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Complications due to uterine leiomyomata in chimpanzees have rarely been documented. Here we describe a female chimpanzee that developed severe hydronephrosis in the right kidney due to leiomyoma. Because hysterectomy did not alleviate the hydronephrosis, nephrectomy was elected. After these procedures, the chimpanzee is doing well. Leiomyomata screening programs with treatment algorithms are a useful component of a comprehensive chimpanzee program.

A 10-y-old multiparous rhesus macaque presented for an annual routine physical examination. Clinically, the animal had pale mucous membranes, petechial and ecchymotic hemorrhages in multiple sites, and a laceration at the tail base. Severe pancytopenia was noted on hematologic evaluation. The monkey was seronegative for SIV, simian T-lymphotropic virus, simian retrovirus type D, and Macacine herpesvirus 1. Bone marrow evaluation revealed a paucity of megakaryocytic precursors in a hypercellular marrow with marked erythroid hyperplasia. In light of these findings, the diagnosis was acquired amegakaryocytic thrombocytopenia purpura. Due to the poor prognosis of the syndrome and clinical deterioration of the monkey, euthanasia was elected. A definitive cause of the thrombocytopenia was not identified; however, the syndrome may have developed secondary to a recent spontaneous abortion. To our knowledge, this case represents the first reported observation of acquired amegakaryocytic thrombocytopenia purpura in a rhesus monkey.

Among 585 sentinel ICR mice (Mus musculus), 8 (7 female, 1 male) had unusual microscopic lesions in the kidney. Light microscopy revealed occasional tubular epithelial cells with large, karyomegalic nuclei that contained intranuclear inclusions and marginated chromatin. These cells were randomly present in the cortex and medulla but were more prominent near the corticomedullary junc tion. Rare pyknotic cells and mild interstitial infiltrates of lymphocytes and plasma cells were associated with occasional foci of abnormal cells. Electron microscopy performed on 2 (1 female, 1 male) of the mice demonstrated intranuclear inclusions composed of abundant flocculent, electron-lucent material. No viral particles or other pathogens were identified. General health monitoring that included serology, microbiology, parasitology, necropsy, and histopathology was negative for pathogens. Polymerase chain reaction-based testing for polyomavirus and immunohistochemistry for adenovirus were performed on 5 of the 7 female mice; all were negative for both viruses. In light of microscopy findings and the lack of evidence for an infectious agent, the tubular lesions were considered degenerative changes, possibly due to a toxic insult. The cause and significance of the findings in these mice can not be explained fully.

During the last half-century pathologists have explored the biologic mechanisms associated with inherited human and veterinary diseases by using inbred and inbred mutant (spontaneous) strains of mice. The first successful gene transfer to mice by pronuclear injection of the herpes simplex virus thymidine kinase gene and rabbit and human beta-globulin genes was achieved in the early 1980s. This accomplishment was followed a few years later with the creation of a mouse bearing a disrupted hypoxanthine phosphoribosyl transferase (hrpt) gene (targeted mutation based on ES cell blastocyst injection). Since then, hundreds of genetically engineered models of biomedical importance have been created. The unprecedented scale and scope of development of engineered models present great opportunities as well as experimental challenges to the investigator. The aim of the present review is to provide a framework of information on engineered mouse models from the perspective of experimental and comparative pathology research. Sections include: 1) a brief historical account of the development of mouse models of disease, with increasing progression of genetic refinement as represented by inbred (spontaneous) and congenic (targeted) mutant strains of mice; 2) a synopsis of spontaneous and targeted mutations, with anecdotal examples of expression of individual genes and interactions between multiple mutant genes; 3) selected examples of targeted mutations of interest to developmental and cancer biologists and immunologists; 4) an overview of the technology of development of transgenic mice; and 5) an introduction to on-line database resources of current multi-species genomic information.

The incidence of primary renal neoplasia in animals is quite low. Carcinomas are the most common primary renal tumors of dogs, cattle, and sheep. Among rabbit tumors, only uterine adenocarcinomas occur more frequently than do embryonal nephromas. However, spontaneous renal cell carcinomas in laboratory rabbits have only been reported once previously. We here report a second occurrence of a renal cell carcinoma in the laboratory rabbit.