AFIP Wednesday Slide Conference - No. 25
March 31, 1999
- Conference Moderator:
Dr. Wallace B. Baze, Diplomate, ACVP
The University of Texas MD Anderson Cancer Center
Science Park, Department of Veterinary Sciences
Bastrop, Texas 78602.
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Case I - 96-309 (AFIP 2638284)
- Signalment: Two-month-old, white-faced, female lamb.
- History: Six lambs from a flock of 100 were affected
with neurologic signs that were non-responsive to thiamine treatment.
This lamb presented with propulsive circling to the left, proprioceptive
deficits in all four limbs, unilateral blindness OS, ventral-medial
displacement OS, dorsal strabismus, and seizure-like twitching
of the head. The lamb was euthanized and necropsied.
- Gross Pathology: Gross lesions were confined to the
brain. The left cerebrum was diffusely enlarged with transfalcine
herniation. The left gyri were enlarged and lacked definition.
- Laboratory Results: Liver copper was 1.77 ppm wet
weight (normal range is 25-100 ppm wet weight).
- Contributor's Diagnoses and Comments:
- 1. Unilateral acute cerebral cortical necrosis and cerebral
- 2. Multifocal necrosis and calcification of cerebral vessels.
Etiology: Copper deficiency.
- Histologic changes were confined to the left cerebrum and
thalamus. Widespread vacuolation was present throughout the cerebral
cortex with prominent clear spaces around capillaries and neurons
(cytotoxic edema). Numerous neurons had shrunken eosinophilic
cytoplasm with nuclear pyknosis and karyolysis (ischemic nerve
cell change). Capillaries were prominent, with swollen endothelium
and increased numbers of both straight and branched capillaries.
Necrosis, mineralization and the accumulation of neutrophils
and pyknotic nuclear debris were present in the media of several
- Copper is a co-factor in many important enzymes including
superoxide dismutase, cytochrome oxidase (c and aa3), lysyl oxidase,
and ascorbic acid oxidase. Copper deficiency in sheep is associated
with a myriad of clinical signs including anemia, decreased immune
responsiveness, decreased growth rate, achromotrichia, inadequate
keratinization of wool with loss of crimp, increased parasitism,
lameness, spontaneous fractures, diarrhea, and reduced fertility.
One of these syndromes usually predominates in a given flock.
- Neurologic diseases associated with copper deficiency in
lambs include swayback (congenital copper deficiency), enzootic
ataxia (delayed-onset ataxia), and cerebral edema. 2 Fetal copper
deficiency results in bilaterally symmetric lesions in the cerebral
white matter (centrum semiovale and corona radiata) that range
from small focal changes to extensive lesions that can result
in cavitation (porencephaly or hydranencephaly). Half of affected
lambs have grossly visible lesions while the remaining ones have
only microscopic changes. Lesions develop prior to significant
myelinization, so evidence of myelin degradation is sparse. Laminar
neuronal necrosis can be found in the cerebral cortex overlying
areas of affected white matter.
- Lambs that develop enzootic ataxia are normal at birth but
develop a swaying hind limb ataxia by 6 months of age. CNS lesions
are microscopic and affect neuronal populations in the brain
stem and spinal cord. The most consistently affected neurons
are in the red and vestibular nuclei, reticular system of the
medulla, ventral motor neurons in the spinal cord and the thoracic
nucleus (nucleus dorsalis or Clarke's column). Affected neurons,
which are those normally rich in cytochrome oxidase, undergo
chromatolysis. Accompanying the neuronal changes is bilateral
symmetrical degeneration of white matter mainly affecting the
dorsal spinocerebellar tracts and their extension into the caudal
cerebellar peduncles and the spinal cord tracts adjacent to the
ventral median fissure. Electron microscopy indicates the lesions
are a primary axonal degeneration and secondary myelin degeneration.
- A unique form of copper deficiency is recognized in England
as severe cerebral edema with herniation.3 Similar to the lamb
presented here, cerebral edema may be unilateral, but there are
no differences in cerebral copper levels between the affected
and unaffected sides of the brain. Examination of brains of affected
lambs under ultraviolet light reveals autofluorescence, similar
to cerebral cortical necrosis due to thiamine deficiency. The
neurologic symptoms are thought to reflect a rapid increase in
intracranial pressure due to cerebral edema while the ischemic
nerve cell change is regarded as secondary to pressure induced
- Plasma copper levels in lambs are low at birth but rise to
adult levels by 1 to 7 days of age. The primary reserve of copper
is the liver, and blood copper concentrations remain near normal
until hepatic copper concentrations are markedly decreased. Since
serum copper is a poor indicator of copper deficiency, the preferred
diagnostic sample is hepatic copper concentration.5 Copper deficiency
may be due to dietary deficiency or decreased copper absorption
from the large intestine of sheep. Excess molybdenum or sulfates
can lead to the formation of insoluble cupric molybdates or copper
thiomolybdates in the rumen. Excessive calcium, especially limestone,
and iron reduce copper absorption. Excess cadmium and zinc reduce
hepatic copper concentrations probably through both decreased
absorption and competition with copper for hepatic metallothionein.
- AFIP Diagnoses:
- 1. Cerebrum: Neuronal necrosis, cortical, acute, diffuse,
with edema, breed unspecified, ovine.
2. Cerebrum, vessels: Necrosis and mineralization, multifocal.
Note: Some sections contain small numbers of lymphocytes
and plasma cells multifocally in the meninges.
- Conference Note: Participants identified similar histopathological
changes as described by the contributor, and considered various
causes of metabolic polioencephalomalacia in the differential
diagnosis, including nutritional deficiencies (thiamine, copper),
water deprivation/salt excess, and several toxicities (lead,
amprolium, thiaminase containing plants, excess dietary sulfur).
- Menke's disease in humans is an X-linked recessive disorder
in which there is severe hypocupremia due to defective intestinal
absorption of copper; copper levels are high in the intestinal
wall, but decreased in the liver and brain. The disease shares
many clinicopathological features with copper deficiency in animals,
and is characterized by severe mental retardation, growth retardation,
and skin abnormalities that cause the hair to have a kinky or
- Contributor: Department of Pathology, Cornell University,
Ithaca, NY 14853.
- 1. Maas J, Smith BP: Copper deficiency in ruminants. In:
Large Animal Internal Medicine, 2nd edition, Smith BP, ed., pp.
904-908, Mosby, St. Louis, MO, 1996.
- 2. Summers BA, Cummings JF, DeLahunta A: Degenerative diseases
of the central nervous system. In: Veterinary Neuropathology,
Summers BA, Cummings JF, DeLahunta A, eds., pp. 273-277, Mosby,
St. Louis, MO, 1995.
- 3. Roberts HE, Williams BM: Cerebral oedema in lambs associated
with hypocuprosis and its relationship to swayback. I. Field,
clinical, gross anatomical and biochemical observations. J Comp
Pathol 76:279-283, 1966.
- 4. Roberts HE, Williams BM: Cerebral oedema in lambs associated
with hypocuprosis and its relationship to swayback. II. Histopathological
findings. J Comp Pathol 76:285-290, 1966.
- 5. Puls R: Copper, sheep. In: Mineral Levels in Animal Health,
Puls R, ed., 2nd edition, pp. 105-109, Sherpa International.
- 6. Gould DH: Polioencephalomalacia. J Anim Sci 76:309-314,
- 7. Duchen LW, Jacobs JM: Nutritional deficiencies and metabolic
disorders. In: Greenfield's Neuropathology, Adams JH, Duchen
LW, eds., 5th ed., pp. 850-852, Oxford University Press, New
- 8. Jones TC, Hunt RD, King NW: Nutritional deficiencies.
In: Veterinary Pathology, 6th ed., pp. 805-806, Williams and
Wilkins, Baltimore, MD, 1997.
Case II - HN1311 (AFIP 2651908)
- Signalment: Five-year-old, male, French bulldog.
- History: This dog was referred to an animal hospital
at the beginning of April because the dog showed depression since
the end of March. Arrhythmia was recognized. Dirofilaria immitis
was not detected in the blood sample, and abdominal and thoracic
radiographs showed no abnormalities. Rectal temperature was 38.6°C.
The dog had been treated with dexamethasone sodium phosphate
to reduce the clinical signs. However, dyspnea and tiring on
exercise recurred over the following three weeks. At the beginning
of May, the dog showed severe bradycardia (heart rates: 40-50
beats per minute) and collapsed with severe dyspnea. Because
the dog demonstrated decerebrate rigidity before death, necropsy
was performed to examine the central nervous system.
- Gross Pathology: The brain showed moderate edematous
swelling accompanied by flattening of the cerebral cortical gyri
and narrowing of the sulci. The posterior portion of the cerebellar
vermis was mildly herniated through the foramen magnum. In transverse
section through the mamillary bodies, a single mass, measuring
1.5 x 2.0 x 1.5 cm, was found, located primarily in the moderately-dilated
right lateral ventricle. The increased cerebrospinal fluid was
cloudy, pinkish, and mucinous in viscosity. The mass was soft,
gelatinous, and grayish white.
Laboratory Results: None.
- Contributor's Diagnosis and Comments: Cerebrum: Malignant
oligodendroglioma, French bulldog, canine.
- Microscopically, the tumor consists of diffuse proliferation
of neoplastic oligodendroglial cells. The neoplastic cells have
small, round, hyperchromatic nuclei with poorly stained cytoplasm,
and the cells infiltrate into the cortex. Rarely, atypical astrocytes
are scattered among the neoplastic oligodendrocytes. The neoplasm
has abundant vascular proliferation with occasional glomeruloid
pattern, and there is severe multifocal extensive necrosis, with
thrombosis and hemorrhages. Neoplastic oligodendroglial cells
generally infiltrate into the adjacent white matter and perivascular
spaces. Perivascular cuffing and satellitosis of neurons by neoplastic
cells are often seen. Mitotic figures are frequently observed
at the periphery of the neoplasm.
- Immunohistochemistry demonstrated that the neoplastic oligodendrocytes
were positive for S-100 protein, vimentin, neuron specific enolase
(NSE), and neurofilament protein (NFP). Myelin basic protein
(MBP) and glial fibrillar acidic protein were not detected in
these cells. Small numbers of GFAP-positive astrocytes that had
oval, large nuclei and abundant eosinophilic cytoplasm were noted
around proliferated vessels.
- Oligodendroglioma appears to be the most common primary brain
tumor in middle-aged and old dogs. A predilection for brachycephalic
dog breeds, such as the present case, has been recognized in
glial tumors. The tumor is usually located in the cerebral white
matter, particularly around the lateral ventricles. Clinically,
the dogs show depression, blindness, ataxia, and change in temperament
from nerve damage. Microscopically, oligodendrogliomas have a
very characteristic honeycomb pattern, and the tumor cells have
small, round, hyperchromatic nuclei with poorly stained cytoplasm.
Occasionally, multifocal mineralization and proliferation of
blood vessels are also observed throughout the neoplasm.
- The neoplasm was considered to be malignant because of the
findings of frequent mitotic figures, nuclear pleomorphism, glomeruloid
vascular tufts, and extensive necrosis. The results of immunohistochemical
staining of canine oligodendroglioma with antibody against MBP
are generally negative. Many oligodendrogliomas show a mixture
with GFAP-positive astroglial cells. The interpretation of the
finding is controversial whether the astrocytes indicate a capacity
for immature oligodendrocytes to express astrocytic differentiation
or reactive astrocytes. In our case, the astrocytes within the
neoplasm appear to be reactive astrocytes since we could not
find intermediate cells, and the cells proliferated especially
preferentially around the proliferating blood vessels.
- AFIP Diagnosis: Cerebrum: Oligodendroglioma, anaplastic,
French bulldog, canine.
- Conference Note: This case was studied in consultation
with the Department of Neuropathology. All conference participants
identified a primary central nervous system (CNS) neoplasm of
glial origin. The diagnosis of high grade astrocytoma was considered
based on histomorphologic findings of a poorly circumscribed,
infiltrative neoplasm with extensive areas of necrosis, relatively
high mitotic rate, and prominent proliferation of glomeruloid
- In immunohistochemical studies performed at the AFIP, neoplastic
cells were negative for synaptophysin and neurofilament protein
(NFP). While the majority of the neoplasm was negative for glial
fibrillary acidic protein (GFAP), there were a few GFAP-positive
cells, most often located adjacent to vessels.
- Anaplastic (malignant) oligodendroglioma and astrocytoma
share several histomorphological features, including high cellularity,
necrosis, high mitotic rate, and prominent proliferation of glomeruloid
vessels; thus, distinguishing between these two glial neoplasms
may be difficult. As noted by the contributor, the presence of
intermingled astrocytic cells is common in anaplastic oligodendrogliomas
and may further complicate the histologic picture. Fortunately,
neoplastic cells in oligodendrogliomas generally have distinguishing
features such as round, hyperchromatic, nuclei surrounded by
small amounts of clear to lightly stained cytoplasm, and distinct
cell borders. In addition, the branching capillary proliferation
("chicken-wire" pattern) is characteristic of an oligodendroglioma.
These histologic features combined with results of immunohistochemistry
support the diagnosis of oligodendroglioma in this case.
- Contributor: Laboratory of Comparative Pathology,
Graduate School of Veterinary Medicine, Hokkaido University,
Sapporo 060-0818, Japan.
- 1. Rubinstein LJ: Tumors of neuroglial cells. In: Atlas of
Tumor Pathology: Tumors of the Central Nervous System, Rubinstein
LJ, ed., 2nd series, Fascicle 6, pp. 85-104, Armed Forces Institute
of Pathology, Washington DC, 1972.
- 2. Summers BA, Cummings JF, DeLahunta A: Tumors of the central
nervous system. In: Veterinary Neuropathology, Summers BA, Cummings
JF, DeLahunta A, eds., pp. 370-373, Mosby, St. Louis, MO, 1995.
- 3. Bailey CS, Higgins RJ: Characteristics of cisternal cerebrospinal
fluid associated with primary brain tumors in the dog: A retrospective
study. J Amer Vet Med Assoc 188:414-417, 1986.
- 4. Taylor RF, Bucci TJ: Oligodendroglioma in a dog. J Small
Anim Pract 13:41-46, 1972.
- 5. Triolo AJ, Howard MO, Miles KG: Oligodendroglioma in a
15-month-old dog. J Amer Vet Med Assoc 205:986-988, 1994.
- 6. Vandevelde M, Fankhauser R, Luginbuhl H: Immunocytochemical
studies in canine neuroectodermal brain tumors. Acta Neuropathol
- 7. Wilson RB, Beckman SL: Mucinous oligodendroglioma of the
spinal cord in a dog. J Amer Anim Hosp Assoc 31:26-28, 1995.
- 8. Koestner A, et al.: Histological classification of tumors
of the nervous system of domestic animals. In: World Health Organization
Histological Classification of Tumors of Domestic Animals, Schulman
FY, ed., 2nd series, volume 5, pp. 17-21, Armed Forces Institute
of Pathology, Washington DC, 1999.
Case III - 10376-98 (AFIP 2640589)
- one 2x2 gross color photo transparency
- Signalment: Ovine, male, cross-bred, 2-week-old.
- History: This lamb became lethargic within 8 hours
of being let out to pasture for the first time. He did not nurse
but seemed more alert after treatment with antibiotic and B-vitamin
injections. Two days after the onset of clinical signs, he began
circling to the left, and by the next day he was non-ambulatory,
laterally recumbent, and paddling with opisthotonos and nystagmus.
The lamb was humanely euthanized.
- Gross Pathology: The cerebrum was edematous, and the
cerebellar vermis was slightly herniated through the foramen
magnum. On transverse section, bilaterally symmetric areas of
hemorrhage and malacia were observed in the cerebellar peduncles,
midbrain including rostral colliculi, thalamus, internal capsule,
and basal ganglia. Using a standard dipstick test, the urine
was positive for glucose.
- Laboratory Results: None.
- Contributor's Diagnosis and Comments: Cerebellar peduncles:
Necrosis, hemorrhage, and edema, bilaterally symmetric, acute,
consistent with ovine focal symmetrical encephalomalacia caused
by Clostridium perfringens type D toxin(s).
- This case is an example of ovine focal symmetrical encephalomalacia.
Necrotic lesions were acute enough that the primary inflammatory
cell response was neutrophilic. The pathogenesis of lesions in
the brain of affected lambs involves increased capillary permeability
associated with binding of epsilon toxin and swelling of astrocyte
end-feet. Toxin production occurs in the gut where proliferation
of Clostridium perfringens type D is favored by certain changes
in diet. Glucosuria is associated with hyperglycemia.
- AFIP Diagnosis: Cerebellum, peduncles: Necrosis, hemorrhage,
and edema, bilaterally symmetrical, extensive, breed unspecified,
- Conference Note: Clostridium perfringens is an anaerobic,
spore-forming, Gram-positive bacillus that causes disease through
elaboration of exotoxins within the gastrointestinal tract. There
are five strains of the organism (types A, B, C, D, and E) based
upon the elaboration of one or more of four exotoxins designated
as alpha, beta, epsilon, and iota. Alpha toxin is a phospholipase
C that is produced by all five strains of C. perfringens and
causes hemolysis and necrosis. Clostridium perfringens types
B and C produce beta toxin which is associated with increased
vascular permeability and necrosis. Epsilon toxin is elaborated
by types B and D as a nontoxic protoxin and is converted to a
potent toxin by proteolytic enzymes, leading to increased vascular
permeability and tissue necrosis. Iota toxin is produced by type
E as a protoxin and is converted to an active form by proteolytic
enzymes, causing increased vascular permeability and necrosis.
- Enterotoxemia caused by C. perfringens type D is a common
disease of sheep and goats, and has been reported in calves.
In sheep, the disease most frequently occurs in fattening lambs
and is known as "overeating disease", or as "pulpy
kidney disease" (named for the rapid postmortem autolysis
of the kidneys in some animals dying from the condition). In
sheep, the disease is predominately characterized by central
nervous system (CNS) signs and lesions, exemplified by the cerebellar
changes in this case. In the gastrointestinal tract, there is
peritoneal hemorrhage, mucosal congestion of the intestines,
and superficial desquamation of the intestinal epithelium; numerous
bacilli are found in the intestinal contents. In goats, the disease
primarily occurs in the gastrointestinal tract, and CNS signs
and lesions occur less frequently than in sheep. Additionally,
lesions in the gastrointestinal tract of goats more commonly
affect the colon, rather than the small intestine.
- Contributor: Animal Disease Diagnostic Laboratory,
ADDL-1175, Purdue University, West Lafayette, IN 47907.
- 1. Summers BA, Cummings JF, de Lahunta A: Degenerative diseases
of the central nervous system. In: Veterinary Neuropathology,
Summers BA, Cummings JF, de Lahunta A, eds., pp. 269-270, Mosby
Year-Book, St. Louis, MO, 1995.
- 2. Jones TC, Hunt RD, King NW: Diseases caused by bacteria.
In: Veterinary Pathology, Jones TC, Hunt RD, King NW, eds., 6th
ed., pp. 420-422. Williams & Wilkins, Baltimore, MD, 1997.
- 3. Barker IK, Van Dreumel AA, Palmer N: The alimentary system.
In: Pathology of Domestic Animals, Jubb KVF, Ken-nedy PC, Palmer
N, eds., 4th ed., vol. 2, pp. 241-244, Academic Press, San Diego,
- 4. Uzal FA, Kelly WR: Effects of the intravenous administration
of Clostridium perfringens type D epsilon toxin on young goats
and lambs. J Comp Path 116:63-71, 1997.
- 5. Uzal FA, Kelly WR: Experimental Clostridium perfringens
type D enterotoxemia in goats. Vet Pathol 35:132-140, 1998.
Case IV - 98-6312 (AFIP 2641154)
- one 2x2 photo transparency
- Signalment: 22-month-old, spayed, female, Australian
- History: There was onset of seizures at 14 months
of age, with gradual progression of thoracic limb weakness, spontaneous
nystagmus, and incoordination.
- Gross Pathology: There was marked bilateral atrophy
of scapular muscles of thoracic limbs. Foci of malacia, 2 to
5 mm in diameter, were found in the midbrain, pons, medulla oblongata
and cerebellum involving the caudal colliculi, lateral vestibular
and lateral cuneate nuclei, and the entire gray matter of the
- Laboratory Results: MRI demonstrated hyperechoic lesions
associated with malacic foci.
- Contributor's Diagnosis and Comments: Poliomyelomalacia,
- This dog was submitted for necropsy with a tentative diagnosis
of hereditary polioencephalomyelopathy based on the clinical
signs and supportive MRI findings. Postmortem findings in this
dog were strikingly similar to those previously described. To
date, this disorder has been reported in the literature affecting
three Australian Cattle Dogs. Similar to this dog, previous dogs
had initial signs of seizures, with progression of neurologic
signs to thoracic limb weakness and stiffness, followed by lateral
recumbency. In addition to the spinal cord lesions, this dog
had grossly apparent malacic lesions affecting multiple nuclei
in the brain stem and cerebellum. The severe spinal cord changes
were restricted to the cervical intumescence in this dog. However,
in previously described cases, the lumbosacral intumescence was
- Lesions in the previous dogs were bilaterally symmetrical
and identified in the caudal colliculi, lateral vestibular nuclei,
lateral cuneate nuclei, and lateral reticular nuclei, extending
into the ventral gray columns of C1 and the cervical and lumbosacral
intumescences. The lesions in the spinal intumescences were the
most severe. Early lesions consisted of degenerative changes
of vacuolation within myelin sheaths and glial cells, with astrocyte
and microglial proliferation, which were identi-fiable microscopically
but not grossly. The gross lesions in the grey matter of the
spinal cord had microscopic changes of rarefaction of neuropil
which was reduced to a loose meshwork of blood vessels, astrocytic
processes, and naked axons. A remarkable feature was the retention
of large motor neurons in the rarefied neuropil, which is also
present in this case.
- The affected dogs in the previous report were produced by
non-affected parents. Pedigree analysis showed that the affected
dogs were genetically closely related. Testing for simple autosomal
recessive inheritance indicated consistency with a disease controlled
by a simple Mendelian autosomal recessive gene with complete
penetrance. The genetic rela-tionship of the dog in this case
to the previous cases is unknown, and siblings in this mating
could not be located or were unaffected.
- The pathogenesis of lesion development in this poliomyeloencephalopathy
is unknown. The bilaterally symmetrical na-ture of the lesions
suggests a neurodegenerative process or toxicosis. It is unlikely
ischemic in nature, as large motor neurons were surviving in
the malacic lesions. Other malacic diseases in animals include
focal symmetrical spinal poliomalacia syndrome of sheep (cause
unknown), focal symmetrical spinal poliomalacia of pigs associated
with sele-nium toxicosis, polioencephalomalacia of ruminants,
thiamine deficiency in carnivores, nigropallidal encephalomalacia
of horses associated with ingestion of Centaurea sp., salt poisoning,
leukoencephalomalacia of horses associated with fumonisins, and
AFIP Diagnosis: Spinal cord: Poliomyelomalacia, bilaterally
symmetrical, with sparing of motor neurons, Australian Cattle
- Conference Note: The neurodegenerative disorder that
affects young Australian Cattle Dogs is characterized by bilateral
and symmetrical encephalomyelopathy. The pathogenesis is unknown;
however, an autosomal recessive mode of inheritance is suspected.
Mitochondrial abnormalities were observed ultrastructurally in
astrocytes in the recent study of affected dogs, and mitochondrial
injury may play a role in the disease process. The CNS lesions
have some resemblance to the human condition known as Leigh's
- Leigh's disease is characterized by early onset (less than
two years), although adolescent and adult forms have been described.
Grossly, lesions predominately occur in the gray matter, are
frequently symmetrical, and particularly affect the basal ganglia,
diencephalon, and brain stem. Lesions are also often observed
in the cerebellum and spinal cord. Microscopically, the lesions
are characterized by vascular endothelial proliferation, astrocytosis,
and the presence of macrophages. There is the appearance of "loosening
of the neuropil", with relative sparing of neuronal perikarya.
Several biochemical abnormalities have been identified in Leigh's
disease, and most of them are associated with impairment of mitochondrial
function. If the pathogenesis of the encephalopathy of Australian
Cattle Dogs is determined to be related to primary mitochondrial
dysfunction, the condition may serve as an important animal model
for the study of related human conditions.
- Contributor: Kansas State University, Diagnostic Medicine/Pathobiology,
1800 Dension, VCS Bldg., Manhattan, KS 66506.
- 1. Brenner O, de Lahunta A, Summers BA, Cummings JF, Cooper
BJ, Valentine BA, Bell JS: Hereditary polioencephalomyelopathy
of the Australian Cattle Dog. Acta Neuropathol 94:54-66, 1997.
- 2. Jubb KVF, Huxtable CR: The nervous system. In: Pathology
of Domestic Animals, Jubb KVF, Ken-nedy PC, Palmer N, eds., 4th
ed., vol. 1, pp. 338-350, Academic Press, San Diego, CA, 1993.
- 3. Duchen LW, Jacobs JM: Nutritional deficiencies and metabolic
disorders. In: Greenfield's Neuropathology, Adams JH, Duchen
LW, eds., 5th ed., pp. 847-850, Oxford University Press, New
- Wednesday Slide Conference Coordinator:
- Ed Stevens, DVM
Captain, United States Army
Registry of Veterinary Pathology*
Department of Veterinary Pathology
Armed Forces Institute of Pathology
(202)782-2615; DSN: 662-2615
- * The American Veterinary Medical Association and the American
College of Veterinary Pathologists are co-sponsors of the Registry
of Veterinary Pathology. The C.L. Davis Foundation also provides
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