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 ), 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 dis- ease 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., , 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 isolate of ADV in ferrets to be document- weeks of life developed rapid viral replication in the ed with published DNA sequence data.32,34 alveolar type II epithelial cells of the lungs.17,29,30 Direct A multiple-ferret home in Dallas, Texas, experienced viral damage rather than immune-mediated disease the loss of 2 of 11 ferrets in the spring of 2000.5 Both caused severe, fulminant, and often fatal pneumoni- ferrets tested positive for antibody using CIEP and had tis.17,29,30 The behavior of this acute infection of neona- microscopic tissue changes consistent with AD. One of tal mink is more reminiscent of feline subgroup par- these ferrets (a 5-year-old male) had an endpoint anti- vovirus infections (e.g., canine parvovirus, feline body titer of 256 by CIEP,35 hypergammaglobulinemia parvovirus, mink virus) than the persistent in- (32%), muscle twitches, and seizures; the liver and kid- fection of adult mink with ADV. ney showed extensive lymphoplasmacytic cellular infil- trates typical of AD. Glomerulonephritis was also iden- Ferrets tified in the kidney. Two of the remaining nine ferrets Aleutian disease in ferrets was originally considered in this home also tested positive using CIEP; the other primarily a subclinical problem. One 1978 report and seven ferrets had not been tested when this article was all studies of AD in ferrets published since 1990, how- written. ever, have described overt clinical disease.1–3,31 Clinical syndromes included chronic wasting disease3,31 and DISEASE TRANSMISSION neurologic disease consisting of posterior paresis or Natural horizontal transmission of ADV among paralysis.1–3 Virus isolated from the spleen of an infect- mink is likely to occur by either the oral or aerosol ed ferret (ADV-F3) was amplified by PCR for DNA se- route.36–38 AD has been experimentally transmitted be- quencing.32 The DNA sequence of a small segment of tween mink by inoculation with whole blood, serum, the capsid protein that makes up the virus “shell” urine,25,37,39 feces, saliva, and bone marrow from infect- showed that ADV-F was 88% to 89% identical to some ed mink.37 previously sequenced pathogenic strains of mink Vertical transmission of ADV has also been shown to ADV.32 DNA sequence differences confirmed that occur in mink.36,40 Dams with either progressive or ADV-F was dissimilar to isolates identified in mink.32 nonprogressive subclinical infections were shown to Clinical syndromes seen during a 1998 outbreak of have high numbers of infected kits.36 The risk for ADV AD in a ferret shelter in San Antonio, Texas, included infection in kits born to dams with nonprogressive sub- generalized wasting and respiratory, neurologic, and car- clinical infections was less than that for kits born to diac forms of disease in ADV-positive ferrets.4 Ferrets dams with progressive AD.36 Dams infected with ADV with chronic wasting disease had small kidneys on before mating had a higher percentage of dead and re- necropsy and glomerulonephritis on microscopic exami- sorbed fetuses compared with dams infected after ex- nation. Respiratory disease in affected ferrets included pected embryo implantation.40 severe coughing, right middle lung lobe consolidation The natural route of transmission of AD among fer-

GENERALIZED WASTING I POSTERIOR PARESIS I VERTICAL TRANSMISSION Compendium February 2001 Small Animal/Exotics 181

TABLE I Submitting Samples for Counterimmunoelectrophoresis Testing for Anti–Aleutian Mink Disease Parvovirus Antibodya

Company Cost Accepted Sample Payment Results United Vaccines, Inc. $15 first ≥10 µL whole Prepayment is required; 48-hr turnaround; ATTN: Customer Service sample; blood or serum, send check or credit results are reported as 2826 Latham Dr. $10 each preferably in a card information with positive, negative, or no Madison, WI 53713 additional capillary tube sample sample (if tube breaks) Phone: 800-283-6465, sample 608-277-2030 aExpress overnight shipping recommended.

rets is unknown. Horizontal transmission is suspected, majority of mink and ferrets infected with ADV pro- but whether infectious ADV is present in urine, feces, duce antibodies against both capsid and nonstructural or saliva of infected ferrets is unknown. This informa- proteins,41 the lack of nonstructural protein detection tion is critical to help companion ferret owners prevent has not been a problem.b An antibody titer based on the transmission of the virus from infected to noninfected most dilute sample that continues to test positive (end- ferrets in their homes. It is likewise important for ferret point titer) would be helpful to clinicians, particularly clubs in terms of establishing rules regarding the admis- when retesting patients suspected of having AD. An in- sion of infected animals in ferret shows. Vertical trans- creasing magnitude of antibody titer likely indicates ac- mission in ferrets has been suspected1 but not studied. tive, ongoing infection. Testing additional dilutions us- Knowledge of the mechanisms of horizontal and verti- ing the CIEP assay is possible but would likely increase cal transmission is crucial for ferret breeders to be able the expense of the test. to make decisions about acquiring new ferrets for As mentioned, CIEP cannot distinguish among im- breeding programs, monitoring breeding ferrets, and munoglobulin subclasses. In ADV-infected mink, IgM placing young jills and hobs in companion homes. increases as soon as 6 days after inoculation and peaks Disease transmission is an area that needs to be re- at 15 to 18 days after inoculation.8 IgG is not detected searched. Detection of infectious virus in blood or cell- until at least 12 days after infection but is consistently free body fluids may help identify ferrets that are cur- increased by 30 days after infection.8 IgG levels remain rently shedding the virus. This information would also increased long after IgM levels have returned to nor- be valuable in learning more about ADV transmission mal.8 The appearance of antibodies of different sub- in ferrets. classes has not been studied in detail in ferrets. Needed improvements in antibody testing include reporting DIAGNOSTICS endpoint titers and distinguishing between IgM and Counterimmunoelectrophoresis is the standard for de- IgG subclasses. New diagnostic tests should be devel- tecting anti–ADV antibodies in mink and ferrets.41 This oped to complement the CIEP by providing these addi- test is a precipitation reaction42 between antibody in tional data, thereby helping clinicians determine the serum samples and a commercial viral antigen43 (Table stage and severity of infection. I). It detects antibodies directed against the capsid pro- Hypergammaglobulinemia (excessive antibody pro- teins comprising the protective “shell” around the viral duction without neutralization of the virus) is a hall- genomic DNA. A simple positive or negative result is mark of AD in mink6 and can develop in infected fer- given. CIEP has primarily been used for test-and-slaugh- rets.1–3,19,31 Serum protein electrophoresis is used to ter programs on mink ranches, in which more detail compare γ-globulin levels with the rest of the serum than a positive or negative result has been unnecessary. proteins. Most commercial laboratories conduct this The currently available CIEP assay is a reliable screen- test and require serum. Care must be taken during sam- ing test, and false-positive results are not induced by ple collection because hemolysis can interfere with the vaccines against mink enteritis virus or other . b However, CIEP has a few limitations when used to di- After this manuscript was accepted for publication, the authors learned that a new assay for antibodies directed against the non- agnose AD in companion ferrets: It does not detect anti- structural proteins of ADV is now commercially available bodies directed against the ADV nonstructural pro- through Avecon, Inc. To our knowledge, there are no pub- teins,1,41 provide endpoint antibody titers, or distinguish lished reports of the assay protocol or the sensitivity and speci- among immunoglobulin subclasses. Because the vast ficity of the test. For more information, see www.avecon.com.

COUNTERIMMUNOELECTROPHORESIS I HYPERGAMMAGLOBULINEMIA 182 Small Animal/Exotics Compendium February 2001

test. The typical cost is $30 to ferrets to verify the presence $35, and results are generally of ADV in necropsy speci- available in 2 to 5 days. A γ- mens. globulin level exceeding 20% of total serum protein is con- TREATMENT sidered hypergammaglobu- Test-and-slaughter pro- linemia.22 The presence of hy- grams have been used to de- pergammaglobulinemia in a crease the incidence of AD on ferret that tested positive on mink ranches and are ex- CIEP and has clinical signs of tremely effective when used wasting or neurologic disease conscientiously.48 Treatment strongly supports a presump- for individual mink infected tive diagnosis of AD.3 with ADV has been limited Horizontal transmission of Figure 2—(A) Normal mink kidney. (B) Lymphoplasma- to experimental reports of im- AD was documented in the cytic cellular infiltrates are typical microscopic changes munosuppressive therapy us- 1960s by means of transmis- seen in the interstitium of the renal cortex of mink infect- ing levamisole,49 cyclophos- sion studies.37 The inocula- ed with pathogenic strains of Aleutian mink disease par- phamide,50 and an interferon tion of uninfected mink with vovirus (ADV). (C) Normal mink liver. (D) Cellular infil- inducer (polyinosinic-polycy- whole blood, serum, saliva, fe- trates are also commonly seen in the periportal areas of tidilic acid [poly IC])51 to de- ces, and urine39 from infected the liver of ADV-infected mink. Ferrets infected with crease hypergammaglobulin- ADV can have lesions similar to those shown here (origi- mink was shown to cause emia and the deposition of nal magnification, ×200). AD.37 Advanced molecular antigen–antibody complexes. biology techniques may allow Levamisole (1 mg/kg) was the detection of viral nucleic acid by testing ferret body added to feed for three treatment periods of 14 days fluids. Serum from experimentally infected mink is each with a 14-day rest period between each treat- routinely tested for viral DNA using PCR.24,43,44 PCR ment.49 Body weight may have increased slightly in the has also detected viral DNA in the urine of mink in- treated group, and hypergammaglobulinemia was re- fected with a highly pathogenic strain of ADV as early duced in some treated animals.49 No statistical analysis as 14 days after inoculation.25 When testing serum24,44 was done in this study, and the variation within the or urine,25 PCR assays may be positive weeks before groups suggested that statistical significance was unlike- mink show any clinical signs of disease. Nevertheless, ly. However, no detrimental side effects associated with mink with progressive disease can test negative when levamisole were mentioned.49 PCR is used to detect ADV DNA in serum. In contrast, cyclophosphamide (10 mg/kg intraperi- Histopathology is perhaps the best method for con- toneally [IP], three times weekly for 13 weeks) was very firming AD in a ferret identified as ADV-positive using effective in suppressing host antibody responses and de- CIEP. Microscopic changes in the organs of ADV-in- position of immune complexes in the kidneys.50 Cy- fected mink include lymphoplasmacytic cellular infiltra- clophosphamide was also used at 10 mg/kg IP twice tion in the liver, kidneys, spleen, and lymph nodes (Fig- weekly for 8 weeks.50 This lower dosage was not as ef- ure 2).45 Evidence of glomerulonephritis and arteritis fective as was the higher dosage, but both were associat- may be seen as well. In early reports of ferret AD,19,20 in- ed with significant negative side effects, including de- fected ferrets showed only massive periportal lympho- pression, anorexia, cyanosis, and leukopenia in treated cytic infiltrates. More recent microscopic examination mink.50 Levels of virus replication were not affected by of tissue from ferrets suspected of having AD, however, cyclophosphamide treatment, indicating that direct vi- have included portal lymphoplasmacytic hepatitis, inter- ral damage to the host is not the cause of classic AD. stitial lymphoplasmacytic nephritis, membranoprolifera- Poly IC (30 mg/kg IP twice weekly for 4 weeks and tive glomerulonephritis, and lymphoplasmacytic gastri- then once weekly for 3 weeks) was given to experimen- tis.5 Ferrets with neurologic signs have been described as tally infected mink.51 γ-Globulin levels were decreased having nonsuppurative encephalomyelitis2,3 and astro- in poly IC–treated mink compared with control ani- cytic hypertrophy in the gray matter of the spinal mals 6 weeks after infection, but this beneficial effect cord,1–3 often without lesions consistent with glomeru- was no longer seen at 12 weeks postinoculation.51 Mi- lonephritis.1,2 In situ hybridization has been used to croscopic changes in target organs appeared to be identify viral DNA and replicating DNA in tissue from blunted in poly IC–treated mink, but study results infected mink.46,47 This technology can be adapted to were not statistically significant.51 Although the use of

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these drugs has not been reported in ADV-infected fer- boxes, bedding, and carpeting contaminated with virus rets, it may be reasonable to consider using immuno- particles—particularly when accompanied by such or- suppressive oral prednisone therapy to decrease im- ganic material as feces—may serve as prolonged sources mune-mediated consequences of AD in carefully of virus for uninfected ferrets. selected companion ferrets. A prospective clinical trial Contaminated environmental conditions would espe- should be done to determine whether this treatment cially exist at ferret shows if ADV-shedding ferrets are would be helpful for ferrets with AD. present. With the current lack of knowledge regarding Treatment of AD in ferrets will continue to be limit- the pathogenesis of AD in ferrets and the limitations in ed to supportive care until more definitive therapy is identifying virus-shedding ferrets, there is no way to determined. Intravenous or subcutaneous fluid therapy guarantee the safety of all ferrets at ferret shows. Re- may be necessary to maintain hydration. Maintaining a stricting entries to ferrets with negative CIEP tests 3 to positive nutritional plane via temporary syringe or tube 4 weeks before the show would be prudent. The best feeding may be needed in sick ferrets. Studies have protection for valuable AD-free breeding stock and shown that ADV-infected mink have a decreased ability companion ferrets is to eliminate their exposure to oth- to mount a humoral immune response.50 Thus moni- er ferrets of questionable ADV status. toring ADV-infected ferrets for opportunistic infections and treating with appropriate antibiotics are important. ACKNOWLEDGMENTS The authors thank Jeff Mauldin, BA, University of DISEASE PREVENTION Georgia, and Jim Wolfinbarger, National Institute of No vaccine against AD in mink or ferrets is currently Allergy and Infectious Disease, National Institutes of available. In fact, the presence of additional antibodies Health, Rocky Mountain Laboratories, Hamilton, MT, directed toward capsid proteins exacerbates the chronic for technical support. They also thank the ferret owners immune-mediated form of AD in mink.52,53 Despite this who graciously provided samples from their pets for re- negative data, anticapsid antibodies have been shown to search purposes. blunt the acute form of AD seen in mink kits,54 and an- tibodies generated against one of the nonstructural pro- REFERENCES teins (NS1) partially protected mink from immune-me- 1. Welchman DB, Oxenham M, Done SH: Aleutian disease in diated AD—but not infection—in a recent vaccine domestic ferrets: Diagnostic findings and survey results. Vet trial.53 Therefore, there is still hope that a vaccine Rec 132:479–484, 1993. against ADV can be developed. Vaccine strategies must 2. Rozengurt N, Stewart D, Sanchez S: Diagnostic exercise: Ataxia and incoordination in ferrets. Lab Anim Sci 45:432– avoid generating anticapsid antibodies in adult animals 434, 1995. and thus must focus on alternative targets for stimulat- 3. Palley LS, Corning BF, Fox JG, et al: Parvovirus-associated ing protective immunity. The expansion of the field of syndrome (Aleutian disease) in two ferrets. JAVMA 201: vaccinology in the past 10 years has brought promising 100–106, 1992. new technology that adds practicality to the hope of de- 4. Gates L: Unpublished data, Universal City Animal Hospital, Universal City, TX, 1997. veloping an effective vaccine against ADV in ferrets. 5. Murray J: Unpublished data, Animal Clinic of Farmers Until an effective vaccine becomes available, the best Brach, Dallas, TX, 2000. recommendations for preventing the spread of AD 6. Eklund CM, Hadlow WJ, Kennedy RC, et al: Aleutian dis- among ferrets are isolation of uninfected ferrets from ease of mink: Properties of the etiologic agent and the host ADV-infected ferrets and environmental cleaning. 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Hadlow WJ, Race RE, Kennedy RC: Comparative vived for 5 to 10 months.55 Complete drying was help- pathogenicity of four strains of Aleutian disease virus for pas- ful in inactivating the virus, and thus mechanical clean- tel and sapphire mink. Infect Immun 41:1016–1023, 1983. ing was as strongly recommended as was disinfection 10. Hadlow WJ, Race RE, Kennedy RC: Royal pastel mink re- 55 spond variously to inoculation with Aleutian disease virus of for environmental control. In all likelihood, ADV can low virulence. J Virol 50:38–41, 1984. survive in the environment in a similar fashion. There- 11. Hartsough GR, Gorham JR: Aleutian disease in mink. Natl fore, food and water bowls, toys, cages, carriers, litter- Fur News 28:10–11, 1956.

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Aleutian disease of mink II. Enhancement of tissue lesions c. albumin:globulin ratio. following the administration of a killed virus vaccine or pas- d. Western blot analysis. sive antibody. J Immunol 109:1–7, 1972. 53. Aasted B, Alexandersen S, Christensen J: Vaccination with 5. Which of the following statements regarding transmis- Aleutian mink disease parvovirus (AMDV) capsid proteins sion of ADV among ferrets is true? enhances disease, while vaccination with the major non- structural AMDV protein causes partial protection from dis- a. ADV has been proven to be shed in the urine, fe- ease. Vaccine 16:1158–1165, 1998. ces, and saliva of ferrets. 54. Alexandersen S, Larsen S, Cohn A, et al: Passive transfer of b. The mode of transmission of ADV among ferrets is antiviral antibodies restricts replication of Aleutian mink dis- unknown at this time. ease parvovirus in vivo. J Virol 63:9–17, 1988. c. ADV is known to be spread in the air. 55. Uttenthal A, Lund E, Hansen M: Mink enteritis parvovirus: d. Transmission from dam to kit is known to occur in Stability of virus kept under outdoor conditions. Acta Pathol ferrets. Microbiol Immunol Scand 107:353–358, 1999. 6. Which of the following factors does not affect the About the Authors manifestations of clinical AD? Dr. Stevenson is affiliated with the Departments of Small a. host genetics c. host immune status Animal Medicine and Medical Microbiology/Parasitology, b. viral strain d. host temperature College of Veterinary Medicine, University of Georgia, Athens. Dr. Gates owns Universal City Animal Hospital, 7. Which of the following statements regarding ADV in Universal City, Texas. Dr. Murray is affiliated with the Ani- mink is true? a. Kits infected with ADV develop severe gastritis and mal Clinic of Farmers Branch, Dallas, Texas. Dr. Bloom is glomerulonephritis. affiliated with the Laboratory of Persistent Viral Diseases, b. Classic disease in adults includes chronic wasting, National Institute of Allergy and Infectious Diseases, Na- glomerulonephritis, high antibody titers, and hy- tional Institutes of Health, Rocky Mountain Laboratories, pergammaglobulinemia. Hamilton, Montana. Dr. Stevenson is a Diplomate of the c. Classic disease in adults includes acute, severe American College of Veterinary Surgery. bloody , similar to that seen with canine parvovirus. d. Kits develop chronic wasting, glomerulonephritis, ARTICLE #5 CE TEST high antibody titers, and hypergammaglobuline- mia. The article you have read qualifies for 1.5 con- tact hours of Continuing Education Credit from 8. Which of the following statements regarding ADV in the Auburn UniversityCE College of Veterinary ferrets is true? Medicine. Choose only the one best answer to each a. Isolation of AD-free ferrets from ferrets with ques- of the following questions; then mark your an- tionable antibody status is the best way to prevent swers on the test form inserted in Compendium. transmission. b. Current tests can guarantee that a ferret is not shedding ADV. 1. AD, an immune-mediated, chronic viral infection of c. Because ADV-F likely dies very rapidly in the envi- mink, ferrets, and related animals, is caused by a ronment, cleaning and disinfection are not impor- a. coronavirus. c. retrovirus. tant. b. picornavirus. d. parvovirus. d. It is unlikely that ADV-F can survive in food and water bowls, cages, carriers, and carpets. 2. The CIEP assay detects a. antigen. c. antibodies. 9. Treatment of ADV in ferrets b. immune complexes. d. CD8+ lymphocytes. a. involves potent antiviral agents. b. requires DNA viral sequencing. 3. The two most common clinical syndromes of AD in c. consists of supportive care and possibly immuno- ferrets are suppressant agents. a. cardiomyopathy and urinary tract infection. d. is not necessary because a vaccine is available. b. glomerulonephritis and posterior paresis. c. uveitis and adrenal gland disease. 10. Most ferrets that become infected with ADV d. thyroid disease and glomerulonephritis. a. are asymptomatic but maintain low antibody titers. b. become acutely ill and die suddenly. 4. Hypergammaglobulinemia is detected using c. are immunosuppressed and chronically affected a. serum electrophoresis. with opportunistic infections. b. total serum protein determination. d. suddenly become aggressive.