Joint Pathology Center Veterinary Pathology Services WEDNESDAY SLIDE CONFERENCE 2014-2015 Conference 9 9 November 2014 CASE I: AFIP-2 (JPC 4004343). left half of the cerebrum. No other gross lesions have been observed in the other organs of the deer Signalment: Male white-tailed deer, age examined. unknown, Odocoileus virginianus. Laboratory Results: The antigen ELISA for History: The animal has been submitted to CWD was negative, A. pyogenes and P. multocida necropsy with a history of CNS signs were isolated from the brain, and the result of ("Disoriented, weak, antlers caught in shrub"). fecal float showed rare strongyle-type ova and Strongyloides. No other ancillary tests have been Gross Pathology: The gross pathology of the performed on other organs. deer examined revealed inadequate body fat and 2.5 cm abscess filled with pus in the center of the 1-1. Cerebrum, deer: Centrally within the section, there is a focal, well-demarcated cellular infiltrate. (HE 6.3X) 1 WSC 2014-2015 antler pedicle (where the antler protrudes from the skull) or j u n c t i o n s b e t w e e n cranial bones that are referred to as “sutures”. Mortality generally occurs from fall (following velvet s h e d d i n g ) t h r o u g h spring (shortly after antler casting). Thus, the period when bucks are developing antlers or when antlers have hardened is when they are most susceptible to this disease.1 Certain buck behaviors, such as aggressive sparring and fighting, can cause damage to the antler pedicle and/or other parts of the skull that can predispose them to brain abscesses.1 Different studies, from 1996-2008, showed that 1-2. Cerebrum, deer: The cellular infiltrate is composed of degenerate neutrophils and abundant cellular debris, consistent with an abscess. (HE 196X) the intracranial abscesses were Histopathologic Description: Brain (cerebrum): diagnosed as the cause There is locally extensive necrosis of the nervous of death or illness in white-tailed deer examined tissue containing cellular debris with bacterial by the diagnostic laboratories across portions of colonization. The necrotic area is surrounded by a the United States and Canada. The bacterium wide zone of inflammatory cells, mainly Arcanobacterium pyogenes was the primary cause composed of neutrophils with fewer lymphocytes of infection.1,2,3,5 and macrophages. There is diffuse intravascular lymphocytic cuffing. The clinical signs include several behavioral characteristics associated with the neurological Contributor’s Morphologic Diagnosis: system, such as “circling” or loss of coordination. Encephalitis, locally extensive, necrotizing, Often times, deer can become emaciated, which is subacute with granulation tissue (capsule) characterized by excessive weight loss or having a formation and bacterial colonization. “deteriorated” appearance. Bucks also may have a puss-like substance located around the antler Contributor’s Comment: Brain abscess-related pedicle that leaks through openings in the skull. It mortality is a growing concern of deer managers is not known whether this disease can be and biologists across the country. Brain abscesses transmitted between deer or other animals through are caused by a variety of bacteria (primarily direct contact or other sources. Also, it is Arcanobacterium pyogenes) that naturally inhabit important to note that deer with brain abscesses the skin of deer, as well as other animals.1,2,3,5 are not recommended for consumption.1 These bacteria typically enter the brain through lesions and skin abrasions associated with the 2 WSC 2014-2015 numbers of brain abscesses occurring in mature males. Recently, a study of 26 collared bucks over 2.5 years old identified brain abscess as the cause of death in 35% of cases, likely related to the increased competition among mature bucks.5 Arcanobacterium pyogenes is the most commonly cultured isolate from brain abscess, being the only isolate in almost 50% of cases.2 The bacterium has been through a series of name changes, and has recently been reclassified as Trueperella pyogenes based on DNA sequencing and mass spectrometry.4 Contributing Institution: Animal Disease Research and Diagnostic Laboratory-Veterinary & 1-3. Cerebrum, deer: Cerebral abscesses lack a capsule due to the lack Biomedical Sciences Department of fibroblasts in the brain; there are areas of liquefactive necrosis infiltrated by large numbers of Gitter cells in the adjacent white matter. South Dakota State University (HE 256X) http://www.sdstate.edu/vs/ The clinical, gross examination and ancillary tests References: findings were compatible with the previous 1. Basinger R. Brain Abscesses – A potential studies. thorn in the side of intensive deer management programs. Westervelt Wildlife Service. 2009;9:26– Note: Multiple blocks were used for the slides 31. submission; therefore, not all the participants will 2. Baumann CD, Davidson WR, Roscoe get the same copy of the slides. DE, Beheler-Amass K. Intracranial abscessation JPC Diagnosis: Brain, midbrain: Abscess, in white-tailed deer of North America. J Wildl focally extensive, with gliosis, spongiosis, Dis. 2001;37(4):661–70. nonsuppurative perivascular cuffing, and 3. Hattel AL, Shaw DP, Love BC, Wagner DC, numerous colonies of bacilli. Drake TR, Brooks JW. A retrospective study of mortality in Pennsylvania captive white-tailed Conference Comment: The contributor deer (Odocoileus virginianus): 2000–2003. J Vet highlights the disease pathogenesis in this case as Diagn Invest. 2004;16:515–521. associated with antler development and biologic 4. Hijazin M, Hassan AA, Alber J, et al. behavior in this species. A second possible Evaluation of matrix-associated laser desorption pathogenesis discussed by conference participants ionization-time of flight mass spectrometry is a hematogenous route, likely subsequent to oral (MALDI-TOF MS) for species identification of infection. Oral mucosal damage or severe dental bacteria of genera Arcanobacterium and disease could potentially lead to bacterial emboli Trueperella. Vet Microbiol. 2012;157(1-2): seeding in the brain and inducing a lesion such as 243-245. is observed in this case. 5. Karns GR, Lancia RA, Deperno CS, Conner MC, Stoskopf MK. Intracranial abscessation as a For a deer exhibiting neurologic symptoms, the natural mortality factor for adult male white-tailed differential of Listeria monocytogenes must also deer (Odocoileus virginianus) in Kent County, be considered. Lesions of listeriosis are typically Maryland, USA. J Wildl Dis. 2009;45(1):196– smaller (microabscesses) and confined to the 200. brainstem. There is an increasing trend for hunters and property owners to allow bucks to reach a more mature age before harvesting to improve herd health and antler quality.1 Associated with the trend is the unintended consequence of increased 3 WSC 2014-2015 CASE II: 66400 (JPC 4048574). coalescing areas of petechial hemorrhage. Atrioventricular and semilunar valves are Signalment: 8 year-old female African black- unremarkable. footed penguin. Histopathology: Multifocal areas of History: This penguin has a history of degeneration, necrosis and inflammation centered intermittent seizures, mild anemia, severe on capillaries disrupt approximately 20 – 30% of leukocytosis and hyperglobulinemia. Recently the the left and right ventricular myocardium. Areas penguin presented with increasing frequency of of degeneration and necrosis are characterized by seizures, acute facial swelling, lethargy, pale cardiomyocytes with extensive vacuolation inappetance and weight loss (BCS 3/9). The of the sarcoplasm (degeneration), loss of cross penguin was treated with supportive care as well striations, fragmented, hypereosinophilic fibers, as doxycycline, enrofloxacin, itraconazole, pyknotic nuclei, scattered karyorrhectic nuclear terbinafine, and amphotericin B for suspected debris (necrosis) and occasional degenerate aspergillosis and avian malaria. The penguin did heterophils. Multifocally, surrounding blood not respond to therapy and ultimately died. vessels are infiltrated by moderate numbers of macrophages, lymphocytes, plasma cells, and Gross Pathology: The animal is in poor body heterophils. Multifocally, within these areas of condition and there are minimal subcutaneous fat inflammation, there are numerous endothelial stores. A focally extensive, 5 x 5 cm focus of wet, cells displaying abundant vacuolated cytoplasm gelatinous subcutaneous tissue (edema) is noted often expanded by oval to round, 15 – 25 µm thin over the keel. Upon opening the coelomic cavity, wall (1 µm) cysts (schizont) containing between approximately 100 ml of transudate primarily 15 – 30 1 – 2 µ m, round, basophilic located within the pleura surrounding the heart apicomplexans (merozoites). Some sections contain a focal, 1 – 2 mm, intravascular aggregate of basophilic to granular material surrounded by layers of fibroblasts, myoepithelial cells, fibrin, and scattered erythrocytes (thrombus), which occludes 80% of a medium caliber artery. Scattered lymphocytes are present within the endocardium. Multifocally separating muscle fascicles and in between blood vessels there are moderate amounts of edema, scattered hemorrhage and numerous small foci of fibrin localized in and around necrotic endothelial cells. Morphologic Diagnosis: Heart, myocarditis, necrotizing, chronic, multifocal, moderate with lymphohistiocytic and heterophilic infiltrate, fibrin deposition, edema, hemorrhage, thrombosis and intra- endothelial, extra-erythrotic schizonts. 2-1. Heart, penguin: The myocardium contains