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Model No. 33
Reprinted
from:
THE AMERICAN JOURNAL OF PATHOLOGY
7 1:2, 345—348, May 1973
Persistent Viral Infections
Human Disease:
Immunologically Mediated Glomerulonephritis and Arteritis,
Dysgammopathies
Animal Disease:
Aleutian Disease of Mink
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 Ore-
gon and was named the Aleutian mink; this mutation is homozygous reces-
sive for the Aleutian gene a. In the early 1950’s, a disease involving the kid-
neys, liver and lymphoid tissues of aa mink was recorded,’ 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 parenchvma, 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 dis-
ease. 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 y-globulin and
complement (CS)
.5
Deposition of y-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 ultrastruc-
turally as electron-dense granular deposits subendothelially and, less fre-
© 1973 The American Association of Pathologists and Bacteriologists
Printed in the U.S.A.
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