< >  Literature Reports of MORTALITY RATE for Rabies (with special reference to Raccoons):

Mortality Rate (Percentage of the Species Population that die)

General

• 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).

General

• The outcome of exposure of an individual to rabies virus may be affected by: (B395.2.w2)
  • Virus strain; (B395.2.w2)
  • Dose of virus; (B395.2.w2)
  • Route and site of exposure (intramuscular inoculation, site of such inoculation, inhalation of virus in an aerosol, ingestion of infected material); (B395.2.w2)
    • Inoculation into tissues of the head and neck appears to not only cause disease after a shorter period than does inoculation into the hind leg, but also to be more likely to result in disease. (B395.2.w2)
  • Animal species; (B395.2.w2)
  • Intraspecific differences. (B395.2.w2)
• There is a very high fatality rate in individuals showing clinical signs. (B47)
  • Reports of survival of e.g. individual dogs after development of clinical signs of rabies is extremely rare, such that basically rabies is considered invariably fatal after the onset of clinical signs. (J63.5.w1)
  • A proportion of infected animals do not develop clinical disease but merely seroconvert. (B47)
  • Human mortality after development of clinical signs is effectively 100%; there are three documented cases of individuals surviving clinical rabies. (B47)
    • In 2004, a 15-year-old girl in the USA survived clinical rabies; this was the first confirmed survivor in a human who had never received any vaccination or any PEP prior to onset of clinical illness. (N7.53.w2)
  • In one incident in sheep, 17 of 22 animals bitten by a rabid carnivore died. (B362.w8)
• Not all animals die after natural (or artificial) exposure to rabies virus. (B395.2.w2)
  • Asymptomatic seroconversion can occur. (B336.76.w76)
  • Animals of various species in rabies endemic areas, including dogs, skunks, raccoons, mongooses and vampire bats, have been found healthy and with neutralising antibodies, indicating abortive infection (infection without the development of fatal encephalitis). (B47)
  • In one experiment with 47 dogs inoculated with rabies virus, 39 died, while eight dogs remained healthy for more than two years, did not develop detectable neutralising antibodies, but were resistant to challenge with high dose rabies and developed high antibody titres after the challenge. (J13.45.w1)
  • Opossums (Didelphis virginiana - Virginian opossum) appear to be only rarely infected with rabies. (B420.XII.w12)
    • Experimental infection with a fox rabies virus produced rabies in only one of three opossums inoculated intracerebrally and none of 18 animals inoculated intramuscularly at 16,000 MICLD₅₀. (P21.64.w1)
    • Experimental infection of 34 opossums with three different rabies virus strains at high doses and by various routes (including intramuscular, intracerebral and others) resulted in signs of CNS disease in only four individuals, and from only one animal was a transmissible agent lethal for mice recovered. (J13.21.w1)
  • Birds experimentally infected with rabies usually show few or no signs of infection, and recover. (J1.24.w7)
  • Elephas maximus - Asian Elephant: All known rabid elephants have died. (J3.144.w2, J12.9.w1, J12.61.w1, B212.w41)
  • In the single reported case of natural rabies in a Pan troglodytes - Chimpanzee, the individual died. (J4.162.w2)

For Procyon lotor - Common Raccoon

• Raccoons appear to have "intermediate" susceptibility to rabies: much more resistant than foxes, and more resistant than skunks, but much less resistant than opossums (Didelphis virginiana - Virginian opossum). (D222.5.w5, B395.2.w2)
• Raccoons may acquire subclinical, immunising infection (J63.5.w1)

Mortality of raccoons due to raccoon rabies variant

"The rabies virus variant associated with raccoons appears to be highly adapted to this species and distinguishable from other viral variants isolated from terrestrial carnivores serving as reservoirs." (J279.1.w2)

• Further information on the existence and identification of the raccoon-associated rabies variant is provided in:
  • Surveillance for Rabies in Raccoons - Rabies Virus Isolates
  • Rhabdoviridae- Rabies virus (Viral Species) - Viral Type Diversity

• Survival of infected raccoons is indicated by high (20-30%) prevalence of seropositive individuals in raccoon populations which have experienced a rabies epizootic, and by persistence of antibody in individual raccoons and the population. (J101.98.w1)
• It has been estimated that about 20% of raccoons in the endemic area of Pennsylvania develop immunity when exposed to rabies virus. (J13.50.w1)

• In raccoons inoculated with a rabies strain isolated from the salivary gland of a raccoon in Florida in 1961, eight of 15 animals died of rabies, including two of three inoculated with 11,000 mouse lethal dose 50% (MICLD₅₀), 2/3 inoculated with 9,000 MICLD₅₀, 1/3 inoculated with 7,000 MICLD₅₀, 0/3 inoculated with 5,000 MICLD₅₀ and 3/3 inoculated with 3,000 MICLD₅₀. (B358.4.w4)
• In raccoons experimentally inoculated intramuscularly with a suspension from the salivary gland of a naturally infected raccoon from Pennsylvania, at 10^4.2 MICLD₅₀, six of ten raccoons died. (B360.16.w16)
• A study comparing survival of raccoons with and without oral vaccination determined that 100% of raccoons were susceptible to a dose of 10^4.9 MICLD₅₀ of a pool of saliva from naturally infected raccoons (original titre 10^6.2 MICLD₅₀/mL) injected into the masseter muscle (0.5 ml of a 1:10 dilution in 2% horse serum). (J1.38.w2)
• One of eleven control raccoons, all of which were negative for rabies virus neutralising antibodies, survived intramuscular inoculation of 0.5 mL street rabies virus (from a naturally infected raccoon from Pennsylvania, virus titre 10^4.5 MICLD₅₀ per ml) into the masseter muscle. (J62.60.w1)
• One of four control colony-bred raccoons, which lacked any antibodies to rabies virus, survived challenge with a known lethal dose (>5 LD₅₀) of street rabies virus isolated from a raccoon from Virginia. (J20.165.w1)

Effect on the population

• In Florida, the raccoon population on Long Boat Key "declined drastically" during the raccoon rabies epidemic there. (B358.4.w4)
• In Baltimore, Maryland, a study was conducted of road-killed and live-trapped raccoons before, during and after a rabies epizootic moved through the city. Road-kill data indicated that the population did not change from 1984 to 1985 but declined in 1986 and 1987 (road kill data for other species remained static); it was suggested that the rabies epizootic, in conjunction with increased city and private individual control of raccoons, contributed to a decline in the Baltimore raccoon population. (J1.26.w5)
  • The first case was detected March 1985, with peaks in January and March 1986, and ending in May 1987; 0/49 raccoons tested in 1984 were rabies-positive, 27/202 in 1985 (13% positive), 63/152 in 1986 (41%) and 5/35 in 1987 (14%). It was noted that from mid-1985 only raccoons which were either suspected of being rabid or were involved in potential exposures of humans or domestic animals were tested for rabies. The centre of rabies activity shifted slightly from west to east during 1985 to 1987. The study showed that raccoons were associated with single-unit residential areas (i.e. detached houses) mainly on the north and west perimeters of the city; higher than expected trapped and road-killed numbers were found in these areas, probably due to high human-raccoon overlap. Smaller numbers from multi-unit residential areas (townhouse areas) probably indicated lower utilization of such areas by raccoons. It was noted that, except for near streams or open areas, multi-unit, inner city residential areas provided few raccoons while the major habitat for raccoons in Baltimore is probably combinations of single-unit housing or multi-unit housing adjacent to parklands or cemeteries and close to streams, with areas of commerce and industry providing poor habitat.  Annual trapping results were 349, 411, 293 and 97 for 1984, 1985, 1986 and 1987; the number in 1987 was significantly lower than the number in 1984-1986; the increase in trapping effort (traps used by 92, 98, 189 and 156 households in the four years and lower captures per household (3.8, 4.2, 1.5 and 0.6 over the four years, also suggest a decline in the population. Peak captures occurred in July to September in most years and peak numbers removed dead or injured from streets occurred in July to October. (J1.26.w5)
• In Centre County, Pennsylvania, in an area enzootic for raccoon rabies, a comparison of survival rates of radiotagged adult raccoons from 23 August 1987 to 26 March 1988, including times before, during and after the harvest season, did not find any differences in survival rates between raccoons which had been vaccinated (intramuscular injection of 1.0 ml inactivated rabies virus vaccine (Rabguard-TC, Norden Laboratories, Lincoln, Nebraska, USA) and those which had not been vaccinated. No deaths from rabies were diagnosed in the study populations during the period of the study and it was not known whether rabies was not present, present but not detected, or present but natural immunity or vaccine-induced immunity was providing protection. (J1.26.w10)
• In Washington D.C. as a whole, prevalence data indicated peaks in rabies in 1983 (initial epizootic) and in late 1986/1987 and late 1991/1992. In a study in an urban national park in Washington, D.C., in which there was a very high raccoon density, there was evidence of decreased raccoon density during and after the 1987 rabies resurgence, compared to density in 1984 to 1985 during a period of low rabies prevalence. Also, survival of juvenile raccoons was lower during the nine-month period of the original epizootic, compared with either the following nine months (z = 1.73, one sided p< 0.05) or the same period in 1989 to 1990 (z=3.01, one-sided p<0.005); survival of adults was not demonstrated to be significantly reduced in this population during the initial epizootic, possibly at least in part due to the efficacy of the immunisation programme (all raccoons captured May 1983 to October 1984, and afterwards all radio-collared raccoons, were immunized experimentally with a killed vaccine (IMRAB, Mieureux Laboratories, Paris, France). (J30.76.w1)
• At the National Zoological Park's Conservation and Research Center (CRC) in Front Royal, Virginia, between April 1980 and June 1981, 35 of 145 marked raccoons died/were found dead (24%). Of these, 29 were too decomposed for any diagnosis; the others were proven to have died from rabies. The relatively high mortality combined with diagnoses of rabid raccoons "suggests that the die-off was due to the epizootic of rabies." During July to September, four of 90 were found dead, with one proven rabid. (P103.1983.w1)
• On Wolfe Island, Ontario, Canada, population density decreased by 71% during a rabies outbreak: from 1,067 raccoons (mean 8.4/kmē) prior to the outbreak to 305 (mean 2.4/kmē) following the outbreak. In parts of the island in which rabies was detected, mortality was 78%. This compared to 50% normal annual mortality for Ontario raccoons in rabies-free areas, suggesting "that rabies had an additive mortality effect on the population." (J1.43.w1)
• Reductions in occurrence of rabid raccoons at the end of an epizootic in a given area are probably due to high mortality rates from rabies. (J91.57.w1, J135.97.w3)

Mortality of raccoons due to other rabies variants

• Raccoons are much more resistant to rabies than are foxes. During a regional epizootic of fox rabies along the Georgia-Florida border (prior to raccoon rabies reaching this area) serum neutralising antibodies were present in about 8.5% of raccoons compared with in only 4.6% of gray foxes. (B358.4.w4)

Experimental data:

• A study using a strain of rabies from a fox salivary gland, isolated in Alabama, found that raccoons were about 1,000-fold more resistant to this isolate than were foxes and about 10-fold more resistant than Mephitis mephitis - Striped skunk. (B358.4.w4)
  • Intramuscular inoculation with fox salivary gland suspension from an Alabama rabid fox caused the deaths of 0/3 raccoons inoculated with 10^0.2 MLD₅₀, 0/3 raccoons inoculated with 10^1.2 MLD₅₀, 2/4 raccoons inoculated with 10^2.2 MLD₅₀, 4/7 raccoons inoculated with 10^3.2 MLD₅₀, and 5/7 raccoons inoculated with 10^5.2 MLD₅₀. (B360.16.w16, P21.64.w1)
• A study comparing survival of raccoons with and without oral vaccination found that a total of 2/17 (12%) of control unvaccinated raccoons survived when injected intramuscularly with 0.3 ml of 1 x 10^5.6 MICLD₅₀/mL street rabies (MD5951 strain, originally isolated from a dog). Raccoons which died following infection were all negative for virus in salivary glands. Raccoons (unvaccinated or vaccinated) succumbed within 11 to 41 days. It was noted that survivorship of vaccinated raccoons did not always correlate with virus neutralising antibody titre: some orally vaccinated raccoons in the third trial with a high virus neutralisation titre succumbed while others without a detectable serological response survived. (J1.25.w4)
• All five non-vaccinated raccoons injected intramuscularly with 0.5 ml of 1 x 10^5.5 MICLD₅₀/mL street rabies (MD5951 strain, originally isolated from a dog) died within 10 to 26 days of inoculation. (J1.26.w8)
• A study (unpublished) found 10^1.8 MICLD₅₀ of a New York City/Georgia (NYC/GA) canine rabies strain from fox salivary glands to be a raccoon lethal dose. (J1.28.w8)
• Raccoons inoculated into the masseter muscle with 10^2.4, 10^3.4 or 10^4.8 MICLD₅₀ of skunk rabies virus isolated from a naturally-infected Mephitis mephitis - Striped skunk all survived an observation period of 92 days. Two of three individuals which had received the highest dose developed serum neutralising antibodies. It was noted that the raccoons had survived doses higher than those required to kill skunks or foxes. (J1.28.w8)
• Raccoons which had survived inoculation into the masseter muscle of 10^4.8 MICLD₅₀ of skunk rabies virus isolated from a naturally-infected Mephitis mephitis - Striped skunk and developed serum neutralising antibodies subsequently survived inoculation with 10^3.2 MICLD₅₀ New York City/Georgia canine strain rabies virus (NYC/GA) from fox salivary glands, whereas raccoons which had not developed serum neutralising antibodies when inoculated with skunk rabies did not survive. (J1.28.w8)
• Two raccoons inoculated into the masseter muscle with 10^5.9 mouse intracerebral lethal dose₅₀ (MICLD₅₀) of skunk rabies virus isolated from a naturally-infected Mephitis mephitis - Striped skunk from Iowa, USA, both survived an observation period of 273 days with no adverse effects. No virus was isolated from saliva samples taken at 25 to 273 days after inoculation. In contrast all five skunks inoculated with 10^0.7 or 10^2.1 MICLD₅₀ died within 35 days of inoculation. One of the raccoons developed a virus neutralising antibody titre of 5.7 days by 25 days after inoculation; this had declined to a titre of less than 5.0 by day 57. (J1.29.w10)
• Five raccoons experimentally inoculated in the masseter muscle with a canine rabies virus isolate (MD 5951, at 0.3 ml of culture with 10^6.9 MICLD₅₀ per mL), all succumbed or required euthanasia within 17 days. (J212.8.w1)
• When raccoons were inoculated by intramuscular injection into the masseter muscle with either 2,500 or 15,000 mouse lethal dose 50 (MLD50) of saliva from a coyote infected with bat rabies from Mexican free-tailed bats Tadrida brasiliensis mexicana) (the coyote had been infected by inoculation with saliva from a coyote which had been infected by a non-bite route following exposure to a cave of the bats), the raccoon inoculated with the lower dose seroconverted (tested at 104 days) while the raccoon inoculated with the higher dose developed furious rabies after 29 days. No virus was found in the salivary glands of either raccoon, but virus was found in the brain of the raccoon which had developed rabies. (J13.27.w3)
• When raccoons were inoculated by intramuscular injection into the masseter muscle with either 832 or 4,000 mouse lethal dose 50 (MLD50) of saliva from rabid Mexican free-tailed bats Tadrida brasiliensis mexicana, the raccoon inoculated with the higher dose developed furious rabies after 15 days and showed clinical signs for 22 hours prior to death. No virus was found in the salivary glands of either raccoon, but virus was found in the brain of the raccoon which had developed rabies. (J13.27.w4)
• Raccoons (along with various other species) did not develop rabies, although one raccoon appeared to seroconvert, after being bitten by red bats Lasiurus borealis infected with red bat rabies. No intramuscular inoculation experiment was carried out in the raccoons. (J13.27.w5)