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CASE I – 3967 (AFIP 2739117)
Signalment: Adult wild, 62-72 cm total length, pre-spawning female and male sockeye salmon (Oncorhynchus nerka).
History: During the 1999 spawning run of the Harrison and Adam rivers in British Columbia, Canada, a massive sustained die-off of adult sockeye salmon (O. nerka) was observed from late August through October.
Gross Pathology: Adult salmon were in good body condition. Aside from multiple superficial cutaneous abrasions and lacerations that were attributed to physical excoriation associated with migration, and small numbers of adult nematode parasites (Anisakis spp.) within the coelomic cavity of multiple fish, there were no other overt internal or external lesions.
Laboratory Results: Aerobic bacterial and viral cultures of multiple tissues failed to yield any significant pathogens. Trace mineral analysis of liver and skeletal muscle was within the normal reference range for adult Pacific salmon. Pooled liver, kidney, and spleen were negative by polymerase chain reaction for infectious hematopoietic necrosis virus (IHNV), viral hemorrhagic septicemia (VHSV), infectious salmon anemia virus (ISAV), Piscirickettsia salmonis, and Enterocytozoon salmonis.
Contributor’s Diagnosis and Comment: Posterior kidney: Glomerulonephritis, segmental to diffuse, subacute, moderate, with tubular epithelial necrosis, protein casts, and endothelial and mesangial protozoal parasites.
Histopathology of all submitted salmon revealed consistent lesions in the kidneys. In the initial phase of the migration, throughout the posterior kidney the capillaries of virtually all the renal glomeruli were variably distended and occluded by dense accumulations of immature protozoal parasites. Small numbers of similar developmental stages were present within the gills of select fish, and an early developmental stage of the parasite was noted in the lateral ventricle of the brain in a single fish. In addition to developmental stages within the glomerular tufts, during the latter stages of the migration there were a large number of mature parasitic spores noted within the lumina of numerous renal tubules. In more severely affected fish, there was diffuse thickening of the glomerular basement membrane and scattered tubules, with focal to segmental coagulative necrosis of renal tubular epithelia and occasional proteinaceous tubular casts.
The parasite was speciated as Parvicapsula minibicornis, a myxosporean pathogen previously observed in sockeye salmon from Horsefly River, BC in 1978. The parasite was described in spawning wild sockeye salmon stocks from Weaver Creek, BC in November 1996. The life cycle of this parasite has not yet been determined; however, based on extrapolation from other related myxosporean parasites, it is likely a complex life cycle that requires an intermediate invertebrate host.
Although osmoregulation, acid-base balance, and nitrogenous waste elimination are accomplished predominantly by the gills of fish, there is still a prominent renal component for homeostasis that is particularly important in freshwater environments. Due to the extent of glomerular involvement, and subsequent tubular epithelial cell necrosis in spawning fish, this parasite likely would have contributed significantly to impaired renal function.
AFIP Diagnosis: Posterior kidney: Protozoa, numerous, glomerular and intratubular, with multifocal tubular degeneration and necrosis, etiology consistent with phylum Myxozoa, sockeye salmon (Oncorhynchus nerka), piscine.
Conference Comment: Myxozoans are parasites primarily found in aquatic tubificid worms and poikilothermic vertebrates such as fish. Species identification of myxozoans is typically performed by examination of spore morphology in wet-mount preparations, and can now be confirmed by polymerase chain reaction or in situ hybridization assays. In fish, the infective spores usually produce few clinical signs and little inflammation. Pathogenic infections occur when large numbers of space-occupying pseudocysts or feeding trophozoites result in renal tubular damage and necrosis.
Other diseases in young salmonids infected with myxozoans include whirling disease caused by Myxobolus cerebralis, and proliferative kidney disease caused by the PKX agent, phylum Myxozoa.
Contributor: British Columbia Ministry of Agriculture, 1767 Angus Campbell Road, Abbotsford, BC, Canada V3G2M3
References: 1. Kent ML, Whitacker DJ, Dawe SC: Parvicapsula minibicornis n. sp. (Myxozoa, Myxosporea) from the kidney of sockeye salmon (Oncorhynchus nerka) from British Columbia, Canada. J Parasitol 83(6):1153-1156, 1997
2. Raverty SR, Kieser D, Bagshaw J, St. Hilaire S: Renal infection with Parvicapsula minibicornis in wild sockeye salmon (Oncorhynchus nerka) from the Harrison and Adams rivers in British Columbia. Can Vet J 41:317-318, 2000
CASE II – P2G2 (AFIP 2744075)
Signalment: 2.5-month-old, male laboratory mouse (Mus musculus).
History: Unilateral right scrotal swelling was observed for about a month.
Gross Pathology: The right testis was markedly enlarged (1.4x1.0x1.0 cm). The normal contralateral testis measured 0.8x0.5x0.5 cm and its external surface was mottled light brown-red. When bisected, the testicular parenchyma bulged over the cut surface, and the tissue was smooth, soft, and tan with multifocal, dark red areas.
Laboratory Results: None.
Contributor’s Diagnosis and Comment: Testis: Teratoma.
The testicular parenchyma is replaced by a non-delineated, unencapsulated, and infiltrative mass composed of several intermingled tissue types representing the three germ layers. The types of tissue present and their proportions vary in different areas of the mass but, in general, nervous tissue (ectoderm) is the most abundant element. Mature nervous tissue contains neurons and lesser numbers of small cells interpreted as glia, as well as multiple cystic or collapsed and somewhat tortuous spaces lined by ciliated, simple cuboidal epithelium, consistent with ependyma.
Other identifiable mature elements include adipose tissue, skeletal muscle, and bone with a marrow cavity containing trilinear hemopoietic tissue (mesoderm), and respiratory epithelium (endoderm) with prominent goblet cells outlining irregular spaces. Islands of immature tissue are composed of densely, or less commonly, loosely aggregated sheets and clusters of undifferentiated, anisokaryotic and anisocytotic cells with spindled, oval, and irregular vesicular to coarsely granular nuclei, often with prominent magenta nucleoli. There is scant to moderate amount of eosinophilic and amphophilic cytoplasm which is often vacuolated. Cytoplasmic margins are indistinct, and obvious multinucleated cells are encountered. Within the immature tissue, there is multifocal rosette formation suggestive of neural differentiation, and the mitotic rate is high (>5/HPF). Microhemorrhages, which appear to be more concentrated in the immature tissue, degeneration, necrosis and dilated lacteals are present multifocally throughout the mass. Residual seminiferous tubules are atrophic with markedly reduced numbers of spermatozoa.
Spontaneous testicular tumors are very rare in mice and most of the reported cases are of Leydig cell origin. Teratoma, seen mostly in Strain 129, appears to be the second most common tumor. Teratoma is defined as a complex tumor of germ cell origin showing elements of more than one germ layer. The incidence of spontaneous testicular teratoma varies among the different sublines of Strain 129 (1% in most sublines to 30% in the 129/Sv-ter). In 129/Sv-ter mice, spontaneous teratogenesis begins during the early stages of gonad differentiation and the earliest tumors were identified in the gonadal ridges of 14 day-old embryos.
A mutation in the ter gene, which enhances the inherited predisposition to spontaneous testicular teratocarcinomas in Strain 129, has been identified. A study of 42 testicular teratomas in Strain 129 mice did not reveal an age group in which the tumors predominated. An apparent relationship between the age of the tumor-bearing mouse and the type of tumor tissue found was observed, and the sequence of tissue differentiation was thought to be similar to that of normal development.
AFIP Diagnosis: Testis: Teratoma, mouse (Mus musculus), strain not specified, rodent.
Conference Comment: Teratoma is defined as “a complex tumor showing elements of more than one germ layer in various stages of maturation and often arranged in such a manner as to suggest abortive organ formation.” Teratoma of the testis is exceedingly rare in domestic animals. In the horse, its presence is thought to prevent the normal descent of the testis; hence, it is more commonly found in a cryptorchid, rather than scrotal testis. As in childhood teratomas, the tumors in young horses are usually benign.
The importance of recognizing and being able to succinctly describe a teratoma, to include identifying the various germ layers, for aspiring veterinary pathology residents, was discussed in conference. The contributor has provided an excellent example of such a description.
Contributor: Experimental Animal Center, The Weizmann Institute of Science, Rehobot, Israel 76100
References: 1. Ladds PW: Testes. In: Pathology of Domestic Animals, ed. Jubb KVF, Kennedy PC, Palmer N, 4th ed., vol. 3, pp. 510. Academic Press, San Diego, CA, 1993
2. Mostofi FK, Bresler VM: Tumours of the testis. In: Pathology of Tumours in Laboratory Animals, ed. Tursov VS, vol. II–Tumors of the Mouse, pp. 325-338. IARC Publishing, Lyon, France, 1979
3. Noguchi T, Noguchi M: A recessive mutation (ter) causing germ cell deficiency and a high incidence of testicular teratomas in 129/Sv-ter mice. J Natl Cancer Inst 75(2):385-392, 1985
4. Rivers EN, Hamilton DW: Morphologic analysis of spontaneous teratocarcinogenesis in developing testes of Strain 129/Sv-ter mice. Am J Pathol 124:263-280, 1986
5. Stevens LC, Little CC: Spontaneous testicular teratomas in an inbred strain of mice. Proc Natl Acad Sci 40:1080-1087, 1954
CASE III – 980508 (AFIP 2752417)
Signalment: Adult male cynomolgus macaque (Macaca fascicularis), nonhuman primate.
History: Physical examination of the monkey found him to be in good health and free of simian retrovirus infection by Raji tissue culture assay. After transfer to animal housing within a biosafety level-4 (BSL-4) suite, with a time period allowed for acclimation, the monkey was then sedated and blood was sampled for baseline data. He was then inoculated intramuscularly with 140 plaque-forming units (PFU) of Marburg virus Musoke strain (dose determined by back titration). The monkey was clinically monitored daily. Blood samples were obtained under sedation on days 3, 5 and 7 post inoculation (PI). By day 7 PI, clinical signs included anorexia and widespread cutaneous petechial hemorrhages. On day 9 PI, the animal was found to be moribund, with a body temperature of 95.7° C. After obtaining a terminal blood sample, the monkey was euthanized and transferred to the BSL-4 necropsy room for complete necropsy.
Gross Pathology: Lesions included petechial rash, hepatomegaly with prominent reticular pattern, splenomegaly and lymphadenopathy.
Laboratory Results: Data are provided for days 0 (baseline), 7, and 9 PI. Virus isolation and titration of blood on days 7 and 9 PI yielded high level viremia (8.32 and 8.0 log PFU per ml blood, respectively). Virus isolation and titration of a liver sample obtained at necropsy on day 9 PI was 9.9 log PFU per gram liver. A limited serum biochemistry panel and a hematology panel were conducted in the BSL-4 clinical laboratory. Blood films for differential counts were treated with gamma irradiation and counted manually outside of containment. Data are as follows:
Automated serum biochemistry:
Albumin: 3.0 g/dL (day 0); 2.5 g/dL (day 9)
AST: 28 U/L (day 0); 1018 U/L (day 9)
Direct Bilirubin: <0.1 mg/dL (day 0); 1.8 mg/dL (day 9)
Total Bilirubin: 0.3 mg/dL (day 0); 1.8 mg/dL (day 9)
Blood Urea Nitrogen: 16 mg/dL (day 0); 15 mg/dL (day 9)
Creatinine: 1.0 mg/dL (day 0); 1.3 mg/dL (day 9)
Total Protein: 7.5 g/dL (day 0); 5.4 g/dL (day 9)
Automated hematology:
WBC (x103): 6.5 (day 0); 3.9 (day 7); 9.6 (day 9)
RBC (x106): 6.3 (day 0); 6.3 (day 7); 5.4 (day 9)
Hgb: 14.0 (day 0); 13.8 (day 7); 11.9 (day 9)
Hct: 41.5 (day 0); 41.4 (day 7); 37.9 (day 9)
MCV: 65.6 (day 0); 65.3 (day 7); 69.9 (day 9)
MCH: 22.1 (day 0); 21.8 (day 7); 22.0 (day 9)
MCHC: 33.7 (day 0); 33.3 (day 7); 31.4 (day 9)
PLT (x103): 478 (day 0); 304 (day 7); 297 (day 9)
Differential blood counts:
Segs (%): 73 (day 0); 92 (day 7); 76 (day 9)
Bands (%): 1 (day 0); 0 (day 7); 5 (day 9)
Lymph (%): 22 (day 0); 8 (day 7); 8 (day 9)
Mono (%): 2 (day 0); 0 (day 7); 2 (day 9)
Eos (%): 1 (day 0); 0 (day 7); 0 (day 9)
Baso (%): 1 (day 0); 0 (day 7); 0 (day 9)
Atypical Lymph (%): 0 (day 0); 0 (day 7); 7 (day 9)
Immature Myeloid: (%): 0 (day 0); 0 (day 7); 2 (day 9)
Contributor’s Diagnoses and Comment: 1. Liver, parenchyma: Hepatocellular degeneration, disseminated, moderate, characterized by hepatocellular swelling, cytoplasmic “ground glass” appearance, lipid droplets, brown pigment (bile) stippling, with intracytoplasmic eosinophilic inclusion bodies, occasional individual cell necrosis, and binucleated hepatocytes, etiology experimental Marburg filovirus infection.
2. Liver, portal triads: Infiltrates, leukocytic, multifocal, mild, comprising hypersegmented neutrophils, eosinophils and mononuclear cells.
3. Liver, sinusoids and blood vessels: Leukocytes, circulating, numerous, comprising hypersegmented neutrophils, apoptotic cells, mitotic figures, and large mononuclear cells.
There is moderate hypoproteinemia with mild hypoalbuminemia. Transaminase is severely elevated, likely referable to liver dysfunction. There is predominantly conjugated hyperbilirubinemia, suggesting cholestasis. Renal function is unchanged. There is mild leukopenia, followed by mild leukocytosis at the time of death, with absolute lymphopenia. The presence of circulating myelopoietic precursor cells is suggestive of premature release from the bone marrow.
Immunohistochemical staining of hepatic sections, using a mixture of Marburg virus-specific monoclonal antibodies as the primary antibody and an indirect immunoperoxidase labeling procedure, demonstrated immunoreactive material interpreted to be viral antigen within circulating monocytes, plasma, Kupffer cells, and endothelial cells. Most hepatocytes were outlined by immunoreactive material interpreted to be viral antigen present within the space of Disse and bile canaliculi, and bound to hepatocellular margins. In addition to stippled pigmentation (possibly bile) noted in the sections lacking specific primary antibody treatment (specificity control), hepatocytes had punctate cytoplasmic immunoreactivity, interpreted to be viral antigen.
Possible differential diagnosis for the etiology of the microscopic hepatic lesion that should be considered include Ebola virus, orthopoxvirus, paramyxovirus, morbillivirus, and flavivirus. Hepatic infection with Ebola virus is morphologically indistinguishable and can be differentiated only on the basis of virus isolation, serology and immunohistochemistry. Marburg and Ebola viruses are serologically distinct filoviruses. Disseminated monkey pox occasionally induces inclusion bodies in the liver of experimentally infected monkeys, but inclusion body morphology differs from that of filoviruses. Measles virus infection (and perhaps other exotic morbilliviruses or paramyxoviruses) may induce inclusion bodies that would have to be differentiated. Yellow fever virus infection in the liver induces formation of Councilman bodies that would need to be distinguished from viral inclusions.
Marburg virus is named for the site of the first outbreak in Marburg, Germany in 1967. Animal handlers and laboratory workers having occupational exposure to infected African green monkeys (imported from Uganda) developed zoonotic infections, with subsequent transmission to health care providers caring for them. There were concurrent outbreaks of human infection in Frankfurt, Germany and Belgrade, Yugoslavia, also traced to infected African green monkeys.
Other names for Marburg virus are vervet monkey virus and African green monkey virus. There have been several instances of human Marburg viral infection contracted in Africa since the original outbreaks in Europe, most recently in Durba, Democratic Republic of Congo in 1998-2000. The reservoir and natural vectors, if any, are unknown. African green monkeys, very susceptible to infection with high fatality rate, may be incidental hosts, as are humans. Asian macaques are also very susceptible to experimental infection.
Although the pathogenesis is not well established, antigen presenting cells (blood monocytes and fixed macrophages) appear to be the initial site of viral infection, with subsequent spread to the liver and other organs. The liver is the apparent target organ of viral infection. As demonstrated in the submitted case, the virus rapidly replicates to very high levels in the blood and liver, overwhelming (or evading) innate immune defenses. Likewise, infection is uncontrolled by the early primary specific immune response. Death is likely due to acute hepatic failure, possibly complicated by terminal shock (so-called “cytokine storm”).
There is no licensed vaccine or specific antiviral therapy currently available. The human case fatality rate ranges 20-80%, depending on the level of supportive care available to infected patients. Because of its high fatality rate and the absence of treatment and prophylaxis, Marburg virus is classified as a biosafety level-4 agent, and can only be handled safely under maximum containment conditions. Besides its zoonotic potential, Marburg virus is a potential endemic infectious disease threat to military operations in certain parts of the world, and is a potential biological warfare threat.
The monkey in the submitted case was part of a pilot study in ongoing animal model development. The goal of the research project is to provide a nonhuman primate efficacy model system in which to assess prospective military prophylactic and therapeutic modalities that may, in turn, predict protection in humans against Marburg viral infection.
AFIP Diagnoses: 1. Liver: Swelling and vacuolar degeneration, hepatocellular, diffuse, moderate, with scattered single cell necrosis, eosinophilic intracytoplasmic inclusions, and edema, cynomolgus macaque (Macaca fascicularis), nonhuman primate.
2. Liver, large vessels: Immature hematopoietic cells, intravascular.
Conference Comment: Several secretory products from Marburg virus-infected monocytes and macrophages, such as TNF-alpha, gamma interferon, macrophage-specific interleukins, proteases, and oxygen radicals, have a cumulative effect in mediating increased endothelial permeability, induction of the coagulation cascade, activation of endothelial adhesion molecules for leukocytes and platelets, and immunosuppression. Hemorrhagic manifestations and shock can develop, but are not seen in all cases.
Filoviral infections in humans and nonhuman primates are characterized by minimal host immune response, with an absolute lymphopenia, as seen in this case. Lymphopenia and lymphoid depletion in monkeys are believed to be a result of lymphocyte apoptosis. Release of soluble mediators from filovirus-infected or activated cells, damage to the fibroblastic reticular cell conduit system, and interaction of viral proteins with lymphocytes have been proposed as triggers for apoptosis. Filoviral replication within monocytes and macrophages, but not lymphocytes, has been shown.
Contributor: U.S. Army Medical Research Institute of Infectious Diseases, 1425 Porter Street, Frederick, MD 21702-5011
References: 1. Feldman H, Bugany H, Mahner F, Klenk H-D, Drenckhahn D, Schnittler H-J: Filovirus-induced endothelial leakage triggered by infected monocytes/macrophages. J Virol 70(4):2208-2214, 1996
2. Geisbert TW, Hensley LE, Gibb TR, Steele KE, Jaax NK, Jahrling PB: Apoptosis induced in vitro and in vivo during infection by Ebola and Marburg viruses. Lab Invest 80(2):171-186, 2000
3. Geisbert TW, Jaax NK: Marburg hemorrhagic fever: report of a case studied by immunohistochemistry and electron microscopy. Ultrastr Pathol 22:3-17, 1998
4. Ignat’ev GM, Strel’tsova MA, Agafonov AP, Kashentseva EA: Mechanisms of protective immune response in monkeys with Marburg fever. Russian Progress in Virology 3:18-24, 1995
5. Kissling RE, Murphy FA, Henderson BE: Marburg virus. Ann NY Acad Sci 174:932-945, 1970
6. Klenk H-D, Feldman H: Symposium on Marburg and Ebola Viruses, [selected abstracts], Marburg, Germany, Oct. 1-4, 2000
7. Schou S, Hansen AK: Marburg and Ebola virus infections in laboratory non-human primates: a literature review. Comp Med 50(2):108-123, 2000
8. Seki S, Habu Y, Kawamura T, Takeda K, Dobashi H, Ohkawa T, Hiraide H: The liver as a crucial organ in the first line of host defense: the roles of Kupffer cells, natural killer (NK) cells and NK1.1 Ag+ T cells in T helper 1 immune responses. Immunol Rev 174:35-46, 2000
CASE IV – 2181180 (AFIP 2741213)
Signalment: 2.5-year-old, neutered male, domestic shorthair cat, feline.
History: This cat had a history of intermittent gastric problems for 2 years. Two weeks prior to presentation, the cat had become lethargic and anorectic. The referring veterinarian had palpated a 4-cm mass in the anterior abdomen and referred the cat to the Michigan State University Veterinary Teaching Hospital. Exploratory surgery revealed a mass adjacent to the pylorus, pancreas, and common bile duct, with some involvement of regional lymph nodes. A gastroduodenostomy was performed and tissue was biopsied. Shortly after surgery, the cat died and was submitted for necropsy.
Gross Pathology: At necropsy the animal weighed 9 lb and was in a fair to poor state of nutrition. The chest and abdominal cavities contained serosanguinous fluid. There was a nodular, firm mass in the proximal duodenum that was 5x3x3 cm in size. The common bile duct emptied into the mass. The liver was pale with an accentuated lobular pattern. A jejunal section was anastomosed to the pylorus. The entire small intestinal wall was thickened. Lungs were congested and edematous.
Laboratory Results: Tissues were not taken for culture at the time of necropsy.
Contributor’s Diagnoses and Comment: 1. Granulomatous to pyogranulomatous and scirrhous mural gastritis and enteritis, with intralesional fungi
2. Chronic lymphadenitis
3. Hypertrophic cardiomyopathy
The wall of the pylorus had an irregular intramural mass that extended from a focally intact mucosa, with expansion of the submucosa to the serosa by two decidedly different inflammatory processes. One region was solid with variably sized aggregates of pale staining macrophages associated with irregular collagen with mixed mononuclear cells. In the aggregates of macrophages were prominent fungal organisms that were focally dematiaceous and dimorphic. The fungi in macrophages had large, somewhat yeast-like, round to bullous forms with occasional extensions by septate hyphae. The second region was composed of irregularly intertwined foci of dense, band-like collagen, which on closer examination was intertwined with mats of fungal hyphae that were primarily non-septate with irregular, right angle branching and highly variable in diameter. The regions between the fungal mats contained mixed neutrophils and macrophages. In these sections, the mucosa of the stomach and the duodenum acquired at necropsy was ulcerated. Periodic acid-Schiff (PAS) and Gomori’s methenamine silver/hematoxylin & eosin staining enhanced the organisms. The extreme variability of the fungal organisms made definitive identification impossible. Unfortunately, cultures were not obtained. Examination of other necropsy tissues also confirmed a hypertrophic cardiomyopathy and a mild chronic hepatitis. The lymph nodes had fibrosis in subcapsular and medullary regions, but no evidence of fungi.
Unfortunately, the biopsy findings were not indicated to the necropsy pathologist by the VTH, nor was the death of the cat indicated to the biopsy pathologist. Therefore, an opportunity to definitively diagnose the fungal etiology was missed, and fresh tissues were not acquired. The histology of the duodenum and the pylorus had identical regions with mats of hyphae, but the duodenal sections did not have the more granulomatous regions seen in the pylorus, nor the large yeast-like forms. The low-power view of the lesions was highly suggestive of a scirrhous variant of mast cell tumor, seen with some frequency in the cat. Other differentials possibly included a mural scirrhous carcinoma or adenocarcinoma, also seen in cats, though generally not in cats of this age. A search of PubMed failed to find a single reference for mycotic gastritis or enteritis in the cat. Therefore, this case is unique, but would have been enhanced by definitive identification of the fungus. Because of the morphologic variability, zygomycosis, phaeohyphomycosis and chromomycosis were considered as rule outs. In spite of the obvious, the pathologist should always consider the possibility of an infectious agent as the etiology for a segmental mass, and retain fresh tissues.
AFIP Diagnosis: Duodenum: Enteritis, transmural, pyogranulomatous to granulomatous, diffuse, moderate, with numerous fungal hyphae, cat, domestic shorthair, feline.
Conference Comment: Mycotic gastritis is usually secondary to focal mucosal disruption, such as occurs with necrosis, ulceration, or infarction. Neoplastic disease, immune suppression from viral infection or systemic corticosteroid administration, or antibiotic therapy that disrupts normal gastric or intestinal microflora can provide conditions that promote mycotic invasion and colonization. Intestinal mycoses in cats have been reported as a sequel to feline panleukopenia infection.
Failure of macrophage recognition and immune processing of fungal invaders is involved in systemic dissemination and the establishment of deep fungal infections. Normal neutrophil activity and T cell-mediated stimulation of macrophages are required for resolution of mycotic lesions.
Contributor: Animal Health Diagnostic Laboratory, P.O. Box 30076, Lansing, MI 48909-7576
References: 1. Barker IK, van Dreumel AA, Palmer N:
The alimentary system. In: Pathology of Domestic Animals,
ed. Jubb KVF, Kennedy PC, Palmer N, 4th ed., vol. 2,
pp. 63, 255-256. Academic Press, San Diego, CA, 1993
*Sponsored by the American Veterinary Medical Association, the American College of Veterinary Pathologists and the C. L. Davis Foundation.
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