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At least 19 recordsLinked to original sources
PubMed1978

Endogenous mink (Mustela vison) type C virus isolated from sarcoma virus-transformed mink cells.

A previously described type virus stock (designated PP-1R), isolated by cocultivating baboon cells with mink cells transformed by Kirsten sarcoma virus (64J1), has been further cloned and characterized. End point-diluted stocks of PP-1R have been obtained that are free of focus-forming activity and lack both Kirsten sarcoma and primate type C viral sequences. Nucleic acid hybridization experiments show that the cloned virus (MiLV) is an endogenous, genetically transmitted virus of the mink (Mustela vison). MiLV replicates in canine, feline, and 64J1 mink cells but not in an untransformed mink cell line. Multiple viral gene copies can be detected in the DNA of normal mink cells in culture and in normal mink tissues; related endogenous viral genes are also detected in several related Mustela species. The virus codes for a p30 protein very closely related antigenically to that of feline leukemia virus but contains p15 and p12 proteins that are antigenically distinct. The mink cell line, Mv1Lu, and its Kirsten sarcoma-transformed derivatives, 64J1, express relatively low levels of type C viral RNA related to MiLV and normally do not produce detectable levels of MiLV p30 protein or complete, infectious viral particles. Infection of sarcoma virus-transformed mink cells with baboon type C virus, however, can augment the level of expression of endogenous mink viral RNA and can result in the synthesis and packaging of mink viral RNA and p30 antigen in extracellular virions. Since the Mv1Lu cell line and its tranformed derivatives have become widely used in studies of retroviruses, the possibility of activating endogenous mink viral genes should be considered by investigators working with these cells.

Animals↗
PubMed1976

Transmissible mink encephalopathy. Reduced spongiform degeneration in aged mink of the Chediak-Higashi genotype.

Mink which are 18 months or older and are dying of transmissible mink encephalopathy (TME) have been found to have a marked reduction in spongiform degeneration of the brain if they are homozygous for the Aleutian gene and thus exhibit the autosomal recessive disorder known as the Chediak Higashi (CH) syndrome. CH mink younger than 1 year, and young or old non-CH mink have a typical lesion profile with widespread microvacuolation of the neuropile. Whereas aged CH mink have reduced spongiform degeneration at both the light and electron microscopic level, there is no other apparent alteration in the TME disease process. The length of incubation, clinical signs, astrocytic response, and brain concentration of the TME agent are comparable to those seen in non-CH mink. We conclude that spongiform degeneration is a secondary change in TME and speculate that vacuolation may be the result of lysosomal enzymes causing an increase in ganglioside catabolism.

Age Factors↗
PubMed1977

Pathologic analysis of mink mortality in New England mink.

The underlying cause of death of a group of New England mink, which died in 1969 to 1970 was explored. PCB and chlorinated hydrocarbon pesticide levels were measured. Aroclor 1254 levels in these mink were elevated 73 fold over levels in healthy mink in 1974. DDT levels were elevated 5 times and DDE 3 times over those control animals. Gross pathology revealed desions of the lungs, liver and kidneys. There lesions were confirmed microscopically. The lungs of the New England mink showed inflammation and congestion. Areas of inflammation were also present in the liver. Massive areas of necrosis were seen in the kidneys, both in the medullary and cortical areas. Kidney involvement was greater than any other organ. P.A.S. positive material was seen in each of these organs with the kidneys showing largest amounts of this material. Since the New England mink did not show lesions of the G.I. tract, did not exhibit fatty degeneration of the liver, which PCB toxicity is known to induce in mink and because they showed areas of congestion, inflammation and positive P.A.S. material, PCB's were not considered the toxic agent. However, fungus or bacterial infection might be the causative agent.

Adipose Tissue↗
PubMed1975

Aleutian disease of mink: the antibody response of sapphire and pastel mink to Aleutian disease virus.

The specific antiviral antibody response of sapphire and pastel mink to Pullman strain of ADV has been examined. Sapphire mink inoculated with from 300,000-3 LD50 developed high levels of specific antibody and AD. Pastel mink inoculated with parallel doses of ADV also produced antibody but did not develop AD. The low incidence of AD in pastel mink inoculated with Pullman strain of ADV is probably related to factors other than antiviral antibody.

Aleutian Mink Disease↗
PubMed2024

Characterizing the gut microbiome of diarrheal mink under farmed conditions: A metagenomic analysis.

This study aimed to comprehensively characterize the gut microbiota in diarrheal mink. We conducted Shotgun metagenomic sequencing on samples from five groups of diarrheal mink and five groups of healthy mink. The microbiota α-diversity and Kyoto Encyclopedia of Genes and Genomes (KEGG) orthology did not show significant differences between the groups. However, significant differences were observed in microbiota β-diversity and the function of carbohydrate-active enzymes (CAZymes) between diarrheal and healthy mink. Specifically, The relative abundance of Firmicutes was lower, whereas that of Bacteroidetes was higher in diarrheal mink. Fusobacteria were enriched as invasive bacteria in the gut of diarrheal mink compared with healthy mink. In addition, Escherichia albertii was identified as a new bacterium in diarrheal mink. Regarding functions, nicotinate and nicotinamide metabolism and glycoside hydrolases 2 (GH2) family were the enhanced KEGG orthology and CAZymes in diarrheal mink. Furthermore, the diversity and number of antibiotic-resistant genes were significantly higher in the diarrheal mink group than in the healthy group. These findings enhance our understanding of the gut microbiota of adult mink and may lead to new approaches to the diagnosis and treatment of mink diarrhea.

Animals↗
PubMed1975

The influence of genotype on the development of glomerular lesions in mink with Aleutian disease virus.

In an attempt to document progression rate differences in the development of glomerular lesions in mink infected with Aleutian disease virus (ADV), the glomeruli of Aleutian and non-Aleutian mink experimentally infected with ADV were evaluated by light, fluorescent, and electron microscopy. The animals were also examined for the presence of interstitial infiltrate, neutrophils, and arterial lesions. One hundred percent of the Aleutian mink had glomerular cell proliferation and interstitial infiltrate, while 95% of the Aleutian and 41% of the non-Aleutian mink had neutrophilic infiltrates and arteritis, respectively. Of the non-Aleutian mink, 91, 83, 42, and 12.5% had glomerular cell proliferations, glomerular neutrophils, interstitial infiltrate, and arterial lesions in, that order. All the Aleutian mink had glomerular depositions of gamma-globulin (IgG) and complement (C3), whereas 75% of non-Aleutian mink had deposits of IgG and C3. One hundred percent of both genotypes had glomerular deposits of immunoglobulin M (IgM). Ultrastructural glomerular changes consisting primarily of depositions of granular electron-dense material on basement membranes were observed in Aleutian mink 6 weeks after infection and 12 weeks after infection in non-Aleutian mink. These findings document progression rate differences in the development of glomerular lesions in Aleutian disease-affected Aleutian and non-Aleutian mink. Further, they emphasize the need for exploration of pathogenetic mechanisms involved in progression rate differences in lesion development.

Aleutian Mink Disease↗
PubMed1978

Effectiveness of immunization with single and multi-component vaccines prepared from a common antigen (OEP), protease and elastase toxoids of Pseudomonas aeruginosa on protection against hemorrhagic pneumonia in mink due to P. aeruginosa.

Toxoids of protease and elastase of Pseudomonas aeruginosa were successfully prepared by treatment with 8% formalin plus 0.2 m lysine and by 4% formalin respectively. The two toxoids proved sufficiently potent to elicit high antibody titers as estimated by both the enzyme-neutralizing and passive hemagglutination tests. The effectiveness of immunizing minks with a single component-vaccine consisting of the common antigen (OEP) of P. aeruginosa or the protease toxoid (PT) or the elastase toxoid (ET) and with the two (PT and ET) or the three (OEP, PT and ET) component-mixed vaccines, on hemorrhagic pneumonia in minks due to the bacteria was investigated. Female Sapphire minks, 3.5 months old, were used in two experiments performed in 1975 and 1976. Minks were immunized three times in one month with a total of 1 mg of each of the three antigens in the case of a single component vaccine and with a total of 2 or 3 mg (equal amounts of each component) in the case of the two or three component vaccines. Two or three weeks after the last immunization, challenge exposure with strain No. 5 was carried out by intranasally inoculating an inoculum containing serial dilutions of 10(3) -10(10) of live bacteria. Summarizing the results of the two experiments, in the case of controls, nonimmunized minks and minks immunized with potassium aluminum sulfate (potash alum) alone, the LD50 values were approximately 10(3) -10(4) with no significant difference between the two. In the case of OEP-vaccinated minks, the LD50 value was about 10(6) and thus clearly differed from those of the controls. In minks immunized with the three-component-vaccine, however, the LD50 value was about 10(8) -10(9), which indicated that the three-component-mixed vaccine was remarkably more effective than the single OEP vaccine component. In minks immunized with either PT or ET or both, the LD50 values were about 10(8) -10(9). The effectiveness of the vaccine made with ET or PT alone is discussed in the text. The pathological findings of the minks which died or survived are described.

Animals↗
PubMed1978

Characteristics of inapparent Aleutian disease virus infection in mink.

Inapparent of nonprogressive Aleutian disease virus (ADV) infection is a subclinical but persistent virus infection of mink. Mink with the inapparent type of ADV infection when subjected to stress did not develop the progessive form of the disease. However, when challenged with a large dose of the virus, these mink did develop progressive Aleutian disease indicating that they were not highly resistant to the virus. Sera of mink with either the progressive of the inapparent type of ADV infection did not neutralise the virus. The anti-ADV antibody activity in mink with inapparent type of ADV infection was in the IgG fraction of the serum the same as in mink with progressive Aleutian disease. These data indicate that the resistance of the mink with inapparent infection as compared to mink with progressive Aleutian disease was not due to a difference in the class of immunoglobulin response to the virus. However, mink with progressive Aleutian disease showed a greatly increased immunoglobulin response.

Aleutian Mink Disease↗
PubMed1977

Current status of PCB toxicity to mink, and effect on their reproduction.

Experiments were conducted from 1968 to 1974 to investigate reproductive complications and mortality in mink fed Great Lakes coho salmon and to ascertain the effects of polychlorinated biphenyls (PCB's) on this fur bearer. The results of mink feeding trials indicated that coho salmon, as such, were not responsible for the loss of reproduction in the adult, or the kit mortality. Mink diets that contained other species of Great Lakes fish caused similar reproductive complications, but to a lesser degree. Rancidity, mercury poisoning and chlorinated hydrocarbon pesticide contamination of the fish were all discounted as being responsible for the problem. The clinical signs and lesions noted in mink that died while receiving diets that contained Lake Michigan coho salmon were very similar to those observed in mink fed on rations that contained supplemental PCB's. These included anorexia, blood stools, fatty liver, kidney degeneration, and hemorrhagic gastric ulcers. Analyses of tissues from mink that died when fed 30% Lake Michigan coho salmon or 30 ppm supplemental PCB diets showed similar PCB residues. PCB toxicity experiments revealed that mink are very sensitive to these compounds and that the lethal dose varied inversely with the chlorine content of the PCB's although only Aroclor 1254 exerted a detrimental effect on reproduction when fed at a low level (2 ppm) for 8 months. The reproductive failure encountered in feeding mink Lake Michigan coho salmon and Aroclor 1254 was shown to be of a non-permanent nature.

Animal Feed↗
PubMed1977

Detection of inapparent Aleutian disease virus infection in mink.

The normal serum gamma-globulin centration of mink from the Ontario Veterinary College field station was 13.2 +/- 2.6% of total serum proteins. Mink serum gamma-globulin concentrations above 21%, which represented 3 standard deviations above the normal mean, were considered to be hypergammaglobulinemic. About 39% of pastel mink infected naturally with Aleutin disease virus (ADV) exhibited an inapparent or nonprogressive infection. These nonprogressivley infected mink had serum gamma-globulin values below 21% andhad antibody titers less than 256 if tested by the couterimmunoelectrophoresis technique. Mink maintained inapparent infection for at least 10 months after infection with ADV. Neither gross nor histopathologic changes were present in the mink with inapparent ADV infection. The virus persisted in blood, mesenteric lymph nodes, kidney, liver, and spleen of mink with non-progressive infection, although the amount of virus present probably was small.

Aleutian Mink Disease↗
PubMed1978

Transmission of Aleutian disease from mink with inapparent infections.

In apparent or nonprogressive Aleutian disease virus infection was considered a subclinical but persistent viral infection in which infected mink did not develop tissue lesions, hypergammaglobulinemia, or high antibody titers. Transmission of Aleutian disease virus from mink with this type of infection was measured. Mink with inapparent Aleutian disease appeared healthy and had normal gamma-globulin values, but were capable of transmitting the disease by direct and indirect horizontal contact. The risk of direct or indirect horizontal transmission from mink with inapparent infection was less than from mink with progressive Aleutian disease. Infection also was directly transmitted from the dam to the kits, but again the risk of infection from dams with inapparent infection was less than from dams with progressive Aleutian disease. Mink infected from their dams before weaning developed the disease more slowly than mink which became infected after weaning.

Aleutian Mink Disease↗
PubMed1978

Isolation and characterization of an endogenous type C RNA virus of mink (Mv1Lu) cells.

Cells of the established MvlLu mink line spontaneously released a reverse transcriptase-containing virus after long-term passage in tissue culture. By molecular hybridization, DNA of normal mink cells was found to possess extensive nucleotide sequence homology with a reverse-transcription product of the viral genome, demonstrating that the new isolate was an endogenous virus of mink origin. The mink virus shared antigenic determinants with the major structural proteins of known mammalian type C viruses. Double-antibody competition radioimmunoassays were developed by utilizing the purified major structural protein, p30, of the mink endogenous virus. The virus was shown to possess antigenic determinants unique from those of other known mammalian type C viruses. It exhibited a higher degree of immunological cross-reactivity with endogenous rat type C and horizontally transmitted feline leukemia viruses than with other mammalian type C viruses tested. The finding that mink cells can remain nonvirus producing for many cell generations argues that there normally exists some cellular restriction to endogenous virus expression in this species.

Animals↗
PubMed1978

Comparison of the lesions of Aleutian disease in mink and hypergammaglobulinemia in ferrets.

Gross and microscopic lesions of Aleutian disease (AD) in mink and hypergammaglobulinemia in ferrets were compared. Both conditions were characterized by widespread proliferation of plasma cells, but proliferation was more prominent in mink infected with AD. Arteritis did not occur in hypergammaglobulinemic ferrets. Minimal or no glomerular alterations occurred in infected ferrets, but were severe in mink infected with AD. Bile duct proliferation was more prominent in diseased mink. Tissue alterations suggested that AD in Aleutian genotype mink is more rapidly progressive than is AD in ferrets, causing overt clinical disease and death. In contrast, hypergammaglobulinemia in ferrets appeared to progress more slowly, with little clinical evidence of disease. This is probably the result of a paucity of glomerular lesions in ferrets. Possible mechanisms to explain the differences in the development of lesions are discussed.

Aleutian Mink Disease↗
PubMed1975

[Pathogenesis of aleutian mink disease. VII. Chronic hepatitis with bile duct proliferation].

Aleutian disease is a chronic persistent viral infection of mink characterized by hypergammaglobulinema, generalized plasmacytosis, sclerosing glomerulonephritis, polyarteritis, and plasma cell hepatitis with bile duct proliferation. The development of hepatic lesions was studied both light- and electron-microscopically in mink experimentally infected with Aleutian disease virus. Fifteen normal and 99 mink experimentally infected with Aleutian disease virus were used. Experimental mink were killed in intervals from 3 weeks to 23 months after infection, and liver sections were processed for both light- and electron-microscopic studies. Experimentally infected mink developed portal and intralobular lymphocytic and plasmacytic infiltrates in the liver 3 weeks after infection. Four to five weeks after infection there was evidence of early bile duct proliferation that began as an outgrowth of the portal bile ducts. Three to five months after infection a marked bile duct proliferation was present in some of the portal triads and adjacent liver lobules; but there was no tendency of these lesions to progress into biliary cirrhosis. Ultrastructural characteristics of proliferating bile duct cells were marked deformation, formation of multiple cell layers, reduction in the number of microvilli and desmosomes, and infiltration of the epithelial cells by lymphoid cells and plasmacytes. The hepatic lesions either develop by direct virus stimulation or by the deposition of virus-antibody complexes.

Aleutian Mink Disease↗
PubMed1979

Abnormal retino-geniculate and geniculo-cortical pathways in several genetically distinct color phases of the mink (Mustela vison).

Several genetically distinct color phases of mink, which all show an abnormal reduction of pigment in the retinal pigment epithelium and which also show abnormalities of the retinofugal pathways, have been studied. Autoradiographic methods have been used to demonstrate the retino-geniculate pathways, and retrograde degeneration or the retrograde transport of horseradish peroxidase has been used for the geniculo-cortical pathways. The retino-geniculate abnormality is mild in some of the color phases and extremely severe in others, but within any one color phase the variability is relatively low. Although the severity of the abnormality varies between color phases, a rather specific pattern of abnormal geniculate innervation is recognizable for mink in general and this is distinct from that found in Siamese cats. In the abnormal mink the size of geniculate lamina A1 is reduced and there is an abnormal crossed input going to the intermediate sectors of this reduced layer. Layer C1 also receives an abnormal crossed input, but this is more variable than that going to A1 and there appears to be little correspondence, retinotopically, between the normal inputs to layers A1 and C1. In some of the abnormal mink there are interruptions within the cytoarchitectionically definable layer A1, and opposite these gaps reduplications of layer A are commonly seen, as though there is an intrinsic geniculate mechanism for generating the characteristic multilaminar geniculate structure. However, there are also numerous examples of fusions between layers receiving afferents from the same eye, and these demonstrate that the development of geniculate lamination must also be under the influence of the retinal inputs. The geniculo-cortical pathway shows a normal topography in most of the mink. Abnormal geniculo-cortical projections, comparable to the "Boston" pattern of Siamese cats are extremely rare, and their occurrence could not be correlated with the severity of the retino-geniculate abnormality or with the laminar pattern in the lateral geniculate nucleus. We suggest that the development of one or the other pattern of geniculo-cortical projection may depend upon the relative timing of the two mechanisms that produce the geniculate lamination.

Animals↗
PubMed1979

Toxic effects of dietary polybrominated biphenyls on mink.

Serial levels of fireMaster FF-1, a commercial mixture of polybrominated biphenyls (PBB), and tissues from chickens and a cow that had previously consumed PBB were fed to mink to ascertain the chronic effects of the commercial and "metabolized" form of this compound on mink. Diets that contained 6.25 ppm (or more) PBB were lethal to adult mink within 10 months. One to 2.5 ppm dietary PBB fed for 9 months had an adverse effect on litter size, kit weight at birth, and kit survival. The data suggest that the PBB derived from contaminated beef and poultry was more toxic than the original PBB. The clinical signs of PBB poisoning in mink were food rejection, weight loss, and unthrifty appearance, and fatty infiltration of the liver. Based on these findings, mink must be considered highly susceptible to PBB toxicity. PBB residue levels 60 times the amount in the diet were found in the adipose tissue of the PBB-treated animals.

Animals↗
PubMed1979

Characterization of a retrovirus isolated from normal mink cells co-cultivated with a dog mammary tumour.

A retrovirus antigenically distinct from known type C, B and D viruses was isolated from normal mink (Mustela vison) lung cells that had been co-cultivated with 5-iododeoxyuridine- and dexamethasone-treated dog mammary tumour cells. Cytogenetic studies of the virus-releasing co-culture showed mitotic figures identical to the normal mink cell line (MvlLu) with the exception of a low frequency of cells with extensive chromosomal breakage and uncoiling. The new virus bands at a buoyant density of 1.16 g/ml, contains 60S RNA and a reverse transcriptase which prefers Mn2+ over Mg2+ for the synthesis of DNA. This enzyme utilizes poly(rA).oligo(dT) more efficiently than poly(dA).oligo(dT) and is also able to synthesize DNA copies from the endogenous RNA. Morphologically, it is a typical type C virus. Filtered virus readily infects mink, dog and other mammalian cells indicating the amphotropic nature of its cell growth requirement. Hybridization studies showed that normal mink DNA contains multiple copies of proviral sequences of this newly isolated virus. Serological analyses indicate that the mink endogenous virus contains in its core protein, in addition to the interspecies type-C determinant, an antigenic component related to one of the determinants found in the feline leukaemia virus p30 protein. This determinant is not present in the Rauscher leukaemia virus, RD114 virus or simian sarcoma virus.

Animals↗