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CASE I – A5 2006 (AFIP 2737400)
Signalment: 6-week-old, female, broiler chicken (Gallus domesticus)
History: None.
Gross Pathology: Chicken is undersized compared to others in the flock. The spleen is twice the normal size. Upon section, the spleen contains an eccentrically located white mass that extends from the inner capsule of one side. Other organs are grossly unremarkable.
Laboratory Results: None.
Contributor’s Diagnoses and Comment: 1. Myofibrosarcoma (spleen)
2. Glomerulopathy, cardiomyopathy, and enteric myopathy
3. Retroviral inclusions (glomeruli, heart, enteric smooth muscle)
An unencapsulated and infiltrative mass partially replaces the spleen. The mass is composed of intersecting bundles of spindle cells that contain abundant amounts of eosinophilic cytoplasm and are accompanied by collagen fibers. Cytoplasmic margins are indistinct. Tumor cells contain pleomorphic, but commonly elongated oval to fusiform nuclei that often exhibit mitoses. The surrounding red pulp sinuses are markedly congested with erythrocytes that obscure the normal splenic architecture. The cytoplasm of tumor cells stains with smooth muscle actin, desmin, and vimentin.
Glomerular mesangia are multifocally enlarged; in some glomeruli there is moderate peripheral mesangial sclerosis. In other glomeruli, the walls of glomerular capillaries and the peripheral mesangium appear hyaline. Visceral epithelial cells are enlarged and some contain magenta, ovoid, intracytoplasmic, perinuclear, inclusions, as do some adjacent mesangial cells or tubular epithelial cells. Some tubules contain proteinic material. There are occasional interstitial aggregates of mononuclear cells.
Some cardiac myocytes appear hyperplastic and some are necrotic. There is sporadic cytoplasmic vacuolization. Numerous myocytes and some Purkinje cells contain multiple intracytoplasmic magenta inclusions that are occasionally present in “spilled coin” arrays.
Rare smooth muscle cells of the enteric tunica muscularis contain elongated perinuclear intracytoplasmic inclusions. In some sections, there are areas where cells of the tunica muscularis are partially necrotic and contain vacuolated, lightly basophilic cytoplasm. Some of these areas contain necrotic granulocytes.
Splenic sarcomas are commonly identified in young chickens. This is a common type, although neurofibrosarcomas are also commonly seen. Most young chicken sarcomas have accompanying retroviral inclusions in specific sites.
AFIP Diagnoses: 1. Spleen: Spindle cell sarcoma, broiler chicken, avian.
2. Heart, cardiomyocytes; small intestine, tunica muscularis, myocytes; and kidney, glomeruli: Eosinophilic intracytoplasmic inclusion bodies, multifocal, few.
3. Kidney: Glomerulonephritis, membranous, global, multifocal, moderate, with minimal interstitial fibrosis and lymphocytic infiltrates.
Conference Comment: The genus Alpharetrovirus, of the family Retroviridae, contains the avian type C retroviruses, such as avian leukosis virus and avian sarcoma virus. Exogenous avian type C retroviruses can be grouped into 3 categories based on the ability to replicate their genome. Replication-competent viruses possess a standard complement of the gag, pol, and env genes found in all retroviruses, which code for various viral proteins. Replication-defective viruses acquire the v-onc gene in rapidly induced malignant tumors, but lose part of their genome in doing so and depend on the helper activity of another oncovirus for productive replication. Replication-competent rapidly transforming viruses (e.g., Rous sarcoma virus) don’t require a helper virus to induce the very rapid development of sarcomas.
Procedures to definitively identify the intracytoplasmic inclusion bodies were not done in this case. Immunohistochemistry performed at the AFIP, was not helpful in determining the cell of origin of the splenic neoplasm; neoplastic cells were negative for smooth muscle actin and desmin. Masson’s trichrome staining revealed very little collagen within the neoplasm. Following the conference, this case was reviewed in consultation with Dr. H. L. Shivaprasad of the University of California, Davis, Fresno Branch Veterinary Diagnostic Laboratory. Dr. Shivaprasad noted that many of the glomeruli are immature, as would be expected in a young chicken, and that avian glomeruli normally have more mesangial cells than mammalian glomeruli. He agreed with the contributor that there is a glomerular lesion and favored a diagnosis of membranous glomerulonephritis. The role of retroviruses in such renal lesions is unknown. Dr. Shivaprasad also noted that the changes present in the kidney are seen fairly commonly in broiler chickens without evidence of retroviral infection.
Contributor: U. S. Department of Agriculture-Food Safety Inspection Service, Eastern Laboratory, Pathology, P.O. Box 6085, 950 College Station Road, Russell Research Center, Athens, GA 30604
References: 1. Gilka F, Spencer JL: Viral matrix inclusion bodies in myocardium of lymphoid leukosis virus-infected chickens. Am J Vet Res 46:1953-1960, 1985
2. Kaliner G: Intracytoplasmic myocardial inclusions in chickens. Zentralblatt für Veterinarmedizin (Reihe A) 21(9):774-78, 1974
3. Murphy FA, Gibbs EPJ, Horzinek MC, Studdert MJ: Retroviridae. In: Veterinary Virology, 3rd ed., pp. 364-380. Academic Press, New York, NY, 1999
4. Steffens WL, Goodwin MA, Ard MB: Immunogold for detection of avian leukosis/sarcoma virus in formalin-fixed heart and kidney. Avian Pathol 26:45-52, 1997
CASE II – 00-0101 (AFIP 2736966)
Signalment: Five-year-old, spayed female Chihuahua, canine.
History: Acute onset of bloody diarrhea followed by death within 12 hours. There was a recent history of dietary change.
Gross Pathology: The dog was in good body condition. Bloody, liquid fecal material was present on the hairs of the perineum. There was a dark red area on the stomach wall. The small intestine had a red/gray serosa and was filled with thick, red/black fluid. The large intestine was empty.
Laboratory Results: A heavy growth of Clostridium perfringens was recovered from the small intestine. PCR analysis of the isolate was positive for genes for both alpha toxin and enterotoxin (enterotoxigenic type A).
Contributor’s Diagnosis and Comment: Enteritis, hemorrhagic, necrotizing, acute, diffuse, severe.
Etiology: enterotoxigenic Clostridium perfringens type A
Hemorrhagic enteritis in dogs is characterized by acute onset of bloody diarrhea, vomiting, and hemoconcentration. If untreated, the disease can progress to complete circulatory collapse and death in less than 24 hr. Young dogs (2–4-years-old) and toy breeds are more commonly affected, but hemorrhagic enteritis may occur in dogs of any age or breed. The lesions and clinical signs have been compared to and resemble those of experimental endotoxic shock, anaphylaxis, and immune-mediated bowel disease, but a definitive relationship has not been established to any of these. Clostridium perfringens, in high numbers, has been cultured from the intestines of some dogs with hemorrhagic enteritis and is proposed to be the cause of this syndrome. Some reports describe the colonization of the villi by bacteria as being morphologically compatible with Clostridium perfringens, as noted in our case. Little information is available regarding the genotype(s) of the organisms recovered in these cases. Recent development of PCR methods for genotyping of Clostridium perfringens should help improve our understanding of the role of this organism in canine hemorrhagic enteritis.
AFIP Diagnosis: Small intestine: Necrosis, villar, diffuse, with focal hemorrhage and numerous surface-adherent bacilli, Chihuahua, canine.
Conference Comment: Of the five types of Clostridium perfringens, designated types A-E based on their production of the four major exotoxins, C. perfringens type A is the most common. Enteric proliferation of this type is recognized as a cause of hemorrhagic enteritis in several species including black-footed ferrets, chickens, horses, pigs, lambs, goats, calves, and man. Clinical signs and histologic lesions are caused by a lecithinase known as alpha toxin, the major toxin produced by C. perfringens type A. Alpha toxin is both hemolytic and cytotoxic by virtue of its effects on cell membranes. Enterotoxin, the principal toxin involved in foodborne illness, is released upon lysis of sporulating cells.
Enteric bacterial overgrowth may develop with alterations of enzymatic activity in the intestinal brush border and enterocyte lysosomes. Necrosis of enterocytes is also seen with Escherichia coli, canine parvovirus type 2, and coronavirus infections, as well as with cryptosporidiosis, coccidiosis, and arsenic and lead toxicoses.
Nucleic acid probes and multiplex polymerase chain reaction assays are reported as being useful in rapidly and efficiently screening isolates from cases of hemorrhagic enteritis for the simultaneous detection of C. perfringens major toxins and enterotoxin genes.
Contributor: Arizona Veterinary Diagnostic Laboratory, Department of Veterinary Science and Microbiology, The University of Arizona, 2831 N. Freeway, Tucson, Arizona 85705
References: 1. Burrows CF, Batt RM, Sherding RG: Diseases of the Small Intestine. In: Textbook of Veterinary Internal Medicine, ed. Ettinger SJ, Feldman EC, vol. 2, pp. 1169-1232. WB Saunders Co., Philadelphia, PA, 1995
2. Meer RR, Songer JG: Multiplex polymerase chain reaction assay for genotyping Clostridium perfringens. Am J Vet Res 58:702-705, 1997
3. Prescott JF, Johnson JA, Patterson JM: Haemorrhagic gastroenteritis in the dog associated with Clostridium welchii. Vet Rec 103:116-117, 1978
4. Sasaki J, Asahina M, Makara M, Shishido S, Okada K: Hemorrhagic enteritis associated with Clostridium perfringens type A in a dog. J Vet Med Sci 61(2):175-177, 1999
5. Turk J, Fales W, Miller M, Pace L, Fischer J, Johnson G, Kreeger J, Turnquist S, Pittman L, Rottinghaus A, Hosser H: Enteric Clostridium perfringens infection associated with parvoviral enteritis in dogs: 74 cases (1987-1990). J Am Vet Med Assoc 200(7):991-994, 1992
CASE III – 3 (AFIP 2663373)
Signalment: 10-year-old, gelding, quarterhorse, equine
History: This horse was presented to the California Veterinary Diagnostic Lab in early May with a 5-week history of weight loss, severe generalized dermatitis, fever, dependent edema of the hind limbs, preputial sheath and ventral abdomen, and enlargement of numerous superficial lymph nodes. The horse’s clinical signs were unresponsive to antibiotic therapy (trimethoprim and sulfadiazine), corticosteroids and betadine baths, so euthanasia and subsequent necropsy were performed. Additional history included exposure to pasture containing a mixture of grasses and broadleaf plants, including Vicia sp., during the winter prior to presentation.
Gross Pathology: The horse was thin with severe alopecia. There was crusting and scaling that was most severe over the face (particularly around the eyes, ears, and muzzle) and serous exudate in the axilla and on the preputial sheath. These changes spared the oral mucosa and mucocutaneous junctions. Numerous small, subcutaneous nodules were present on the neck and shoulders and variably sized flat annular lesions were present on the perineum and thighs. Multiple, 0.5 cm, firm, white nodules were present throughout all of the lung lobes. The superficial (retropharyngeal, superficial cervical, prescapular, inguinal) and internal (hepatic, mesenteric, renal, mediastinal) lymph nodes were enlarged and homogeneously white-tan with loss of recognizable cortical and medullary architecture. Additional changes included conjunctivitis and blepharitis, severe dependent edema of the legs, abdomen, and preputial sheath, and seborrhea on the withers, shoulders, back and ventral abdomen.
Laboratory Results: The horse had a normocytic, normochromic anemia (PCV = 19.5%), mild monocytosis (1.860/m l), and hyperfibrinogenemia (600 mg/dl). Samples from the lung and liver were negative for pathogenic bacteria. Small numbers of Trichophyton equinum were isolated from skin samples. AGID for equine infectious anemia was negative and a pooled organ sample (lymph node, liver, spleen, brain, lung) was negative for cytopathic viruses. Fluorescent antibody microscopic examination of skin samples was negative for epidermal deposition of IgG and complement.
Contributor’s Diagnosis and Comment: Skin: Mild to severe diffuse granulomatous dermatitis and panniculitis with multifocal intracorneal pustules and ulcers.
Etiology: Vicia benghelensis
Sections of the skin, liver, lung, spleen, kidney, lymph nodes, gastrointestinal tract, brain, heart, trigeminal ganglia, adrenal gland, and pancreas were stained with hematoxylin and eosin and were examined histologically. Sections from the skin contained mild to very severe inflammation, which in mildly affected areas was primarily centered around blood vessels and nerves in the deep dermis and panniculus and in severely affected areas extended from the superficial into the deep subcutis. Inflammation in the latter regions multifocally replaced or widely separated dermal collagen and adnexal structures and in some areas extended into the outer epithelial layer of the adnexa. The infiltrates contained numerous epithelioid macrophages, plasma cells, lymphocytes, and fewer multinucleated giant cells. The stratum corneum was multifocally expanded due to mild to moderate orthokeratotic hyperkeratosis and it contained large intracorneal pustules, some of which contained bacteria. Thick serocellular crusts covered multifocal ulcers.
Similar foci of granulomatous inflammation were also seen along the endocardium and in the myocardium, in periportal and random areas within the liver, in perivascular regions in the subcapsular and superficial cortical regions of the kidneys, and within the examined lymph nodes. In the brain, similar inflammation was present in the neuropil adjacent to the lateral ventricle. Moderate mixed mononuclear inflammatory cell infiltrates surrounded bronchioles and medium and large vessels throughout the lungs. Inflammation within the lungs was associated with multifocal fibrinoid necrosis of vessel walls and invasion of the vascular smooth muscle and adventitia by similar granulomatous infiltrates.
Examined tissue sections were negative for infectious agents with special stains (Gram’s, periodic acid-Schiff, acid-fast, and Gomori’s methenamine silver).
Generalized cutaneous crusting and scaling with alopecia, in addition to multisystemic granulomatous inflammation, characterize systemic granulomatous disease (SGD) of horses, or equine sarcoidosis. The cause for the development of equine SGD is often not determined. In one report of systemic granulomatous disease in two cattle and a second report in one other horse, SGD was associated with the ingestion of Vicia sp., often called hairy vetch. Various species of vetch are found in many areas of California, but ingestion of the plant appears to be an uncommon cause of systemic granulomatous disease in large domestic animals. Due to the relative abundance of this plant in California and the paucity of reports of associated disease, disease in these animals may truly represent an unusual response to the ingestion of this plant. It may, on the other hand, be due to our inability as practitioners to recognize the disease entity, or may be associated with a failure in identifying exposure of the animal to the plant through the clinical history or during the post-mortem examination (i.e., gross, histo, or toxicological testing). The pathogenesis of vetch-associated granulomatous disease is not known and may be due to multiple factors.
AFIP Diagnosis: Haired skin: Dermatitis and panniculitis, granulomatous, diffuse, severe, with ulceration, hyperkeratosis, and intracorneal microabscesses, quarterhorse, equine.
Conference Comment: In some sections of skin, severe granulomatous inflammation diffusely infiltrates the dermis and extends into the subcutis. In other sections, the inflammatory infiltrate is primarily perivascular in the deep dermis and panniculus, with only mild to moderate periadnexal infiltrates in the superficial dermis. The epidermis has multifocal intracorneal microabscesses and is occasionally ulcerated with an overlying serocellular crust.
Similar systemic granulomatous disease in cattle has been attributed to hairy vetch toxicosis and to ingestion of citrus pulp. In cattle there is often a prominent eosinophilic inflammatory component. A delayed type hypersensitivity to one or more plant constituents has been proposed to stimulate the inflammatory response.
Contributor: University of California, Davis, School of Veterinary Medicine, California Veterinary Diagnostic Laboratory System, P.O. Box 1770, Davis, CA 95617-1770
References: 1. Anderson CA, Divers TJ: Systemic granulomatous inflammation in a horse grazing hairy vetch. J Am Vet Med Assoc 183:569-570, 1983
2. Griffiths B, Done SH: Citrinin as a possible cause of the pruritus, pyrexia, and hemorrhagic syndrome of cattle. Vet Rec 129:113-117, 1991
3. Johnson B, Moore J, Woods LW, Galey FD: Systemic granulomatous disease in cattle in California associated with grazing hairy vetch (Vicia villosa). J Vet Diagn Invest 4:360-362, 1992
4. Woods LW, Johnson B, Hietala SK, Galey FD, Gillen D: Systemic granulomatous disease in a horse grazing pasture containing vetch (Vicia sp.). Vet Pathol 4:356-360, 1992
CASE IV – 340/97 (AFIP 2734403)
Signalment: 26-month-old, male, white German noble goat, caprine.
History: In an experimental study, male white goats at the age of 14 weeks were fed semisynthetic copper deficient food (0.9 mg/kg dry weight) for 20 months. A supplementation of increasing amounts of ammoniumtetramolybdate (10-40 mg/kg d.w.) was added during the last two months of the study. The animals were euthanized at 23-months-old.
Gross Pathology: The most obvious macroscopic difference was the lower body weight and fat content of the carcasses of animals in the experimental group compared with the control. A red-yellow, moderately swollen liver with a well-filled gallbladder was typical for goats suffering from copper deficiency and molybdenosis. The hair showed a normal structure. Achromotrichia could not be detected because the goats were white. The bones appeared normal and radiographs revealed no signs of osteoporosis.
Laboratory Results: Chemical analyses showed a considerable decrease of hepatic copper, with only slightly lowered levels for Mg, P and S. The levels for Al, Fe and Pb were extremely elevated at 500-1600%. Increased hepatic concentrations were also seen for Ca, Co, Se, Zn, Cd, Mn and Mo. Hematology was characterized by a severe microcytic, hypochromic anemia with very low hemoglobin concentrations and hematocrit values. Clinical chemistry showed increased values of total bilirubin, GLDH and ASAT, but lowered levels of cholesterol, thyroxin and ceruloplasmin.
Contributor’s Diagnoses and Comment: 1. Liver: Moderate chronic degenerative hepatosis with moderate bile duct proliferation and bridging portal fibrosis, moderate portal and periportal hemosiderosis in macrophages and hepatocytes, mild subacute-chronic reactive interstitial lymphoplasmacellular hepatitis.
2. Pancreas: Eosinophilic degeneration and necrosis with severe irregularity of the exocrine pancreas (not submitted).
3. Skin: Chronic dermatosis characterized by moderate orthokeratotic epidermal and infundibular hyperkeratosis, atrophy of the epidermis and the integumentary appendages (not submitted).
The gastrointestinal tract, kidneys, cardiovascular system, lymphatic tissues, testes, bones and nervous system were without any specific morphological lesions.
Copper and molybdenum are essential but antagonistic trace minerals that must be present in the diet in a balanced relation. Copper deficiency can be caused by a lack of copper in feed and water or by a genetic disease in man (Menke’s disease) and mice.
Molybdenum toxicity has been a problem in certain areas of Europe, Australia, New Zealand, Texas, California and Nevada and is associated with alkaline soil, granithic mountain areas or ranches surrounding coal or uranium mines. Molybdenosis leads to secondary copper deficiency and it has been suggested that the underlying biochemical events take place within the gastrointestinal tract where the interactions among copper, molybdenum and sulphur are maximal. This may explain the differences in toxicity between ruminants and non-ruminants induced by the same dose of molybdenum in diet.
While lesions of the liver are typically described in copper intoxication, morphological alterations of the liver caused by copper deficiency or molybdenosis are rarely reported. In the rat, molybdenum stimulates an accumulation of lipids and phospholipids within the hepatocytes by inhibiting mitochondrial phosphorylation leading to degeneration and focal necrosis. In our study, a mild fatty degeneration of the liver, hepatocellular necrosis, portal bridging fibrosis, bile duct proliferation and hemosiderosis were observed. Fe, Al, and Pb values were extremely elevated and may have caused hepatocellular damage as well. The lesions in the liver may also be responsible for the maldigestion. The intensity of the histopathological alterations may be caused by the duration of our study.
Defects affecting the cardiovascular system and the skeleton of copper deficient animals are related to disorders of lysyl oxidase. Lesions at the growth plates of distal extremities appeared in goats with molybdenosis on day 70 of the experiment, but after 235 days no lesions were present. This is supported by the absence of radiographic or histological bony lesions in our study.
Achromotrichia and defective hair structure in ruminants have been linked with a lack of tyrosinase. In the animals investigated in our study, structural alterations of the hair did not occur and an achromotrichia could not be observed because the goats were white-haired. A moderate hyperkeratosis and atrophy of the skin and the integumentary appendages were obvious. No other author reported these findings and we could not find an explanation of these alterations because the endocrine system appeared histomorphologically normal.
Degeneration, acinar irregularity, and loss of basement membranes in the exocrine pancreas is caused by depleted cytochrome oxidase activity and enhanced monoamine oxidase activity and has been described in copper deficient cattle, rats and guinea pigs.
Ceruloplasmin is an oxidase that catalyses the oxidation of amines and iron. It is formed in the liver and deficiency leads to anemia as observed in our study.
Neurological symptoms caused by disorders of dopamine ß-hydroxylase are cardinal signs of severe copper deficiency of sheep and rats, and are induced intrauterine or during the perinatal period. Cytochrome oxidase catalyses the final and irreversible step of the mitochondrial electron transport chain. It is an important key in energy production and seems to be responsible for alterations in gut, heart, pancreas, and brain.
It can be summarized that pathological findings in our long-term study of copper deficiency, and the effect of molybdenum supplementation in goats, are mainly caused by the effects of insufficient activity of lysyl oxidase (skin), cytochrome oxidase (liver, pancreas) and ceruloplasmin (hemosiderosis) activity. No achromotrichia and nervous symptoms appeared, indicating that tyrosinase and dopamine ß-hydroxylase may be less affected in the goats of our study. The age of the animals, the duration of the study and the fact that goats are less sensitive to copper deficiency and molybdenosis than other ruminants may explain the differing results found in our study compared with other reports.
This study was performed with economic support from the Swedish Environmental Protection Agency, Stockholm, Sweden.
AFIP Diagnosis: Liver: Degeneration, hepatocellular, diffuse, moderate, with lipid-type vacuolar change, bridging portal fibrosis, biliary hyperplasia, and granular, green-brown pigment, goat, white German noble, caprine.
Conference Comment: The mechanism responsible for maintenance of the inverse relationship of copper and molybdenum levels in the body is complex and not completely understood; however, one of the important clinical outcomes of molybdenosis is a secondary copper deficiency. Of the various dietary trace minerals present in the body, only copper, iodine, iron, selenium, and zinc are associated with well-characterized deficiency states.
The complex clinical signs and necropsy findings associated with copper deficiency are best understood in relation to the biochemical functions of the copper-containing enzymes. The variety and extent of clinical signs such as anemia, depigmentation and achromotrichia, osteoporosis and malformed growth plates, liver changes, general debilitation and weakness, brain and spinal cord demyelination, and diarrhea due to mucosal lesions and ulcerations are thought to be related to the degree of copper-dependent enzyme activity. As a cofactor, copper is involved in a variety of oxidative enzymes of diverse function. Deficiencies of this element may effect electron transport (cytochrome oxidase), absorption of iron and its utilization in hematopoiesis (ceruloplasmin), tyrosine degradation and pigmentation (tyrosinase), neurotransmitter metabolism (dopamine hydroxylase) or cross linkage of elastin and tropocollagen (lysyl oxidase). Copper and molybdenum concentrations in the diet and stored in organs, the dietary ratio of Cu:Mo concentrations, and the duration and extent of the deficiency or excess will influence the clinical profile and severity of tissue damage.
Perl’s iron stain demonstrated abundant hemosiderin in hepatocytes and Kupffer cells.
Contributor: Institut für Veterinär-Pathologie, An den Tierkliniken 33, Leipzig, Germany 04301
References: 1. Coulson WF, Barlow RM, Cancilla PA, Weissman N, Linker A, Waisman J, Carnes WH: Cardiovascular system in naturally occurring copper deficiency and swayback in sheep. Am J Vet Res 27:815-818, 1967
2. Dollahite JW, Rowe LD, Cook LM, Hightower D, Mailey EM, Kyzar JR: Copper deficiency and molybdenosis intoxication associated with grazing near a uranium mine. Southwest Vet 26:47-50, 1972
3. Fell BF, Dinsdale D, El-Gallad TT: Gut pathology of rats dosed with tetrathiomolybdate. J Comp Path 89:495-513, 1979
4. Fell BF, Farmer LJ, Farquharson C, Bremmer I, Graca DS: Observations on the pancreas of cattle deficient in copper. J Comp Path 95:573-590, 1985
5. Frank A: ‘Mysterious’ moose disease in Sweden. Similarities to copper deficiency and/or molybdenosis in cattle and sheep. Biochemical background of clinical signs and organ lesions. Sci Total Environ 209:17-26, 1998
6. Hainline BE, Rajagopalan KV: Molybdenum in animal and human health. In: Trace Elements in Health: A Review of Current Issues, ed. Rose J, pp. 150-166. Butterworth, London, England, 1983
7. Irwin MR, Poulos PW, Jr., Smith BP, Fisher GL: Radiology and histopathology of lameness in young cattle with secondary copper deficiency. J Comp Path 84:611-621, 1974
8. Ishida N, Kawashima R: Histochemical studies of the skin and wool in sheep reared on high molybdenum diet. Jap J Zootech. Sci 45:352-360, 1974
9. Leigh LC: Changes in the ultrastructure of cardiac muscle in steers deprived of copper. Res Vet Sci 18:282-287, 1975
10. Pletcher JM, Banting LF: Copper deficiency in piglets characterized by spongy myelopathy and degenerative lesions in the great blood vessels. J South Afr Vet Assoc 3:43-46, 1983
11. Suttle NF, Field AC, Barlow RM: Experimental copper deficiency in sheep. J Comp Path 80:151-162, 1970
12. Sharma AK, Parihar NS: Pathology of experimental molybdenosis in goats. Ind J Anim Sci 64(2):114-119, 1994
13. Sharma AK, Parihar NS: Clinicopathology of induced molybdenum toxicity in young goats. Ind J Anim Sci 64(2):120-125, 1994
14. Suttle NF: The role of comparative pathology in the study of copper and cobalt deficiencies in ruminants. J Comp Path 99:241-258, 1988
15. Suttle NF, Angus KW: Experimental copper deficiency in the calf. J Comp Path 86:595-608, 1976
16. Suttle NF, Field AC, Barlow RM: Experimental copper deficiency in sheep. J Comp Path 80:151-162, 1970
17. Waisman J: The ultrastructure and histochemistry of the myocardium in copper-deficient pigs. Fed Proc 31:627, 1972
18. Ward GM: Molybdenum toxicity and hypocuprosis in ruminants:
a review. J Anim Sci 46:1078-1085, 1978
*Sponsored by the American Veterinary Medical Association, the American College of Veterinary Pathologists and the C. L. Davis Foundation.
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