Seventy-nine spontaneous neoplasms in Dunkin-Hartley guinea pigs were observed over a 9-year period in the Fort Detrick guinea pig colony. Sixty-three of the neoplasms were found during approximately 8,500 necropsies performed on animals under 27 months of age. The remaining 16 tumors were in 34 breeders maintained after 27 months of age on a natural life-span study. Of this group, 10 (29.4%) developed neoplasms by the termination of the study, when the animals were 80 months of age. The skin tumor, trichofolliculoma, of which there were 29, comprised the largest tumor classification.

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189Summary A case of opocephaly in inbred guinea-pig strain 2jN and another in strain 13jN, a conjoined twin and an opocephaly concurrent with conjoined twins in the Dunkin-HartleyjFD strain are described. The incidence of congenital malformations in the inbred strain 2jN and strain 13jN was 0,0013 and 0,0073 % respectively. The incidence in the random-bred Dunkin-HartleyjFD strain was 0'0007%.Spontaneous congenital malformation of the guineapig have rarely been reported (Hoar, 1976). This is especially remarkable in view of the enormous numbers of guinea-pigs that are constantly being raised as laboratory animals. In a recent review of Case I. A conjoined twin Dunkin-HartleyjFD strain guinea-pig was found dead shortly after birth. The female twins had a single head with a broad face and 2 eyes. The upper abdomen was shared; the lower abdomen and hind quarters were separate and normally developed (Fig. ]). The fused thoracic cavities had 2 sterna, but only] normal respiratory system of larynx, trachea and lungs. There was a

The cause of a fatal condition characterized by hemorrhagic cardiomyopathy, hemothorax, and coagulation defects in hysterectomy-derived male mice was investigated. Microscopic heart alterations included multifocal hemorrhage and necrosis with variable degrees of acute inflammation and fibroplasia that were most severe in the region of the atrioventricular junction. A spontaneous outbreak was arrested by increasing menadione Na-bisulfite (vitamin K) in the feed to 20 ppm. The complete syndrome including hemorrhagic cardiomyopathy was readily reproduced in germ-free male mice given a vitamin K-free diet, and in conventional male and female mice given Warfarin in the diet. We concluded that the cause of this condition was vitamin K deficiency.