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Canine Distemper Virus Author: R.C TITLE: CANINE DISTEMPER VIRUS AUTHOR: R.C. PEARSON and J.R. GORHAM PUBLICATION: VIRUS INFECTIONS OF CARNIVORES. VIRUS INFECTIONS OF VERTABRATES, VOL 1, PG. 371 DATE: 1987 INTRODUCTION For Paramyxoviridae, Morbillivirus, family description please see p. 123. Distemper is an acute or subacute contagious disease of mink and other Mustelidae. The etiologic agent is the same paramyxovirus that causes canine distemper. Distemper in mink is manifested by signs of catarrhal inflammation, systemic infection, central nervous system disturbance or a combination of these. The first report of distemper in mink appeared in the fur industry trade journals in the early 1930s. Mink distemper has a worldwide distribution. In addition to a high case-fatality rate, surviving mink may exhibit varying degrees of pelt damage. The disease will remain a threat to ranch-raised mink populations as long as feral species and unvaccinated dogs disseminate the virus. VIRUS PROPERTIES Physical and chemical characteristics See the chapter on canine distemper for details. Although canine distemper virus (CDV) is heat and light sensitive outside the host, it is maintained by low ambient temperatures for several days. Shen and Gorham (1980) showed that pathogenic CDV survived for 48 hours at 25'C and 14d at 5'C. Antigenic properties Mink immunized with one strain or attenuated vaccine are resistant to other CDV strains (Hartsough and Gorham, 1953). Field evidence has suggested a variation between the strains with regard to incubation period, signs and severity of the disease. Appel et al. (1981) found that ferrets inoculated intraperitoneally with equal amounts of virus died within 2 weeks using the Snyder Hill strain, within 4 weeks using the R252 strain and within 4-6 weeks using the A75-17 strain. EPIZOOTIOLOGY Infected dogs are the most important source and reservoir of CDV for ranch- raised mink. Another source of distemper outbreaks is unvaccinated mink breeding stock, recently introduced or returned to a farm (Hartsough and Gorham, 1953, Parker et al., 1961; Ott et al., 1965). Feral animals such as skunks (Jamison et al., 1973). raccoons (Parker et al., 1961; Karstad and Budd, 1964), and foxes (Hartsough and Gorham, 1953) trans- mit CDV to mink with ease. Although Gorham and Brandly (1953) found that CDV could not be transmitted by flies, the viremia that occurs during the disease allows for the possibility that bloodsucking arthropods could serve as vectors. PATHOGENESIS The most significant means of transmission is by exposure to airborne saliva and nasal exudate aerosols over short distances (Gorham and Brandly, 1953). The gastrointestinal tract is not a portal of entry. Transplacental transmission has been documented in the dog, but Hagen et al. (19,-O) exposed pregnant mink to an attenuated CDV and failed to recover virus from the fetuses. Crook et al. (1958) determined that the incubation period was 9-14d in aerosol- infected mink and ferrets. He detected viremia 2 d PI in ferrets and 3 d PI in mink. Gorham and Brandly (1953) and Crook et al. (1958) had evidence for a carrier state when they found virus in nasal exudate from 5-51 d PI after all signs had abated or until the death of the animals. High titers of virus were obtained from the lungs on d 10 (Crook et al., 1958), whereas only moderate titers were present in liver and brain. Low titers were recovered from pooled kidneys and bladders, adrenals, thyroids, salivary glands and skeletal muscles. Viruria may occur when the virus replicates in the urinary bladder epithelium (Gorham and Brandly, 1953). Virus detected in the skin scurf on d 5 PI may have been due to contamination by nasal or conjunctival exudates. An outbreak of CDV is manifested by mink first exhibiting catarrhal symptoms followed by neurologic signs. Occasionally this sequence is reversed (Hartsough and Gorham, 1953; Hartsough, 1974). Mortality rate is variable in adult mink and is around 90% in kits (Gorham et al., 1972). Distemper is always fatal in ferrets. DISEASE SIGNS Very young mink often die without developing signs of distemper. Nine-14 d after exposure, most infected mink have squinty, swollen, watery eyes and a serous nasal discharge (Fig. 127). In 2-3d , this discharge becomes purulent, accumulates as brown granular material adhering to the skin, and within 1-2 d completely closes the eyes and occludes the nostrils (Fig. 128). The skin on the chin becomes hyperemic and papules or ulcers may develop on the lips (Budd et al., 1966). The mink may have a normal appetite until the eyes are stuck shut. At that time, anorexia, emaciation, and dehydration may occur and persist for days or weeks depending upon the severity of the infection. Budd (1981) reported that ferrets have signs similar to those of mink. She noted that the normal rectal temperatures of tractable laboratory ferrets ranged from 37.7-39.1'C. When infected with distemper, the body temperature increased to 41'C, 3-5d PI. Animals may be febrile for 3 or more days, but become hypothermic before death. One week after the eye signs appear, the mink's feet may become swollen 2-3 times their normal size. In some instances, the head may appear swollen. On the surface of the foot pads, severe inflammation manifests itself as small scabs. This inflammation may extend up to the legs and if the animal lives long enough, may cause wrinkled, crusty, thickened skin over the whole body. Small pustules may occasionally be seen between the hind legs. Loss of hair is common. The thickened skin of the pads causes the toes to spread in the characteristic "snowshoe" foot appearance (Fig. 129; Budd et al., 1966). Diarrhea may occur later in the disease. Urinary incontinence may result in the pelt being moistened ventrally. At this time the mink may go into a coma and die in a terminal convulsion. It may also recover while the catarrhal signs subside. Although the animal may have a good appetite and appear normal for a period of days or weeks, it may later die in a "screaming fit" signifying neurotropic distemper. Affected mink may froth at the mouth, chew violently on the wire mesh, roll around the cage and scream sharply. The duration of the convulsions varies from less than 1 hour to 2 d. The mink usually dies after 1 or 2 attacks. Veterinarians have observed CDV outbreaks in which the attack rate was much greater in pastel mink than in the natural dark mink. In these instances, the pastel mink were represented in sufficient numbers and had equal opportunity for exposure. Hansen (1971) reported similar findings from a CDV outbreak in Denmark. Non-vaccinated pastel mink and kits experienced a greater mortality than other types. Thus, the mink genotype may influence susceptibility to CDV. PATHOLOGY External catarrhal lesions and skin rash are usually the only gross signs. If a mink dies of neurotropic distemper, external signs are usually absent. The only lesion recorded at necropsy of most mink and ferrets is an enlarged spleen (Budd et al., 1966; Gorham et al., 1972). It is not possible to diagnose distemper by examining the thoracic or the abdominal viscera; however, the thymus is atrophied. Occasionally the lungs of mink, ferrets and weasels are congested or consolidated in foci or whole lobes (Pinkerton, 1940; Keymer and Epps, 1969). Lesions of secondary infection are rarely seen at necropsy. The histologic lesions of distemper in mink and ferrets closely resemble those of the dog. Inclusion bodies are not present in the early stage but are a feature in epithelial cells later during the course of the disease. They are seen in the epithelium of the urinary bladder, trachea, bile ducts, salivary and adrenal glands, astrocytes of the CNS and macrophage/phagocytic cells of lymph nodes and spleen (Watson and Plummer, 1942; Wisnicky and Wipf, 1942; Crook and McNutt, 1959). The inclusion bodies are usually intracytoplasmic but may be intranuclear or both. They are eosinophilic with hematoxylineosin staining and may be variable in size and shape. They are usually not seen in neurotropic distemper. Pinkerton (1940) noted focal pneumonitis in mink with hyperplastic and often multinucleate histiocytes in the alveolar walls. He also found giant cells in bronchiolar epithelium and in the lumen of alveoli which contained both intranuclear and intracytoplasmic inclusion bodies. Tajima et al. (1971) reported that lymphoid cells, containing intranuclear and intracytoplasmic inclusion bodies, underwent degeneration and necrosis whereas reticular cells in the lymph nodes became hyperplastic. IMMUNE REACTION A life-long immunity to CDV is obtained by mink that completely recover from infection or that are properly vaccinated (Cabasso et al., 1957; Burger and Gorham, 1964). Although [gA, IgG, IgM and CMI responses are known for the dog, they have not been described for mink or ferrets. Hansen and Lund (1972) found that modified live CDV induced production of neutralizing antibodies in mink at a titer range of 500--1,000 four weeks after vaccination. At this time the mink were challenged with the Snyder Hill strain with no mortality. They also showed that maternal antibodies interfered with vaccination of kits. Four week old kits from vaccinated dams had a mortality rate of 8% when challenged with a high dose of the CDV strain of Snyder Hill. When kits of vaccinated dams were vaccinated 5-8 weeks of age, 60%-70% died of distemper when challenged. Kits that had been vaccinated at 11 weeks of age were immune to challenge. LABORATORY DIAGNOSIS Distemper is tentatively diagnosed in mink and ferrets by evaluation of clinical signs, but laboratory confirmation is necessary in most cases using histopathologic or immunofluorescent evidence, or ferret inoculation (Hartsough and Gorham, 1953). Frequently CDV infected mink show no signs of disease.
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