WAM 602 - 1 - 04-7C CETACEAN NECROPSY REPORT UNIVERSITY OF NORTH CAROLINA AT WILMINGTON◦UNIVERSITY OF TENNESSEE◦ NORTH CAROLINA STATE UNIVERSITY Date: 30August 2004 Species: Stenella clymene Location: North Topsail Island, NC Sex: M TL: 202 cm GROSS REPORT REPORTING INSTITUTION: University of North Carolina at Wilmington GROSS NECROPSY EXAMINATION REPORT FIELD NUMBER WAM 602 SPECIES Stenella clymene RECOVERY DATE 30 August 2004 NECROPSY DATE 30 August 2004 LOCATION North Topsail Island, NC LAT/LONG 34.517406N / 77.365422W SEX M TL 202cm WT 92kg CONDITION 1 HISTORY WAM and DAP received page at 07:45 from Gretchen Lovewell (NMFS Beaufort) of a live stranded dolphin on North Topsail Island. The onsite contact was with Topsail Island Communications, so WAM called them and they said they had a police officer onsite and that the animal was alive and rolling in the surf. WAM left immediately and arrived on scene at 08:15. The animal was alive and the public had now secured the animal and were supporting it in the surf. WAM assessed and determined the animal was an adult male Stenella clymene, an extremely rare animal for this region. WAM called the VABLAB and informed them of the live animal- they had the truck packed and were ready to leave. WAM called Ari Friedlaender as he was driving to Wilmington from Raleigh. He detoured and headed to Topsail Island. WAM contacted Blair Mase Guthrie and discussed the options for transport, and concluded that there were few to none with a pelagic dolphin from a declared UME. DAP had been in contact with Craig Harms (NCSU) and found that he was driving to Raleigh to teach so we started UNCW UT NCSU
Transcript
WAM 602 - 1 - 04-7C
CETACEAN NECROPSY REPORT
UNIVERSITY OF NORTH CAROLINA AT WILMINGTON◦UNIVERSITY OF TENNESSEE◦ NORTH CAROLINA STATE UNIVERSITY
Date: 30August 2004 Species: Stenella clymene Location: North Topsail Island, NC Sex: M TL: 202 cm
GROSS REPORT REPORTING INSTITUTION: University of North Carolina at Wilmington
GROSS NECROPSY EXAMINATION REPORT
FIELD NUMBER WAM 602 SPECIES Stenella clymene RECOVERY DATE 30 August 2004 NECROPSY DATE 30 August 2004 LOCATION North Topsail Island, NC LAT/LONG 34.517406N / 77.365422W SEX M TL 202cm WT 92kg CONDITION 1
HISTORY WAM and DAP received page at 07:45 from Gretchen Lovewell (NMFS
Beaufort) of a live stranded dolphin on North Topsail Island. The onsite contact was with Topsail Island Communications, so WAM called them and they said they had a police officer onsite and that the animal was alive and rolling in the surf. WAM left immediately and arrived on scene at 08:15. The animal was alive and the public had now secured the animal and were supporting it in the surf. WAM assessed and determined the animal was an adult male Stenella clymene, an extremely rare animal for this region. WAM called the VABLAB and informed them of the live animal- they had the truck packed and were ready to leave. WAM called Ari Friedlaender as he was driving to Wilmington from Raleigh. He detoured and headed to Topsail Island. WAM contacted Blair Mase Guthrie and discussed the options for transport, and concluded that there were few to none with a pelagic dolphin from a declared UME. DAP had been in contact with Craig Harms (NCSU) and found that he was driving to Raleigh to teach so we started
UNCW
UT NCSU
WAM 602 - 2 - 04-7C discussing euthanasia options with Dr. Terra Kelley, a wildlife veterinary resident working with Craig. She agreed to come to the beach and conduct an assessment on site. DAP, EMM and ASF arrived at ca. 09:30 and Dr. Kelley arrived at ca. 10:30. At this point we had the animal in a stretcher and were restraining it just above the surf line. Respirations were monitored continuously from this point on. WAM would have rather kept the animal in the water, but as the surf was rolling in from 4-6’ decided to protect the people assisting with the animal as much as possible.
The decision was made to euthanize the animal after Dr. Kelley arrived and we prepared the scene for this outcome. Sedative included 100mg of Xylazine and 40mg of Acepromazine injected IM at 11:31:24. We waited 15 minutes for the anesthesia to take effect. The animal went through moderate arching and twitching that slowed after 10 minutes. At 11:46:09 a cardiac needle was inserted and ca. 60cc of blood was drawn and transferred to purple and red top tubes. At 11:47:30, 20ml euthanasia solution was started. The animal took two short breaths, the blowhole closed and all motion ceased. At 11:49:15 it was pronounced dead. The carcass was then wrapped in the stretcher and carried ca. 250m down the beach to a crossing and was loaded into the truck for transport. Initially, the animal was going to go to UNCW for necropsy. In discussions w/ Blair Mase Guthrie she suggested that we try to get a head scan if at all possible, so we decided to take the carcass to Raleigh. As we were heading to the highway Craig Harms called and said the scanning facility was booked for the rest of the afternoon and were not going to be able to fit in the scan. We changed plans and headed south again to UNCW for necropsy. The necropsy was started at 14:30 after external photos and morphometrics were concluded by EMM, ASF, MMB, CJH, BCB and volunteers from the UNCW Marine Mammal Stranding Network. The head was removed intact within 30 minutes and was wrapped multiple bags and immersed in slush ice, where it remained for the rest of the night. The necropsy was completed at 20:00 and the lab was cleaned and finished at 21:00.
WAM left Wilmington at 05:00 on 31 August to transport the head to
Raleigh. The scan was conducted from 08:30 to 09:00 and the necropsy was begun at 10:30. The blubber was dissected cleanly and the ears were removed and fixed whole. Blubber samples were collected for lipid typing. The ptyregoid and dorsal orbital sinuses were opened and investigated for parasites. The brain was removed intact and sectioned to grossly assess a region of hemorrhage noted during the scan. The head dissection was completed at 13:30. I had lunch with Craig and Mac and left Raleigh at 14:00 arriving at UNCW at 17:30. I re-bagged all of the tissues in the vacuum sealer and secured the tissues in the ultracold at 18:30.
On 1 September all histopath and blood samples for viral analysis were
shipped Fed Ex.
NECROPSY External exam: There were no obvious lesions on the external surface. The eyes were slightly roughened and there was minor bleeding on the ventral surface of the flukes
WAM 602 - 3 - 04-7C from sand abrasion. The dorsal fin had a large healed “bite” removed from the caudal trailing edge. Internal exam: The animal was placed on the gurney right side down. Blubber thickness was collected on the left side. The head was removed within 30 minutes and the remaining carcass was rolled multiple times during necropsy. Blubber: The blubber was less than 1cm over the whole animal and did not express much lipid when folded or compressed. Musculoskeletal: There is loose blood expressed from the right scapula and pectoralis. The synovial fluid in the right and left glenohumeral joint is pink raspberry color. In the head, there is subcutaneous hemorrhage at the blubber acoustic fat interface on the right mandible- region (6x4cm) of ecchymotic hemorrhage extends dorsally to maxilla and melon on right side. Blood was expressing from the right lateral head muscle when cut. CNS/Brain: The brain was scanned and then removed whole and fixed. The scan showed a region of darkening in the right rear quadrant. There was no obvious lesion on gross exam, but suggest rigorous histopath investigation is required. Spinal cord was removed at the atlas/axis and fixed. Pituitary: The pituitary was removed whole and fixed- no obvious lesions. Circulatory: Small 1mm bubbles were noted, and pressed back and forth, in the circulation of the right jugular. Heart: left ventricle firm in rigor, AV valves open—again suggesting rigor, thus wall thickness measurements of heart not taken; NVL on surface. Both left and right AV valves look normal. Collected fixed samples from left and right ventricles, left and right atria. Pericardial lymph- similar to lung lymph (see below). Lungs: Right- lung has a bifurcation of the leading edge suggesting a vessel traveling through the bifurcation. The lung is heavy, wet, dark red in color. The cranial/ventral margin is deflated (similar in appearance to lungs of young animals). Upon palpation small 5mm circular nodules evident in deep tissues. Lung is uniformly dark red in color throughout, very consolidated. Small, very firm nodules appeared calcified. Collected culture swab. Right lung lymph- weight was 13g; slightly less than one half of cross sectional face is muddy brown with small lighter tan areas throughout.
WAM 602 - 4 - 04-7C Left- lighter than right, but still wet, soppy, dark pink red in color, airway contents bloody, some foam. Cranial ventral margin deflated as well. Few/ rare small (~5mm) nodules, were collected. Left lung lymph- weight was 7g, which is half the size of the right; all of this lymph node is similar in cross section to the lesions described for the right. GI Tract:No foodstuffs found from all chambers. Fore- stomach is contracted to a ball dorsally. There is loose bile in the fore-stomach. There are 3 ulcers located at the caudal margin of the fore-stomach. The main-stomach is contracted with thick green bile found. Pyloric-stomach is thin walled and enlarged with cross section of 3cm by length of 20cm and filled with gas. Colonic lymph nodes were tan colored and unremarkable. Pancreas: The surface of the pancreas displays two areas where vessels are obvious and the surrounding tissue is dark red (looks like varicose veins). The pancreas doesn’t feel fibrotic to the touch. The color is light pink, appears normal. % of cross section that appears fibrotic: Section 1
Section 2
Section 3
Section 4
Section 5
Section 6
5% 10% 5% 5% 5% 5% Section 6 has an area of varicose vein like discoloration throughout its depth. Pancreatic Lymph Node: The whole lymph node looked fibrotic and active throughout. At one terminus of the node approximately 75% of the cross section was dark brown/black in color with small areas that were lighter tan throughout. Mesenteric Lymph Node: The mesenteric lymph node has an odd shape. The lymph node chain is irregular in shape and almost appears to be folded upon itself along its length. The cranial margins of the node are firm to the touch and it appears fibrotic across all cut surfaces. Rare small (<1mm) dark pigmented areas were seen (parasites??). Upon cross-section, the color was mottled from areas of white (fibrosis) to dark tan. Large piece sampled for histology. Pre-scapular Lymph Node: Right and left pre-scapular lymph nodes are edematous. Right lymph node, upon cross-section, is highly variable in color ranging from dark red to tan, to small areas of gravelly, peppery color. The right node is active, the cortex is involuted. The left lymph node is similar in appearance to the right node. Liver: The liver was normal. It had sharp caudal margins and a uniform steel blue-black color. There were no surface irregularities. Collected a cranial and caudal sample for histology. Collected culture swab. Kidneys: NVL; no obvious fat; overall color is darker than “normal”. Collected culture swab.
WAM 602 - 5 - 04-7C Spleen: The spleen was the size of a small lime (appears small?) and the visceral peritoneum appears thickened. Collected culture swab. Adrenals: Left- cortex appears moderately thickened. There appear to be areas of involution into the medulla. The cortex is brown to brick red in color and the medulla is light pink. Sampled for histology. Right- appears similar, but the cortex is not as thick as on the left adrenal. Reproductive Tract: The testes were large and firm suggesting the male was seasonally producing sperm. The epididymes were filled with copious sperm. Epididymis, testes and prostate sampled. Parasites: Mild Crassicauda was found in the external right obliques. One Phyllobothrium in the blubber at the anus. Six Monorrhygma in the mesentery of the right testis. Other: Bladder is enlarged and thickened, bladder wall is ~1cm thick. Thyroid has NVL. Thymus is atrophied, very small in size.
SUMMARY A live stranding that was euthanized on the beach. The necropsy produced no obvious gross lesions that suggest reason for stranding, although systemic lymph node irregularities noted. The animal had not fed for a long time with no foodstuffs found and a dark sticky bile found throughout all stomach chambers. The head was transported to Raleigh, was scanned and finished the necropsy. CAUSE OF DEATH: Await histopath results. This report was generated by: _______________________________ UNCW Marine Mammal Program
TISSUES COLLECTED Frozen: Skeleton (incl. skull) Skin Blubber B (dorsal and ventral separately), G, H NIST (blubber, liver, kidney -80) Dorsal fin Epaxial muscle at dorsal fin Epaxial muscle at anus Epaxial muscle at sternohyoid 10% Buffered Formalin: Dorsal skin Ventral skin Prescapular lymph node Right epaxial muscle Liver: caudal and cranial sections Left adrenal Spleen Mesenteric lymph node (not in cassette)
WAM 602 - 6 - 04-7C Dorsal aorta Spinal cord Colonic lymph Colon Right lung Left lung Right lung lymph node Left lung lymph node Pericardial lymph Prostate Epididymis Kidney Testis Bladder Stomach ulcer Stomach, main Stomach, pyloric Duodenum Pancreatic lymph node Pancreas: normal area and an area with varicose vein-like section Fixed at NCSU during head dissection: Lymphoid tissue at base of larynx Pharyngeal mucosa Skeletal muscle from larynx Brain Pituitary 70% ETOH: skin Skeletal: frozen at UNCW for later transport to Smithsonian Other: Samples for Tracy Romano: normal suite in -80 Cultured tissues: Lung Kidney Spleen Liver Blood: 60 cc’s whole blood; CBC & chem panel, serum to Dr Saliki, remaining serum frozen in -80
PHOTOS/VIDEO: at UNCW (in MMSN folder and on CD in folder) ASSOCIATED DATA SHEETS Marine Mammal Stranding Report Level A data sheet Mass Dissection data sheet Blubber mass/ thickness data sheet Evaluation of Human Interaction Delphinid Specimen Record Cetacean body surface area data sheet Necropsy Summary Sheet List of samples
WAM 602 - 8 - 04-7C “Colonic Lymph Node” (slide 2): Separating a fibrovascular and muscular stroma, there is a 2.2 cm in diameter metazoan with a 5 micron, eosinophilic tegument, lining smooth muscle, absence of gastrointestinal tract, and solid parenchymus body (cestode) surrounded by neutrophils, eosinophils, foamy to epithelioid macrophages, lymphocytes and plasma cells (Figure 1). There are extravasated erythrocytes, fibrin exudation, aggregates of hemosiderophages, and irregular basophilic material (dystrophic mineralization).
Figure 1. Serosa, Colon. 20x. HE. Cestode (arrow) is surrounded by mixed inflammatory cells and basophilic, granular debris (mineral) (double arrows).
Colon (slide 2): There is a mild increase in lymphocytes, plasma cells, and eosinophils within the lamina propria. There is a diffuse, mild, goblet cell hyperplasia. At one margin, there is a coagulum of hyalinized collagen with interspersed extravasated erythrocytes, and numerous, small vascular channels. Skeletal Muscle (slide 2): Two sections are examined. No significant histologic findings. Lung Lymph Node (slide 3): There is moderate lymphoid follicle hyperplasia and macrophages are increased within medullary sinuses. Mutifocal, loosely aggregated macrophages containing abundant, 1 to 2 micron, black granules (anthracosis) and birefringent crystalline structures (silicosis) are randomly present within the cortex (Figure 2).
crystalline structures are present within the same macrophages containing carbon pigment.
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Thyroid Gland (slide 3): Follicles are of varying caliber and lined by a single layer of cuboidal epithelium. Approximately 70% of follicles contain an eosinophilic, homogenous colloid. Left Lung Lymph Node (slide 4): Lymphoid follicles are mildly hyperplastic. Medullary sinuses are expanded by macrophages, fewer erythrocytes, and edema. There is a focal aggregate of multinucleated giant cells with abundant eosinophilic cytoplasm and 4 to 8 eccentric nuclei. There are scattered macrophages within intracytoplasmic, granular, black pigment (anthracosis). Spleen (slide 4): Periarteriolar lymphoid sheaths are mildly reactive with prominent macrophages in the follicular center. There is a mild plasmacytosis. There is scattered extramedullary hematopoiesis and small numbers of macrophages with intracytoplasmic brown, granular pigment (hemosiderophages). The red pulp is moderately depleted of erythrocytes. Artery (slide 5): No significant histologic findings. Pericardial Lymph Node (slide 5): Abundant mature collagenous tissue separates lymphoid follicles. Lymphoid follicles are hyperplastic and within the germinal center of one follicle, there is abundant eosinophilic, homogenous material (hyalosis vs. amyloid). There is edema, increased macrophages, erythrocytes, and erythrocytophagia in the medullary sinuses. Aorta (slide 5): No significant histologic findings. Testis (slide 5): Seminiferous tubules are lined by germ cells with evident maturation into spermatozoa. Pancreatic Lymph Node (slide 6): There is moderate deposition of fibrous connective tissue separating lymphoid follicles. Lymphoid follicles are mildly hyperplastic with macrophages increased within the center. There are multifocal, poorly organized macrophages and multinucleated giant cells. There are multifocal macrophages with intracytoplasmic, irregular round, variably-sized, black pigment (anthracosis). Heart (slides 7, 9, 10, 12): In slides 7 and 12, there is focal loss of cardiomyocytes with replacement by mature connective tissue (Figure 3). In slide 10, there is a focal sprinkling of lymphocytes in the ventricular interstitium and a single medium-caliber artery with 4 loosely packed concentric whorls of fibroblasts surrounding the vessel.
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Figure 3. Heart. 100x. HE. There is focal loss of cardiomyocytes with replacement by fibrous connective tissue. Lung (slides 7 and 15): There is multifocal to coalescing flooding of alveolar and bronchiolar lumina by lightly eosinophilic homogenous fluid (edema), beaded material (fibrin), and extravasated erythrocytes (Figure 4). There is marked mucosal ulceration of a bronchiole which is filled with eosinophils, neutrophils, lymphocytes, plasma cells, and macrophages admixed with fibrin and cellular debris. At the center of the inflammatory infiltrate, there is a tangential section of a nematode that is 40 to 50u in diameter with a 4 to 6 micron cuticle, coelomyarian-polymyarian musculature, and a completed digestive tract (Figure 5). In slide 15, there are three coalescing granulomas that range from 4 mm to 6mm (Figure 6). Granulomas have a central core of mineral surrounded with associated macrophages, lymphocytes, plasma cells, neutrophils, and fewer eosinophils. There is associated interstitial fibrosis and smooth muscle hypertrophy of associated alveolar septal walls.
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Figure 4. Lung. 200x. Airways are filled with erythrocytes and eosinophilic fluid (serum and fibrin).
WAM 602 - 13 - 04-7C Figure 5. Lung. 20x. This bronchiole is completely occluded by inflammatory cells, fibrin, and a single intraluminal nematode.
Figure 6. Lung. 20x. Granulomas in the lung with a central core of mineral. Blubber (slides 8 and 11): No significant histologic findings. Adrenal Gland (slide 8 and 9): There is mild, multifocal extramedullary hematopoiesis within the cortex. Duodenum (slide 8): There is moderate lamina proprial infiltrate of plasma cells and fewer eosinophils. The superficial mucosa is sloughed. Intestine (slide 8, 10, 11): There is a moderate to marked infiltrate of eosinophils, plasma cells, and lymphocytes within the lamina propria with occasional exocytosis into sloughed mucosal epithelium. There are two aggregates of eosinophils and fewer macrophages within the mucosa surrounding a central core of eosinophilic granular to globular material (degranulated eosinophils, Splendore-Hoeppli material) (Figure 7). There is a sprinkling of eosinophils within the muscularis mucosa. Within the submucosa, there is an approximately 1.0 cm in diameter granuloma composed of a central core of eosinophilic debris and mineral surrounded by numerous fibroblasts, epithelioid macrophages, and lymphocytes, plasma cells, and fewer eosinophils.
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Figure 7. Intestine. 200x. HE. Within the mucosal layer, there is a granuloma with a central eosinophilic core (Splendore-Hoeppli material). Eosinophils infiltrate the intestinal mucosa displacing crypts (arrows). Urinary Bladder (slide 9): Multifocally, there are extravasated erythrocytes and an eosinophilic coagulum with occasional golden, granular pigment adhered to the superficial urothelium (Figure 8). Occasionally, sperm is present within this eosinophilic coagulum In these regions, superficial epithelial cells have deeply eosinophilic cytoplasm and hyperchromatic nuclei.
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Figure 8. Urinary Bladder. 400x. HE. There is an eosinophilic coagulum with interspersed sperm and erythrocytes. Esophogastric junction (slide 9): There are multifocal lymphoplasmacytic infiltrates within the muscularis mucosa and at the junction of the basal layer and muscularis mucosa. There are multifocal (2) granulomas within the muscularis mucosa. Granulomas are composed of epithelioid macrophages, mineral, and surrounding lymphocytes and plasma cells. Within the gastric mucosa, there are two, small aggregates of multinucleated giant cells with a faintly golden intracytoplasmic structure. Gut-associated lymphoid follicles are mildly hyperplastic. Liver (slides 10 and 14): There is diffuse, mild to occasionally moderate biliary hyperplasia. There is a mild increase in portal fibrous connective tissue and hepatic arteriolar walls are thickened. Nearly 45% of hepatocytes contain an granular brown, intracytoplasmic pigment (ceroid-lipofuscin vs. iron). There is focal, nodular hepatoceullar, cytoplasmic vacuolation (lipid accumulation). Pancreas (slides 11 and 14): There is moderate congestion. Prostate (slide 12): There are occasional plasma cells within the interstitium. Glandular cells are high cuboidal with abundant foamy cytoplasm. Kidney (slide 12): There is mild, multifocal interstitial fibrosis with associated lymphocytes and plasma cells (Figure 9). Within one affected region, there is granular black pigment. A few tubules near this region contain eosinophilic, proteinic fluid (tubuloproteinosis) (Figure 10).
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Figure 9. Kidney. 200x. HE. There is loss of proximal tubules with replacement by fibrous connective tissue and infiltration by lymphocytes and plasma cells.
Figure 10. Kidney. 400x. HE. There is proteineic fluid within tubules (tubuloproteinosis). Mesenteric Lymph Node (slide 13): Lymphoid follicles are separated by fibrous connective tissue and smooth muscle. Multifocally, there are granulomas composed of a central, granular eosinophlic core (Splendore-Hoeppli reaction) and surrounded by multinucleated giant cells, epithelioid macrophages, fewer eosinophils, and lymphocytes and plasma cells. Rarely, within the eosinophilic matrix, there are longitudinal sections of whole or fragmented nematode larvae (Figure 11). Larvae are 10 to 15 microns in diameter with basophilic, round internal structures and a tapered posterior.
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Figure 11. Mesenteric Lymph Node. 400x. HE. There are granulomas within the mesenteric lymph node with associated multinucleated giant cells (circle). Within the center of the poorly-organized granuloma, there is eosinophilic granular material (Splendore-Hoeppli reaction) (star) which results from localized antigen-antibody reactions and a single nematode larvae (arrow). Main Stomach (slide 14): There are increased lymphocytes and plasma cells within the mucosa. Pancreas (slide 14): No significant histologic findings. Vas Deferens (slide 15): Numerous spermatozoa fill lumina. Forestomach (slide 16): There is a transition from intact to eroded to ulcerated mucosal epithelium. In regions of epithelial ulceration, there are large accumulations of viable and degenerate neutrophils and fewer macrophages within a matrix of fibrin, extravasated erythrocytes and pyknotic nuclear debris. There is a mild, loosely organized proliferation of plump fibroblasts and vascular channels with plump endothelial lining (reactive). Within the submucosa, there is moderate edema which is most pronounced around vascular spaces. Eosinophils, neutrophils, lymphocytes, plasma cells, and fewer macrophages are strewn within the submucosa with a predilection for perivascular regions. Spinal Cord (slide 17): There is a mild to moderate, multifocal perivacular cuffing with expansion of Virchow-Robins spaces by lymphocytes and fewer plasma cells and macrophages (Figure 12). There is also globular eosinophilic fluid (serum) and few extravasated erythrocytes. Inflammation is typically within
WAM 602 - 18 - 04-7C the gray matter. There is multifocal demyelination of ventral and dorsal tracts characterized by swelling of myelin sheaths and dissolution and degeneration of axons (Figure 13). Occasionally, macrophages are present within individual swollen myelin sheaths (digestion chambers) and have dense eosinophilic cytoplasm and hyperchromatic nuclei. Occasional neurons have moderate amounts of cytoplasmic, brown, granular pigment (ceroid-lipofuscin).
Figure 12. Spinal Cord. 400x. HE. There is perivascular cuffing by lymphocytes and plasma cells within Virchow-Robins spaces (arrow). A neuron contains intracytoplasmic, brown, granular pigment (ceroid-lipofuscin) (circle).
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Figure 13. Spinal Cord. 400x. HE. There is expansion of myelin sheaths and degeneration of axons (arrows). Brain (NCSU Slides 5-10) (Report generated by Dr. Mac Law): Slides 5-10, Brain and spinal cord: At all levels of the brain and C1 spinal cord, there is moderate to severe perivascular cuffing, characterized by expansion of Virchow-Robbins spaces by predominantly lymphocytes and plasma cells (Figure 14). Scattered, multifocal areas of the adjacent neuropil contain small aggregates of similar inflammatory cells; a few of these areas show focal necrosis along with small numbers of macrophages, and there are areas of marked gliosis with prominent, swollen astrocytes. However, no apparent demyelination is noted in the white matter. Occasional, multifocal areas of the meninges are mildly thickened by lymphocytes and plasma cells. There is mild to moderate neuronal lipofuscinosis. Additional Tissues Examined: Slides 1 and 2, red tissue from laryngeal area: presumptively normal tonsillar lymphoid follicles and adjacent salivary gland tissue. Slide 3, dark red linear tissue: normal glandular tissue (parathyroid?). Slide 4, right periorbital tissue: lymph node, with essentially normal lymphoid follicles.
WAM 602 - 20 - 04-7C DIAGNOSIS: Nonsuppurative meningoencephalitis and myelitis. COMMENTS: The lesions are suggestive of a viral cause, such as morbillivirus or other encephalitis virus. The perivascular cuffing appeared to be somewhat more severe caudally, especially in sections of hippocampus and caudally into the brain stem and cerebellum. Interestingly, there is not obvious white matter degeneration/demylenation, and no inclusion bodies were noted. In addition, although it is difficult to assess without lymphoid tissues from an age-matched control animal, there is no obvious lymphoid necrosis or depletion from lymphoid follicles.
Figure 14A and 14B. Brain. There is marked perivascular cuffing by plasma cells and lymphocytes. Serum exudes from the leaky vessel wall (orange arrow) and there is rarefaction (spongy) gray matter surrounding the vessel (block arrow) (A).
1.Urinary Bladder:Intraluminal hemorrhage and mild, focally extensive, urothelial hyperplasia. 2.Prostate: Prostatitis, plasmacytic, multifocal, minimal. 3.Kidney: Interstitial nephritis, lymphoplasmacytic, multifocal, mild to moderate with occasional tubuloproteinosis and interstitial fibrosis.
WAM 602 - 22 - 04-7C FINAL DIAGNOSES/INTERPRETATIVE SUMMARY 1.Nonsuppurative meningoencephalomyelitis. 2.Verminous pneumonia. 3.Gastroenteritis. 4.Interstitial nephritis. Systemic disease in this thin animal involved the nervous, respiratory, lymphoreticular, digestive, cardiovascular, and urogenital system and varied from severe to incidental lesions. The most striking and debilitating lesions involved the central nervous system (brain and spinal cord) and were inflammatory in nature. These changes are similar to other cetaceans examined to this point (4 Oct 2004) in the UME. Given the animal’s body condition, it was likely that this is a chronic condition rather than one that resulted in instantaneous disease and illness. A viral etiology is likely. Additional diagnostics are needed for absolute confirmation. Verminous pneumonia , gastroenteritis, and to a lesser degree, interstitial nephritis were likely contributory to this animal’s ill thrift, while the verminous lymphadenitis, lymph node anthracosis, prostatitis, and cardiac fibrosis were considered incidental findings. COMMENT The cause of morbidity in this cetacean is attributed to systemic disease involving the nervous, respiratory, digestive, and to a lesser degree, urinary system. The non-suppurative (lymphocytes, plasma cells, no neutrophils or eosinophils) meningoencephalomyelitis is the change that most severely affected this animal with the other lesions contributing to its debilitation. Inflammatory changes with the brain were similar to other cases reported in the UME with inflammation generally targeting the gray matter in the spinal cord and brain with minimal neuronal necrosis. As with the other cases, a viral etiology is suspected. The list of potential agents is large and includes Morbillivirus, Herpesvirus, Enterovirus, Flavivirus, Alpha-herpesvirus, Paramyxovirus, Adenovirus, or an unidentified viral agent. Identifying the agent may be a difficult task should “routine” testing for Herpesvirus, Morbillivirus, and Enterovirus prove unsuccessful. The absence of inclusions (Herpesvirus, Morbillivirus, Adenovirus) and synctia (Morbillivirus) does not fully support these viral agents. PCR, Immunohistochemistry, and viral isolation could prove very beneficial in these cases. Submission of fresh tissue for viral isolation may also be recommended. While considered much less likely, bacteria, toxins, and parasitic (aberrant migration) agents are mentioned for the sake of completeness. There was evidence of a verminous pneumonia which is not an uncommon finding. The pulmonary hemorrhage, edema, and fibrin exudation represents a fairly acute response in this animal and may represent a separate response from the parasitic infiltration. Inflammation of the duodenum, jejunum, and forestomach was observed and may have led to inanition and malabsorption (supporting the gross findings of lack of contents). Finally, there were scattered foci of interstitial infiltrates within the kidney. This is a non-specific change that may be a result of prior infection. This was not a diffuse or severe change and likely had a small effect upon renal function.
WAM 602 - 23 - 04-7C Anthracosis and larval migration (mesenteric) were observed in the lymph nodes. Anthracosis and silicosis represents inhalation of carbon and silicon particulates from anthropogenic sources. While the reaction may be locally severe, unless there is a marked inflammatory response in the lung resulting in the production of cytokines and fibroblast growth factors, the effect upon the animal is minimal. I have observed mesenteric granulomas in a number of cetaceans and the cause has always eluded me until this case. This may represent a typical migration pattern or an aberrant migration of a gastrointestinal nematode like Anisakids. In humans, this migration is considered abnormal and represents an extragastrointestinal migration.1
Granulomas were observed in the serosa of the colon, esophagus, and pancreatic lymph node. A causative agent, a cestode, was found in the serosa of the colon and likely, the esophageal granuloma has a similar causation. The pancreatic lymph node granuloma may be the result of parasitic migration, bacterial or fungal infection. An etiologic agent was not evident. 1A case of extragastrointestinal anisakiasis involving a mesocolic lymph node Kim HJ, Park C, Cho SY. Korean J Parasitol 35 (1): 63-66 (Mar 1997), PENDING TESTS-PATHOLOGIST
TEST PURPOSE SITE RESULT Histology, Brain NCSU Received 1
Oct2004 DATE: REPORTING PATHOLOGISTS: Prelim: 4 Oct 2004 David S. Rotstein, DVM, MPVM, DACVP Mac Law, DVM, PhD, DACVP (Brain)
