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C O N F E R E N C E 5 26 September 2018 Joint Pathology Center Veterinary Pathology Services WEDNESDAY SLIDE CONFERENCE 2018-2019 C o n f e r e n c e 5 26 September 2018 CASE I: 1505184 (JPC 4066664-00). Gross Pathology: Autopsy of the euthanized herdmate (heifer B) revealed severe crusting Signalment: 14-month-old Holstein heifer. and ulcerative dermatitis and stomatitis including the following locations: History: Two 14-month-old Holstein heifers perineal/perivulvar, periocular, mammary, were presented to the large animal clinic as perinasal/perioral and tongue. In addition, representatives from a heard outbreak, which large raised to crateriform ulcers with affected five other heifers on the farm who adherent diphtheritic membranes were had more severe signs and had subsequently present throughout the rumen, as well as died or were euthanized. This heifer (heifer generalized lymphadenopathy, splenomegaly A) died immediately prior to transit to the and corneal edema. Autopsy of the clinic, and had no known clinical signs. Her spontaneously dead heifer (heifer A) revealed live herdmate (heifer B) had a 2-week- meningeal edema and hyperemia with duration of clinical signs of unthriftiness, oral cerebellar coning, consistent with cerebellar and cutaneous ulcers with ptyalism, and ocular signs including squinting, epiphora, and corneal ulcers. On physical exam, this heifer B was tachycardic and tachypneic with a rectal temperature of 103° Fahrenheit and generalized peripheral lymphadenomegaly. Heifers involved in the outbreak were also reported to have had cloudy eyes and appeared to be blind. Also housed in close physical proximity to the heifer herd were 5 sheep that had recently lambed. No treatments were performed at this time, and Cerebellum and trachea, ox. Sections of cerebellum and due to suspicion for malignant catarrhal trachea are submitted for examination. Congestion and fever, the live herdmate was euthanized hemorrhage within the cerebellar leptomeninges as well as the tracheal submucosa are evident at low without further clinical diagnostics or magnification. (HE, 5X) treatment. 1 herniation. The brain did not autofluoresce virus (Indiana or New Jersey strains) or under exposure to ultraviolet light. epizootic hemorrhagic disease of deer virus. Virus isolation performed on fresh lung, Laboratory results: A panel including liver, kidney and spleen sections harvested serology and PCR tests was submitted on immediately postmortem were negative for blood drawn from the live heifer (heifer B) bovine viral diarrhea virus (BVDV) and immediately prior to euthanasia. A nested infectious bovine rhinotracheitis (IBR) virus. PCR test was positive for ovine herpesvirus- 2 malignant catarrhal fever (MCF) virus, and Microscopic Description: Cerebellum, negative for the alcelaphine herpesvirus-1 Trachea (heifer A): Within the cerebellar and 2 MCF viruses. Coronavirus PCR tests leptomeninges and tracheal mucosa and performed on intestinal contents were also submucosa, there is marked vasculitis with negative. ELISA serology tests detected edema, multifocal to coalescing lympho- antibodies for bluetongue virus; however, histiocytic infiltrates and hemorrhagic foci. PCR tests performed on serum for The vasculitis is characterized by moderate bluetongue virus were negative. No serum numbers of lymphocytes, histiocytes, plasma antibodies were detected by ELISA for foot cells and neutrophils that expand the tunica and mouth disease virus, vesicular stomatitis adventitia and transmigrate through the walls Cerebellum, ox. Higher magnification of the leptomeninges with abundant hemorrhage, and a lymphohistiocytic infiltration which extends down into Virchow-Robin’s Space. There is protein and cellular debris in the wall of a small arteriole (vasculitis) and an infiltrate of lymphocytes and plasma cells in the leptomeninges as well as the adjacent Virchow-Robins’ space. (HE, 215X) 2 of varying caliber arterioles and venules. Segments of vascular walls demonstrate pyknosis and karyorrhexis with fibrinoid necrosis and hemorrhagic foci that are also scattered within the cerebellar parenchyma. Numerous discrete clear vacuoles surround Purkinje cells, which often demonstrate cytoplasmic hypereosinophilia (degeneration). The tracheal mucosal Trachea, ox. There is segmental necrosis of ciliated epithelium is multifocally attenuated, with epithelium, and infiltration of the mucosa and underlying submucosa with numerous lymphocytes, and fewer loss of apical cilia, or necrotic and denuded histiocytes and neutrophils. There is also submucosal and replaced by eosinophilic and hemorrhage and edema. (HE, 216X) karyorrhectic debris, necrotic neutrophils and extravasated erythrocytes. Similar Contributor’s Morphologic Diagnoses: inflammatory populations surround and Cerebellum: Moderate-severe lympho- infiltrate seromucinous glands. histiocytic meningitis and segmental necrotizing vasculitis with multifocal acute- The kidney and urinary bladder from heifer A subacute hemorrhage. had similar vascular changes as described above in addition to multifocal associated Trachea: Moderate multifocal acute erosive interstitial inflammation with tubular and ulcerative tracheitis with severe necrosis and regeneration in the kidneys, and lymphohistiocytic necrotizing vasculitis, ulceration of the transitional epithelium of perivasculitis and adenitis. the urinary bladder with submucosal hemorrhage. Similar vascular changes and Contributor’s Comment: Malignant inflammatory infiltrates were also present in catarrhal fever (MCF) is a highly fatal the cutaneous, oral and rumen lesions of lymphoproliferative viral disease reported heifer B, and the choroid of both eyes. In skin worldwide affecting many wild and captive and mucosal lesions, inflammatory infiltrates species of the order Artiodactyla.5,9 The MCF often extended from the submucosa and virus group comprises ten gamma- dermis into the overlying herpesviruses, belonging to the recently epidermis/epithelium, occasionally blurring assigned Macavirus genus4,6,7, six of which the basement membrane. The epidermis and are naturally pathogenic.5,8 These include squamous mucosa of the tongue and rumen alcelaphine herpesvirus-1 (AIHV-1), frequently contained deep erosions to ulcers alcelaphine herpesvirus-2 (AIHV-2), ovine covered by waves of serocellular crusts herpesvirus-2 (OvHV-2), caprine containing colonies of bacteria, grit and herpesvirus-2, (CpHV-2), MCF of white- fragments of plant material. In other regions tailed deer (Odocoileus virginianus) (MCFV- there was multifocal keratinocyte necrosis WTD), and ibex-MCFV. Experimental within all layers of the epidermis/epithelium infection with hippotragine herpesvirus-1 characterized by cytoplasmic hyper- (HipHV-1) in domestic rabbits (Oryctolagus eosinophilia with loss of intercellular cuniculus) is documented, but no natural desmosomes and pyknosis. Marked infections have been reported.5,9 Non- paracortical hyperplasia was observed within pathologic members include: gemsbok-MCF, enlarged peripheral lymph nodes of heifer B. muskox-MCF, and aoudad-MCF, also named 3 after their respective carrier species.5,9 generalized lymphadenopathy are Identified natural host species including characteristic of the intestinal form, and wildebeest (Connochaetes taurinus), severe nasal mucosal inflammation and domestic sheep (Ovis aries), wild and hemorrhagic gastroenteritis are characteristic domestic goats (Capra hircus) and roan of the peracute form. Hematuria, stranguria, antelope (Hippotragus equinus) are a source and convulsions can also be seen.9 In cattle of infection for susceptible, poorly adapted infected with OvHV-2, there is usually an species such as American bison (Bison acute onset of clinical signs, but experimental bison), many cervids, and domestic cattle studies show that some animals may present (Bos taurus). with disease months after infection.9 Of paramount economic importance to those Bison are 100 times more likely to become managing bison, deer, and exotic game infected, and 10,000 times more susceptible farms, as well as zoological collections, are to developing MCF than cattle5, but alcelaphine herpesvirus-1 (AIHV-1) and experimentally-induced MCF with OvHV-2 ovine herpesvirus-2 (OvHV-2), the causative in bison yields milder clinical signs agents of wildebeest-associated MCF (WA- (oculonasal discharge, peripheral MCF), and sheep-associated MCF (SA- lymphadenopathy) and vascular lesions MCF) respectively. Susceptibility to (arteritis, phlebitis) than in cattle.9 CpHV-2 infection by pathogenic MCF viruses and harbored asymptomatically in wild and development of disease in non-reservoir domestic goats infects many species of deer hosts varies.5 In general, Bali cattle/banteng and manifests usually as chronic weight loss, (Bos javanicus), white-tailed deer dermatitis and alopecia.5 Goats also harbor (Odocoileus virginianus), Pere David's deer OvHv-2, and may be the source of infection (Elaphurus davidianus), and American bison for white-tailed deer in MCFV-WTD, which are highly susceptible to disease following is now known to affect other cervids such as infection; water buffalo (Bubalus bubalis), the red brocket deer and many cervids are intermediately (Mazama americana).5 CpHV-2 has also susceptible; domestic cattle and pigs (Sus been linked to a recent report of MCF in a scrofa) are mildly susceptible; and fallow captive deer (Dama dama) are resistant.5,9 pudu (Pudu puda). It is important to note that Additionally, laboratory animals such as viral shedding of OvHV-2 and AIHV-1 does rabbits
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