Stevenson-Feb 01 PV Review

178 V Vol. 23, No. 2 February 2001 CE Article #5 (1.5 contact hours) Refereed Peer Review Aleutian Mink FOCAL POINT Disease Parvovirus: #Aleutian mink disease parvovirus (ADV) can cause serious illness Implications for in companion ferrets. KEY FACTS Companion Ferrets I ADV infection can result Universal City Animal Hospital in wasting or neurologic University of Georgia Universal City, Texas syndromes in ferrets, p. 180. M. A. McCrackin Stevenson, DVM, PhD Leo Gates III, DVM I No cure or preventive vaccine Rocky Mountain Laboratories for ADV infection in mink or Animal Clinic of Farmers Branch National Institutes of Health ferrets currently exists, p. 183. Dallas, Texas Hamilton, Montana Jerry Murray, DVM Marshall E. Bloom, MD I Supportive therapy is the current treatment for Aleutian disease in ABSTRACT: Aleutian mink disease parvovirus (ADV) causes disease in mink and ferrets and ferrets, p. 183. can infect such related animals as raccoons, weasels, fishers, martens, and striped skunks. Severe Aleutian disease (AD) in adult mink is characterized by viral persistence, high levels of I Additional research is needed antiviral antibody (which is ineffective at eliminating the virus), and immune-complex disease. to better understand the Death results when virus–antibody immune complexes deposit in the kidneys, producing im- pathogenesis of Aleutian disease mune-mediated glomerulonephritis. Ferrets infected with ADV are usually asymptomatic and in ferrets, improve diagnostic maintain a low antibody titer, but severe disease can occur. Ferrets with clinical signs of AD testing, and develop prevention may have chronic wasting disease (similar to that seen in mink) or neurologic disease (most and treatment options, p. 183. often manifested as posterior paresis or paralysis). leutian mink disease parvovirus (ADV) can infect ferrets and is capable of negatively impacting the companion ferret population. Several reports A of Aleutian disease (AD) in companion1 and research2,3 ferrets have been published during the past decade. In recent years, outbreaks have occurred in a ferret shelter4 and multiple-ferret homes.5,a Despite the perceived increase in disease incidence in ferrets, little is known about incubation, transmission, inter- pretation of diagnostic tests, pathogenesis, treatment, and prevention of AD in ferrets. This article summarizes information about AD in mink and ferrets and provides suggested management options for affected companion ferrets. HISTORY OF ALEUTIAN DISEASE IN MINK Aleutian disease has long been considered primarily a disease of ranch mink aGreenacre C: Personal communication, University of Georgia, Athens, 2000. Compendium February 2001 Small Animal/Exotics 179 (Mustela vison). Highly sus- easier to handle than the some- ceptible Aleutian mink (aa) times ferocious mink.21 Ferrets carry two autosomal recessive were infected with tissue ho- genes for dilute coat color mogenates from infected (producing a gun-metal gray mink20 or were closely housed pelt) that is associated with with infected mink and fer- Chédiak-Higashi syndrome,6 rets.19 Although the ferrets did an inherited disorder of the not develop clinical illness, immune system7 (Figure 1). they did acquire periportal ADV was named after Aleu- lymphocytic cellular infiltrates tian mink because of their in their livers,19,20 thymic hy- unique susceptibility to AD.8 pertrophy,19,22 hypergamma- However, dark-coated mink globulinemia, splenomegaly, that are heterozygous (Aa) or Figure 1—A young adult female Aleutian mink. Note the and mesenteric lymphaden- homozygous dominant (AA) gun-metal gray color of the fur. Aleutian mink carry a opathy.19 Glomerulonephritis are also susceptible to ADV double recessive gene (aa) that is associated with muted and arteritis, hallmarks of AD infection but tend to have coat color and Chédiak-Higashi syndrome. They are in highly susceptible Aleutian lower morbidity and mortali- highly susceptible to infection with Aleutian mink disease mink, occurred in naturally ty compared with Aleutian parvovirus. infected ferrets19 but not in mink.9,10 AD was recognized ferrets experimentally infected as a disease syndrome in 1946 when mink ranchers re- with material from mink.20–22 Mink ADV appeared to alized the economic value of the gray pelts and began persist in the ferrets for 13620 to 180 days.21 actively breeding Aleutian mink for their desirable coat Limitations of these early studies included the inabil- color. The first published description of AD in mink ity to detect and differentiate viral strains19–22 and easily appeared in 1956.11 test for preexisting antibody in the acquired research Before the identification of ADV, distemper and bot- animals.19,20 The overall conclusions of studies conduct- ulism were the primary disease concerns of mink ranch- ed before 1985 were that there were distinct mink and ers. Ranchers commonly made their own autogenous ferret strains of ADV,21,22 the disease progressed more distemper vaccines by homogenizing spleen from dis- slowly in ferrets than in mink,21,22 and the disease and temper-infected mink, making suspensions, and inject- microscopic tissue changes were less severe in ferrets ing all the mink on their ranch. This practice led to a than in mink.20–22 severe outbreak of AD on a Connecticut ranch, with a mortality rate of almost 100% within 6 months.12 Over CLINICAL DISEASE the ensuing decade, suspicions rose that AD was caused Manifestations of clinical disease are likely deter- by a “filterable agent” (i.e., a virus). ADV was isolated mined by virus strain and host genotype and immune and studied during the early 1970s13,14 but was not cor- status. Thus a broad array of clinical signs—ranging rectly characterized as a parvovirus until 1980.15 Exten- from clinical normalcy to nonspecific signs (e.g., lethar- sive molecular characterizations of ADV and studies of gy, anorexia) to specific problems (e.g., uremia; neuro- its pathogenesis in mink have been published over the logic dysfunction; frank hemorrhage of the digestive past 20 years.6,16,17 Although very distantly related to tract, including the mucosa of the oral cavity and in- parvoviruses that cause acute gastrointestinal disease testines)—can be seen. (e.g., canine parvovirus, feline parvovirus, mink enteri- tis virus), ADV is antigenically distinct from these Mink members of the feline subgroup of parvoviruses.18 Aleutian disease was first manifested as a chronic wasting disease of adult Aleutian mink.11 Weight loss, ALEUTIAN DISEASE IN FERRETS poor pelts, lethargy, anorexia, polydipsia, anemia, and Many ferrets (Mustela putorius furo) were probably melena were common clinical signs in affected mink.6 naturally exposed to ADV on mink ranches because Infertility, small litters, and high stillborn rates were some farmers raised mink and ferrets on the same prop- also noted.23 Necropsy examinations of end-stage in- erty. Ferrets were also experimentally infected with ADV fected animals classically showed small, shriveled kid- during the 1960s.19,20 Researchers believed that AD neys; splenomegaly; mesenteric lymphadenopathy; hep- could be developed as an animal model for human im- atomegaly; and blood in the intestinal tract.6 Aleutian mune-mediated diseases but sought an animal that was mink experimentally infected with virulent strains of ALEUTIAN MINK I CHÉDIAK-HIGASHI SYNDROME I CLINICAL SIGNS 180 Small Animal/Exotics Compendium February 2001 ADV tested positive for anti–ADV antibodies (end- and collapse, and serosanguineous pleural effusion. Mi- point titers were 1024 or greater using counterimmu- croscopic examination of necropsy tissue samples re- noelectrophoresis [CIEP]), tested persistently positive vealed hemorrhagic interstitial pneumonia. Neurologic when polymerase chain reaction (PCR) was used to de- signs usually followed respiratory signs by several weeks tect nucleic acid in the serum, were hypergammaglobu- but occurred alone in some ferrets. Neurologic dysfunc- linemic (i.e., more than 20% of total serum proteins tion started as posterior paresis and either remained sta- were γ-globulins), and were azotemic in end-stage dis- ble or progressed to ascending paralysis accompanied by ease.24,25 Virus was found in the cytoplasm of such phago- urinary and fecal incontinence. A few ferrets developed cytic cells as macrophages and dendritic cells26,27 and in heart disease reminiscent of ferret cardiomyopathy, but renal tubular epithelial cells.28 necropsy samples showed arteritis in the cardiac muscle Adult non-Aleutian mink may develop one of three (suspected to have resulted from immune-complex de- general types of ADV infection: progressive AD as de- position) and lymphoplasmacytic infiltrates. Severe an- scribed for Aleutian mink9; persistent nonprogressive terior uveitis also occurred in some ferrets. Uveitis has infection; or nonpersistent, nonprogressive infection also been described in AD-affected mink.33 with eventual clearance of the virus.10 Whether these All of these sick ferrets tested positive for anti–ADV three categories apply to ferrets is unknown. antibody by CIEP, and viral DNA was amplified by The target cells for viral replication are different in PCR using tissue from some of these ferrets.34 DNA se- newborn kits compared with adult mink.17 In contrast quence analysis of these PCR products was identical to to the protracted infection of macrophages and den- that previously reported for ADV-F.32,34 To date, ADV- dritic cells in adult mink, kits infected within the first 2 F is the only

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