Results
AFIP Wednesday Slide Conference - No. 23
March 15 2000

Conference Moderator:
Dr. Wallace B. Baze, Diplomate, ACVP
The University of Texas MD Anderson Cancer Center
Science Park, Department of Veterinary Sciences
Bastrop, Texas 78602

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Case I - 97055 (AFIP2694673)

 

Signalment: Eight-year-old male rhesus monkey (Macaca mulatta)

 

History: Animal died following a six-day illness consisting of progressive depression, anorexia, labored abdominal breathing, coughing, and tachypnea.

a

Case 23-1. Chest radiograph. Diffusely lung fields are infltrated by flocculent fluid densities.

bc

d

Case 23-1. Gross Images. Lungs (b) have a pale tan mottling. Cut section of the fixed lung (c) contains diffusely distributed pale tan 2-3mm foci. Within the white matter of the brain (d) is an 0.3x1.0cm cavitating lesion.

 

Gross Pathology: At necropsy the carcass appeared in good condition. There was moderate scrotal and inguinal edema. The lungs were diffusely hyperinflated and did not collapse when the thoracic cavity was opened. The lungs were gray to white and had pleural vascular distension and a granular texture throughout with disseminated firm nodules, ranging in diameter from 1 to 5 mm. The right middle lung lobe was firm and dark red. The spleen contained a 1 cm in diameter firm, pale-yellow irregular nodule. There was minimal, focal, gastric ulceration and hemorrhage. The right cerebral frontal lobe and left occipital lobe each had 1 cm x 2 cm x 2 cm abscesses.

 

Gross Morphologic Diagnoses:
1. Severe multifocal (miliary) pyogranulomatous pneumonia
2. Severe multifocal pyogranulomatous encephalitis
3. Mild focal pyogranulomatous splenitis
4. Moderate locally extensive subcutaneous edema
5. Minimal focal acute gastric hemorrhage

 

Laboratory Results: Serum collected two days prior to the monkey's death was submitted for Blastomyces dermatitidis titer; the results were 1:32, with greater than 1:8 considered positive.

 

Contributor's Diagnosis and Comments: Severe chronic pyogranulomatous encephalitis with intralesional fungal organisms (consistent with Blastomyces dermatitidis).

 

Other Histologic Diagnoses (slides not submitted):
1. Severe, multifocal, pyogranulomatous pneumonia
2. Mild, pyogranulomatous tracheobronchial lymphadenitis
3. Moderate, focal pyogranulomatous splenitis
4. Minimal focal granulomatous hepatitis

 

All pyogranulomatous lesions contained intralesional fungal organisms consistent with Blastomyces dermatitidis.

 

Etiology: Blastomyces dermatitidis

 

This animal was given an intravenous injection of latex microspheres for experimental purposes, shortly before its illness became clinically apparent. In some slides, microspheres are evident; they appear as refractile, pale yellow, round structures, approximately 30 microns in diameter.

 

Blastomycosis has not been reported previously in nonhuman primates. The acute onset of respiratory signs following the experimental procedure confounded ante-mortem diagnosis. Also confounding diagnosis were the disease's previously unrecognized status in nonhuman primates and the animal's lack of exposure to soil while at our facility from June 1996 until death in February 1997, suggesting the incubation period in this animal was greater than 4.5 years.

e (H&E)f (PAS)

g (PAS)

Case 23-1. Multifocally within the lung, there are fibrotic foci (e,f) that contain neutrophils (f,g), epithelioid cells (f,g), occasional foreign body giant cells (e,f,g), and scattered 8-12u diameter yeast bodies (f,g).

 

AFIP Diagnosis: Cerebrum: Abscesses and pyogranulomas, multifocal, with budding yeast, rhesus monkey (Macaca mulatta), nonhuman primate, etiology consistent with Blastomyces dermatitidis.

Conference Note: Blastomycosis is primarily a disease of humans and dogs but also is seen in other animals, including the cat, horse, sea lion, wolf, ferret, dolphin and polar bear. The disease occurs primarily in the Mississippi-Ohio river basins, the central U.S. Atlantic states, and in the northern border of Ontario and Manitoba in Canada. Blastomyces dermatitidis, the causative agent of North American blastomycosis, is a dimorphic fungus that produces a mycelial growth at room temperature and yeast-like forms in tissue and in culture at 37 degrees Celsius.

 

The organism reproduces by budding and can be found free or within macrophages in affected tissues. Although the lung is considered the most common site of primary involvement, primary cutaneous infections, and disseminated disease can occur. Disseminated disease most commonly affects the lung, lymph nodes, skin, eyes, bone, joints, and subcutaneous tissues. Occasionally, primary cutaneous infection may occur from a puncture wound in the skin. However, because skin lesions more commonly result from disseminated infection, cutaneous blastomycosis should arouse suspicion of systemic disease. Pulmonary lesions are sometimes resolved by the time the sites of disseminated infection become apparent.

 

The differential diagnosis discussed during the conference included cryptococcosis, histoplasmosis, aspergillosis, coccidioidomycosis, African histoplasmosis (Histoplasma capsulatum var. duboisii) and South American blastomycosis (Paracoccidioides braziliensis). Cryptococcus neoformans is characterized by a wide, carminophilic capsule. Histoplasma capsulatum is much smaller than Blastomyces, and has narrow-based budding. Aspergillus sp. often present as narrow, septate hyphae that branch dichotomously at acute angles. Coccidioides immitis is larger, and reproduces by endosporulation rather than budding. Histoplasma capsulatum var. duboisii has similar size and shape to Blastomyces dermatitidis, but the former has uninucleate yeast-like cells narrower based buds while the latter has multinucleate yeast-like cells and broad based buds. South American blastomycosis reproduces in tissue by multiple budding.

 

Contributor: Wake Forest University School of Medicine, Department of Pathology, Section on Comparative Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1040

 

References:

1. Cote E, Barr SC, Allen C, Eaglefeather E: Blastomycosis in six dogs in New York State. J Amer Vet Med Assoc 210(4):502-504, 1997

2. Dungworth DL: The respiratory system. In: Pathology of Domestic Animals, eds. Jubb KVF, Kennedy PC, Palmer N, 4th ed., vol. 2, pp. 667, Academic Press, San Diego CA, 1993

3. Jones TC, Hunt RD, King NW: Diseases caused by fungi. In: Veterinary Pathology, 6th ed., pp. 505-547, Williams and Wilkins, Baltimore MD, 1997

4. Legendre AM: Blastomycosis. In: Infectious Diseases of the Dog and Cat, 2nd ed., pp. 371-377, WB Saunders Co, Philadelphia, PA, 1998

5. Wilkinson LM, Wallace JM, and Cline JM: Disseminated blastomycosis in a rhesus macaque (Macaca mulatta). Vet Pathol 36(5):460-462, 1999

 

 

Case II - MC99-7 ( AFIP 2694669)

 

Signalment: 2½-year-old male rhesus monkey (Macaca mulatta)

 

History: This monkey was humanely sacrificed due to persistent diarrhea, significant weight loss (>20%), and a generally poor condition.

 

Gross Pathology: The lungs were relatively firm and poorly collapsible, with multiple patchy foci of congestion and hemorrhage.

Contributor's Diagnoses and Comments:
1. Interstitial pneumonitis, subacute, patchy, moderate.
2. Syncytial giant cell infiltrate, primarily alveolar, patchy, moderate-marked.
3. Amorphous, foamy to granular amphophilic alveolar material consistent with Pneumocystis (most sections).
4. Alveolar proteinosis & fibrin exudation, patchy, mild.
5. Angitis, subacute, multifocal, mild.

 

This monkey had been inoculated IV 9 months previously with SIV/Delta B670. Most of the microscopic findings are characteristic for, and the direct result of, lentivirus (SIV) infection. These lesions, especially the distinctive syncytial cell formation (in which viral antigens and particles are demonstrable) are not typical of lentivirus infection in sheep, goats or humans with HIV. Pneumocystis carinii is an important opportunistic respiratory pathogen the environmental source of which is not always known. It is commonly seen in conjunction with the immunosuppression created by SIV and is noted with significant frequency (>50%) during later stages of macaque lentivirus infection.

 

The lentivirus (SIV) pulmonary infection was confirmed postmortem by immunohistochemistry and Pneumocystis organisms were visualized by GMS staining and also confirmed by immunohistochemical evaluation.

 

AFIP Diagnoses:

1. Lung: Pneumonia, interstitial, lymphoplasmacytic and histiocytic, diffuse, mild, with syncytial cells and edema, rhesus monkey (Macaca mulatta), nonhuman primate.
2. Lung: Pneumonia, interstitial, lymphohistiocytic, mild, with intraalveolar foamy material (atypical fungi), etiology consistent with Pneumocystis carinii.

Conference Note: Simian immunodeficiency virus (SIV) is a member of the Lentivirus genus in the family Retroviridae along with human immunodeficiency virus, equine infectious anemia virus, ovine lentivirus, bovine immunodeficiency-like virus, and feline immunodeficiency virus. In addition to the lungs, other organs commonly affected by SIV include brain, lymph nodes, thymus, gastrointestinal tract, and skin. Secondary infections are common with SIV infection and include pneumocystosis, cryptococcosis, toxoplasmosis, candidiasis, mycobacteriosis, nocardiosis, disseminated salmonellosis, and infection with cytomegalovirus, herpes simplex virus, and rhesus gamma herpesvirus.

Pneumocystis carinii is an atypical fungus that is ubiquitous in the environment and can frequently be found in normal lungs without associated lesions. P. carinii is often the first opportunistic infection diagnosed in HIV-1 infected humans, and is the leading cause of death in AIDS.

SIV and the secondary infections that often accompany it are very similar to the situation with human AIDS, making the macaque-SIV model an extremely valuable tool for the study of HIV and AIDS.

 

Contributor: Division of Laboratory Animal, S-1040 BioMedical Science Tower, University of Pittsburgh, PA, 15261

 

References:

1. Baskerville A, Dowsett AB, Cook RW, Dennis MJ, Cranage MP, Greenaway PJ: Interstitial pneumonia in simian immunodeficiency virus infection. J Pathol 167:241-247, 1992

2. Baskerville A, Dowsett AB, Cook RW, Dennis MJ, Cranage MP, Greenaway PJ: Pneumocystis carinii pneumonia in simian immunodeficiency virus infection: Immunohistological and scanning and transmission electron microscopical studies. J Pathol 164:175-184, 1991

3. Baskin GB, Murphey-Corb M, Martin LN, Soike KF, Hu F-S, Kuebler D: Lentivirus-induced pulmonary lesions in rhesus monkeys (Macaca mulatta) infected with simian immunodeficiency virus. Vet Pathol 28:506-513, 1991

4. Bennett BT, Abee CR, Henrickson R: Nonhuman Primates in Biomedical Research - Diseases, pp. 39-43 & 298-299. Academic Press, New York, 1998

5. Cotran RS, Kumar V, Collins T: Pathologic Basis of Disease, 6th ed., pp. 247-248. Saunders, Philadelphia, PA, 1999

6. Vogel AP, Miller CJ, Lowenstine LJ, Lackner AA: Evidence of horizontal transmission of Pneumocystis carinii pneumonia in simian immunodeficiency virus-infected rhesus monkeys. J Infect Dis 168:836-843, 1993

 

 

Case III - S-63504 (AFIP 2715544)

 

Signalment: 5-year-old, rhesus macaque, female, Macaca mulatta

 

History: This domestic purpose-bred macaque was born in 1993 and had an uneventful history in an AAALAC-accredited facility until the autumn of 1998, when she was anorexic. Physical examination revealed hypothermia (96.5(F)), tachypnea (136 breaths/minute), dehydration, decreased body mass, mild hepatosplenomegaly, and upper abdominal tenderness. Thoracic auscultation revealed loud respiratory sounds with labored inspiratory and expiratory components. Apex heart sounds were shifted to the right.

 

Case 23-3. The A/P thoracic radiograph shows marked right sided deviation of the cardiac silouette. The lateral thoracic radiograph shows diffuse fluid density in dorsal lung fields.

 

Thoracic radiographs demonstrated an increased pulmonary interstitial pattern with air bronchograms bilaterally. The cardiac silhouette was shifted to the right. Abdominal radiographs demonstrated hepatomegaly and the presence of excessive gas in the stomach, small intestine, and colon. Supportive treatment, including oral, subcutaneous, and intravenous fluids, antibiotics, and vitamins were administered, but response to treatment was minimal and the monkey was euthanized in late 1998.

 

Gross Pathology:

Body weight at necropsy was 5.5 kg. Numerous petechial and ecchymotic hemorrhages were present in the skin of the forelimbs, the ventral thorax, ventral abdomen, and hindlimbs. The subcutis of the ventral abdomen was edematous.

 

Approximately 100 ml of red fluid and 25 ml of clotted blood were in the right pleural cavity. The right middle and caudal lung lobes were dark red to black and firm. On cut surface a cavitated focus (5x5x10mm) was present in the dorsal aspect of the right caudal lobe; the surrounding tissue was dark red to black and friable. The visceral pleura overlying the cavitated focus was focally adhered to the parietal pleura by means of a circular, tan, 2 cm diameter plaque. The costal surface of the remainder of the right caudal lobe and the right middle lobe were covered with blood and fibrin and diffusely adhered to the parietal pleura. These two lung lobes were also adhered to each other, as well as to the diaphragm, pericardial sac, and mediastinum.

 

Laboratory Results:

Serial hematology and serum biochemistry samples revealed a severe leukocytosis (21 to 35 x103/mm3) with mature neutrophilia (18 to 31 x103/mm3), a developing mild anemia (36%), decreased platelet count (90 to 172 x103/mm3), and marked increases in BUN (265 to 411 mg/dl) and creatinine (8.0 to 15.0 mg/dl).

Pleural fluid was submitted for culture and sensitivity. Corynebacterium ulcerans was isolated and was reported sensitive to a variety of antibacterial agents, including cefazolin, cephalothin, penicillin, erythromycin, gentamicin, tetracycline, trimethoprim/sulfa, vancomycin, nitrofurantoin, sulfasoxazole, and enrofloxacin.

Contributor's Diagnosis and Comments:
Lung: necrotizing bronchopneumonia and fibrinohemorrhagic pleuritis
Etiologic agent: Corynebacterium ulcerans

 

Corynebacterium ulcerans has been isolated from cattle with mastitis and cutaneous infections (Hommez et al. 1999; Hart 1984), nonhuman primates with abscesses, bite wounds, pneumonia, and mastitis (Fox and Frost, 1974; May 1972; Panaitescu et al. 1977), and humans with sore throat, tonsillitis, nasopharyngitis, laryngitis, and pulmonary nodules (de Carpentier et al. 1992; Dessau et al. 1995; McDonald et al. 1997; Hust et al. 1994). Often human infections have been associated with contact with livestock or ingesting unpasteurized dairy products. Based on genomic DNA relatedness, Corynebacterium ulcerans is a distinct species closely related to C. diphtheriae and C. pseudotuberculosis (biovars equi and ovis) (Riegel et al. 1995).

 

Like these related species and biovars, C. ulcerans produces potent exotoxins, specifically diphtheria toxin and necrotizing (C. ovis -like) toxin. Diphtheria toxin is an acidic protein which inhibits protein synthesis by inactivation of elongation factor 2, while necrotizing (C. ovis -like) toxin is a basic glycoprotein, a phospholipase D and a sphingomyelinase, and increases vascular permeability, leading to local edema (Carne and Onon, 1982).

 

Based on the known pathogenesis of C. diphtheriae, it is hypothesized that the inhalation/ingestion of C. ulcerans is followed by local proliferation on the upper and/or lower respiratory tract epithelium, release of toxins, necrosis of the colonized and adjacent epithelium, an intense neutrophilic infiltrate in the underlying tissue, vascular congestion, interstitial edema, and fibrinosuppurative exudation.

 

Corynebacterium ulcerans should be considered in the differential diagnosis when confronted with a nonhuman primate with suspected bronchopneumonia and/or pulmonary abscesses. Therapeutic intervention, if warranted, should include appropriate antimicrobial therapy, based on bacterial isolation and sensitivity testing, diphtheria antitoxin, and supportive care.

 

AFIP Diagnoses:

1. Lung: Pneumonia, suppurative and hemorrhagic, multifocal to coalescing, moderate, with chronic active pleuritis, rhesus macaque (Macaca mulatta), nonhuman primate.
2. Lung: Pneumonia, fibrinous, subacute to chronic, diffuse, with chronic fibrinohemorrhagic pleuritis.

Conference Note: Corynebacteria sp. are Gram positive, generally non-motile, pleomorphic bacilli. With the exception of C. diphtheriae, they are generally part of the normal flora and they are widely distributed in the environment. C. ulcerans is a commensal of horses and cattle.

 

The differential diagnosis discussed in conference included Pasteurella sp., Legionella pneumophila, Actinobacillus sp., and Corynebacterium sp. A Gram's stain demonstrated small numbers of pleomorphic Gram positive bacilli within the affected areas.

 

Contributor: Merck Research Laboratories, Departments of Safety Assessment and Laboratory Animal Resources, West Point, PA and Rahway, NJ.

 

References:

1. Carne HR, Onon OE: The exotoxins of Corynebacterium ulcerans. J Hyg Camb 88:173-191, 1982

2. de Carpentier JP, Flanagan PM, Singh IP, Timms MS, Nassar NY: Nasopharyngeal Corynebacterium ulcerans: a different diptheria. J Laryn Otolo 106:824-826, 1992

3. Dessau RB, Brandt-Christensen M, Jensen OJ, Tonnesen P: Pulmonary nodules due to Corynebacterium ulcerans. Eur Respir J 8:651-653, 1995

4. Fox JG, Frost WW: Corynebacterium ulcerans mastitis in a bonnet macaque (Macaca radiata). Lab Anim Sci 24:820-822, 1974

5. Hart RJC: Corynebacterium ulcerans in humans and cattle in North Devon. J Hyg 92:161-164, 1984

6. Hommez J, Devriese LA, Vaneechoutte M, Riegel P, Butaye P, Haesebrouck F: Identification of nonlipophilic Corynebacterium isolated from dairy cows with mastitis. Journ Clin Micro 37:954-957, 1999

7. Hust MH, Metzler B, Schubert U, Weidhase A, Seuffer RH: Toxische Diphtherie durch Corynebacterium ulcerans. DMW 119:548-552, 1994

8. May BD: Corynebacterium ulcerans infections in monkeys. Lab Anim Sci 22:509-513, 1972

9. McDonald S, Cox D, Allen R, Bixler D, Steele G: Respiratory Diptheria Caused by Corynebacterium ulcerans. Terre Haute, Indiana, 1996. MMWR 46:330-332, 1996

10. Panaitescu M, Maximescu P, Michel J, Potorac E: Respiratory pathogens in non-human primates with special reference to Corynebacterium ulcerans. Lab Anim 11:155-157, 1977.
11. Riegel P, Ruimy R, de Briel D, Prevost G, Jehl F, Christen R, Monteil H: Taxonomy of Corynebacterium diphtheriae and related taxa, with recognition of Corynebacterium ulcerans sp. nov. nom. rev. FEMS Microbiology Letters 126: 271-276, 1995

 

 

Case IV - 97-1185 (AFIP 2694774)

 

Signalment: 6-year-old, American domestic shorthair, castrated male, feline.

 

History: Two weeks prior to presentation at the North Carolina State University Veterinary Teaching Hospital this cat received anesthesia for dental prophylaxis. Recovery from anesthesia was prolonged, and the cat became acutely blind and severely lethargic. Over a 2-week period the cat's appetite decreased, a right head tilt developed, and the cat become progressively lethargic. At the veterinary teaching hospital an ophthalmic examination showed a normal fundus and pupillary light response; however, the menace reflex was absent. Neurological examination revealed occasional circling to the right. Titers for Toxoplasma gondii, Cryptococcus neoformans, feline infectious peritonitis virus, and feline immunodeficiency virus were negative. The owner refused further clinical work-up and the cat was euthanized for necropsy.

Gross Pathology: No significant lesions.

 

Laboratory Results: No significant clinical pathology or microbiology data.

 

Contributor's Diagnoses and Comments:

1. Brain, cerebral cortex and hippocampus: Multifocal, severe, subacute cerebral cortical necrosis with microcavitation and gliosis.
2. Brain, hippocampus: Multifocal, mild lymphocytic meningoencephalitis.

 

Microscopically there are bilateral lesions within the dorsal gyri of the cranial telencephalon, as well as the dorsal, lateral, and ventral gyri of the caudal telencephalon. Affected areas are characterized by neuropil vacuolization, prominent vasculature with perivascular edema, and moderate gliosis composed of astrocytes and large foamy microglia. These regions contain low numbers of ischemic neurons having sharply angular eosinophilic cytoplasm with pyknotic to karyorrhectic nuclei. In some regions the neuropil vacuolation often coalesces to form microcavitations. Similar changes are present within some sections of the hippocampus, predominantly throughout Ammon's horn, and with less severity the dentate gyrus.

 

A variety of etiologies may cause feline cortical neuronal necrosis. Hypoxia, hypoglycemia, heavy metal toxins, and feline ischemic encephalopathy have been implicated in acute neuronal necrosis. There is no corroborating clinical pathology data to suggest hypoglycemia as an etiology in this cat. Lead inclusions are usually evident in hematoxylin and eosin stained sections of brain and kidney; also, there is no history of heavy metal exposure.

 

Global brain ischemia, as may occur with disrupted circulatory conditions, is characterized by neuronal necrosis. With severe hypotension, the brain's perfusion becomes inadequate causing bilateral infarcts at the boundary, or watershed zones, between areas supplied by major arteries. The dorsal gyri are a watershed zone since the anterior cerebral arteries supply the medially located cingulate gyri and the middle cerebral arteries supply the lateral gyri. Sparing of the cingulate and lateral gyri, and lesions predominantly within the dorsal gyri are characteristic of those associated with hypotension, and both are present in this case. The lesions within the lateral and ventral gyri of the caudal telencephalon, and hippocampus do not correspond with watershed zones; however, this distribution may reflect a site-specific sensitivity of these areas to hypoxia.

 

Humans after cardiac arrest can have necrosis within Ammon's horn of the hippocampus, and it appears that ischemia selectively affects the pyramidal neurons of Ammon's horn, while sparing the hippocampal dentate gyrus. Consistent with ischemia in this cat is the necrosis within the hippocampal Ammon's horn with sparing of the dentate gyrus.

 

The histologic changes observed in this case are suggestive of global ischemia. There is a syndrome in cats called feline ischemic encephalopathy (FIE) which can have a histologic presentation similar to that seen in this cat. FIE has an uncertain etiology, however, the lesion distribution suggests an underlying vascular disorder. Cardiomyopathy or aberrant parasite migration by the larvae of Cuterebra sp. have been suggested as etiologies. FIE is typically associated with asymmetrical cerebral atrophy in the lateral gyri, which is the area supplied by the middle cerebral artery. Cases have been documented with no gross lesions, instead having histologic evidence of bilateral cerebral cortical and cerebellar necrosis. Lesions have also been described within the hippocampus and brain stem, as they also are supplied by the middle cerebral artery.

 

The lesions within this cat's dorsal gyri are not a usual feature of FIE, rather, the dorsal gyri lesions are more characteristic of global ischemia. Given the cat's history and recent onset of clinical signs, the brain lesions are probably a direct result of the anesthetic procedure regardless of any preexisting brain disease. Furthermore, monitoring systemic blood pressure is unusual for routine veterinary surgical procedures, thus increasing the chances for hypotension. It remains possible that pre-existent subclinical brain disease was exacerbated by the anesthetic procedure.

 

AFIP Diagnosis: Brain, cerebral cortex and hippocampus: Necrosis, cortical, laminar, multifocal, with segmental hippocampal neuronal loss and gliosis, domestic shorthair, feline.

Conference Note: The contributor has provided an excellent discussion of this case.

 

Contributor: North Carolina State University, College of Veterinary Medicine, 4700 Hills Borough St., Raleigh, NC 27606.

References:

1. Auer RN, Siesj BK: Biological differences between ischemia, hypoglycemia, and epilepsy, Ann Neurology 24:699-707, 1988

2. Bernstein NM, Fiske RA: Feline ischemic encephalopathy in a cat, JAAHA 22:205-206, 1986

3. de Lahunta A: Veterinary Neuroanatomy and Clincal Neurology, 2nd edition, pp. 427-429. Philadelphia, WB Saunders Co. 1983

4. Garcia JH: The Evolution of Brain Infarcts. A Review, J Neuropathol Exp Neurol 51:387-393, 1992

5. King JM: Feline ischemic encephalopathy, Vet Med 91:1062, 1991

6. Palmer AC and Walker RG: The neuropathological effects of cardiac arrest in animals: a study of five cases, J Small Anim Pract 11:779-790, 1970.
7. Summers BA, Cummings JF, de Lahunta A: Veterinary Neuropathology, pp. 237-249. Mosby, Inc., St. Louis, MO, 1995

8. Williams KJ, Summers BA, de Lahunta A: Cerebrospinal cuterebriasis in cats and its association with feline ischemic encephalopathy. Vet Pathol 35(5): 330-343, 1998

 

 

J Scot Estep, DVM
Captain, United States Army
Registry of Veterinary Pathology*
Department of Veterinary Pathology
Armed Forces Institute of Pathology
(202)782-2615; DSN: 662-2615
Internet: estep@afip.osd.mil

* 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.

 

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