Facts about Albino Dobermans
Dr. David Prieur
(updated 6/2/04)
Here are some of the papers
which Dr. Prieur has authored or co-authored, listed here to help demonstrate
his expertise in the field of veterinary genetics and inherited disorders
-- especially including his work with Chediak Higashi syndrome, Maltese
dilution, and the fawn-hooded trait, all disorders of pigment production:
Ahern Rindell, A. J., Murnane, R. D., & Prieur, D. J. (1988).
BETA-Galactosidase activity in fibroblasts and tissues from sheep with
a lysosomal storage disease. Biochemical Genetics, 26(11-12), 733-746.
Tissues and fibroblasts of sheep affected with an inherited, neuronal
lysosomal storage disease expressed a deficiency of beta-galactosidase
activity.....
Ahern Rindell, A. J., Murnane, R. D., & Prieur, D. J. (1989).
Interspecific genetic complementation analysis of human and sheep
fibroblasts with beta-galactosidase deficiency. Somatic Cells and
Molecular Genetics, 15(6), 525-533. Interspecific somatic cell hybrids
were analyzed by genetic complementation to determine if a lysosomal
storage disease in sheep associated with deficiencies of
beta-galactosidase and alpha-neuraminidase was homologous with any 4
beta-galactosidase-deficient human diseases.....
Ahern Rindell, A. J., Prieur, D. J., Murnane, R. D., Raghavan, S. S.,
Daniel, P. F., Mc, C. R. H., Walkley, S. U., & Parish, S. M.
(1988). Inherited lysosomal storage disease associated with
deficiencies of beta-galactosidase and alpha-neuraminidase in sheep.
American Journal of Medical Genetics, 31(1), 39-56.
Amann, J., Ganjam, V. K., & Prieur, D. (1987). Thyroid function and
histology in feline Chediak-Higashi syndrome (CHS). Federation
Proceedings, 46(3), 649.
Amann, J. F., & Prieur, D. J. (1986). Muscle lesions in beige
(Chediak-Higashi syndrome) and heterozygous C57BL/6J mice. Veterinary
Pathology, 23(6), 692-697.
Bell, T. G., Meyers, K. M., Prieur, D. J., Fauci, A. S., Wolff, S. M.,
& Padgett, G. A. (1976). Decreased nucleotide and serotonin storage
associated with defective function in Chediak-Higashi syndrome cattle
and human platelets. Federation Proceedings, 35(3), 807.
Bell, T. G., Meyers, K. M., Prieur, D. J., Fauci, A. S., Wolff,
S. M., & Padgett, G. A. (1976). Decreased nucleotide and serotonin
storage associated with defective function in Chediak-Higashi syndrome
cattle and human platelets. Blood, 48(2), 175-184. T....Serotonin
content in CHS bovine platelets was only about 1.2% of the content in
normal platelets. ATP and ADP contents in bovine CHS platelets were
subnormal. The ATP/ADP ratio in normal platelets was 5.04, as opposed
to 29.38 in CHS platelets. Similar studies were carried out in
platelets from human beings with CHS.
Burns, G. L., Meyers, K. M., & Prieur, D. J. (1984). Secondary
amyloidosis in a bull with Chediak-Higashi syndrome. Canadian Journal
of Comparative Medicine, 48(1), 113-114.
Collier, L. L., Bryan, G. M., & Prieur, D. J. (1979). Ocular
manifestations of the Chediak-Higashi syndrome in four species of
animals. Journal of the American Veterinary Medical Association,
175(6), 587-590. Ocular examinations performed on cattle, cats, mink,
and mice affected with the Chediak-Higashi syndrome (CHS) revealed
photophobia, pale irises, and fundic hypopigmentation associated with
red fundic light reflections. Cats with CHS also had cataracts.
Spontaneous nystagmus was observed in four of nine cats with CHS, and
the duration of induced nystagmus was longer in affected and Siamese
cats than in clinically normal cats of other breeds. Tear secretion
appeared to be normal in all species of animals with CHS. The ocular
manifestations of CHS in these animals were similar to those reported
in man.
Creel, D., Collier, L. L., Leventhal, A. G., Conlee, J. W., &
Prieur, D. J. (1982). Abnormal retinal projections in cats with
Chediak-Higashi syndrome. Investigative Ophthalmology and Visual
Science, 23(6), 798-801. In two Siamese cats with the syndrome,
fragmentation of the A1 layer of the dorsal lateral geniculate nucleus
into several islands was observed by autoradiographic techniques.
Hargis, A. M., Haupt, K. H., Prieur, D. J., & Moore, M. P. (1985).
Animal model of human disease: dermatomyositis. Familial canine
dermatomyositis. American Journal of Pathology, 120(2), 323-325.
Hargis, A. M., Haupt, K. H., Prieur, D. J., & Moore, M. P. (1985).
A skin disorder in three Shetland sheepdogs: comparison with familial
canine dermatomyositis of Collies. Compendium on Continuing Education
for the Practicing Veterinarian, 7(4), 306-315. A skin disease closely
resembling familial dermatomyositis of Collies is described in one male
and two female Shetland sheepdogs, all sired by the same father.
Dermatitis first developed at 8-10 weeks of age. The two females had
myositis, but it was prominent in only one. The male was infertile. A
tentative diagnosis of epidermolysis bullosa was discounted because of
the absence of large skin vesicles. The pedigree of the affected dogs
is presented.
Hargis, A. M., Moore, M. P., Riggs, C. T., & Prieur, D. J. (1989).
Severe secondary amyloidosis in a dog with dermatomyositis. Journal of
Comparative Pathology, 100(4), 427-433. A male Collie aged 5 years and
10 months, which developed dermatomyositis at 2 months of age, died
from severe secondary amyloidosis. Amyloid deposition was most severe
in renal glomeruli and produced renal failure. Amyloidosis has been
reported in man with immune-mediated disorders including rheumatoid
arthritis, systemic lupus erythematosus and dermatomyositis. It is
suggested that the inflammation in this case of familial canine
dermatomyositis may have predisposed to the development of amyloidosis.
Hargis, A. M., Prieur, D. J., Haupt, K. H., Collier, L. L., Evermann,
J. F., & Ladiges, W. C. (1986). Postmortem findings in four litters
of dogs with familial canine dermatomyositis. American Journal of
Pathology, 123(3), 480-496. Twenty juvenile to young adult collie and
collie-Labrador retriever crossbred dogs with dermatomyositis and 10
newborn collies were examined. Cutaneous, muscular, and vascular
lesions were present in the juvenile and adult dogs and were most
severe around the head and distal extremities. In more severely
affected dogs, lesions were more generalized, including myositis of
oesophageal muscle and arteritis of skin, muscle, bladder, and
spermatic cord. Although viruses were not isolated from muscle,
crystalline viral-like structures were present in cytoplasm of
endothelial cells within skeletal muscle. The dogs with dermatitis and
myositis consistently had lymphoid hyperplasia, especially of
peripheral lymph nodes. More severely affected dogs were smaller than
less severely affected littermates, and the more severely affected
males had reduced weight of testicles and prostate glands, compared
with body weight. The reduced weight of genital organs was correlated
positively with reduced fertility. A few lymphoid aggregates were
present in or around thyroid glands of 6 of the 20 dogs. There were no
histological signs of glomerular disease in any of the dogs. The
newborn collies had no signs of dermatomyositis. [See also American
Journal of Veterinary Research (1985) 46 (9) 1861-1875].
Hargis, A. M., Prieur, D. J., Haupt, K. H., McDonald, T. L., &
Moore, M. P. (1986). Prospective study of familial canine
dermatomyositis. American Journal of Pathology, 123(3), 465-479.
Familial canine dermatomyositis in collie dogs is a newly recognized
spontaneous disease resembling dermatomyositis in children. In a litter
of 9 collie dogs studied from birth to 7.5 months of age, the onset and
severity of dermatitis and myositis were correlated with increased
serum circulating immune complexes (CICs) and IgG. The immunoglobulin
component of the CICs consisted principally of IgG. All dogs showed
increases in CIC before or at the onset of dermatitis. Myositis
developed later. The CIC reached a peak between 14-18 weeks of age in
all dogs except the most severely affected dog, in which the CICs
continued to increase to 238 µg/ml (controls 30 µg/ml) at 7
months of age. In the moderately affected dogs the CICs reached stable
levels at 14-18 weeks, and in the mildly affected dogs the CICs
decreased to normal after 14-18 weeks. Although the dogs had
electromyographical and repetitive nerve stimulation abnormalities, the
abnormalities did not correlate with severity of dermatomyositis or
increases in CICs or IgG. PM examination at 7.5 months of age showed
that all dogs had myositis and 8 of 9 had dermatitis. Except for 1 dog,
the severity of dermatomyositis was correlated positively with
increases in CICs. A strong positive association between increases in
CICs and IgG, but not IgM or IgA, was generally present. Increased CICs
appear to be involved in the mechanisms that control the development,
severity, and progression of dermatomyositis in collie dogs.
Hargis, A. M., Winkelstein, J. A., Moore, M. P., Weidner, J. P., &
Prieur, D. J. (1988). Complement levels in dogs with familial canine
dermatomyositis. Veterinary Immunology and Immunopathology, 20(1),
95-100. CH50, C4, C2, and C3 levels were measured in 7 dogs with
dermatomyositis and in 22 control dogs. Dogs with dermatomyositis did
not have clinical evidence of active disease at the time of serum
collection for complement assays. No absolute complement component
deficiency was identified in dermatomyositis-affected dogs in this
study; however, a statistical difference in C2 was identified between
control dogs of non-Collie breeds and control Collies, suggesting there
may be a breed difference in complement levels.
Haupt, K. H., Hargis, A. M., Prieur, D. J., Hegreburg, G. A., &
Moore, M. P. (1984). Familial canine dermatomyositis: preliminary
studies on a canine model of human dermatomyositis. [Abstract].
Federation Proceedings, 43(3), 708. Breeding experiments were conducted
with two Collies affected by dermatitis and myositis (also called
epidermolysis bullosa). The condition developed at 7-11 weeks of age in
all 6 puppies of an inbred litter. The mode of inheritance seemed to be
autosomal and dominant.
Haupt, K. H., Prieur, D. J., Hargis, A. M., Cowell, R. L., McDonald, T.
L., Werner, L. L., & Evermann, J. F. (1985). Familial canine
dermatomyositis: clinicopathologic, immunologic, and serologic studies.
American Journal of Veterinary Research, 46(9), 1870-1875. Laboratory
studies were performed on 3 Collies with familial canine
dermatomyositis, 6 progeny from a breeding of 2 of the Collies (incross
litter), and 4 progeny from the breeding of an affected Collie male and
a normal Labrador Retriever (outcross litter). Haematological
abnormalities were leukogram changes consistent with inflammation and,
in 2 severely affected incross dogs, anaemia of inflammatory disease.
Serum muscle enzyme activities were not greatly increased. High
concentrations of immune complexes and proportionally increased total
IgG were present in the serum of moderately and severely affected
incross dogs. The same dogs had weakly positive direct Coombs tests,
and one affected outcross dog had a strongly positive direct Coombs
test. Rheumatoid factor was present in a severely affected incross dog.
A few dogs had polyclonal globulin increases that were attributed to
inflammation. Low antibody titres to canine calicivirus were present in
3 dogs and a low titre to canine coronavirus was present in one dog.
Haupt, K. H., Prieur, D. J., Moore, M. P., Hargis, A. M., Hegreberg, G.
A., Gavin, P. R., & Johnson, R. S. (1985). Familial canine
dermatomyositis: clinical, electrodiagnostic and genetic studies.
American Journal of Veterinary Research, 46(9), 1861-1869. Three
affected Rough Collies (2 male littermates and an unrelated female)
were studied clinically. Experimental matings were carried out with 1
affected male mated to the affected female and also to an unaffected
Labrador Retriever. Semen evaluation indicated that the other male was
infertile. The 6 live progeny from the mating between affected parents
all developed by 7-11 wk of age a similar, but variably severe,
dermatitis and later myopathy. Three of the 4 progeny from the other
mating had milder forms of dermatitis and myopathy. Although pedigree
analysis showed a definite familial tendency for canine
dermatomyositis, there was no evidence for a simple autosomal recessive
or dominant mode of inheritance, due to the variable expression of the
disease.
Haupt, K. H., Prieur, D. J., Moore, M. P., Hargis, A. M., Hegreberg, G.
A., Gavin, P. R., & Johnson, R. S. (1985). Familial canine
dermatomyositis: clinical, electrodiagnostic, and genetic studies.
American Journal of Veterinary Research, 46(9), 1861-1869. Three
Collies with a skin disorder, 6 progeny from a breeding of 2 of the
Collies (incross litter), and the 4 progeny from the breeding of an
affected Collie male and a normal Labrador Retriever female (outcross
litter) were examined. By 7 to 11 weeks of age, all 6 dogs in the
incross litter, developed a qualitatively similar, but variably severe,
dermatitis of the ears, face, lips, tip of the tail, and over bony
prominences of limbs. Later, myopathic signs characterized by
bilaterally symmetrical skeletal muscle atrophy of the head, neck,
trunk, and extremities; facial palsy; decreased jaw tone; stiff gait;
and hyperreflexia were observed in the dogs more severely affected by
the dermatitis. Of the 4 dogs in the outcross litter, 3 had similar,
but milder, dermatitis and myopathy. Cutaneous lesions consisted of
intraepidermal and subepidermal vesicles or pustules with intradermal
infiltration by leukocytes. Muscle lesions included myositis; myofibre
degeneration, regeneration, and atrophy; and fibrosis. A generalized
myopathy in the severely affected dogs was indicated by abnormal
readings on needle electromyograms and normal motor nerve conduction
velocities. Spontaneous needle electromyogram abnormalities were
fibrillation potentials, positive sharp waves, and bizarre
high-frequency discharges. Retrospective and prospective genetic
analyses disclosed a definite familial tendency and indicated an
autosomal dominant component.
Hegreberg, G. A., Padgett, G. A., Prieur, D. J., & Johnson, M. I.
(1975). Genetic studies of a muscular dystrophy of mink. Journal of
Heredity, 66(2), 63-66. Analysis of breeding data on 12 litters from 7
males and 12 females revealed that muscular dystrophy is transmitted in
an autosomal recessive manner. Variation in skeletal muscle fibre
diameter size was the most pronounced and consistent change in
dystrophic mink. Other changes included centralisation of nuclei,
degenerative change, increase in endomysial and perimysial connective
tissue, and regenerative attempts. These changes were not present in
known heterozygotes.
Kahraman, M. M., & Prieur, D. J. (1987). Application of the feline
model of Chediak-Higashi syndrome for prenatal diagnosis via fetal
blood examination. Federation Proceedings, 46(3), 425.
Kramer, J. W., Davis, W. C., & Prieur, D. J. (1975). An inherited
condition of enlarged leukocytic and melanin granules in cats: probable
homology with the Chediak-Higashi syndrome. Federation Proceedings,
34(No.3), 861. The Chediak-Hagashi syndrome (CHS) is an autosomal
recessive condition manifested morphologically by enlarged cytoplasmic
granules in many cell types. CHS has been described in man, mink,
cattle, mice and in a killer whale. A condition in a line of Persian
cats which resembles CHS was recently observed. Enlarged cytoplasmic
granules were present in leucocytes and melanophores in all the Persian
cats (4) with yellow eyes and the 'Blue Smoke' coat colour which were
examined, but were absent in related cats without the specified ocular
and coat colours. Analysis of the pedigree of this family of cats
suggests that the trait is inherited as an autosomal recessive
condition. Round acidophilic cytoplasmic inclusions varying in diameter
from 1 to 2 mu were present in Wright's stained neutrophils. These
inclusions were detected in neutrophils from the myeloblast to the
segmented stage. Electron microscopic cytochemistry revealed enlarged
peroxidase-positive granules which thus correspond to azurophilic
(primary) granules. Hair and skin from these cats contained enlarged
melanin granules as compared to normal cats. Although an increased
susceptibility to infection was not apparent, a bleeding tendency was
present in these cats. The evidence suggests that the condition in
these cats is homologous with CHS.
Kramer, J. W., Davis, W. C., & Prieur, D. J. (1977). The
Chediak-Higashi syndrome of cats. Laboratory Investigation, 36(5),
554-562. Initial clinical, genetic, cytochemical, and ultrastructural
studies were carried out to characterize the Chediak-Higashi syndrome
in cats. Three cats with Chediak-Higashi syndrome were found in a
single line of 27 Persian cats, and three additional affected cats were
produced from two prospective breedings of the original line. The
disorder was characterized genetically as an autosomal recessive
condition. All cats in the line with the combination of yellow eye
color and "blue smoke" hair colour exhibited the disorder. Four of the
five cats examined had bilateral nuclear cataracts as early as three
months of age. No increased susceptibility to infectious disease was
observed. A bleeding tendency was noted. Abnormally large eosinophilic,
sudanophilic, peroxidase-containing granules were observed in the
neutrophiles of the granulocytic series of blood and bone marrow by
electron and light microscopy. Granules of eosinophiles and basophiles
were also enlarged. Light microscopic studies of hair and skin revealed
enlarged melanin granules. These manifestations were similar to those
in man, mink, cattle, mice, and the killer whale with Chediak-Higashi
syndrome. Cats are the sixth species in which this genetic disease has
been reported.
Kramer, J. W., Klaassen, J. K., Baskin, D. G., Prieur, D. J., Rantanen,
N. W., Robinette, J. D., Graber, W. R., & Rashti, L. (1988).
Inheritance of diabetes mellitus in Keeshond dogs. American Journal of
Veterinary Research, 49(3), 428-431. The genetic aspects of inherited,
insulin-dependent diabetes mellitus of Keeshond dogs were studied
retrospectively and in a prospective mating programme. The symbol dm
was used to designate the gene that causes hypoplasia of the islets of
Langerhans. The retrospective study disclosed 4 diabetic dogs;
prospective outcross, backcross, and inbred matings disclosed 49
diabetic dogs. Outcrossing demonstrated that the diabetic phenotype was
displayed readily against a genetic background of a breed other than
the Keeshond. In dogs with the dm/dm genotype, onset of diabetes was
most frequent before the dog was 6 months old, but did occur in some
older dogs. The dm genotype was best described as autosomal recessive.
Kramer, J. W., Davis, W. C., Prieur, D. J., Baxter, J., &
Norsworthy, G. D. (1975). An inherited disorder of Persian cats with
intracytoplasmic inclusions in neutrophils. Journal of the American
Veterinary Medical Association, 166(No.11), 1103-1104. A newly
recognized, heritable disease of Persian cats which is characterized by
eosinophilic, intracytoplasmia inclusions in neutrophils is reported.
Despite absence of clinical disease or history of increased
susceptibility to infection, the features of the disease i.e. the
peroxidase positive, abnormally large primary granules of neutrophils,
enlarged melanin granules, pigment dilation of hair colour (all three
effected animals have blue smoke hair), increased bleeding time and the
believed autosomal recessive mode of inheritance suggest that the
disease is best classified as the Chediak-Higashi syndrome of cats.
McCluer, R. H., Daniel, P. F., Raghavan, S., Ahern Rindell, A. J.,
& Prieur, D. J. (1987). Glycolipids and oligosaccharide
accumulation in the brain of sheep with beta-galactosidase deficiency.
Journal of Neurochemistry, 48(Suppl.), S129.
Menard, M., Meyers, K. M., & Prieur, D. J. (1990). Absence of dense
granule precursors in megakaryocytes from cats with the Chediak-Higashi
syndrome. Veterinary Clinical Pathology, 19(1), 6-7.
Meyers, K. M., Holmsen, H., Seachord, C. I., Gorham, J., & Prieur,
D. (1979). Characterization of platelets from mink and cats with the
Chediak-Higashi syndrome. Thrombosis and Haemostasis, 42(1), 218.
Meyers, K. M., Hopkins, G., Holmsen, H., Benson, K., & Prieur, D.
J. (1982). Ultrastructure of resting and activated storage pool
deficient platelets from animals with the Chediak-Higashi syndrome.
American Journal of Pathology, 106(3), 364-377. The ultrastructure of
platelets from Chediak-Higashi (CH) and normal cattle, mink, and cats
at rest was studied. Platelets from CH animals had virtually no
platelet dense granules. Alpha granules, amorphous membrane-surrounded
structures, mitochondria, and microtubules of CH bovine platelets were
similar in number and appearance to those in normal bovine platelets.
Giant CH granules, present in other cells and considered diagnostic of
the syndrome, could not be identified in platelets from CH animals. The
open canalicular system and dense tubule system were not readily
identifiable in resting bovine platelets. The ultrastructure of normal
and CH cattle platelets was investigated at different stages of
ADP-induced aggregation. After platelets changed shape during the first
phase of aggregation, the ultrastructure of CH platelets was similar to
that of normal platelets. The CH platelets composing the aggregates
during irreversible aggregation were not as activated as normal
platelets, even though the aggregation tracings were similar. Normal
and CH cattle platelets treated with thrombin appeared morphologically
similar and were characterized by centrifugal movement of granules.
Meyers, K. M., Seachord, C. I., Prieur, D., & Holmsen, H. (1979). A
serotonin induced biphasic aggregation by platelets from cats with the
Chediak-Higashi syndrome. Thrombosis and Haemostasis, 42(1), 195.
Miller, L. M., Hegreberg, G. A., Prieur, D. J., & Hamilton, M. J.
(1984). Inheritance of congenital myasthenia gravis in smooth fox
terrier dogs. Journal of Heredity, 75(3), 163-166. The phenotypes with
respect to congenital myasthenia gravis of 132 Smooth Fox Terrier dogs
from 25 matings were analysed.....
Murnane, R. D., Ahern Rindell, A. J., & Prieur, D. J. (1991). Ovine
GM1 gangliosidosis. Small Ruminant Research, 6(1-2), 109-118. Ovine GM1
gangliosidosis is a newly described neuronal lysosomal storage disease
first observed in Suffolk sheep. ....
Murnane, R. D., Ahern Rindell, A. J., & Prieur, D. J. (1991).
Ultrastructural lesions of ovine GM1 gangliosidosis. Modern Pathology,
4(6), 755-762. Ovine GM1 gangliosidosis, an inherited disease of sheep
with deficiencies of beta-galactosidase and alpha-neuraminidase,
storage of GM1 ganglioside, asialo-GM1 and neutral long chain
oligosaccharides in the brain, autosomal recessive inheritance, and
histopathological lesions typical of lysosomal storage diseases, has
been described recently.....
Murnane, R. D., Prieur, D. J., Ahern Rindell, A. J., Parish, S. M.,
& Collier, L. L. (1989). The lesions of an ovine lysosomal storage
disease. Initial characterization. American Journal of Pathology,
134(2), 263-270. An inherited disease associated with deficiencies of
beta-galactosidase and alpha-neuraminidase has been identified recently
in sheep.....
Penner, J. D., & Prieur, D. J. (1986). Homology of Chediak-Higashi
syndrome in humans, cats, and mink. [Abstract]. Proceedings of the
Society for Experimental Biology and Medicine, 181(1), 196.
Penner, J. D., Prieur, D. J., Meyers, K. M., & Gorham, J. R.
(1984). Homology of paracrystal formation and lysosomal abnormalities
in fibroblasts from animals with Chediak-Higashi syndrome. [Abstract].
Federation Proceedings, 43(3), 603.
Prieur, D. J. (1972). Defective function of renal lysosomes in mice
with the Chediak-Higashi syndrome. Dissertation Abstracts
International, 32b(No.8), 4933.
Prieur, D. J., Ahern Rindell, A. J., & Murnane, R. D. (1991).
Animal model of human disease. Ovine GM-1 gangliosidosis. American
Journal of Pathology, 139(6), 1511-1513.
Prieur, D. J., Ahern Rindell, A. J., Murnane, R. D., Wright, R. W.,
& Parish, S. M. (1990). Inheritance of an ovine lysosomal storage
disease associated with deficiencies of beta-galactosidase and
alpha-neuraminidase. Journal of Heredity, 81(4), 245-249. Prospective
and retrospective genetic studies were carried out to determine the
mode of inheritance.....
Prieur, D. J., & Collier, L. L. (1978). Animal model of human
disease: Chediak-Higashi syndrome. Animal model: Chediak-Higashi
syndrome of animals. American Journal of Pathology, 90(2), 533-536.
Prieur, D. J., & Collier, L. L. (1981). Inheritance of the
Chediak-Higashi syndrome in cats. Journal of Heredity, 72(3), 175-177.
The phenotypes with respect to the Chediak-Higashi syndrome (CHS) of
245 cats from 67 matings were analysed. It was determined that the gene
for feline CHS, like that in other species with CHS, is inherited in an
autosomal recessive manner with complete penetrance. The symbol ch is
proposed for the gene for CHS in cats. Additional studies revealed
enlarged periodic acid-Schiff positive granules in renal tubule cells
in CHS cats, which provides further evidence of the homologous nature
of CHS among the various species in which it occurs.
Prieur, D. J., & Collier, L. L. (1981). Morphologic basis of
inherited coat-color dilutions of cats. Journal of Heredity, 72(3),
178-182. The melanin granules in hair of black, smoke, blue,
Chediak-Higashi-smoke and pink-eyed dilution cats were studied. The
hair of black cats contains numerous small dark brown to black melanin
granules uniformly distributed throughout all portions. The basis for
the dilution in smoke cats is a paucity of melanin granules in the
basal portions of the hair. Blue cat hair has a larger basic melanin
granule, some very large but relatively regularly shaped granules, and
a non-uniform distribution of granules. The granules in the blue cat
hair resemble those in the hair of dilute mice. The Chediak-Higashi
trait causes even larger basic melanin granules than the blue dilution,
and enlarged and relatively irregularly shaped granules. The melanin
granules in the hair of the pink-eyed dilution cat are very small, and
are yellowish brown compared with the dark brown to black of those of
black, smoke and blue cats.
Prieur, D. J., & Collier, L. L. (1982). Lesions associated with the
Maltese dilution of cats. [Abnormal melanin granules, an autosomal
recessive trait.]. Laboratory Investigation, 46(1), 66a.
Prieur, D. J., & Collier, L. L. (1984). The Maltese dilution of
cats. Feline Practice, 14(4), 23-25, 28-29. Maltese dilution is a
non-deleterious, autosomal recessive, coat-colour trait, the gene for
which is designated d. Manifestations of Maltese dilution are
summarised.
Prieur, D. J., & Collier, L. L. (1984). Maltese dilution of
domestic cats. A generalized cutaneous albinism lacking ocular
involvement. Journal of Heredity, 75(1), 41-44. The Maltese dilution is
an autosomal recessive trait of cats that dilutes black coat colour to
blue, and orange colour to cream. The pigmented cutaneous and ocular
tissues of Maltese dilution and control cats were examined and compared
by light microscopy. Most of the melanin granules in all of the
pigmented cutaneous tissues of the Maltese dilution cats were
aggregated together into large clumps. However, clumped melanin
granules were absent from intraocular tissues containing
melanin-producing cells of either neural crest or optic cup embryologic
origin. It is concluded that the Maltese dilution trait is a unique
generalised albinism without ocular involvement.
Prieur, D. J., & Collier, L. L. (1987). Neutropenia in cats with
the Chediak-Higashi syndrome. Canadian Journal of Veterinary Research,
51(3), 407-408. Neutropenia is often present in human patients with
Chediak-Higashi syndrome, but has not been reported in affected
animals. This study confirms that affected cats have neutropenia,
whereas unaffected cats genotypically heterozygous for the syndrome do
not. No lysozyme activity was detected in the serum.
Prieur, D. J., Fittschen, C., & Collier, L. L. (1984). Blue
Doberman syndrome of dogs: a deleterious macromelanosomal trait.
[Abstract]. Federation Proceedings, 43(3), 603. The coat colour
dilution of blue Dobermans was due to aggregation of melanin granules
into macromelanosomes. Alopecia may result from impaired hair growth
induced by the massive melanin granules.
Prieur DJ, Gorham JR, Wood RK. (2001). Distribution of tyrosine
aminotransferase activity in mink (Mustela vison). Comp Biochem Physiol
B Biochem Mol Biol, Sep;130(2):251-6. The distribution of the enzyme
tyrosine aminotransferase in tissues of mink, Mustela vison, was
investigated. High levels of enzymatic activity were detected only in
liver, documenting the hepatic-specific nature of this enzyme in this
species. Further studies disclosed that tyrosine aminotransferase is
not absent from non-hepatic tissues because of the lack of the use of a
stabilized buffer, sensitivity to temperature, or due to the presence
of an inhibitor. Collectively, these results suggest that the enzymatic
assay of tyrosine aminotransferase will be unlikely to be an
efficacious approach for identifying mink that are heterozygous for the
autosomal recessive deficiency of this enzyme that is common in dark
mink.
Prieur, D. J., Holland, J. M., Bell, T. G., & Young, D. M. (1976).
Ultrastructural and morphometric studies of platelets from cattle with
the Chediak-Higashi syndrome. Laboratory Investigation, 35(3), 197-204.
This study revealed that the lesions in platelets from cattle with the
Chediak-Higashi syndrome (CHS) are not morphologically analogous to
those present in the other granule-containing cells in cattle and other
species with CHS.
Prieur, D. J., & Meyers, K. M. (1984). Genetics of the fawn-hooded
rat strain. The coat color dilution and platelet storage pool
deficiency are pleiotropic effects of the autosomal recessive red-eyed
dilution gene. Journal of Heredity, 75(5), 349-352. The inheritance of
coat colour, hooded coat pattern, and platelet storage pool deficiency
of fawn-hooded rats was studied by crossing fawn-hooded rats with rats
of other strains. It was determined that the tan coat colour and the
platelet storage pool deficiency are pleiotropic effects of the
autosomal recessive red-eyed dilution (r) gene. The hooded-coat pattern
was determined to be the effect of a different autosomal recessive
gene. It was also demonstrated that the tan coat colour of fawn-hooded
rats is a dilution, and that the shade of the tan coat colour expressed
varied with the underlying coat colour genes.
Stone, D. M., Jacky, P. B., & Prieur, D. J. (1991). The Giemsa
banding pattern of canine chromosomes, using a cell synchronization
technique. Genome, 34(3), 407-412. Cytogenetic investigations were
performed on one Doberman Pinscher and two Boxer dogs. Conventional
homogeneously stained and G-banded metaphases from peripheral blood
lymphocyte cultures synchronised with amethopterin and
bromodeoxyuridine were studied. These procedures permitted the
unequivocal identification of all chromosomes. A chromosome idiogram
was constructed on the basis of the G-banding pattern at the haploid
327-band resolution level. The secondary constrictions and tapering of
the telomeric regions characteristic of several dog chromosomes are
described. Q- and C-banding and staining for nucleolus organiser
regions were also performed, and the salient features are described.
Stone, D. M., Mickelsen, W. D., Jacky, P. B., & Prieur, D. J.
(1991). A novel Robertsonian translocation in a family of Walker
hounds. Genome, 34(4), 677-680. A 5-yr-old female Walker hound having a
narrowed vulva which prevented natural mating was examined
cytogenetically. The modal chromosome number was 77. The chromosome
complement included 2 submetacentric X-chromosomes; a 3rd non-X
submetacentric chromosome had arms homologous with chromosomes 21 ad
33. Cytogenetic analysis of 2 full-sisters with histories of absence of
oestrus disclosed that one had the same translocation and that the
other had a normal female chromosome constitution.....
Wilkerson, M. J., Lewis, D. C., Marks, S. L., & Prieur, D. J.
(1998). Clinical and morphologic features of mucopolysaccharidosis type
II in a dog: naturally occurring model of Hunter syndrome. Veterinary
Pathology, 35(3), 230-233. A 5-year-old male Labrador Retriever had
progressive incoordination, visual impairment, and exercise
intolerance. Coarse facial features, macrodactylia, unilateral corneal
dystrophy, generalized osteopenia, progressive neurological
deterioration, and a positive urine spot test for acid
mucopolysaccharides suggested mucopolysaccharidosis.....This appears to
be the first report of Hunter syndrome or mucopolysaccharidosis type II
in a dog.
Young, D. M., Callis, G. M., Cruea, D. D., & Prieur, D. J. (1985).
Bovine osteopetrosis: a model for skeletal dysplasias of increased
density. Federation Proceedings, 44(3), 745. Examination of 24 cases,
mainly in purebred Angus calves, revealed the condition to be a
modelling defect of fetal chondro-osteogenesis. It appeared to be
inherited as an autosomal recessive trait.
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