Canine distemper is a highly contagious, systemic, viral disease of dogs seen worldwide. Distemper is sometimes confused with other systemic infections
such as leptospirosis, infectious canine hepatitis, or Rocky Mountain spotted fever (Deem et al 2000). Toxins such as lead or organo-phosphate pesticides
can cause similar gastrointestinal or neurologic pathological conditions. Distemper infected animals have a diphasic fever, leukopenia, GI and respiratory
mucous membrane inflammation with excessive secretions, and often have pneumonic and neurologic complications. Neurologic signs due to distemper virus
infection in raccoons are similar to those from rabies. A transient fever usually occurs 3-6 days after infection, and anorexia may develop. This fever stops
for several days before a second fever starts, lasting less a week. Fever may be accompanied by nasal discharge, eye discharge, and anorexia. GI and
respiratory signs may follow and usually include secondary bacterial infections. Hyperkeratosis of the footpads (“hardpad” disease) and nose are common.
Dogs with hyperkeratosis often have neurologic signs. Central nervous system signs include: 1) involuntary twitching leg muscles or facial muscles; 2)
impaired movement or paralysis, in the hind-limbs, followed by paresis and paralysis of all legs; 3) jaw convulsions with chewing movements and salivation
(“chewing-gum fits”) and acute encephalomyelitis. Later seizures become more frequent and severe, and the animal may fall on its side and paddle its legs;
with involuntary urination and defecation. The systemic disease may be as short as 10 days, but the onset of neurologic signs may be delayed for several
weeks or months (Deem et al 2000).
Diagnosis is based upon histopathologic lesions in brain, lung, spleen, and small intestine. Intranuclear and intra-cytoplasmic inclusion bodies are found in
many cells including epithelial cells in the respiratory tract, gastric lining, and the epithelium lining the renal pelvis and urinary bladder. The best tissues for
fluorescent antibody testing and virus isolation of canine distemper virus are lung, brain, stomach, small intestine, kidney, and urinary bladder.
1.1.2 Infectious Agent
Canine distemper is caused by a paramyxovirus closely related to the viruses of measles and rinderpest. The canine distemper virus is a relatively large
(150– 250 nm) single-stranded RNA virus with a lipoprotein envelope, is a morbillivirus in the family Paramyxoviridae (Greene, and Appel. 1990, Swango, L. J.
1995). The enveloped virus is sensitive to lipid solvents and most disinfectants and has limited survivability outside the host animal.
Canine distemper occurs worldwide in domestic, captive and free-ranging carnivores. There is a low risk of canine distemper infecting humans.
Transmission more likely to occur from domestic dogs than from wild carnivores, but people should avoid contact with infected wild animals.
Canine distemper virus infection has been reported in all families of terrestrial carnivores: Canidae (dogs, foxes, wolves), Felidae (domestic cats, African lion,
tiger, leopard, and jaguar), Hyaenidae (captive and free-ranging hyenas), Mustelidae (eg, ferret, mink, skunk), most Procyonidae (eg, raccoon, coatimundi),
Ursidae (Alaska and Russia- polar, Alaska- grizzly, Italy- Marsican brown bears, Florida black bears), and some Viveridae (binturong - Asian Bearcat) (
Gaskin. 1974, Appel, et al. 1994, Blythe, et al. 1983, Cook and Wilcox. 1981, Fix, et. 1989, Gould and Fenner 1983, Piat, B. L. 1950, Truyen et al 1990) O’
Brien, Nash, Wildt, Bush, and Benveniste. 1985, Swango, 1995, Wozencraft, 1993).
1.1.5 Mode of Transmission
The major route of CDV transmission is through aerosol droplet spread of respiratory secretions containing virus. Other body excretions and secretions (e.g.,
urine) can result in infection in susceptible
hosts when aerosolized. Canine distemper is highly contagious, and viral shedding may follow infection
for 60–90 days after infection (Greene and Appel. 1990). Some infected dogs may shed virus for several months. Mother to fetus (transplacental) infection
has been reported in domestic dogs (Krakowka, et al. 1977). The epidemiologic significance in mother to fetus transmission of CD and whether this
transmission can occur in other species are unknown. Usually canine distemper does not survive long in the environment but the virus can survive at lower
temperatures (e.g., 48 hr at 25oC and 14 days at 5oC) and may be transmitted either by direct contact or through inanimate objects (Shen, and Gorham
Distemper virus initially replicates in the lymphatic tissue of the respiratory tract. A cell-associated viremia results in infection of all lymphatic tissues, which is
followed by infection of respiratory, the gastrointestinal and urogenital epithelium, the central nervous system and optic nerves. Disease occurs after the virus
replicates in these tissues. The degree of viremia and extent of spread of virus to various tissues is moderated by the level of specific humoral immunity in
the host during the viremic period.
1.1.6 Incubation period
In dogs, a 14 to 18 day incubation period is reported (Greene and Appel. 1990). An initial transient fever and leukopenia are reported to occur 4 to 7 days
1.1.7 Period of communicability
Canine distemper virus may be shed for 60–90 days (Greene and Appel. 1990). Some infected dogs have shed canine distemper virus for several months.
Canine distemper virus can pass from the mother to the fetus via the placenta in domestic dogs (Krakowka, et al. 1977). Canine distemper is short-lived in
the environment but may be transmitted by direct contact or from inanimate objects, since the virus can survive lower temperatures (e.g., 48 hr at 25oC and
14 days at 5oC) (Shen, and Gorham 1980).
All domestic, captive and free-ranging carnivores may have varying levels of susceptibility.
1.1.9 References Canine Distemper
Appel, M. J. G., and R. J. Montali. 1994. Canine distemper and emerging morbillivirus diseases in exotic species. Proc. Am. Assoc. Zoo Vet. 1994: 336–339.
Appel, M. J. G., Yates R. A., Foley G. L., Bernstein J. J., Santinelli S, Spelman L. H, Miller L. D,. Arp L. H, Anderson M, Barr M, Pearce-Kelling S, and
Summers B. A. 1994. Canine distemper epizootic in lions, tigers, and leopards in North America. J. Vet. Diagn. Invest. 6: 277–288.
Blythe, L. L., Schmitz J. A, Roelke M, and Skinner, S. 1983. Chronic encephalomyelitis caused by canine distemper virus in a Bengal tiger. J. Am. Vet. Med.
Assoc. 183: 1159–1162.
Budd, J. 1981. Distemper. In: Davis, J. W., L. H. Karstad, and D. O. Trainer (eds.). Infectious Diseases of Wild Mammals. Iowa State University Press, Ames,
Iowa. Pp. 31–44.
Cook, R. D., and Wilcox G. E, 1981. A paramyxovirus- like agent associated with demyelinating lesions in the CNS of cats. J. Neuropathol. Exp. Neurol. 40: 328
Deem SL, Spelman LH, Yates RA, Montali RJ. (2000). Canine Distemper in Terrestrial Carnivores: a Review. J Zoo Wildl Med. 2000 Dec;31(4):441-51. Field
Veterinary Program, Wildlife Conservation Society, Bronx, New York 10460, USA.
Durchfeld, B., W. Baumgartner, W. Herbst, and R. Brahm. 1990. Vaccine-associated canine distemper infection in a litter of African hunting dogs (Lycaon
pictus). J. Med., Series B37: 203–212.
Fix, A. S., D. P. Riordan, H. T. Hill, M. A. Gill, and M. B. Evans. 1989. Feline panleukopenia virus and subsequent canine distemper virus infection in two snow
leopards (Panthera uncia). J. Zoo Wildl. Med. 20: 273– 281.
Gaskin, M.. 1974. Canine distemper virus in domesticated cats and pigs. Am. J. Vet. Res. 35: 803–806.
Giesel, O. 1979. Distemper in otters. Berl. Muench. Tieraerztl. Wochenschr. 92: 304. (In German.)
Gould, D. H., and Fenner W. R. 1983. Paramyxovirus- like nucleocapsids associated with encephalitis in a captive Siberian tiger. J. Am. Vet. Med. Assoc. 183:
Greene, G. E., and Appel M. J. 1990. Canine distemper. In: Greene, C. E. (ed.). Infectious Diseases of the Dog and Cat. W. B. Saunders, Philadelphia,
Pennsylvania. Pp. 226–241.
Haas, L., H. Hofer, M. East, P. Wohlsein, B. Liess, and T. Barrett. 1996. Canine distemper virus infection in Serengeti spotted hyaenas. Vet. Microbiol. 49:
Krakowka, S., Hoover E. A., Koestner A., and Ketring, K. 1977. Experimental and naturally occurring transplacental transmission of canine distemper virus.
Am. J. Vet. Res. 38: 919–922.
Mainka, S. A., Xianmeng Q., Tingmel, H, and Appel M.J. 1994. Serologic survey of giant pandas (Ailuropoda melanoleuca), and domestic dogs and cats in the
Wolong Reserve, China. J. Wildl. Dis. 30: 86–89.
Montali, R. J., Bartz G. R, and Bush M. 1987. Canine distemper virus. In: Appel, M. J. (ed.). Virus Infections of Carnivores. Elsevier Science Publishers,
Amsterdam, The Netherlands. Pp. 347–443.
Munson, L., M. Appel J. G, Carpenter M. A, O’Brien S. J, and Roelke-Parker M. 1995. Canine distemper in wild felids. Proc. Am. Assoc. Zoo Vet./Wildl. Dis.
Assoc./ Am. Assoc. Wildl. Vet. 1995: 135–136.
Nowak, R. M. 1991. Order Carnivora. In: R. M. Nowak (ed.). Walker’s Mammals of the World, 5th ed., vol. 2. The Johns Hopkins University Press, Baltimore,
Maryland. Pp. 1045–1219.
O’Brien, S. J., Nash W. G, Wildt D. E, Bush M. E, and Benveniste R. E. 1985. A molecular solution to the riddle of the giant panda’s phylogeny. Nature 317:
Piat, B. L. 1950. Susceptibility of young lions to distemper. Bull. Serv. Elev. Indust. Anim. Afrig. Occid. Fr. 3: 39–40.
Qui, X., and Mainka S. 1993. Review of mortality of the giant panda (Ailuropoda melanoleuca). J. Zoo Wildl. Med. 24: 425–429.
Shen, D. T., and Gorham J. R. 1980. Survival of pathogenic virus at 58C and 258C. Vet. Med. Small Anim. Clin. 75: 69–70.
Swango, L. J. 1995. Canine viral diseases. In: Ettinger, S. J., and E. C. Feldman (eds.). Textbook of Veterinary Internal Medicine: Diseases of the Dog and
Cat. W. B. Saunders Co., Philadelphia, Pennsylvania. Pp. 398–409.
Truyen, U., Stockhofe-Zurwieden N, Kaaden O. R, and Pohlenz J. 1990. A case report: encephalitis in lions. Pathological and virological findings. Dtsch.
Tieraerztl. Wochenschr. 97: 89–91.
Wozencraft, W. C. 1993. Order Carnivora. In: Wilson, D. E., and D. M. Reeder (eds.). Mammal Species of the World, 2nd ed. Smithsonian Institute Press,
Washington, D.C. Pp. 279–384.
Charles E. Gilbert, Ph.D., M.S.
Epidemiology & Toxicology Institute
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