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Campylobacter jejuni was inoculated intravenously into pregnant ewes on gestation days 1 14 and 123 to reproduce ovine abortion. All ewes aborted 7-1 2 days post-inoculation. High numbers of C. jejuni were isolated from ewe tissues (caruncle, bile, cecal feces), fetal tissues, and placenta. C. jejuni colonies were identified in caruncles and placenta by light microscopy and immunoperoxidase techniques. Histologically, inoculated ewes had a severe purulent endometritis with vasculitis. Placentas from inoculated ewes and field cases showed necrosis and purulent inflammation; however, placentas from inoculated ewes had large numbers of bacterial colonies compared to few bacteria found in field cases. Histologically, only one fetus from the inoculated ewes showed lesions (purulent bronchopneumonia), whereas all fetuses from field cases had a distinct bronchopneumonia, and one fetus showed multifocal hepatic necrosis. These results suggest that C. jejuni (serotypes Penner 1 and Lior 2) is an important abortifacient organism for sheep. Campylobacteriosis is a highly contagious and economically significant disease in sheep and is most often caused by Campylobacter fetus subspecies fetus (previously named C. fetus var. intestinalis).15.32 It is characterized by abortion (third trimester), stillbirths, premature births, weak lambs, and occasional ewe deaths due to m e t r i t i~. '~,~~ Grossly, aborted or stillborn fetuses may have no lesions or they may show subcutaneous serosanguineous edema, serosanguineous body fluids, discrete necrotic liver lesions, or bronchopneumonia. Placental cotyledons are enlarged, yellowish, and covered with blood-tinged exudate, while the intercotyledonary stroma is edematous. Microscopically, placental lesions, which are predominant in hilar zones, consist of septa1 necrosis, arteriolitis, leukocyte infiltration, and accumulation of high numbers of bacteria within lacunae, chorionic trophoblasts, and endothelial cells. In humans, Campylobacter jejuni is recognized to be a common cause of acute dia~-rhea,~J~ and is associated with abortion and neonatal sepsis.33 Campylobacter organisms are small, curved, highly motile, noncapsulated, microaerophilic, gram-nega

Five of six immunodeficient Arabian foals that died of adenoviral infection were found to be infected with an intestinal coccidian of the genus Cryptosporidium. Various developmental stages of the organism were found in the microvillous border of the intestinal mucosa. The foals had diarrhea but it was not possible to separate the effects of the cryptosporidial infection from those of the concomitant adenoviral enteritis.

Infiltrative lipomas, similar to those described in man, were diagnosed in 12 dogs of various breeds, sexes, and ages. The neoplasms were poorly delineated, soft enlargements in muscle and connective tissue that caused dysfunction because of mechanical interference or pressure pain. The neoplasms consisted of differentiated fat cells that had infiltrated between or replaced muscle, collagen fibers or both. Single or multiple recurrences followed surgical removal in four of eight dogs: no follow-up was possible in the other four.

Spontaneous paratuberculosis was studied in free-ranging and captive bighorn sheep (Ovis canadensis), and Rocky Mountain goats (Oreamnos americanus). Lesions of paratuberculosis in these species resembled the disease in domestic sheep and goats. Mycobacterium paratuberculosis cultured from bighorn sheep was used to orally infect bighorn x mouflon (Ovis musimon) hybrid sheep, elk (Cervus elaphus nelsoni), mule deer (Odocoileus hemionus), and white-tailed deer (Odocoileus virginianus). Clinical paratuberculosis developed only in mule deer and was characterized by poor growth and diarrhea. Gross lesions were mild in all species. Enlargement of mesenteric lymph nodes was mild to moderate; the wall of the distal small intestine was affected minimally. Focal to diffuse infiltrates of epithelioid macrophages and giant cells occurred in the cortex of mesenteric lymph nodes, around mesenteric lymphatics, and in the intestinal mucosa. Extraintestinal lymph nodes, spleen, liver, and lung were involved in some animals; focal necrosis and mineralization was present in all species but was severe and widespread in the cervids.

The medical records of eight horses with histological evidence of myodegeneration of the masseter muscles were examined. While they were alive their most common clinical signs had included difficulty in eating or opening their mouths, weight loss, difficulty in moving, and noticeable atrophy of the masseter muscles. The serum activities of muscle enzymes were abnormally high in all of the horses. Whole blood and/or liver selenium and vitamin E concentrations were less than the reference ranges in some of the horses. The lesions varied with the stage of the disease and consisted of swelling and discoloration, or muscle atrophy and fibrosis. Histologically, the muscle changes ranged from acute to subacute degeneration, with regenerative changes accompanying ongoing degeneration, to chronic degeneration with fibrotic replacement of muscle tissue. There were changes in the masseter muscle of all the horses, but some had widespread lesions in skeletal muscle, and a few also had myocardial lesions.

Abstract. A dog with a lymphoproliferative disease resembling the Skzary syndrome variant of mycosis fungoides in man had large numbers of circulating morphologically abnormal lymphoid cells, multicentric cutaneous nodules and plaques, and extracutaneous involvement of lymph nodes and viscera. The presence of Pautrier's microabscesses, intracutaneous hyperchromatic cells, and leukemic cells with convoluted nuclei distinguished the disease from other types of cutaneous lymphoma.