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WSC 11-12 Conf 14 Layout Joint Pathology Center Veterinary Pathology Services WEDNESDAY SLIDE CONFERENCE 2011-2012 Conference 14 25 January 2012 CASE I: NADC MVP-2 (JPC 3065874). Gross Pathology: The deer was of normal body condition with adequate deposits of body fat. There Signalment: 5-month-old female white-tailed deer was crusty exudate around the eyes. Multifocal areas (Odocoileus virginianus). of hemorrhage were seen in the heart (epicardial and endocardial), lungs, kidney, adrenal glands, spleen, History: Observed depressed, listless. Physical exam small and large intestines (mucosal and serosal revealed fever (102.5 F), mild dehydration, normal surfaces) and along the mesenteric border, mesenteric auscultation of heart and lungs, no evidence of lymph nodes and iliopsoas muscles. Multifocal ulcers diarrhea. Treated with IV fluids, antibiotics and a non- were present in the pyloric region of the abomasum. steroidal anti-inflammatory drug. Deer died within 5 hours. Laboratory Results: PCR for OvHV-2: positive PCR for EHV: negative PCR for Bluetongue virus: negative PCR for BVD: negative Contributor’s Histopathologic Description: Within the section of myocardium there is accentuation of medium to large arteries due to the infiltration of the vascular wall and perivascular spaces by inflammatory cells. Numerous lymphocytes and fewer neutrophils invade, and in some cases, efface the vessel wall. Fibrinoid degeneration and partially occluding fibrinocellular thrombi are present in the most severely affected vessels. Less affected vessels are characterized by large, rounded endothelial cells and intramural lymphocytes and neutrophils. Within the myocardium are multifocal areas of hemorrhage and scattered infiltrates of lymphocytes and macrophages. 1-1. Heart, white-tailed deer. Necrotizing arteritis characterized by Contributor’s Morphologic Diagnosis: marked expansion of the wall by brightly eosinophilic protein, numerous inflammatory cells, and cellular debris (fibrinoid necrosis). (HE 67X) Myocardium: Arteritis and periarteritis, fibrinonecrotic, 1 WSC 2011-2012 1-2. Heart, white-tailed deer. Higher magnification of affected myocardial artery with effacement of the muscular wall by abundant clinical disease in white-tailed deer8, and an MCF virus subintimal proein, neutrophils, macrophages, and cellular debris (fibrinoid necrosis). (HE 172X) endemic in goats, provisionally known as caprine herpesvirus-2 (CpHV-2) has been associated with chronic alopecia in sika and white-tailed deer.5,6 The lymphocytic, multifocal, acute, moderate to severe, literature on MCF contains descriptions of various with fibrinoid degeneration, thrombosis and manifestations of disease with diverse organ myocardial hemorrhage, white-tailed deer (Odocoileus involvement. The variable nature of disease virginianus). expression is thought to result from multiple regulatory genes in gammaherpesviruses acquired during Contributor’s Comment: Malignant catarrhal fever evolution. Cell type as well as host species may alter (MCF) is the clinical manifestation of the infection of the expression of these genes.6 certain ruminant species with one of a group of pathogenic gammaherpesviruses known as MCF Deer infected with OvHV-2 can have a variety of viruses. Most domestic cattle and numerous exotic clinical signs. Typically, the affected animal is species of ruminants are susceptible to clinical disease lethargic, febrile with diarrhea that is often watery or that may be sporadic or occasionally epidemic in contains blood. Death usually occurs within 48 hours. nature. Clinical disease can range from peracute to Animals that live longer may have excessive watery to chronic and has been reported in various species of mucous discharge from the eyes, mouth and nose. cervidae including white-tailed deer, black-tailed deer, Mucosal erosions or ulceration may be present in the mule deer, reindeer, muntjac deer, sika deer, Shira’s nose, oral cavity or anywhere in the gastrointestinal moose, Pere David’s deer, swamp deer, rusa deer, and tract. Corneal opacity may lead to blindness in one or red deer.1,2,4,6,7,13,14,15 The disease is characterized both eyes. Compared to cattle, MCF in deer is usually primarily by lymphoproliferation, mucosal an acute disease with animals showing few clinical inflammation and vasculitis. Historically, 2 MCF signs before death. Lesions are more hemorrhagic and viruses have been associated with clinical disease, one involve the viscera of the gastrointestinal tract. MCF endemic in wildebeest, known as alcephaline in cattle is less acute and the severity of visceral herpesvirus –1 (AIHV-1), and the other endemic in lesions is decreased. Clinical signs in cattle are sheep, ovine herpesvirus-2 (OvHV-2) known as sheep- variable. Grossly, MCF in cattle produces enlarged associated MCF (SA-MCF). Only AIHV-1 has been lymph nodes, corneal edema, cutaneous crusts and propagated in vitro and partially characterized. hyperemia, oral hyperemia and ulceration, OvHV-2 is the major MCF virus worldwide. Recently, mucopurulent nasal discharge, and erosive or however, 2 additional members of the MCF virus ulcerative lesions throughout the digestive system. group have been associated with clinical disease in deer. An MCF virus of unknown origin that causes Deer acquire the infection through direct or indirect 2 WSC 2011-2012 contact with the reservoir species, most commonly The most common sites for vascular lesions are the sheep. Reservoir species remain infected with the brain and leptomeninges, carotid rete, kidney, liver, virus but do not show any clinical signs. Research adrenal capsule and medulla, salivary gland, and any suggests that deer with MCF do not transmit the virus section of skin or alimentary tract with gross lesions. to other deer. Sheep between the ages of 6 and 9 Lymphocytic infiltrates are also present in the kidneys, months of age shed much more virus than do sheep of periportal areas of the liver, gastrointestinal mucosa, other ages and therefore are considered most dermis, meninges, and heart. Microscopic lesions seen dangerous to deer and other susceptible species.9,10 in other areas are an active proliferation of Nasal secretions are the predominant vehicle by which lymphoblasts in lymph nodes, especially in T cell- virus is spread from sheep to other species.9,10 There is dependent areas of interfollicular and paracortical some evidence that MCF viruses may be spread by zones; and lymphocytic uveitis with exudate from aerosol over significant distances. Research on MCF ciliary processes into the filtration angle, resulting in in bison has documented transmission over distances corneal opacity of the eye.3,12,17 of 2.5 to 3 miles, against prevailing winds and in the absence of common water sources suggesting that In MCF, the virus is usually associated with some mechanisms of transmission remain undefined. lymphocytes in adults, and primary viral replication occurs in small and medium-sized lymphocytes. T- Recent research suggests that some susceptible species lymphocyte proliferation is likely secondary to may be latently infected with virus and that there may infection of large granular lymphocytes, which have T- be recrudescence of disease during periods of stress. suppressor cells and natural killer cell activity. Viral Much remains unknown concerning latent infections in infection and dysfunction of these cells causes susceptible species. The incubation period (time from lymphoproliferation, T-suppressor cell dysfunction, infection to the manifestation of clinical disease) is and necrosis. Thevasculitis is presumed to be immune- unclear and can be quite variable, ranging from a few mediated, but demonstration of immunoglobulin and days to several months. In some species clinical signs complement components has been inconsistent.16 have been seen as late as 8 months after exposure to infected sheep. In the present case deer were housed Contributor: National Animal Disease Center on a pasture that was within 50 yards of a pasture 2300 Dayton Avenue containing sheep. Lambing had occurred on the Ames, IA 50010 pasture approximately 6 months earlier. Six-month-old www.nadc.ars.usda.gov lambs were still present on the sheep pasture. References: Differential diagnosis for diseases that cause ulceration 1. Beatson NS. Field observations of malignant and necrosis of the oral and gastrointestinal mucosa catarrhal fever in red deer in New Zealand. Biol of and hemorrhage in deer and other ruminants include Deer Prod. 1985;22:135-137. epizootic hemorrhagic disease in deer, bluetongue, 2. Brown CC, Bloss LL. An epizootic of malignant bovine virus diarrhea-mucosal disease, rinderpest, and catarrhal fever in a large captive herd of white-tailed vesicular diseases. Important vesicular diseases to deer (Odocoileus virginianus). J Wildl Dis. 1992;28(2): consider are foot and mouth disease and vesicular 301-305. stomatitis, which are grossly indistinguishable from 3. Gelberg HB. Alimentary system and the peritoneum, one another. omentum, mesentery, and peritoneal cavity. In: McGavin MD, Zachary JF, eds. Pathologic Basis of JPC Diagnosis: Heart: Arteritis, necrotizing and Veterinary Disease. 4th ed. vol. 1. St. Louis, MO: proliferative, multifocal, severe, with thrombosis and Elsevier; 2012:1078, 1118. mild multifocal myocarditis. 4. Jessup DA. Malignant catarrhal fever in a free- ranging black-tailed deer (Odocoileus hemionus Conference Comment: Histologically, malignant columbianus) in California. J Wildl Dis. 1985;21(2): catarrhal fever (MCF) typically presents
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