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CASE I – 99-6486 (AFIP 2739540)
Signalment: 1-year-old, male, llama
History: This llama had injured his front leg and the owners noticed swelling at the injury site. The llama was presented 1 week later with extension of the swelling to the ventral neck and thorax and respiratory distress. Intravenous fluids, potassium penicillin, methylprednisolone acetate and dimethylsulfoxide were administered. The llama did not respond and died at the veterinary clinic.
Gross Pathology: The referring veterinarian performed a necropsy. Gross lesions were not described. Kidney, liver, lymph node, lung, spleen and skin were submitted fresh and in 10% buffered formalin.
Laboratory Results: A complete blood count revealed WBC = 7000/dl. Abnormal serum chemistry values were BUN = 60mg/dl, Creatinine = 3.0 mg/dl. A pure culture of Yersinia pestis was isolated from the liver.
Contributor’s Diagnosis and Comment: Pneumonia, necrosuppurative, multifocal, severe, with intralesional gram-negative rods, lung.
Severe, multifocal, acute, necrotizing inflammation with bacterial rods was present in the sections of skin, kidney, spleen, liver and lymph node. This case represents fatal septicemic plague.
Plague is caused by Yersinia pestis, a non-motile, non-spore forming, facultative anaerobic gram-negative, bipolar staining coccobacillus of the family Enterobacteriaceae. It is a disease of antiquity, decimating human populations at various stages in history. Plague continues to be a problem today in many parts of the world, particularly in the western United States, primarily in northern New Mexico. In New Mexico, plague is most commonly found at elevations where piDon and juniper trees flourish. The main reservoir is rock squirrels and prairie dogs. Transmission of Y. pestis between hosts occurs by flea bites, less commonly by contact of the organism with mucous membranes or broken skin, or by inhalation or droplets from animals with pneumonic plague.
Cats acquire the disease most commonly following predation on infected rodents and lagomorphs or by bites from the prey’s plague-infected fleas. Clinical signs include fever, lethargy, dehydration, and cervical, retropharyngeal and mandibular lymphadenopathy. The three forms of plague are bubonic, septicemic and pneumonic.
To the best of our knowledge, this represents the first reported case of plague in a llama. There are reports of plague in camels and a mule deer. The New Mexico State Office of Public Health investigated this case. Three pastures at this facility were found to have prairie dog colonies. The pasture where the infected llama resided had evidence of a prairie dog colony die-off. Prairie dogs are highly susceptible to the infection and entire colonies can be destroyed. Cultures of captured fleas from this farm were negative for Y. pestis. The public health officials presumed the llama contracted the disease from bites of infected fleas of prairie dogs.
AFIP Diagnosis: Lung: Pneumonia, necrotizing, acute, multifocal, embolic, moderate, with colonies of bacilli, llama (Lama glama), camelid.
Conference Comment: Birds, bears, skunks and dogs are relatively resistant to infection with Y. pestis while camels, goats, deer and cats are more susceptible and may serve as a source of infection for humans. Burrowing rodents, such as rock squirrels and prairie dogs, are ideal reservoir hosts for Y. pestis because their social structure allows easy transfer of infected fleas to a large population of new, susceptible animals.
The pathogenesis depends on how the organism enters the body. Following a flea bite, the organism is either destroyed by neutrophils or phagocytized by monocytes. Replication within monocytes results in the production of a capsular envelope that renders the organism resistant to further phagocytosis. Localization of infection in regional lymph nodes precedes release into the bloodstream by 2-6 days. As Y. pestis grows, the lymph nodes become enlarged, soft and fluctuant forming the bubo. Abscess formation allows the organism to disseminate via the lymphatics or bloodstream to other organs, including the lungs.
With ingestion or inhalation of contaminated tissues or fluids, the bacillus enters the body having already acquired the protective capsular envelope from the previous host’s monocytes. Therefore, the disease spreads more quickly, as reflected in the shorter incubation period of only 1-3 days.
Endotoxin plays a key role in infections caused by gram-negative bacteria. The lipopolysaccharide (LPS) component of the outer membrane of gram-negative bacteria is released following degradation of the cell wall. The LPS is composed of a toxic fatty acid (lipid A) core and a complex polysaccharide coat with O antigens unique to each bacterial species. Binding to CD14 on leukocytes and endothelial cells forms an LPS-binding protein complex that can enhance the action of monocytes and macrophages to produce inflammatory mediators, including tissue factor, tumor necrosis factor, interleukin-1, -6, and -8, platelet activating factor, prostaglandins, leukotrienes, proteinases, and toxic oxygen metabolites. Endotoxin release in low doses causes local inflammation; with higher doses, systemic effects such as septic shock can occur. Widespread endothelial injury can trigger the coagulation cascade and lead to disseminated intravascular coagulation.
Contributor: New Mexico Department of Agriculture-Veterinary Diagnostic Services, 700 Camino de Salud, NE, P.O. Box 4700, Albuquerque, NM 87196-9110
References: 1. Christie AB, Chen TH, Elberg S: Plague in camels and goats: their role in human epidemics. J Inf Dis 141(6):724-726, 1980
2. Eidson M, Thilsted JP, Rollag OJ: Clinical, clinicopathologic and pathologic features of plague in cats: 119 cases (1977-1988). J Amer Vet Med Assoc 199:1191-1196, 1991
3. Macy DW: Plague. In: Infectious Diseases of the Dog and Cat, ed. Greene CE, 2nd ed., pp. 295-300. WB Saunders, Co., Philadelphia, PA, 1998
4. Thorne T, Quan TJ, Williams ES, Walshalf TJ, Daniels D: Plague in a free-ranging mule deer from Wyoming. J Wild Dis 23(1):155-159, 1987
CASE II – 00-446 (AFIP 2738737)
Signalment: Adult, male, guinea pig, Cavia porcellus
History: This guinea pig (ear tag number 28) was found dead in its cage approximately 6 weeks after arrival at the laboratory animal facilities at the North Carolina State University College of Veterinary Medicine.
Gross Pathology: Bilaterally, the kidneys are markedly irregular and have a granular appearance with numerous, small pits scattered across the capsular surface.
Laboratory Results: None.
Contributor’s Diagnosis and Comment: Kidney: Segmental nephrosclerosis with mineralization.
Spontaneous segmental nephrosclerosis is a common finding in all breeds of guinea pigs, particularly those greater than 1 year of age. The classic description of gross lesions is that of bilaterally irregular and pitted kidneys. Common microscopic findings include segmental to diffuse interstitial fibrosis, variable glomerulosclerosis, and frequently, dilated protein-filled tubules. Small interstitial aggregates of mononuclear cells are also occasionally described.
The underlying pathogenesis of segmental nephrosclerosis is not known. Autoimmune disease has been proposed as a potential mechanism because of spontaneous deposition of IgG and complement (C3) in the mesangium and a lesser amount in the glomerular basement membrane. However, the role of complement in the disease is not resolved; guinea pigs deficient in C4 do not develop nephritis, but guinea pigs deficient in C3 develop nephritis at similar rates and severity as control animals. Other possible etiologies include infectious agents, high protein diets, genetic predisposition and vascular disease.
The clinical significance of the renal disease is unclear. Many of the animals diagnosed at necropsy with nephrosclerosis did not have clinical signs or clinical pathologic findings of renal failure, although elevations in BUN and creatinine and hyposthenuria are noted in some cases. Occasionally, ascorbic acid deficiencies or metastatic mineralization accompanies the nephrosclerosis. Whether these were primary or secondary diseases was not determined.
AFIP Diagnosis: Kidney: Fibrosis, interstitial, multifocal, mild, with tubular dilatation, tubular proteinosis, and lymphoplasmacytic interstitial nephritis, guinea pig (Cavia porcellus), rodent.
Conference Comment: The lesions of nephrosclerosis are common, generally incidental findings in guinea pigs that share certain similarities with chronic renal disease in dogs and cats. Conference participants described a mild neutrophilic tubulitis present in some sections.
Contributor: North Carolina State University, College of Veterinary Medicine, 4700 Hillsborough Street, Raleigh, NC 27606
References: 1. Bauk L, Stefkovic G: Searching the records for clues about kidney disease. Vet Med 81:1127-1130, 1986
2. Foltz CJ, Cork LC, Winkelstein JA: Absence of glomerulonephritis in guinea pigs deficient in the fourth component of complement. Vet Pathol 31(2):201-206, 1994
3. Percy DH, Barthold SW: Guinea pig: diseases associated with aging. In: Pathology of Laboratory Rodents and Rabbit, pp. 172-176. Iowa State University Press, Ames, Iowa, 1993
4. Schurman SJ, McAdams AJ, Beischel L, Davis AE, Welch TR: CD3 independent glomerulonephritis in guinea pigs: dependence upon primary humoral response. Clin Imm and Immunopathol 74(1):51-58, 1995
5. Steblay RW, Rudofsky U: Spontaneous renal lesions and glomerular deposits of IgG and complement in guinea pigs. J Imm 107(4):1192-1196, 1971
CASE III – P-6652-99 (AFIP 2741888)
Signalment: Pig, crossbred, neutered male, 4-weeks-old
History: Nursery pig was found dead and submitted for necropsy.
Gross Pathology: The lungs were dark red and consolidated. The ventral aspects of the cranial and middle lobes were particularly affected (bronchopneumonia) and were also covered by thin mats of fibrin. Pinpoint pale gray and red foci were widely dispersed beneath the capsule of the liver. Red areas (of hemorrhage) were scatted in the kidneys, particularly near the corticomedullary junction.
Laboratory Results: Actinobacillus suis was isolated from the liver and lungs.
Streptococcus suis type II and IV, Pasteurella multocida, and E. coli were isolated from the lungs.
The lungs were negative for pseudorabies and swine influenza virus by FA.
Contributor’s Diagnosis and Comment: Liver: Hepatitis, necrotizing and suppurative, multifocal, with bacterial colonization and intrasinusoidal and intravascular fibrin deposition, consistent with Actinobacillus suis infection.
Fatal septicemia caused by Actinobacillus suis occurs sporadically in nursery-aged pigs. Actinobacillus suis can be recovered from the tonsils and nasal cavities of clinically normal swine indicating that a carrier state contributes a source of infection. Infection resulting in disease may depend on immune-status and/or predisposing bacterial or viral infections that damage upper respiratory mucosa. Actinobacillus suis is a gram-negative coccobacillary to filamentous bacterium that in culture is hemolytic and catalase positive. Its pathogenesis is probably related to lipopolysaccharide (endotoxin) and, in some strains, a hemolysin (ApxI). In this case, fibrin deposition in portal and central veins may be an indication of disseminated intravascular coagulopathy. Vasculitis was evident in some sections.
AFIP Diagnosis: Liver: Hepatitis, necrotizing, acute, multifocal, embolic, moderate, with colonies of bacilli, crossbred pig, porcine.
Conference Comment: Actinobacillus suis septicemia in young pigs, like other bacterial septicemias, can cause acute death with necrosis, hemorrhages and infarcts in various organs, to include the skin. Vasculitis and thrombosis are mediated by endotoxin. Conference discussion focused on endotoxin and its role in triggering the clotting cascade.
Brown and Hopps stain demonstrated a uniform population of gram negative bacilli. PTAH staining clearly demonstrated intravascular fibrin strands and clumps, consistent with disseminated intravascular coagulation.
The differential diagnosis for bacterial septicemia and embolic hepatitis in young pigs includes Salmonella choleraesuis, Erysipelothrix rhusiopathiae, Actinobacillus pleuropneumoniae, Leptospira pomona, Haemophilus parasuis, Mycoplasma hyorhinis, Escherichia coli, and Streptococcus suis.
Bacteria that typically form large colonies in tissue, as in this case, include Yersinia spp., Actinomyces spp., Actinobacillus spp., Arcanobacter spp., Corynebacterium spp., Clostridium spp., Staphylococcus spp. and Streptococcus spp.
Contributor: Animal Disease Diagnostic Laboratory, Purdue University, West Lafayette, IN 47907-1175
Reference: Taylor DJ: Miscellaneous bacterial infections. In: Diseases of Swine, ed. Straw BE, D’Allaire S, Mengeling WL, Taylor DJ, 8th ed., pp. 624-627, 1999
CASE IV – 98D4766 (AFIP 2739928)
Signalment: Four-year-old, spayed female, domestic shorthair cat, Felis catus
History: The cat was lethargic, depressed and constipated when presented to the referring veterinarian. Supportive treatment was initiated. The cat died five days later. A necropsy examination was requested.
Gross Pathology: The cat was in reasonably good flesh. The lungs contained multiple pale yellow to white nodules. The stomach and duodenum contained several ascarids.
Laboratory Results: The cat tested negative for FeLV prior to death. There was no growth of bacteria from the tissues that were cultured on routine culture media. Blastomyces dermatitidis was isolated from the lungs.
Contributor’s Diagnosis and Comment: Pyogranulomatous pneumonia with intralesional fungi, Blastomyces dermatitidis
Microscopic examination of a section of lung containing a nodule revealed numerous neutrophils, macrophages and multinucleated giant cells within alveolar spaces. In several of the alveolar spaces the inflammatory cells surrounded 8-25 micrometer spherical yeast-like organisms interpreted to be Blastomyces dermatitidis. Occasional macrophages or multinucleated giant cells contained organisms within their cytoplasm. The organisms were readily visible in H&E stained sections and several of the organisms had broad-based budding. The alveolar septa were thickened due to infiltration of neutrophils and macrophages. Hemorrhage, necrosis, infiltration of neutrophils and macrophages, and yeast-like organisms were also observed in the cerebellum, but an insufficient amount of fixed cerebellum was left to submit enough stained slides for all conference participants. No significant microscopic lesions were observed in sections of other organs.
Among domestic animals, blastomycosis occurs mainly in dogs. It is uncommon in cats and other domestic species of animals. Blastomyces dermatitidis is a dimorphic fungus. Mycelial growth occurs at room temperature whereas in tissue it has yeast-like growth. In tissue the organisms are spherical, usually 8-20 microns in diameter but occasionally larger, with a thick double-contoured wall and it reproduces by broad-based budding. It is generally accepted that the source of infection for animals and humans is from growth of the organism on vegetation and that animal to animal or human infection does not occur. The lung is the most common primary site of infection, but primary cutaneous blastomycosis also occurs. Systemic dissemination of infection often occurs.
AFIP Diagnosis: Lung: Pneumonia, pyogranulomatous, focally extensive, moderate, with budding yeast, domestic shorthair cat, feline, etiology consistent with Blastomyces dermatitidis.
Conference Comment: Blastomycosis is a chronic granulomatous and suppurative disease of humans and animals that can show predominantly systemic (pulmonary) or cutaneous signs. Being a dimorphic fungus, infection is usually acquired from inhalation of mold spores with a phase transition to the pathogenic yeast form at body temperature. An adhesion promoting protein, WI-1, is not expressed in the mold form but is up-regulated and controlled transcriptionally during the phase transition to the yeast form at temperatures of 25-37°C.
Pulmonary blastomycosis generally begins as a mild respiratory infection with occasional dissemination to bones, joints, or skin. Untreated systemic blastomycosis is a serious and often fatal disease.
Although clinical signs and characteristic interstitial lung densities may indicate a fungal infection, definitive diagnosis should be based on identification of the causative organisms. Cryptococcus neoformans may be differentiated from Blastomyces by the presence of a thick, carminophilic capsule with the former. Paracoccidioides brasiliensis tissue-form cells with only one bud may be mistaken for blastomycosis if sections are not carefully examined for the characteristic multiple budding or ‘spoke wheel’ forms. Tissue form cells of Histoplasma capsulatum var. duboisii are 2-5 m m in diameter, typically exhibit narrow-based budding, and induce a more histiocytic inflammatory reaction. Clinicopathologically, hypercalcemia has been associated with systemic granulomatous diseases in man and, rarely, with cases of canine blastomycosis. The hypercalcemia has been attributed to the extrarenal metabolism of 25-hydroxycholecalciferol to the active 1, 25-dihydroxycholecalciferol (calcitriol) by mononuclear phagocytes.
Contributor: Auburn University College of Veterinary Medicine, Department of Pathobiology, 166 Greene Hall, Auburn University, AL 36849-5519
References: 1. Breider MA, Walker TL, Legendre AM, VanEe RT: Blastomycosis in cats: five cases (1979-1986). J Amer Vet Med Assoc 193(5):570-572, 1988
2. Chandler FW, Kaplan W, Ajello L: Blastomycosis. In: A Colour Atlas and Textbook of the Histopathology of Mycotic Diseases, pp. 39-41, 158-167. Wolfe Medical Publications Ltd., London, England, 1980
3. Dow SW, Legendre AM, Stiff M, Greene C: Hypercalcemia associated with blastomycosis in dogs. J Amer Vet Med Assoc 188(7):706-709, 1986
4. Dungworth DL: The respiratory system. In: Pathology
of Domestic Animals, ed. Jubb KVF, Kennedy PC, Palmer N, vol.
2, 4th ed., p. 667. Academic Press, Inc., 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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