.368.w1)
  • Luxembourg: ORV started in 1986; there were 137 cases per year before ORV started. Rabies was eliminated in 1999; it was under control after 23 vaccination campaigns and eliminated after 27 campaigns. There were 231 km of border with endemic areas. The whole of the 2419 km territory was covered by the campaigns. (J68.368.w1)
  • Netherlands: ORV using manually distributed Tubingen baits containing SAD-B19, 1988-1991. There were three cases per year on average before vaccination and none after 1988. (B695.24.w24)
  • Poland: ORV started in 1993. There were 2,634 cases per year before ORV started; in 2010 there were 151 cases. Rabies was brought under control after 24 vaccination campaigns; there were 36 campaigns to 2010. The border with endemic areas was 2,200 km and the whole of the 291,133 km territory was covered by the campaigns. (J68.368.w1)
  • Russia: (Kalinigrad Oblast): ORV started in 2007; there were 26 cases before ORV started and there were 43 cases in2010; there were four vaccination campaigns to 2010. The campaigns covered 12,703 km of the 15125 km area (84%) and there were 437 km of border with endemic areas. (J68.368.w1)
  • Slovakia: ORV started in 1993; there were 489 cases per year before ORV started and rabies was eliminated in 2006 after 28 campaigns. The whole of the 45,804 km territory was covered by the vaccination campaigns; there was 1,160 km of border with endemic areas. (J68.368.w1)
  • Slovenia: ORV started in 1989; there were 761 cases per year before ORV started and there were 12 cases in 2010. Rabies was considered under control after 13 campaigns and permanently under control after 37 campaigns; there had been 39 campaigns to 2010. 19047 of the 19167 km2 (99%) was covered by the vaccination campaigns and there was 815 km of border with endemic areas. (J68.368.w1)
  • Switzerland [and Lichtenstein]: ORV started in 1978; there were 1,054 cases per year before ORV started and rabies was eliminated in 1996. Rabies was under control after 19 vaccination campaigns, permanently under control after 35 campaigns and eliminated after 37 campaigns. 18,665 of the 38,875 km2 territory (48%) was covered by the vaccination campaigns. There was 889 km of border with endemic areas. (J68.368.w1)
  • Ukraine: ORV started in 2007; there were 2,929 cases per year before ORV started and 1,862 in 2010, by which time there had been six vaccination campaigns. Vaccination campaigns covered 413,046 of the 558,161 km (59%) territory and there were 1,926 km of border with endemic areas. (J68.368.w1)
  • Overall, more campaigns were required if a greater proportion of the territory was affected with rabies, while fewer campaigns were required to eliminate rabies when countries implemented consistently overlapping campaigns covering most of the rabies-affected area compared with those which did not take this approach. It was also evident that a disproportionately greater effort was required for the final phase of elimination compared to the effort required for initial reduction to less than 50% of the original level. (J68.368.w1)

(J68.368.w1)

In Procyon lotor - Common Raccoon
  • Oral vaccination programmes use Raboval V-RG vaccinia-rabies glycoprotein recombinant virus vaccine, 1.8 mL inside a plastic sachet which is placed inside an extruded fishmeal polymer bait. Tetracycline hydrochloride is present in the bait as a biomarker (deposited in bones and teeth). (J4.213.w4, J249.111.w2)
  • Raccoons have also been successfully immunised by intramuscular injection of an inactivated vaccine (1 mL of Imrab (Rhone-Merieux). (J1.26.w9)
  • Note: vaccination is not effective if the animal is already incubating rabies at the time it is inoculated. Additionally, vaccination may fail occasionally. (J1.43.w2)
Humans
  • Vaccination of humans pre-exposure is recommended for individuals in high-risk occupations such as veterinarians, wildlife biologists, animal control officers, animal handlers and laboratory workers involved in rabies diagnosis, research or vaccine production. (B58.1.w1, B209.1.w1)

    • Vaccination for individuals in high-risk occupations involves three doses of a rabies human diploid cell vaccine, given by deep subcutaneous or intramuscular injection into the deltoid region, on a schedule of injections on days 0, seven and 28. Note: injection into the gluteal region may result in a lower antibody response. (J342.95.w1)

    • For individuals travelling to rabies endemic areas, usually a course of two injections is given, two to four weeks apart by deep intramuscular injection, which should be adequate if post-exposure treatment is expected to be readily available. However, a further dose after six to 12 months is recommended for continued potential exposure. (J342.95.w1)

    • Preexposure vaccination may also be advisable for spelunkers exploring caves with large bat colonies and individuals likely to spend extended periods (30 days or more) in direct contact with mammals in rabies endemic regions where medical care may not be readily available. (B209.1.w1)

CLICK THE LINKS FOR Literature Reports
  • --
  • --
Prophylactic Treatment
Animals
  • Vaccinated animals which have been possibly exposed (e.g. bitten by a suspected rabid animal) should be given a booster vaccination immediately. (B47, B23.20.w15, B336.76.w76)
    • Following re-vaccination, the animal should be observed carefully for any signs of illness which may indicate rabies, for at least 90 days. (B23.20.w15, , B336.76.w76)
    • If e.g. a zoo animal has been previously vaccinated but its vaccinations are out of date, decisions on appropriate actions (re-vaccination and quarantine, quarantine, or euthanasia) must be made on a case basis. (B23.20.w15)
  • Post-exposure prophylaxis of naive, unvaccinated animals which have been bitten or scratched either by an animal known to be rabid, or by a wild carnivore or bat which is not available for rabies testing, is not normally practiced. (B23.20.w15)
Humans

Treatment for rabies after suspected exposure is a combination of prophylactic measures:

Treatment of the wound: 

  • The wound from a bite from a suspected rabid animal should be immediately flushed and cleaned thoroughly using soap and water followed by application to the wound of either ethanol or a quaternary ammonium compound. (B47)
  • Immediate washing of a bite wound and flushing with soap and water, detergent or water alone is recommended. (B47, B58.1.w1, J63.5.w1)
  • All bites and scratches should be immediately washed with soap and water, and irrigated with povidone-iodine solution or another virucidal solution. (N7.48.w4)
  • For deep punctures, a catheter should be placed to flush the wound periodically. (B47)
  • The wound should not be sutured. (B47)

Administration of (human origin) rabies immune globulin:

  • For individuals without prior vaccination:
    • Post-exposure prophylactic treatment with human-origin rabies immune globulin is used in humans bitten by a suspected rabid animal (B47, B58.1.w1).
    • Administration of rabies immune globulin is considered to be the best postexposure prophylactic treatment for individuals without prior vaccination. (B47)
    • Rabies immune globulin should be locally infiltrated into and around the wound site. (B47, J63.5.w1)
    • Up to half of a total dose of 20 IU/kg bodyweight is given in and around the wound, with the remained given intramuscularly. (J342.95.w1)
    • N.B. Individuals who have been vaccinated prior to being exposed should not be given immune globulin due to possible interference with the anamnestic response to human diploid cell rabies vaccine. (B47)
    • Additionally, following administration of immune globulin, a rabies human diploid cell vaccine is given (see below). (J342.95.w1)

Vaccination:

  • Individuals who have not previously been vaccinated are given vaccine on days 0, 3, 7, 14 and 30 after exposure, the first dose being given after administration of immune globulin. (B47, J342.95.w1)
  • Individuals who have already been vaccinated and have adequate antibody titres are re-vaccinated, once on day 0 and once again at some point between day 3 and day 7, by deep intramuscular injection into the deltoid region or, for children, on the anterolateral thigh. (B47, (J342.95.w1))
    • This is essential even for individuals with high antibody titres. (B47)
    • Individuals who have been vaccinated previously but have low or negative titres should be treated as if they have not been vaccinated.
CLICK THE LINKS FOR Literature Reports
  • --
CLICK THE LINKS FOR OVERVIEWS of management techniques available

Return to top of page

Environmental and Population Control Measures

General Environment Changes, Cleaning and Disinfection Environmental disinfection is not a major part of rabies control. However, this virus is easily inactivated by a wide range of detergents and disinfectants. (B47, B209.1.w1, B336.76.w76, B352.2.w2, J15.23.w3)
CLICK THE LINKS FOR Literature Reports
  • --
  • --
CLICK THE LINKS FOR Technique Descriptions, if available
 
Population Control Measures
  • Reduction in population density of wild animal populations, below a threshold necessary for maintenance of the disease in the population, by a variety of lethal methods such as hunting, poisoning or den gassing, has been used to control rabies, particularly when outbreaks have occurred in certain populations. (B58.1.w1, B209.1.w1, B360.26.w26)
  • While there have been some successes at rabies control by population reduction, other programmes have been unsuccessful in reducing the population density sufficiently to stop disease transmission. (B209.1.w1, B360.26.w26) 
    • "Control efforts based on reservoir host species depopulation are not ecologically or morally sound and are ineffective." (B336.76.w76)
    • Attempted eradication of a wildlife host species "is impractical, expensive, and has ecological consequences, which are usually difficult to predict reliably." (B209.1.w1)
    • Population reduction generally results in increased reproduction. (B360.26.w26)
    • In Europe, only two outbreaks appear to have been completely eradicated by fox population reduction (Dijon in 1923, Corsica in 1943). (B360.26.w26)
In Europe
  • Elimination of stray dogs as well as of suspect dogs was important in the elimination of dog rabies (which is still present in Turkey). (B684.6.w6)
  • Note: reduction efforts on fox populations (increased hunting, gassing/poisoning, shooting) of Vulpes vulpes - Red fox was ineffective at controlling rabies in Europe, even when in some cases more than 30% of the population was removed annually. Claims have been made that culling was effective in limited areas. (B684.6.w6)
    • Computer models suggest that fox densities would need to be reduced to below 0.2-1.0 per km2 for this to be effective, and high survival of remaining foxes at such low densities would make maintenance of such low populations problematic. (B684.6.w6)
  • Use of immunocontraceptive agents alongside vaccines might be useful in control. (B684.6.w6)
Literature Reports
  • --
Technique Descriptions, if available
--
Isolation and Quarantine Isolation:
  • If an unvaccinated dog, cat or ferret has been exposed to a rabid animal (or to a wild carnivore or bat which is not available for testing, and the owner is not willing for it to be euthanased, the animal should be placed in strict isolation for six months. (N7.54.w1)
  • A zoo mammal which has not been vaccinated and which has been bitten or scratched either by an animal known to be rabid, or by a wild carnivore or bat which is not available for rabies testing may have its wound treated, then be placed in strict isolation for six months, with careful monitoring for any signs of illness which may indicate rabies. (B23.20.w15)

Quarantine:

  • Strict quarantine regulations are effective in preventing introduction of rabies. (B47)
  • In the USA, it is recommended that wild-caught animals which are susceptible to rabies should be quarantined for at least six months before being placed on exhibit in zoos. (N7.54.w1)
  • "Because of the risk of rabies in wild animals (especially raccoons, skunks, coyotes, foxes, and bats), AVMA, NASPHV and CSTE strongly recommend the enactment and enforcement of state laws prohibiting their importation, distribution, and relocation. (N7.54.w1)
  • Quarantine, registration of dogs, laws regarding use of muzzles and official notification of cases were all important in eliminating dog rabies across most of Europe (still present in Turkey). (B684.6.w6)
CLICK THE LINKS FOR Literature Reports
  • --
CLICK THE LINKS FOR Technique Descriptions, if available
CLICK THE LINKS FOR OVERVIEWS of management techniques available
  • --

Return to top of page

Authors & Referees

Authors Debra Bourne MA VetMB PhD MRCVS (V.w5)
Referee Suzanne I. Boardman (V.w6);  Dr Robert G. McLean (V.w42), Rick Rossatte (V.w95), Dr Claude T Sabeta PhD (V.w167)

To Top of Page