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CASE I – 288-00 (AFIP 2737427)
Signalment: 3-year-old quarter horse gelding
History: Several horses died acutely after several hours of illness.
Gross Pathology: The squamous epithelium of the forestomach was diffusely sloughing, but there was no hyperemia. The urinary bladder mucosa was diffusely covered with petechia and ecchymoses, but there was no hemorrhage into the lumen.
Laboratory Results: Serum chemistry: calcium 9.3 mg/dL (normal 11.2-13.6); BUN 47 mg/dL (10-23); creatinine 2.0 mg/dL (1.2-1.9). About = bale of alfalfa hay, grown in central Arkansas, was presented with the horse containing eight 3-striped blister beetles (Epicauta vittata), or portions of them. Urine from a second horse was also submitted and it had 119 ppb of cantharidin.
Contributor’s Diagnosis and Comment: Ulcerative cystitis due to cantharidin toxicity.
Affected horses often have hypocalcemia and azotemia, as well as hypomagnesemia. The toxin causes acantholysis and systemic effects from gastrointestinal absorption and urinary tract elimination, but the mode of action is unknown. Necrosis and ulceration of the squamous lining of the distal esophagus, forestomach, and urinary bladder are the most commonly reported severe lesions.
In one recent review, no gross lesions were documented in six of twenty-four horses that died of cantharidin toxicity. Two had gastric or esophageal ulceration, fourteen horses had diffuse or segmental hyperemia of the gastrointestinal mucosa, and two had urinary bladder mucosal hemorrhages.
Cantharidin, present in the hemolymph of the beetles, is a potent mucosal irritant. Rarely, lip and oral ulcers may occur from the toxin. The epithelial lining of the esophagus, stomach, and urinary bladder are most sensitive to ulceration from the toxin, but the remainder of the intestine and colon may be affected by hyperemia. As in our case, blister beetles were not found in the ingesta in these horses.
AFIP Diagnoses: 1. Urinary bladder: Ulceration, diffuse, with mucosal fibroplasia and neovascularization (early granulation tissue), quarter horse, equine.
2. Stomach, squamous: Epithelial degeneration, necrosis, and loss, diffuse, moderate, with multifocal, subacute gastritis.
Conference Comment: The clinical signs of cantharidin toxicity in horses, which can range from colic to vague illness and acute death within several hours, result from ingestion of alfalfa hay containing blister beetles. The variation in the severity of clinical signs is attributed to a dose-related response, but the degree of severity also may be influenced by early diagnosis and treatment. In addition to ulcerative lesions of the gastrointestinal tract and urinary system, myocardial degeneration and necrosis may occasionally occur. Cardiac lesions are thought to be due to either direct myocardial toxicity, or the result of violent contractions induced by the toxin. Signs of shock in horses may be subtle, with only visceral and mucosal congestion. Severe shock, collapse, and rapid death in some horses are thought to result from fluctuations in blood calcium and magnesium concentrations. Although there are no recognized pathognomonic lesions, the finding of beetles in hay, or presence of cantharidin in body fluids of a horse with clinicopathologic signs suggestive of cantharidiasis is usually considered confirmatory of the diagnosis.
Contributor: Arkansas Livestock and Poultry Commission Laboratory, #1 Natural Resources Drive, Little Rock, AR 72205
References: 1. Helman RG, Edwards WC: Clinical features of blister beetle poisoning in equids: 70 cases (1983-1996). J Am Vet Med Assoc 211:1018-1021, 1997
2. Jones TC, Hunt RD, King NW: Diseases due to extraneous poisons. In: Pathology of Domestic Animals, 6th ed., pp. 706-707. Williams and Wilkins, Baltimore, MD, 1997
3. Ray AC, Kyle AL, Murphy MJ, Reagor JC: Etiologic agents, incidence, and improved diagnostic methods of cantharidin toxicosis in horses. Am J Vet Res 50:187-191, 1989
4. Schoeb TR, Panciera RJ: Pathology of blister beetle (Epicauta) poisoning in horses. Vet Pathol 16:18-31, 1979
5. Shawley RV, Rolf LL: Experimental cantharidiasis in the horse. Am J Vet Res 45:2261-2266, 1984
CASE II – A992430092 (AFIP 2737419)
Signalment: Male and female hamsters, breed not specified, various ages
History: Breeder reported high morbidity and mortality in hamsters. Acute onset of illness (clinical signs not specified), and death within 24 hours.
Gross Pathology: Eight hamsters of varying age and sex were submitted for postmortem examination. All were dehydrated, and there was fetid, fluid fecal matter adherent to the perineum. The cecum in 6 of the 8 hamsters was distended with gas and contained foamy, tan, semi-fluid content.
Laboratory Results: Routine bacterial culture of large bowel was negative. Electron microscopy of stool samples for the presence of viral particles was negative. Cytotoxicity assay for Clostridium difficile was negative.
Contributor’s Diagnosis and Comment: Typhlocolitis, necrotizing, acute to subacute, with intracellular bacilli.
Etiology: Tyzzer’s disease (Clostridium piliforme, formerly Bacillus piliformis)
Tyzzer’s disease affects a variety of animal species. Lesions can be detected in the terminal small intestine, large bowel, liver and heart, but in hamsters, major lesions are sometimes confined to the intestinal tract. The long, thin bacilli typical of Clostridium piliforme are difficult to visualize with routine hematoxylin and eosin staining, but can readily be observed following silver impregnation such as Warthin-Starry or Steiner procedures. Hamsters appear to be highly susceptible to infection, with high morbidity and mortality.
AFIP Diagnosis: Large intestine: Colitis, subacute, diffuse, moderate, with crypt epithelial hyperplasia, goblet cell loss, and intraepithelial, filamentous bacilli, etiology consistent with Clostridium piliforme, hamster, breed not specified, rodent.
Conference Comment: Hepatomegaly with multifocal, random areas of necrosis is considered the most consistent lesion seen at necropsy in hamsters, gerbils, other laboratory rodents, and foals infected with Tyzzer’s disease. The Gram negative, intracellular, filamentous bacilli are most readily found in hepatic, intestinal epithelial, or myocardial cells bordering areas of necrosis. Reports of Tyzzer’s disease in dogs and cats are relatively rare. Immune status is suspected to play a role in susceptibility to infection.
Contributor: Texas Veterinary Medical Diagnostic Laboratory, 6610 Amarillo Boulevard West, P.O. Box 3200, Amarillo, TX 79116-3200
References: 1. Ikegami T, Shirota K, Goto K, Takakura A, Itoh T, Kawamura S, Une Y, Nomura Y, Fujiwara K: Enterocolitis associated with dual infection by Clostridium piliforme and feline panleukopenia virus in three kittens. Vet Pathol 36(6): 613-615, 1999
Motzel SL, Gibson SV: Tyzzer disease in hamsters and gerbils from a pet store supplier. J Am Vet Med Assoc 197:1176-1178, 1990
2. Waggie KS, Thornburg LP, Grove KJ, Wagner JE: Lesions of experimentally induced Tyzzer’s disease in Syrian hamsters, guinea pigs, mice and rats. Lab Anim 21:155-160, 1987
3. Zook BC, Huang H, Rhorer RG: Tyzzer’s disease in Syrian hamsters. J Am Vet Med Assoc 171:833-836, 1977
CASE III – 00-0343 (AFIP 2741252)
Signalment: Two-week-old, female mixed breed lamb (Ovis aries)
History: The lamb was presented for a swelling in the neck region that had been present for more than a week. On physical examination, the lamb was bright and alert. A nonpainful, movable and firm, 10 X 10 cm, round to elliptical mass was located paramedially on the ventral surface of the neck. The overlying skin was normal. Surgical excision was performed.
Gross Pathology: The mass had a slightly lobulated appearance. It was ovoid, except for an attached caudal tailpiece, and a dorsocranial duct that had been ligated and cut intraoperatively. The center of the mass contained caseous material and pieces of vegetation; one section of vegetation was 10 cm long.
Laboratory Results: An aspirate of the mass, obtained pre-operatively, revealed Gram-positive cocci and Gram-negative rods.
Contributor’s Diagnosis and Comment: Thyroglossal duct cyst with luminal necrosis and suppuration, encapsulated by granulation tissue.
Thyroglossal duct cysts are a common congenital anomaly in children, and are reported to occur in dogs and pigs. During normal embryonic development, a hollow tube grows downward from the foramen cecum, located at the base of the tongue, to form the thyroid gland distally. Unresorbed portions of the thyroglossal duct may persist as cysts or ectopic thyroid tissue.
In the present case, several features are consistent with the diagnosis given. First, the cyst is lined by non-keratinized stratified squamous epithelium, similar to oropharyngeal epithelium. Also, the cyst wall contains numerous primitive epithelial ducts that merge into areas with normal-appearing thyroid follicles. The caudal tail of the mass (not present in section) is composed of normal thyroid tissue. It is probable that pieces of grass, reaching the oropharynx of the lamb, migrated down the thyroglossal duct, resulting in an abscess.
AFIP Diagnosis: Fibrovascular tissue: Ectopic thyroid gland and squamous epithelial-lined cyst (thyroglossal duct cyst), with chronic-active inflammation, ulceration, and granulation tissue, mixed breed lamb, ovine.
Conference Comment: Remnants of the thyroglossal duct can be found on the ventral midline anywhere from the oropharynx to the mediastinum. They are lined by multi-layered epithelium that often forms follicles filled with eosinophilic colloid. If any portion of the thyroglossal duct remains patent after birth, a cyst may form, often not becoming clinically evident for several months. Neoplastic transformation occurs uncommonly, resulting in papillary carcinoma.
Thyroglossal duct cysts must be differentiated from other midline pharyngeal pouch cysts such as parathyroid cysts, branchial cysts, ultimobranchial duct cysts, follicular cysts, and salivary mucoceles.
Contributor: Massachusetts Institute of Technology, Division of Comparative Medicine, 77 Massachusetts Avenue, Cambridge, MA 02139
References: 1. Capen CC: The endocrine glands. In: Pathology of Domestic Animals, ed. Jubb KVF, Kennedy PC, Palmer N, 4th ed., vol. 3, p. 309. Academic Press, Inc., New York, NY, 1993
2. Cotran RS, V Kumar, and T Collins: Robbins Pathologic Basis of Disease, 6th ed., p 1147. WB Saunders Co., Philadelphia, PA, 1999
3. Al-Ani FK, Vestweber J: The embryologic origin of thyroglossal duct cysts. Vet Med:271-272, 1986
CASE IV – MSU1 (AFIP 2737401)
Signalment: Thirty-week-old, female, Arbor Acres broiler-breeder chicken (Gallus gallus)
History: In a four-house complex of broiler-breeder birds (20,000 hens, 2,000 cocks per house), hen mortality was higher than expected and egg production was lower than expected. Six hens were submitted live for necropsy examination.
Gross Pathology: Four of six birds had more than adequate fat reserves. Three birds had multiple small, white foci in the liver, kidney, and ovary, respectively. Other organs were unremarkable.
Laboratory Results: Liver, kidney, and ovary were processed for DNA extraction by SNAP Miniprep Kit and tested for avian leukosis virus (ALV) subgroup J provirus using the polymerase chain reaction assay. The tissues were positive for ALV subgroup J with a very clean, specific band.
Contributor’s Diagnosis and Comment: Myelocytomatosis, ovary - Gallus gallus
The ovary section had stromal architecture disrupted and replaced by a neoplastic process. Neoplastic cells consisted of compact groups of clone-like myelocytes containing large vesicular nuclei. Mitotic figures were occasionally observed. Cytoplasm was packed with spherical, acidophilic granules.
Myelocytomatosis, myeloid leukosis, and myelocytoma are neoplastic conditions caused by retrovirus subgroup J of avian leukosis virus (ALV) that uses myelocytes as target cells. Meat-type chickens are the primary host. It is believed that ALV subgroup J is a recombinant exogenous form of ALV. Being an exogenous virus, it can spread horizontally by contact with infected chickens.
Although other ALV subgroups can be endogenous as a provirus, and carry a viral oncogene that inserts into host DNA to induce tumors, ALV subgroup J has not been shown to carry a viral oncogene (v-onc). Instead, ALV subgroup J becomes oncogenic when the virus (myc or v-myc) inserts itself near the normal proto-oncogenes of chickens. The viral long term repeats (LTR) cause dysregulation of the normal c-myc gene to induce tumor formation. Thus, normal proviral genomes under the control of cellular regulatory genes, which are totally silent in normal birds, may have normal control and regulation disrupted, leading to tumor formation. Progeny infected as embryos with ALV subgroup J are immunotolerant, viremic, and life-long shedders. Stress plus immunosuppression promotes tumor expression and virus shedding in those birds. Since first isolated in 1988, the retrovirus of myelocytomatosis has become a major economic factor in broiler-breeder birds.
AFIP Diagnosis: Ovary: Myelocytoma, broiler-breeder chicken, breed not specified, avian.
Conference Comment: All members of the family Retroviridae possess the enzyme reverse transcriptase, which is necessary for the transcription of proviral DNA from mRNA. ALV-related retroviruses are identified by six subgroups: A, B, C and D (exogenous viruses), E (endogenous) and J (recombinant). Apparently, the J subgroup of avian leukosis virus arose from genetic recombination between an exogenous and endogenous avian leukosis virus. Each subgroup possesses various viral oncogenes that largely determine the pathogenesis. Subgroups A, B, and J are common in the field; subgroups C and D are rare.
In myelocytomatosis, bone marrow intersinusoidal spaces are filled with primitive myeloid stem cells and neoplastic myelocytes that appear to arrest their differentiation at the non-granulated or granulated myelocyte level. Neoplasms often extend through the periosteum, forming distinctive soft, friable nodular masses, often at costochondral junctions. Extramedullary neoplasms, as in this case, may arise by metastasis. Histologically, solid masses on scant stroma are composed of uniform myelocytes with large, vesicular nuclei and a distinct nucleolus. Occasionally, the cytoplasm is packed with eosinophilic granules. A common feature of the neoplastic myelocytes is the formation of a cohesive, invasive proliferation of cells into parenchymatous organs.
Contributor: Murray State University, Breathitt Veterinary Center, 715 North Drive, P.O. Box 2000, Hopkinsville KY 42241-2000
References: 1. Fadly AM, Schat KA, Spencer JL: Avian tumor viruses symposium. Am Assoc Avian Pathol, 40th annual meeting, Reno, NV, 1997
2. Owen RL: Update on ALV-J and remaining issues. 48th Annual New England Poultry Health Conference, pp.15-16, 2000
3. Payne LM, Fadly AM: Neoplastic diseases/leukosis/sarcoma group. In: Diseases of Poultry, ed. Calnek BW, pp. 414-466. Iowa State University Press, Ames, IA, 1997
4. Zavala G, Fadly AM, Glisson JR: Avian Leukosis Virus Subgroup
J. Intl Poult Expo, Westbrook, ME, 1998
*Sponsored by the American Veterinary Medical Association, the American College of Veterinary Pathologists and the C. L. Davis Foundation.
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