Hi Everyone! This information is what I have compiled about Aleutian - its
not much and in "medicalese" a lot, but I hope this helps.
 
According to Dr. Elizabeth Hillyer, Aleutian disease, or AD, is caused by a
parvovirus.  It was first reported in ranch-bred mink in the 1950's and was
named after mink homozygous for the aleutian gene, which typically develop
the most severe forms of the disease.  Ferrets can be infected with mink
strains of the AD virus and there is at least one ferret-specific strain of
the AD virus.  The infection in both ferrets and mink is characterized by
viral persistence associated with non-neutralizing antibody.  However,
ferrets infected as adults usually do not develop AD virus-associated
disease.
 
The classic form of AD in mink is in immune complex-mediated disease.
Affected mink show severe hypergammaglobulinemia, glomerulonephritis,
arteritis, plasmacytosis, and progressive wasting.  Death occurs within 5
months of infection in Aleutian mink, which are susceptible to all strains
of the virus.  Depending on the viral strain and host genotype and immune
status, non-Aleutian mink may clear the AD virus, become inapparent
carriers, or develop progressive disease similar to that seen in Aleutian
mink.  Decreased fertility, abortion, and neonatal interstitial pneumonitis
may also be associated with AD virus infection in this species.  Ranch mink
are regularly screened for AD, there is no vaccine for the disease.
 
Ferrets that are experimentally infected with mink strains of AD virus
develop virus-specific antibody and show evidence of persistent infection
for up to 180 days.  however, they do not usually develop the severe disease
seen in mink when they are inoculated with either ferret or mink strains fo
AD virus.  In clinical practice, ferrets can be seropositive for AD virus
without ever developing signs of the disease.  S.  Brown screened over 500
shelter ferrets in Illinios during the 1980's and found that approximately
10% tested seropositive on counterimmunoelectrophoresis.  Only two of these
animals went on to develop signs of disease consistent with AD.
 
AD typically manifests as a wasting disease in ferrets.  Weight loss,
lethargy, pallor, hepatomegaly, splenomegaly, melena, rear leg or
generalized weakness, and neurologic signs are all possible findings.  A
presumptive diagnosis of AD in ferrets is based on the presence of the
typical clinical signs in conjunction with hypergammaglobulinemia and a
positive antibody titer.  Hypergammaglobulinemia is usually pronounced, with
gamma globulins representing more than 20% of total protein, and serum
protein electrophoresis shows a monoclonal spike.
 
The two most common tests for AD virus antibody are
counterimmunoelectrophoresis and immunofluorescent antibody tests.
Counterimmunoelectrophoresis is used for screening mink and is rapid, highly
specific, and inexpensive (contact United Vaccines, 1-608-277-2030) The
immunofluorescent antibody test may be more sensitive than
counterimmunoelectrophosesis.
 
Two case reports describe naturally occurring AD in ferrets.  In one report,
four ferrets aged 2 years or older developed a chronic, wasting disease;
mild hepatomegaly and splenomegaly were present at necropsy.  Histologic
findings varied in severity but included splenic reticuloendothelial cell
hyperplasia, lymphocytic-plasmacytic infiltration in hepatic portal areas,
periportal fibrosis, bile duct hyperplasia, and membranous
glomerulonephritis.  The second case reports AD in two 2 yo castrated male
ferrets, both of which had positive AD virus antibody titers on both
counterimmunofluorescent antibody testing.  Clinical and necropsy findings
in these two animals illustrate the spectrum of disease possible in
association with AD virus.  The first ferret showed anorexia, cachexia,
hypochromic microcytic anemia, progressively increasing hyperglobulinemia,
and tarry feces.  Histologic evaluation at necropsy revealed a
mild-to-severe inflammatory infiltrate composed mostly of plasma cells
interspersed with lymphocytes in multiple organs, including the meninges,
choroid plexus, liver, thyroid gland, heart, salivary glands, common bile
duct, pancreas, kidneys, lungs, and lymph nodes.  The second ferret tested
positive for posterior pareseis;laboratory testing revealed hypoalbuminemia
and hypergammaglobulinemia.  Clinical signs that developed in this animal
included intermittent head tremor, diarrhea, and fecal/urinary incontinence.
On histopathologic exam, infiltrations of plasma cells and lymphocytes were
found in the doudenum, stomach, salivary gland, liver, thyroid gland, lungs
and right atrium; disseminated, nonsuppurative, lymphoplasmacytic
encephalomyelitis was present.
 
There is no specific treatment for ferrets with AD.  Provide supportive care
and be sure that the ferret is on a good diet.  The course of the disease is
typically chronic.  Remember that infected animals can serve as a potential
source of infection for other ferrets.There is no vaccine for the disease.
 
Please remember that this info was gathered in the late 1980's, but all the
information that I have on the disease - their may be newer treatments that
I am not aware of, or other signs of the disease.  To my knowledge, no
current vaccine exists and most vets are not aware of it - probably due to
the fact the disease was first discovered in mink.  IMHO this sounds like a
real nasty virus - as bad, if not worse than ECE.  At least in my
experience, ECE is not fatal, even after infecting 350+ ferrets.
 
Lisa
[Posted in FML issue 1845]