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At least 37 records · Page 2Linked to original sources
PubMed1977

Anticoccidial activity of eight compounds in domestic mink.

Eight compounds were tested for anticoccidial activity in 44 domestic mink (Mustela vision). A treatment group consisted of 4 mink exposed to 2 inoculumns of sporulated oocysts on day 0 and day 22 of the experiments. Each inoculum contained 2,000 Isospora laidlawi, 2,000 Eimeria vision, and 2,000 Eimeria sp. One compound was administered to each treatment group; a control of 4 juvenile mink and a control group of 4 adult mink were designated. All treatments were given each day for 30 days after the initial exposure, except lincomycin which was administered for 14 days. In juvenile mink (3 to 4 months old), amprolium at dose level of 0.012% and sulfaquinoxaline at dose level of 0.024% in the water inhibited almost all of the oocyst production when compared with that of the control group. Lincomycin injected at dose level of 5 mg/day/mink was ineffective in suppressing oocyst production. In adult mink (2 to 4 years) monensin sodium at dose level of 0.012% a commercial antiobiotic-sulfonamide mixture at dose level of 0.49%, and lasalocid solium at dose level of 0.01% in the feed inhibited almost 100% oocyst production. Lasalocid sodium at dose level of 0.10% in the feed was lethal to 3 to 4 mink. Sulfamethazine at dose level of 0.014% and sulfathiazole at 0.014% in the feed had limited anticoccidial activities.

Amprolium↗
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↗
PubMed1976

Toxic and carcinogenic effects of nitrosodimethylamine in mink.

In a feeding experiment, 96 mink divided into four groups were kept on diets in which each animal received from 0.04-0.07 mg/kg bw NDMA/day. After four months' feeding the mink were still in good health. Except for 20 mink kept for breeding, the animals were skinned. They showed no gross lesions; however, in the livers of mink receiving a total of 16-21 mg/kg bw NDMA some of the smaller hepatic veins were partially occluded. The 20 remaining mink and their offspring were all kept on the same diet, which included 10% herring meal with a NDMA content of 7.2-7.8 mg/kg. After 233 experimental days and a total intake of 26 mg/kg bw NDMA one male died of liver fibrosis and occlusive changes in the hepatic veins. The remaining 16 in the parent group and 22 in the F1 group developed haemangiomatous liver tumours after a total intake of 25-87 mg/kg bw NDMA. The carcinogenic action of NDMA on mink appears to be nearly 100% if the exposure time is long enough and if the dose is near to the hepatotoxic level.

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 disease of mink: identification of nonpersistent infections.

Aleutian disease virus usually produces a persistent infection and progressive immune comples disease in mink of the Aleutian genotype. Study of Aleutian disease virus infection in non-Aleutian mink showed that about one-quarter developed nonpersistent infections by the virus, and that the nonpersistence was not genetically determined by the host. The nonpersistently infected mink developed only a transient elevation of serum gamma globulin, and much lower specific Aleutian disease virus antibody titers than persistently infected mink. No lesions were found in the nonpersistently infected mink.

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↗
PubMed1979

Susceptibility of mink to certain viral animal diseases foreign to the United States.

Mink (Mustela vison) were inoculated with viruses: African horse sickness (AHS), African swine fever (ASF), bovine herpes virus II (BHV2), foot-and-mouth disease (FMD), goat pox (GP), hog cholera (HC), peste des petits ruminants (PPR), rinderpest (RP), swine vesicular disease (SVD), vesicular exanthema of swine (VES) and vesicular stomatitis (VS). Their susceptibility was measured by development of clinical signs, virus isolation and detection of precipitin and/or virus neutralizing antibodies. SVD virus produced a lesion in one mink. Virus was isolated from mink inoculated with SVD, FMD and BHV2. Neutralizing and/or precipitin antibodies were detected in mink inoculated with ASF, FMD, GP, RP, SVD and VS viruses. Mink were not susceptible to AHS, HC, PPR and VES viruses.

African Horse Sickness↗
PubMed1979

Protection against hemorrhagic pneumonia of mink by Pseudomonas aeruginosa multicomponent vaccine.

An attempt to prevent epidemics of hemorrhagic pneumonia in mink due to Pseudomonas aeruginosa was made in the course of epidemics with injection of the multicomponent vaccine consisting of common protective antigen (OEP) of P. aeruginosa mixed with toxoids of protease and elastase of the bacillus. Enzootics of hemorrhagic pneumonia, due to P. aeruginosa serotype 8, broke out from August to October 1977 in a total of 13 sheds of 3 farms (A, B and C) which were located in the northeast area of Hokkaido. These farms were raising 7,452, 2,553 and 10,639 mink respectively. The mortality rate of the mink on farms A, B and C were 11.8%, 13.0% and 1.0% respectively. The vaccination was performed on the 3 farms 5, 8 and 21 days after the onset of the disease. Inoculation of each mink with 200 micrograms or 100 micrograms of each of the three components of the multicomponent vaccine was effective in most of the male and female groups of mink. The period required for revealing the effect of the vaccination was very short, in some cases only a few days. Administration of the vaccine 21 days after the onset of the enzootic was also effective.

Animals↗
PubMed1975

[Isolation of reoviruses from mink].

In this first report of the isolation of reovirus from mink, isolates were obtained from 18 to 26 young mink with viral enteritis, by using cultures of cat kidney cells. The isolated also produced cytopathic changes in cell cultures of mink kidney, dog kidney, piglet kidney, calf kidney, bovine embryonic kidney and calf testis. A characteristic feature was the formation of eosinophilic inclusion bodies in the cytoplasma of culture cells. Haemagglutination tests were negative with erythrocytes from cat, rabbit, pig, horse and cattle. Attempts to infect old and young mink, kittens and ferrets with tissue culture material failed. It was not known to what extent this second infection with reovirus influenced the course of mink viral enteritis.

Animals↗
PubMed1977

Effects of the common protective antigen (OEP) and toxoids of protease and elastase from Pseudomonas aeruginosa on protection against hemorrhagic pneumonia in mink.

The effects of common protective antigen (OEP) of Pseudomonas aeruginosa strain N10 (serotype 5) and OEP plus toxoids of protease and elastase from P. aeruginosa strains IFO 3080 and IFO 3455 were studied during an enzootic of hemorrhagic pneumonia caused by P. aeruginosa serotype 3 in mink. The overall mortality rate in non-vaccinated mink was 24.8% (524 mink). It was highest in male kittens, followed by female kittens and adults. OEP (1,000 millimicrong) plus toxoids (each 1,000 millimicrong of protease toxoid and elastase toxoid) was significantly protective in every stable or farm regardless of sex or age. It was also effective in a stable where the vaccine was administered 12 days after the onset of the disease. OEP (1,500 millimicrong) alone produced a similar effect in a majority of mink, but was less effective in some stables. OEP plus toxoids was significantly more effective than OEP alone in protecting mink against hemorrhagic pneumonia due to P. aeruginosa.

Age Factors↗
PubMed1976

Effect of common protective antigen vaccination to protect mink from challenge exposure with Pseudomonas aeruginosa.

The protein portion of endotoxin (OEP), or common antigen of Pseudomonas aeruginosa prepared from strain N10 of P aeruginosa, was examined as a possible vaccine against this organism in mink. Mink were given OEP vaccine and challenge exposed by instillation with the inoculum into the nostril. They survived after this exposure with 4 median lethal (LD50) doses of strain NC-5 (protease negative, elastase negative) or with 160 LD50 doses of strain 5 (protease positive, elastase positive). Strain NC-5 belonged to TYPE 5 AND strain 5 belonged to type 8 (according to the serotyping method of Homma). Strain N10, the source of OEP, belonged to serotype 5. Thus, the mink vaccinated with OEP vaccine were able to stand challenge exposure to both homologous and heterologous serotype strains. More mink given OEP vaccine survived the challenge exposure by intranasal spraying with virulent strain 5 than did those in the nonvaccinated control group, with a significant difference. When the surviving mink of the vaccinated group were rechallenge exposed with 300 or 3,000 LD50 doses of the same strain a month later, most of them survived.

Administration, Intranasal↗
PubMed1977

[Aneuploidy and polyploidy in the bone marrow cells of minks of different genotypes, ages and fertility].

An analysis of aneuploidy and polyploidy in bone marrow cells of female minks of different genotype and age has shown that in young minks with unsatisfactory reproductive characteristics, and in old females, the frequency of aneuploid and polyploid cells is significantly higher as compared to that in minks having a good reproductive capacity. The increase in aneuploidy level takes place mainly in the form of hypoploidy, and an increase of the frequency of polyploid cells is accompanied by a parellel increase of the proportion of cells with a low degree of ploidy. A correlation between frequencies of appearance of aneuploid and polyploid cells in minks is observed (r = 0.69 +/- 0.27). On the basis of original and bibliographic data, a hypothesis on a genetically determined instability of karyotype in mutant minks is argumented.

Age Factors↗
PubMed1978

San Miguel sea lion virus fed to mink and pigs.

Mink became infected with San Miguel sea lion virus when fed ground meat from seal carcasses showing vesicular-like lesions in the skin. The mink also contracted the infection when they were fed San Miguel sea lion virus infected pig meat or cell culture propagated virus. San Miguel sea lion virus infection in mink was inapparent but the virus was isolated from blood and rectal swabs. Pigs treated similarly with the same virus preparations given to mink developed a severe vesicular disease syndrome similar to that produced by vesicular exanthema of swine. In a separate trial, pigs fed a large sample of commercial ground seal meat did not develop disease signs or antibodies. Further work is needed to assess the hazard of introducing San Miguel sea lion virus into swine on the same premises when potentially San Miguel sea lion virus infective seal meat is fed to mink.

Animal Feed↗
PubMed1979

Multiple myeloma in a mink handler following exposure to Aleutian disease.

Aleutian disease of mink is a viral illness characterized by systemic plasmocytosis and hypergammaglobulinemia. Some affected mink develop a monoclonal gammaglobulin spike and Bence-Jones proteinuria. A case of multiple myeloma in a mink handler with a 15-year history of exposure to Aleutian mink is presented. Previously reported cases of possible Aleutian disease (AD) in man are discussed and the pathogenesis of AD reviewed. Aleutian disease virus (ADV) may produce asymptomatic infection in exposed individuals. Available data suggest symptomatic disease in humans is extremely rare.

Aged↗
PubMed1978

Eradication of Aleutian disease of mink by eliminating positive counterimmunoelectrophoresis test reactors.

The counterimmunoelectrophorsis test was applied on three Aleutian disease virus-infected mink ranches for the detection of specific Aleutian disease virus antibody. All mink on the ranches were tested during the pelting season and before the breeding season for 4 consecutive years. Aleutian disease has been eliminated from the three commercial mink ranches by culling out all mink that were positive for Aleutian disease virus antibody.

Aleutian Mink Disease↗