Abstract. Necropsy of 2 white-tailed deer fawns who died acutely revealed diarrhea and melena in case No. 1 and no gross changes in case No. 2. Histologically, the livers of both deer displayed multifocal coagulative necrosis, with infiltrations of neutrophils, macrophages, and lymphocytes. By Warthin-Starry staining, bundles of filamentous bacteria were identified within hepatocytes at the periphery of the necrotic foci in case No. 1. There was multifocal myocardiocyte necrosis in case No. 1 and multifocal lymphoid necrosis of the Peyer's patches in case No. 2. Clostridium piliforme 16S ribosomal ribonucleic acid gene was detected in both livers by polymerase chain reaction (PCR) with C. piliforme-specific primers. The liver copper levels in both cases were normal to slightly elevated. The kidney copper level in case No. 2 was elevated. This represents the first published cases of Tyzzer's disease in deer, a novel use of PCR for the diagnosis of C. piliforme infection, and a possible association between copper toxicosis and Tyzzer's disease.

Abstract.A retrospective study revealed intestinal plasmacytosis in 53 of 102 rabbits used in various experimental studies and as controls. The breeds affected included New Zealand white (n = 46), Dutch-belted (n = 6), and Watanabe (n = 1) rabbits. Sex predisposition was not found in any breed. The mean (+ SD) ages were 3.1 I 1.4 years for New Zealand white rabbits, 1.3 +. 1.1 for Dutch-belted rabbits, and 2 years for the Watanabe rabbit. The severity increased with animal age. The incidence was higher ( P < 0.05) in rabbits used in antibody production and cholesterol studies. The lesions were characterized by multifocal to diffuse infiltration of well-differentiated plasma cells in the intestinal mucosa. Electron microscopic examination revealed typical plasma cell morphology of the infiltrating cells. Small intestine and cecum were the major sites affected. In severe cases, colon, rectum, trachea, esophagus, mesenteric lymph node, and spleen were also involved.Key words: Cecum; intestine; plasmacytosis; rabbits.The gut is continuously challenged immunologically with a myriad of dietary, microbial, and other environmental antigens and/or mi tog en^.^.^,^.^.^ As a part of the host mucosal immune system, gut-associated lymphoid tissues consist of inductive sites, e.g., Peyer's patches, appendix and solitary lymphoid nodules, and effector sites, e.g., the lamina propria.1.2,4.8 Under antigenic stimulation, naive T and B lymphocytes in the inductive sites undergo activation and differentiation into antigen-specific effector and memory T and B cells, including plasma cells. Activated T and B cells home to the effector sites via local and/or systemic circulation to mount a mucosal immune r e s~o n s e .~. * .~ Normally, plasma cells in the intestinal lamina propria constitute the largest plasma cell pool in the body, and most of these cells produce antigen-specific IgA.9 In this report, we describe plasma cell hyperplasia in the intestinal mucosa in 53 (52%) of 102 rabbits.Among the 102 rabbits studied retrospectively, 80 were New Zealand white (NZW), 14 were Dutch-belted (DB), and eight were Watanabe (WN) rabbits. The rabbits were supplied by eight commercial vendors. They were used or were planned to be used in various studies from 1988 to 1994 (Table 1). The rabbits were either found dead or euthanatized for evaluation of the concomitant diseases, e.g., anorexia, uterine carcinomas, mammary gland tumors, and pneumonia. Tissues were fixed in 10% neutral buffered formalin, embedded in paraffin, and stained with hematoxylin and eosin (HE). Selected tissue samples were fixed in Karnovsky's fixative for transmission electron microscopy. Histologic diagnosis of intestinal plasmacytosis was established by estimation: 1) if >50% of the infiltrating cells in the lamina propria were plasma cells and 2) if the plasma cells infiltrated >25% of the lamina propria area in depth and/or length on a given histologic section (Figs. 1-4). Data were analyzed with a two-tailed t-test (Statwork@, Cricket, Philadelphia PA) and x2 test.I...

In the present case the rapid development of the fibrous stricture of the pyloric antrum and the pyloric stenosis can be seen by comparison of the two barium-meal examinations done 16 days apart. This clearly excludes a congenital abnormality. Summary A case of pyloric stenosis and fibrous stricture of the pyloric antrum developing in under two months in a child after swallowing compound ferrous sulphate tablets is described. Death was due to acute suppurative peritonitis following jejunostomy.The literature on ferrous sulphate poisoning and fibrous stricture of the stomach due to the ingestion of corrosive poisons is briefly reviewed.

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