AFIP Wednesday Slide Conference - No. 7
October 30 1996

Conference Moderator: LTC Gary M. Zaucha
Diplomate, ACVP
U.S. Army Medical Research Institute of Infectious Disease
Bldg. 1425
Fort Detrick, MD 21702-5011

Return to WSC Case Menu

Case I - 96031474 (AFIP 2551105)

Signalment: One-year-old ewe.

History: Died acutely. Vaccinated for clostridial disease and tetanus. Multiple tissues submitted for evaluation.

Gross Pathology: The heart and lungs were submitted intact. Approximately 20- 25% of the lung parenchyma contained petechiation and ecchymotic hemorrhages. The lungs were firm and glistening. According to the clinician, there were multiple black spots in the omentum, multifocal areas of hemorrhage in the kidneys, and no apparent enlargement of the spleen.

Laboratory Results: Lung sections were submitted for routine bacteriology. Bacillus anthracis was cultured and confirmed by a Gram stain followed by mouse inoculation. The mice died in less than 22 hours. Subsequent testing on inoculated mice spleens included: String-of-pearls, gamma phage reaction, Gram stain, and both cell wall and capsule flourescent antibody(antiserum for FA were obtained from Dr. John Ezzel, USAMRIID, Fort Derrick, Maryland). All tests were positive for B. anthracis.

Contributor's Diagnosis and Comments:

Lung, bacteremia, hemorrhagic, necrotizing, peracute to acute, severe.
Spleen, bacteremia, hemorrhagic, congested with extensive accumulation of large gram positive bacilli, peracute to acute, severe.

Grossly, as reported by the clinician, there was a lack of splenic enlargement. Histologically, B. anthracis appeared to comprise a majority of the spleen's sectional mass. In addition, the lungs contained numerous organisms, both in multifocal aggregates as well as surrounding bronchioles. The spleen and lung tissue contained minimal inflammation compared with the extensive bacterial population present. In the literature, anthrax in sheep takes a more rapid course than other ruminants, resulting in less of an inflammatory reaction.1 The composition of the spleen in sheep with more collagen in the splenic capsule may play a role in the lack of splenic enlargement seen.3

AFIP Diagnosis: 1. Lung: Pneumonia, interstitial, peracute to acute, diffuse, moderate, with multifocal hemorrhage, fibrin, and myriad bacilli, breed not specified, ovine.
2. Spleen: Splenitis, peracute to acute, diffuse, moderate, with lymphocytolysis, fibrin, and myriad bacilli.

Conference Note: Bacillus anthracis is a a large, 1 m X 3-6 m, gram-positive, rod-shaped bacterium that forms spores on exposure to air or oxygen, particularly when large numbers of bacilli are excreted in the terminal stage of the disease. The spores may remain viable in soil for 15 years, and under experimental conditions in the laboratory for 50 years. Areas of enzootic anthrax have alkaline soil with a high nitrogen level from decaying vegetation, alternating periods of rain and drought, and temperatures in excess of 15.5C. Ruminants are most susceptible to the disease which is a brief septicemic form. Humans are intermediate, and horses, pigs, dogs and cats are less susceptible with frequent localized infections (pharynx, skin, intestine, lungs). Sources of infection other than soil include contaminated animal products (bone meal, wool, hair, hides, and vegetable (peanut) proteins). In 1992, there were reported cases of post-vaccinal anthrax in cattle after the use of the Sterne strain of B. anthracis, a product routinely used in Australia to prevent losses attributable to anthrax outbreaks.

The anthrax bacillus possesses three primary, plasmid-encoded virulence factors: a poly-D-glutamic acid capsule, and lethal and edema toxins. Lethal toxin is composed of two proteins, lethal factor (LF) and protective antigen (PA). Edema toxin is composed of an edema factor (EF), a calmodulin-dependent adenylate cyclase, and PA. Edema toxin is presumed to be responsible for the edema seen around cutaneous lesions and other sites of infection. Intravenous injection of a PA-LF combination (lethal toxin) causes death. Neither LF nor EF is active without PA. On the molecular level, it has been reported that the PA does not bind LF or EF. Instead, upon binding to surface receptors of target cells, an unidentified, cell-associated protease cleaves the PA, releasing a 20-kDa fragment (in- vitro study) . The activated fragment retained at the cell surface binds LF or EF, and the complex enters the cell by endocytosis. It has been demonstrated that PA exists in the blood of infected animals primarily as a complex with LF. Cleavage of PA is catalyzed by a calcium-dependent, heat-labile serum protease. Other than being complexed to PA, LF appears to be unaltered during the course of anthrax infection. The ubiquitous protective antigen-cleaving protease has been identified in primates, horses, goats, sheep, dogs, cats, and rodents.

Edema toxin (EF + PA) has been shown to raise intracellular cAMP levels in many types of eukaryotic cells, suggesting that most cells possess PA receptors and internalized EF. In contrast, lethal toxin (LF +PA) has been shown to be highly cell-type specific. The less well understood biologic effect of lethal toxin appears to be directed toward inhibition of macrophage function. PA + LF mixtures are highly toxic to mouse macrophages in vitro. It is thought that lethal toxin may alter membrane permeability. Lethal factor is a central nervous system (CNS) depressant.

Although edema and lethal toxins impair the immune system by damaging cells, the major mechanism for evasion of the host immune defense is the B. anthracis capsule. The highly negatively charged ploy-D-glutamate capsule physically inhibits phagocytosis and interferes with opsonization.

Contributor: Department of Veterinary Pathology, College of Veterinary Medicine, Oklahoma State University, Stillwater, OK 74078


1. Gleiser CA: Pathology of anthrax infection in animal host. Fed Proc 26:1518- 1521, 1967.

2. Timoney JF, et al.: The genus Bacillus. In "Hagan and Bruner's Microbiology and Infectious Diseases of Domestic Animals". 8th Ed., p.206. Ithaca, New York, Comstock Publishing Associated, 1988.

3. Valli, VEO: The Hematopoietic System. In Pathology of Domestic Animals. Jubb KVF, Kennedy PC and Palmer N (eds): Academic Press, San Diego, 4th ed.,
vol 3, pp. 240-243, 1993.

4. McGee ED, et al.: Anthrax in a dog, Vet Pathol 31:471-473, 1994.

5. Ezzell J; Wilhelmsen C: Bacillus anthracis in: Pathogenesis of Bacterial Infections in Animals. edited by Gyles C. and Thoen C., 2nd ed., pp 36-41, 1993.

6. Salmon, D. D. and Ferrier, G. R. Post vaccination occurrence of anthrax in cattle, Vet Rec, 130, 140-141, 1992.

International Veterinary Pathology Slide Bank:
Laser disc frame #19369.


Case II - 96-9009 (AFIP 2549681)

Signalment: Six-year-old male English Setter.

History: The dog was presented to the referring veterinarian for a one day duration of lethargy, anorexia, diarrhea, and suspected weight loss. Initial lab work revealed a non-regenerative anemia (PCV 20%) and thrombocytopenia (20,000/ul). The case was referred to Angell Memorial Animal Hospital for further evaluation. Physical exam findings included pale mucous membranes and a painful abdomen. Complete blood count and blood chemistry revealed non-regenerative anemia (HCT 15%, reticulocyte count 0.8%, total protein 6.0 g/dl), panleukopenia (WBC 3.9 x 103/ul: segs 3.0 x 103/ul; lymphs 0.3 x 103 /ul), thrombocytopenia (6,000/ul), and very slightly elevated ALT (91 U/L) and ALKP (145 U/L). Renal values were normal. Radiographs indicated hepatosplenomegaly. Ultrasound-guided fine needle aspirates of the spleen and liver revealed extramedullary hematopoiesis. A bone marrow aspirate was hypoplastic with an increase in immature megakaryocytes. Twelve days later anemia (9.1%) and thrombocytopenia (5000/ul) persisted. The dog was given a matched whole blood transfusion, had an acute transfusion reaction, and died.

Gross Pathology: The liver and spleen were diffusely enlarged. The prescapular lymph nodes were also enlarged.

Laboratory Results: See above.

Contributor's Diagnosis and Comments: Prescapular lymph node: Acute megakaryoblastic leukemia.

Description: The normal architecture is replaced by numerous pleomorphic megakaryocytes and megakaryoblasts with clusters of attendant small lymphocytes and plasma cells. The majority of the blast cells are round to irregularly shaped with a central, irregularly shaped nucleus with finely granular to clumped chromatin, moderate nuclear to cytoplasmic ratio, and occasionally granular amphophilic cytoplasm. Frequently blast cells are binucleate or multinucleate and measure 30-55 microns in diameter. These large blast cells have abundant, finely granular cytoplasm.

A neoplastic infiltrate of similar appearing cells was present in the liver, spleen, lung, marrow, adrenals, and pancreatic vessels. The sign of panleukopenia, thrombocytopenia, and non-regenerative anemia reflect bone marrow failure. Although no special stains or immunohistochemistry were pursued to further diagnose this case, the massive infiltration of visceral organs with megakaryocytes and the predominance of the same cell type in the marrow indicated that the dog had megakaryocytic leukemia.

Acute leukemia is a marrow-based neoplasm that may involve any of the hematopoietic, lymphoid or mononuclear phagocytic cells systems. Cases of megakaryocytic leukemia in any species of animal, including humans, are rare. Patients usually present in good body condition, possibly with a fever, subcutaneous hematomas, gastrointestinal hemorrhage, hepatosplenomegaly, pancytopenia, anemia, and thrombocytopenia. Interestingly, dogs usually exhibit thrombocytopenia, whereas cats present with thrombocytosis. The course of the disease is usually very rapid due to myelophthisis and rapid bone marrow failure. Megakaryoblasts, comprising 70 to 90% of the blast cells, quickly replace the bone marrow. Consequently, erythroid and myeloid series cells are decreased early in the disease. It is believed that myelofibrosis results from stromal proliferation caused by PDGF and TGF- and from fibrin deposition due to the procoagulant property of the cytoplasm of the tumor cells. Many of the patients also develop disseminated intravascular coagulation (DIC). The clinical manifestations of the disease in this dog followed the generally recognized course observed in other forms of leukemia in which anorexia, lethargy, and weight loss may be the primary signs.

Megakaryoblastic leukemia is one of several types of myelogenous leukemias. In 1987, based on the French-American-British system, the acute myeloid leukemias were classified into seven groups designated M1 through M7, in which M7 was represented by acute megakaryoblastic leukemia. Abnormal proliferation of megakaryocytes has more often been associated with myeloproliferative disorders such as polycythemia vera and chronic megakaryoblastic leukemia. This may partly be due to the difficulty in differentiating megakaryoblasts from immature cells of other hematopoietic linages by light microscopy. Acute megakaryoblastic leukemia is believed to be a defect at the stem cell level in megakaryoblast differentiation. During normal development, megakaryoblasts are stimulated to differentiate and proliferate by meg-CSF, PDGF, and thrombopoietin.

Case reports of acute megakaryoblastic leukemia in dogs and cats have been infrequently published in the veterinary literature. The incidence of this form of acute myeloid leukemia in animals is believed to 1% of all AMLs. This value may be artificially low due to imprecise characterization of blast forms. Several of the cases reported in dogs occurred secondary to experimental exposure to gamma irradiation, in which a radiation- induced defect in the stem cell of the marrow was suspected.

In humans, acute megakaryoblastic leukemia accounts for 8-10% of all leukemias. The disease affects patients of a wide age range, but usually has two clinical peaks: adults and young children, particularly those with Down's syndrome. In one review it was reported that nearly 30% of children with acute megakaryocytic leukemia had Down's syndrome. It is also seen in adults associated with irradiation or as a transformation of another form of myeloproliferative disorder. Molecular analysis has linked cytogenetic abnormalities at chromosome 21q and the translocation t(1;22) (p13;q13) to acute megakaryoblastic leukemia.

Identification of immature monocytic cells and proper classification of acute leukemias by Wright's stained smears alone may be very difficult. Evaluation by electron microscopy and immunohistochemistry is important for the classification of myeloid leukemias. Megakaryocytes characteristically stain with PAS and alpha-naphthyl acetate esterase. They will also be negative for Sudan-black and myeloperoxidase. Using immunohistochemistry these cells stain with platelet-specific antibodies to GPIIb/IIIa and vWF. As these techniques are used more frequently in the study of animal leukemias, an increase in monocytic and mixed cell types may be noted.

Treatment of acute leukemias generally offers poor results. Protocols in human medicine usually include chemotherapy and bone marrow transplantation. Chemotherapy may be made difficult based on the expression of the multidrug resistance gene (mdr-1P- glycoprotein) found in a megakaryoblastic cell line, CMK.

AFIP Diagnosis: Lymph node, prescapular: Megakaryoblastic leukemia, English Setter, canine.

Conference Note: The conference participants agreed with the contributor's diagnosis. The conference discussion centered on the histomorphologic and staining characteristics of megakaryocytic cells as described above. Neoplastic megakaryocytes frequently stain positively for Factor VIII-related antigen as well.

Contributor: Angell Memorial Animal Hospital, Pathology Department, 350 S. Huntington Ave., Boston, MA 02130.

1. Messick J, Carothers M, Wellamn M: Identification and characterization of megakaryoblasts in acute megakaryoblastic leukemia in a dog. Vet Pathol 27:212-214, 1990.

2. Cain GR, et al: Platelet dysplasia associated with megakaryoblastic leukemia in a dog. J Am Vet Med Assoc 188:529-530, 1986.

3. Shull RM, DeNovo RC, McMracken MD: Megakaryoblastic leukemia in a dog. Vet Pathol 23: 533-536, 1986.

4. Burton S, et al: Acute megakaryoblastic leukemia in a cat. Vet Clin Pathol 25: 6- 10, 1996.

5. Hamilton TA, et al: Cytosine arabinoside chemotherapy for acute megakaryocytic leukemia in a cat. J Am Vet Med Assoc 199:359-361, 1991.

6. Innes DJ, et al: Megakaryocytic leukemia: identification utilizing anti-factor VIII immunoperoxidase. Amer J Clin Pathol 77:107-110, 1981.

7. Darbes J, et al: Demonstration of feline and canine platelet glycoproteins by immuno and lectin histochemistry, Histochemistry 100: 83-91, 1993.

8. Colbatzky F, Hermanns W: Acute megakaryoblastic leukemia in one cat and two dogs. Vet Pathol 30: 186-194, 1993.

9. Koike, T: Megakaryoblastic leukemia: the characterization and identification megakaryoblasts. Blood 64; 683-692, 1984.

10. Tolle DV, et al: Circulation micromegakaryocytes preceding leukemia in three dogs exposed to 2.5R/day gamma radiation. Vet Pathol 20: 111-114, 1983.

11. Cain GR, Kawakami TG, Jain NC: Radiation-induced megakaryoblastic leukemia in a dog. Vet Pathol 22: 641-643, 1985.

12. Jain NC, Blue JT, Grindem CB, Harvey JW, et al: Proposed criteria for classification of acute myeloid leukemias in dogs and cats. Vet Clin Pathol 20: 63-82, 1992.

International Veterinary Pathology Slide Bank: None


Case III - D96-1221Y (AFIP 2549479)

Signalment: 4.5-year-old, Springer Spaniel/Labrador Retriever cross, spayed female, canine.

History: This dog was listless and sleeping more than usual. Clinical signs progressed to disorientation, circling, head pressing and abnormal posturing. On physical examination, temperature, pulse and respiration were normal, attitude was disoriented, gait was hypermetric, neck was dorsoflexed and paddling occurred when lying on her side. The dog went into respiratory arrest and died.

Gross Pathology: Petechiae and grayish discoloration were noted on the sectioned surface of the brain stem and piriform lobe of the cerebral cortex.

Laboratory Results: Serum titer for toxoplasmosis and the cryptococcus latex agglutination test were both negative.

Contributor's Diagnosis and Comments: Severe multifocal granulomatous meningoencephalomyelitis.

The lesions observed in the brain of this dog are consistent with what has been described for granulomatous meningoencephalomyelitis in the dog. In all sections, with the exception of the piriform lobe of the cerebral cortex, the lesions were primarily inflammatory in nature whereas in the piriform lobe, a more concentrated population of whirling epithelioid histiocytic cells might lead one to conclude that this areas exhibited a form of the disease called "neoplastic reticulosis." Nevertheless, this lesion is believed to be inflammatory in nature and the cause of this condition in dogs has not been elucidated. In this case, no etiologic agent was identified.

AFIP Diagnosis: Brain: Meningoencephalitis, histiocytic and lymphoplasmacytic, multifocal to coalescing, severe, mixed-breed, canine.

Conference Note: Conference participants agreed that this lesion is consistent with the disease known as granulomatous meningoencephalitis (GME) of dogs. Microscopically, there are dense aggregates of cells arranged in perivascular whorls. The perivascular cuffs are composed of histiocytes and varying numbers of lymphocytes, and plasma cells in a network of reticulin fibers (demonstrated with a reticulin stain). In some areas, the perivascular cells are predominantly lymphocytic, while in other regions, histiocytic cells are most numerous. A panel of special stains for infectious agents failed to demonstrate microorganisms.

Granulomatous meningoencephalomyelitis is a sporadic, idiopathic, progressive inflammatory disease of the CNS that has been described in various animals including dogs, cats, horses, and cattle, but is most prevalent in dogs. This disease appears to have a world-wide distribution, with recent reports coming from the US, Australia, New Zealand, Switzerland, and the UK. GME appears to occur more commonly in toy breed dogs, particularly poodles and terriers. The majority of confirmed cases occurred in young to middle-aged dogs (1 to 8 years of age). GME occurs in both sexes; however, there appears to be a higher prevalence in females.

The etiology and pathogenesis are unknown; however, the lesion resembles experimental allergic encephalomyelitis, which suggests a possible immunologic basis. Recent immunohistologic studies have shown that many lymphocytic and lymphoblastic cells are immunoglobulin-bearing. There are also morphologic similarities between GME and viral encephalomyelitis. It has been suggested that GME may represent an altered host response to canine distemper virus or rabies virus. Distemper and rabies-like inclusion bodies have been described in CNS lesions of dogs with GME. However, attempts to demonstrate CDV antigen in cases of GME have been unsuccessful, and GME occurs in rabies-free countries. Another speculation on the cause is a retrovirus, perhaps contaminating and spread by canine vaccines.

Lesions are confined to the CNS with involvement primarily of the white matter of the cerebellum, caudal brain stem, and cervical spinal cord, but lesions are often disseminated in the brain. In the brain and/or spinal cord, soft gray oval lesions with irregular or well-defined margins may be discerned on gross sectioning. Sometimes, the cut surface of the CNS has a granular, mottled appearance with finger-like projections. Meninges may appear thickened and cloudy; occasionally, optic nerves are enlarged grossly. Internal hydrocephalus may be present in some dogs.

Contributor: University of Minnesota, College of Veterinary Medicine, Department of Veterinary Diagnostic Medicine, 1333 Gortner Avenue, St. Paul, MN 55108.

1. Russo ME: Primary Reticulosis of the Central Nervous System in Dogs. J Am Vet Med Assoc 174:492-500, 1979.

2. Thomas JB, Eger C: Granulomatous Meningoencephalomyelitis in 21 Dogs. J Small Anim Pract 30:287-293, 1989.

3. Sorjonen DC: Clinical and histopathological Features of Granulomatous Meningoencephalomyelitis in Dogs. J Am Anim Hosp Assoc 26:141-147, 1990.

4. Tipold A, Pfister H, Zurbriggen A, Vandevelde M: Intrathecal Synthesis of Major Immunoglobulin Classes in inflammatory Diseases of the Canine CNS. Vet Immunol and Immunopathol 42:149-159, 1994.

5. Jubb KVF, Kennedy PC, Palmer N, eds: Inflammation in the central nervous system. In Pathology of Domestic Animals, Academic Press, Inc., 4th ed. Vol 1:426-427, 1993.

6. Summers BA, Cummings JF, de Lahunta A: Granulomatous meningoencephalitis. In Veterinary Neuropathology, Mosby, St. Louis, 110-111, 1995.

International Veterinary Pathology Slide Bank:
Laser disc frame #3937, 3938, 8061, 8062, 20973, 20974.


Case IV - 960531.7 (AFIP 2550444)

Signalment: Cat, "Chartreux", male, 2-years-old.

History: Fever, progressive anorexia and prostration, weight loss; several cases in a cattery (pure bred "chartreux" grey cats). This cat was sacrificed.

Gross Pathology:
- 50 ml peritoneal yellowish effusion
- parietal and perihepatic (Glisson's hepatic capsule) peritoneum: whitish thickening - tiny (<1mm) intrahepatic white foci.

Laboratory Results: Serology positive for feline infectious peritonitis (1/16000). Hemogram: Leukocytosis (24,500/ l) due to neutrophilia (19,500/ l, no anemia.

Contributor's Diagnosis and Comments:
1. Parietal peritoneum: Peritonitis, subacute, diffuse, severe.
- moderately exudative and fibrinous.
- granulomatous, with polymorphic mainly histio - lymphocytic cellular infiltration and lympho-plasmacytic perivasculitis.

2. Liver: Exudative, fibrinous and histio-lymphocytic granulomatous perihepatitis with superficial degenerative hepatocytic foci.
-Granulomatous multifocal interstitial (periportal) and perivascular hepatitis.
- hemosiderosis, moderate, mainly in Küpffer cells.

3. Kidney: Glomerulitis, diffuse, mainly proliferative or membrano-proliferative (we considered the intraglomerular flowing back of the proximal epithelium as an artifact due to contraction of the modified flocculus during formalin fixation)

Etiological diagnosis: feline infectious peritonitis infection - subacute moderately effusive form - glomerulonephritis associated.

Feline infectious peritonitis (FIP) is a fatal, systemic disease described in domestic cats and in wild Felidae throughout the world. The etiologic agent is a single-strand RNA virus belonging to the family Coronaviridae. FIP is seen mainly in cats between 6 months and 3 years of age and there is no sex predilection. The disease has been subdivided into two forms. The classical effusive form is characterized by fluid effusions in peritoneal and/or pleural cavities. The less common non-effusive form consists of pyogranulomatous lesions in visceral organs with minimal exudation.

The clinical signs of the effusive form are chronic fever, anorexia, weight loss, depression and abdominal distension. Cats with pleural involvement can present with dyspnea. Ocular and CNS symptoms are relatively rare. Anemia and or icterus can develop.

Non-effusive FIP may be regarded as more chronic and smoldering as compared with the effusive form. Cats present granulomatous inflammatory reactions in the peritoneal cavity, eyes, CNS, and present signs specific to affected organs. Central nervous system signs are variable; weakness or paralysis of the hind limbs is the more frequent.

Hematologic changes are similar in the two forms: leukocytosis associated with an absolute neutrophilia is described. A mild to moderate non-regenerative anemia is also common. The plasma proteins are often elevated principally due to hyperglobulinemia.

Most of the cats with effusive form finally die. At necropsy, peritonitis is present in most animals. Marked effusion can be found. The fluid is clear and pale to deep yellow. Small, firm and white foci of inflammation are visible in kidneys, liver and pancreas.

In the non-effusive form, inflammatory foci are present in the abdominal or thoracic organs or restricted to the eyes or nervous system. Microscopically, the main lesion is a generalized vasculitis accompanied by a cellular infiltrate around blood vessels. This infiltrate consists of lymphocytes, plasma cells, macrophages and neutrophils in variable proportion.

AFIP Diagnosis:

1. Skeletal muscle with serosal surface: Serositis, pyogranulomatous and fibrinous, diffuse, moderate, with vasculitis, Chartreux, feline.
2. Liver: Peritonitis, pyogranulomatous and fibrinous, diffuse, moderate, with subcapsular and portal hepatitis and vasculitis.
3. Kidney: No significant lesions.

Conference Note: The conference participants agreed that the lesions in this cat are consistent with feline infectious peritonitis virus (FIPV) infection. The glomerular changes coded by the contributor were not present in the sections examined at the conference.

The pathogenesis of FIPV infection is not completely understood. Transmission most likely occurs through either the fecal-oral or respiratory routes. After infection, the virus replicates in local lymphoid tissues and a primary viremia develops. The virus replicates in macrophages, which spread the virus to many parts of the body.

The disease is antibody-mediated and complement-dependent. The clinical outcome is dependent of the levels of cellular and humoral immunity within the host. The disease has been described as having three clinical forms: effusive, non-effusive, and a mixed form. The effusive form occurs in cats that develop humoral, but not cellular immunity. It has been postulated that antibody coating enhances the uptake of virus by phagocytic cells. Since FIPV prefers this intracellular environment, the net effect is to enhance virus replication. Antibody might also react with antigen and complement producing an Arthus-like reaction. Complement-mediated activation of terminal clotting factors, together with vascular lesions that consume platelets and clotting factors, causes a coagulopathy in cats with effusive FIP.

Non-effusive FIP is thought to occur in cats that develop humoral immunity, and partial cellular immunity; partial cellular immunity limits the level of virus replication and dissemination. The granulomatous lesions of non-effusive FIP occur around small foci of virus-laden macrophages. Non-effusive FIP occurs with 1/4 the frequency of the effusive form. A recent article describes an uncommon intestinal form of non-effusive FIP that grossly resembled a neoplasm and occurred within the colon or at the ceco-colic junction.

Recovery from FIPV infection is presumed to be due to strong cellular immunity. It appears, however, that FIPV may persist as a latent or sequestered infection which may be reactivated when the established immunity is compromised by agents such as feline leukemia virus, feline immunodeficiency virus, neoplasia, administration of corticosteroids, surgery, and parasitism. Approximately 50% of cats with clinical FIP test positive for feline leukemia virus infection.

Contributor: Ecole Vétérinaire d'Alfort, laboratoire d'Anatomie Pathologique, 7, Avenue du Général de Gaulle, 94704 MAISONS ALFORT - FRANCE.

1. Pedersen NC: An overview of feline enteric coronavirus and infectious peritonitis virus infections. Feline Pract, 23, pp. 7-20, 1995

2. Jubb KVF, Kennedy PC, Palmer N (eds): Pathology of Domestic Animals, 4th ed., Vol. 2, pp. 438-441, 1993.

3. Hoskins JD: Coronavirus infection in cats. Comp Cont Ed Pract Vet, 13, pp.567-586, 1991.

4. Weiss RC: Feline infectious peritonitis and other coronaviruses. In "The cat, Diseases and Clinical Management, Vol. 1, RG Sherding (ed), pp. 333-335, Churchill Livingstone, 1989.

5. Weiss RC, Scott FW: Pathogenesis of feline infectious peritonitis: pathologic change and immunofluorescence. Am J Vet Res, 42, pp. 2036-2048, 1981.

6. Hayashi T, et al: Pathology of non-effusive type feline infectious peritonitis and experimental transmission. Jpn J Vet Sci, 42, pp. 197-2120, 1980.

7. Montali RJ, and Strandberg JD: Extraperitoneal lesions in feline infectious peritonitis. Vet Pathol, 9, pp. 109-121, 1972.

8. Wolfe LG, Griesemer RA: Feline infectious peritonitis: Review of gross and histopathologic lesions. J Am Vet Med Assoc, 158, pp. 987-993, 1971.

9. Harvey CJ, Lopez GW, Hendrick MJ: An uncommon intestinal manifestation of feline infectious peritonitis: 26 cases (1986-1993), J Am Vet Med Assoc, Vol. 209, No. 6, 1996.

International Veterinary Pathology Slide Bank:
Laser disc frame #538, 539, 728, 729, 737, 1132, 1308, 1309, 1889, 2156, 2157, 2493, 4216, 4217, 5016, 5017.

Lance Batey
Captain, VC, USA
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 substantial support for the Registry.

Return to WSC Case Menu