History: This animal was in good condition at the time of slaughter.
Gross Pathology: There were several ovoid white nodules
(5-6 mm) projecting from the esophageal muscle.
Contributor's Diagnosis and Comments: Sarcocysts in esophageal
muscle.
Cause: Sarcocystis gigantea (ovifelis).
Conference Note: As noted by the contributor, some of the sections viewed in conference contained a degenerate cyst surrounded by granulomatous inflammation.
Over 90 species of Sarcocystis have been recognized in mammals, birds, and reptiles, and at least 14 of these are regularly found in muscle of domestic animals.2 Often clinical disease does not occur. The severity of clinical signs varies with the species of parasite, the age of the infected animal, and the number of sporocysts ingested. In lambs experimentally infected with varying doses of S. tenella, effects included anemia, anorexia, decreased weight gain, fever, and death.1 Spontaneous sarcocystosis in sheep can present as a neurological disorder, affecting up to 10% of a flock. Affected sheep show muscle weakness, hindlimb paresis, and ataxia; some become recumbent, and occasionally sheep die without any premonitory signs.1
All Sarcocystis species have an obligatory two-host life cycle. Definitive hosts are carnivores, which are usually clinically unaffected. They prey on the herbivorous intermediate hosts. Upon being ingested by carnivores and released from mature cysts, zoites invade the intestinal epithelium and develop into gamonts. Fertilization occurs, followed by the formation of oocysts, which sporulate within the carnivore's intestine. These infective oocysts are shed in the feces. Susceptible herbivores then ingest oocysts or sporocysts, and sporozoites are released in the intestine and migrate into arterioles, where first generation merogony occurs in endothelial cells. Merozoites released from these meronts undergo second generation merogony in capillary endothelium throughout the body. Upon subsequent liberation, these merozoites enter circulating mononuclear cells and undergo endodyogeny (third generation merogony). Finally, zoites from second and third generation meronts enter the heart, skeletal muscle, or neural tissue (varies with species) and develop into immature noninfective sarcocysts containing unicellular metrocytes. These metrocytes produce bradyzoites that are infective for the definitive host, and whose presence characterizes a mature sarcocyst.3
Contributor: Department of Pathology and Microbiology, Faculty of Veterinary Medicine, University of Montreal, P.O. Box 5000, St. Hyacinthe, (Quebec), Canada J2S 7C6
References:
International Veterinary Pathology Slide Bank:
Laser disc frame #13666-68, 13677, 15217, 21461
Signalment: 35-year-old, male, chimpanzee (Pan troglodytes).
History: This animal was owned by a local private zoo, euthanized and presented for necropsy with history of chronic intermittent diarrhea and recent severe anorexia and weight loss that was nonresponsive to therapy.
Gross Pathology: The postmortem interval was 12-15 hours. There was minimal subcutaneous and intra-abdominal adipose tissue. There was moderate and diffuse mesenteric and visceral lymph node enlargement. There were 10-20 multifocal 0.2-2.5 cm, white, raised papillary foci within the proximal duodenum. The pancreas was small and firm. The duodenal and proximal to midjejunal mucosa was thickened and segmentally reddened. The distal colonic mucosa was segmentally reddened. The liver was friable and had a slightly increased lobular pattern. The gallbladder was moderately distended and the contents were opaque. The kidneys were unremarkable. There was moderate to marked generalized muscle atrophy.
Laboratory Results:
4 days ante mortem 1 day ante mortem Human Male* Units
| Parameter | 4d b/f death | 1d b/f death | Normal Range |
| WBC | 14.3 | 11.1 | 3.9-10.6 x 103/ul |
| RBC | 5.61 | 4.77 | 4.4-5.9 x 106ul |
| Hemoglobin | 13.9 | 12.2 | 13.3-17.7 g/dl |
| Hematocrit | 45 | 42 | 39.8-52.2 % |
| MCV | 81.2 | 76.7 | 81-100 fl |
| MCH | 24.8 | 25.6 | 26.6-33.8 pg |
| MCHC | 30.9 | 25.6 | 31.5-36.3 g/dl |
| Seg. Neut. | 9.724 (68%) | 7.548 (68%) | 1-8-7.0 x 103/ul |
| Band Neut. | 1.143 (1%) | -- | 0.0-0.7 x 103/ul |
| Lymp. | 3.289 (23%) | 2.775 (25%) | 1.1-4.8 x 103/ul |
| Mono. | 0.715 (5%) | 0.555 (5%) | 0.0-0.8 x 103/ul |
| Eosino. | 0.429 (3%) | 0.222 (2%) | 0.0-0.4 x 103/ul |
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Direct fecal exam: No parasites seen
Fecal Giardia ELISA test: Negative
Fecal aerobic culture: No Salmonella, Shigella, or Campylobacter
species isolated.
Fecal anaerobic culture: No Clostridium species isolated.
Contributor's Diagnosis and Comments: Pancreas: Severe chronic diffuse pancreatic exocrine atrophy and fibrosis.
Additional diagnoses (tissue not provided):
Skeletal Muscle: Moderate chronic multifocal muscle fiber atrophy.
Duodenum: Multiple adenomatous polyps.
Intestine: Moderate chronic multifocal eosinophilic enteritis
with intralesional nematodes (Enterobius vermicularis)
Liver/Gallbladder: Mild chronic diffuse lymphocytic and plasmacytic
cholangitis.
Moderate multifocal hepatocellular fatty change.
Kidney: Mild chronic multifocal interstitial nephritis.
Heart: Moderate chronic multifocal myocardial fibrosis.
Histologic examination of the pancreas revealed diffuse acinar cell atrophy and loss. The remaining pancreas is composed primarily of variably sized aggregates of islet cells intermixed with pancreatic ducts surrounded by a moderately cellular fibrous connective tissue. There are a few scattered foci of fat necrosis and variable scattered collections of lymphocytes and plasma cells. The diffuse atrophy and fibrosis are most likely sequelae to chronic pancreatitis.
The clinical pathologic findings of a marked increase in serum creatinine, phosphorus, and BUN in the presence of a slight metabolic acidosis are suggestive of significant renal disease; however, the histologic findings indicate only mild renal disease. The azotemia is presumed to be predominantly prerenal and a result of decreased renal perfusion. The marked elevation in creatinine is out of proportion to the elevation in BUN and in the absence of significant renal disease may be a result of the lipemia and/or hemolysis, or may be further falsely increased because of noncreatinine chromogens such as ketones from the massive protein catabolism. The observed cardiac fibrosis suggests that cardiac output may have been altered and may have contributed to the reduction in renal perfusion. The very low amylase may reflect the massive loss of acinar tissue.
Chronic pancreatitis can have a variable presentation and most dogs and cats have a history of chronic weight loss in the presence of a vigorous appetite. In humans it can present as repeated attacks of mild to moderately severe abdominal pain or persistent and intractable abdominal pain. In some cases the local disease may be clinically silent until either exocrine pancreatic insufficiency (EPI) or diabetes develops. There are no consistent hematologic or serum chemistry profile changes in EPI; the serum amylase and lipase values are frequently within normal ranges, and undigested fats are not consistently found in the feces; thus the diagnosis of chronic pancreatitis requires a high index of suspicion. The definitive test for EPI in dogs and cats is to measure serum trypsin-like immunoreactivity.
Conference Note: As the contributor noted, measurement of trypsin-like immunoreactivity (TLI) has become established as the method of choice for diagnosing exocrine pancreatic insufficiency (EPI) in the dog. This test measures trypsinogen, which is synthesized exclusively by the pancreas. The serum level depends on pancreatic mass, so pancreatic atrophy leads to reduced serum levels. In cats, recent studies have demonstrated decreased serum TLI with EPI; however, diagnostic criteria have not been established for this species.5 False-negative results for EPI can occur with concurrent pancreatitis and with renal failure.4
Other serum tests sometimes used to diagnose EPI include the BT-PABA test and measurements of cobalamin and folate. In EPI, folate is increased and cobalamin is decreased. However, false positive results can occur due to bacterial overgrowth, which causes a similar change in levels of these vitamins. With severe, diffuse small intestinal disease, both values are decreased.4 The BT-PABA test indirectly measures chymotrypsin levels, which are decreased in cases of EPI.
Contributor: Department of Comparative Pathology, New England Regional Primate Research Center, Harvard Medical School, One Pine Hill Drive, P. O. Box 9102, Southborough, MA 01772
International Veterinary Pathology Slide Bank:
Laser disc frame #6581-2, 6627-8.
Signalment: 3-day-old, male, Golden Retriever cross, dog (Canis familiaris)
History: The pup was one of 8 in a litter from a Golden Retriever cross bitch, heterozygous for Golden Retriever muscular dystrophy (GRMD). From birth the pup was unable to suckle from the bitch and, unlike its littermates, failed to gain weight. Despite supplementary feeding the pup died at 3 days of age.
Gross Pathology: The trapezius, diaphragm, sternocephalicus, abdominal muscles and tongue showed white streaking throughout the length of the muscles. There was an acute aspiration bronchopneumonia.
Laboratory Results: Serum creatine kinase at 1 day old: 306,200 U/L
Genomic amplification of canine dystrophin gene exon 7-specific polymerase chain reaction products (harvested from blood) identified the point mutation in the consensus splice acceptor site in intron 6 of the canine dystrophin gene associated with Golden Retriever muscular dystrophy (GRMD) (R.J.Bartlett et al 1996).
Contributor's Diagnosis and Comments: Skeletal muscle,
tongue: Severe, diffuse, polyphasic muscle necrosis and regeneration,
Golden Retriever cross, canine.
Etiology: X-linked inherited dystrophin deficiency: GRMD
Cardiac Muscle: No abnormality.
Heart: No abnormality detected.
Tongue: There were few areas of normal striated muscle within the tongue. Variation in fiber size associated with muscle degeneration and regeneration was a prominent feature. Degenerate muscle fibers appeared swollen with increased eosinophilia, whereas regenerating muscle fibers were narrow with variable cross sectional diameter and occasional central nuclei. Evidence of muscle regeneration was also demonstrated by prominent clusters of plump myonuclei lining up along the edge of myofibers.
Segmental necrosis of muscle fibers was often accompanied by increased basophilia due to mineralization. Areas of increased tissue basophilia were associated with infiltrates of macrophages and skeletal muscle precursor cells associated with myofiber regeneration.
GRMD is a genotypic and phenotypic homologue of Duchenne muscular dystrophy (DMD) (B.J Cooper et al 1988). In both humans and dogs with dystrophin deficiency there is phenotypic variation in the clinical progression of the disease between individuals. One manifestation of dystrophin deficiency recorded in dogs is a lethal neonatal form (J.McC Howell et al 1994; B.A Valentine et al 1988). Pups presenting with this form of the disease usually have serum creatine kinase levels greater than 1000 times the normal adult range at birth, and die before 14 days of age (B.A Valentine et al 1988; J.McC Howell et al 1994). At post mortem there is severe muscle necrosis and mineralization consistently involving the diaphragm and intercostal muscles (J.McC Howell et al 1994). Muscles severely affected by necrosis and mineralization in this pup included the tongue, trapezius, intercostal and sternocephalicus muscles. Cardiac lesions are usually absent until after 3 months of age (B.A Valentine et al 1989).
Conference Note: The normal function(s) of dystrophin, and the mechanism by which dystrophin deficiency results in cardiac and skeletal muscle degeneration, are not known. This protein is most abundant in skeletal, cardiac, and smooth muscle cells, and is linked to an integral membrane glycoprotein. Valentine et al suggest that it is a cytoskeletal protein, possibly involved in membrane stabilization.
In addition to the canine model presented here, a murine mutant, mdx, is also X-linked and lacks dystrophin, and thus is considered to be an animal model for DMD. Although histopathologic changes in both models are similar, the mdx mouse develops little or no detectable weakness, so it is a poor clinical model for DMD.2
Contributor: School of Veterinary and Biomedical Sciences, Murdoch University, Murdoch, Western Australia, 6150
International Veterinary Pathology Slide Bank:
Laser disc frame #9137-8, 9142-3
Signalment: 5-year-old, female, Friesian, bovine.
History: Four of 200 pasture-fed dairy cows that had been supplementally fed maize silage died a week after aborting late term fetuses. Principal clinical signs included profuse vaginal discharge and labored breathing for two days prior to death.
Gross Pathology: The submitting veterinarian described patchy consolidation of all lung lobes, particularly in the ventral aspect, and diffuse pulmonary congestion and edema. There was recent fibrinous pleurisy and excessive straw-colored pleural exudate that clotted on exposure to air.
Laboratory Results: Mortierella wolfii was cultured from samples of fresh lung.
Conference Note: When the infected placenta separates from the uterine attachments, hematogenous dissemination of fungi occurs. Widespread growth of fungal hyphae occurs in pulmonary capillaries and larger blood vessels, resulting in necrotizing vasculitis and thrombosis, which leads to infarction and necrosis of pulmonary parenchyma.
Other fungi within the phylum Zygomycota, primarily Mucor and
Rhizopus species, can also opportunistically invade the lung and
cause similar lesions. Likewise, several species of Aspergillus,
in the phylum Ascomycota, can cause severe acute pulmonary lesions
in mammals and birds. Although there are morphologic differences
in the various groups of fungi, definitive etiologic diagnosis
requires fungal culture, immunohistochemistry, or molecular techniques.
Contributor: New Zealand Registry of Animal Pathology, Batchelar
Animal Health Laboratory, P.O. Box 536, Palmerston North, New
Zealand
Terrell W. Blanchard
Major, VC, USA
Registry of Veterinary Pathology*
Department of Veterinary Pathology
Armed Forces Institute of Pathology
(202)782-2615; DSN: 662-2615
Internet: blanchard@email.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.