Mast cell tumors are among the most commonly seen tumors of the skin in dogs and are more highly aggressive than mast cell tumors of other species. Some breeds display a markedly higher incidence of mast cell tumor development than others and appear to have some genetic predisposition. Recently, mutations have been found in canine mast cell tumor tissues and cell lines within the juxtamembrane domain of the protooncogene c-KIT In previous studies utilizing a small number of cases, no association between the presence of a mutation and the breed of dog or grade of the tumor could be identified. An expanded study with a larger sample set was performed to explore this possibility. The juxtamembrane domain of c-KIT was amplified using the polymerase chain reaction from genomic DNA preparations of 88 paraffin-embedded mast cell tumors from selected breeds. Mutations, consisting of duplications and deletions, were found in 12 of the tumors. A significant association was found between the presence of a mutation and a higher grade of tumor but not between breed and grade or between breed and the presence of a mutation.

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We evaluated the effects of feeding farm-raised mink (Mustela vison) diets containing polychlorinated biphenyl (PCB)-contaminated fish from the Housatonic River (HR; Berkshire County, MA, USA) on adult reproductive performance and kit growth and survival. Diets contained 0.22-3.54% HR fish, providing 0.34-3.7 microg total PCBs (TPCB)/g feed wet wt (3.5-68.5 pg toxic equivalence [TEQ]/g). Female mink were fed diets before breeding through weaning of kits. Twelve kits from each treatment were maintained on their respective diets for an additional 180 d. Dietary PCBs had no effect on the number of offspring produced, gestation period, or other measures of adult reproductive performance. Mink kits exposed to 3.7 microg TPCB/g feed (68.5 pg TEQ/ g) in utero and during lactation had reduced survivability between three and six weeks of age. The lethal concentrations to 10 and 20% of the population (LC10 and LC20, respectively) were estimated to be 0.231 and 0.984 microg TPCB/g feed, respectively. Because inclusion of PCB-contaminated fish that composed approximately 1% of the diet would reduce mink kit survival by 20% or more, it is likely that consumption of up to 30-fold that quantity of HR fish, as could be expected for wild mink, would have an adverse effect on wild mink populations.

Brief communications 303 perimental placentitis. Bacterial replication occurs in rough endoplasmic reticulum. Am J Pathol 124:226-237. for Brucella abortus strain RB5. Vet Pathol 33:615. [Abstr.] 4. Chitwood MB, Lichtenfels JR: 1972, Identification of parasitic metazoa in tissue sections. Exp Parasitol 32:461-464. 5. Ewalt DR: 1989, Comparison of three culture techniques for the isolation of Brucella abortus from bovine supramammary lymph nodes. J Vet Diagn Invest 1:227-230. 6. Ewalt DR, Payeur JP, Martin MB, et al.: 1994, Characteristics of a Brucella species from a bottlenose dolphin (Tursiops truncatus). J Vet Diagn Invest 6:448-452. 7. Farrell ID: 1974, The development of a new selective medium for the isolation of Brucella abortus from contaminated sources. Res Vet Sci 16:280-286. 8. Fleischman RW, Squire RA: 1970, Verminous pneumonia in the California sea lion (Zalophus californianus). Pathol Vet 7:89-101. 9. Foster G, Jahans KL, Reid RJ, et al.: 1996, Isolation of Brucella species from cetaceans, seals, and an otter.

The effects of feeding ranch mink (Mustela vison) diets containing polychlorinated biphenyl (PCB)-contaminated fish (88 gold fish [Carassius auratus] weighing a total of 70.3 kg and 16 carp [Cyprinus carpio] weighing a total of 77.3 kg) collected from the Housatonic River (HR; Berkshire County, MA, USA) in October 1999 on organ weights and histology and hepatic concentrations of total PCBs (sigmaPCBs) and 2,3,7,8-tetrachlorodibenzo-p-dioxin toxic equivalence (TEQ) were evaluated. Diets contained 0.22 to 3.54% HR fish, which provided 0.34 to 3.7 microg sigmaPCBs/g feed (3.5-69 pg TEQ/g feed). Female mink were fed the diets eight weeks before breeding through weaning of kits at six weeks of age. Offspring were maintained on their respective diets for an additional 180 d. The dietary concentration of PCBs that caused a decrease in kit survival (3.7 microg EPCBs/g feed [69 pg TEQ/g]) resulted in a maternal hepatic concentration of 3.1 microg sigmaPCBs/g wet weight (218 pg TEQ/g). Organ weights were not consistently affected. Mandibular and maxillary squamous cell proliferation was apparent in 31-week-old juveniles exposed to as low as 0.96 microg sigmaPCBs/g feed (9.2 pg TEQ/g). Juveniles in this treatment group had a liver concentration of 1.7 microg sigmaPCBs/g wet weight (40 pg TEQ/g). Because inclusion of PCB-contaminated fish, which comprised approximately 1% of the diet, resulted in mandibular and maxillary squamous cell proliferation, it is possible that consumption of up to 30-fold that quantity of HR fish, as could be expected for wild mink, would result in more severe lesions characterized by loss of teeth, thus impacting survivability.