Tritrichomonas foetus is the causative agent of bovine trichomonosis. This protozoan is found in the preputial cavity of bulls and is transmitted to cows during coitus. Currently, the diagnosis of this parasite is based on microscopic examination of preputial washings or scrapings, but it was recently recognized that other trichomonads similar in size, shape, and motility to T. foetus can be present in preputial samples. Despite the serious consequences of an incorrect diagnosis for bovine trichomonosis, the precise speciation of these other trichomonads has remained uncertain. Here, a total of 12 non-T. foetus isolates were microscopically examined. On the basis of morphological criteria, seven of these isolates were identified as Tetratrichomonas sp., whereas four other isolates coincided with the description of Pentatrichomonas hominis. In the last isolate, a third non-T. foetus species was identified as belonging to the genera Pseudotrichomonas or Monocercomonas: the first time that species of either of these genera have been reported in preputial samples. To confirm these data, small subunit rRNA gene sequences were obtained by PCR from the 12 trichomonad isolates. These new sequences were analysed in a broad phylogeny including 72 other parabasalid sequences. From our phylogenetic trees, we confirmed the taxonomic status of non-T. foetus organisms isolated from preputial samples (Tetratrichomonas, Pentatrichomonas, and Pseudotrichomonas) and suggested the existence of two Tetratrichomonas species, despite their morphological similarity. The route of transmission of the non-T. foetus organisms identified in the bovine preputial cavity is discussed and we confirm that the PCR assay using the previously described T. foetus-specific primers TFR3 and TFR4 could be a useful alternative method for the diagnosis of bovine trichomonosis.

An outbreak of salmonellosis in foals occurred on a large Thoroughbred farm in California. Only foals less than 8 days of age exhibited clinical signs, which included depression, anorexia, and diarrhea. Three foals died from septicemia. The agent responsible was Salmonella ohio, which is rarely involved in salmonellosis in horses. During the course of the outbreak, S. ohio was isolated from 27 of 97 mares (27.8%) and 34 of 97 foals (35.1%). Mares were the presumed source of infection for foals. The absence of clinical signs in mares allowed for increased exposure of foals through environmental contamination. Although foals continued to become infected after strict control measures were adopted, none became ill. Salmonella serotypes of seemingly low virulence can produce serious disease outbreaks.

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Abstract. Two 6-month-old raccoon kits, which had been rescued and fostered in preparation for return to the wild, became acutely ill and died 3 weeks before scheduled release. At necropsy, the kits had grossly enlarged livers and spleens, diffusely consolidated lungs, and generalized lymphadenopathy. Histologically, extensive infiltrates of macrophages containing yeast organisms were identified in lung, liver, kidney, spleen, lymph nodes, intestinal tissues, brain, adrenal gland, bone marrow, and thymus of both animals. Histiocytic inflammation with accompanying fibrosis was widespread, with necrotic foci evident in lungs, spleen, and intestinal sections. Fungal organisms were observed on sheep blood agar plates; however, repeated subcultures to fungal media designed to induce conidial structures for fungal identification were unsuccessful. Partial DNA sequencing of the 28S ribosomal RNA gene of the blood agar isolate identified 100% homology with Ajellomyces capsulatus (anamorphic name Histoplasma capsulatum). The kits were rescued and fostered in the San Francisco Bay area and it is likely that the exposure to H. capsulatum occurred in this area. Histoplasma sp. infection in wild mammal species is often used as an indication of spore contamination of a geographic region. Northern California is not known to be an endemic region for H. capsulatum, which is not a reportable disease in this state. The presence of severe, disseminated disease and the need for molecular identification associated with the isolate from a nonendemic region identified in the present report may indicate genetic adaptation and altered characteristics of this agent and may warrant further investigation.