Contributed by:
James B. Henson, DVM, PhD and John R. Gorham, DVM, PhD,
Department of Veterinary Pathology, College of Veterinary Medicine Agricultural
Research Service, US Department of Agriculture, Washington State University,
Pullman, Wash.
Biologic Features
In the early 1940’s a spontaneous mutation with a dark blue coat color (resembling that of the Aleutian fox) occurred in ranch-raised mink in Oregon and was named the Aleutian mink; this mutation is homozygous recessive for the Aleutian gene
a. In the early 1950’s, a disease involving the kidneys, liver and lymphoid tissues of
aa mink was recorded,1 and was called Aleutian disease (AD). It first seemed that only Aleutian mink were affected; however, it has been shown that all genotypes of mink were susceptible to the disease, but
aa mink develop more severe disease with a more rapid course. It appears that a small percentage of non-Aleutian mink may either recover or live for years with AD.
Clinically, AD is characterized by gradual loss of weight, anemia, uremic ulceration of the oral mucosa and rarely nervous signs. The gross lesions include emaciation, hepatomegaly with small pinpoint pale foci scattered through the
parenchyma, generalized lymphadenopathy with the spleen and lymph nodes 2 to 4 times normal size, nephritis characterized by enlarged kidneys with widespread petechiae early in the course and by shrunken pale kidneys with cortical cysts during the later stages. Histologically there is widespread proliferation and infiltration of plasma cells in practically all organs (Figure 1)
2,3,4
These cells are mostly perivascular early in the disease. The plasmacytosis leads to a marked hypergammaglobulinemia, which may exceed 50% of the total serum proteins. The glomeruli in affected kidneys are relatively avascular and contain large amounts of slightly granular, eosinophilic material (Figure 1). The latter represents a proliferation of the mesangeal cells and mesangeal matrix as well as deposited
gamma-globulin and complement (CS)
.5
Deposition of gamma-globulin and CS along the glomerular capillary basement membranes and in the mesangeal areas (Figure 2) are seen by fluorescent
microscopy.6 These deposits can be visualized ultrastructurally as electron-dense granular deposits subendothelially and, less fre-
© 1973 The American Association of Pathologists and Bacteriologists
Printed in the U.S.A.
