Faecal carriage of salmonella was investigated in 320 hedgehogs from Moss municipality in south-eastern Norway, Askøy, Bergen and Os municipalities in central-western Norway, and five municipalities in south-western and central Norway. The sampling in Moss was carried out 1 year after a human outbreak of salmonellosis, whereas the sampling in Askøy, Bergen and Os was carried out during a human outbreak. Both outbreaks were caused by Salmonella Typhimurium 4,5,12:i:1,2. No salmonella were detected in the hedgehogs from south-western (0/115) and central (0/24) Norway. Thirty-nine percent (39/99) of the animals sampled on Jeløy, and 41% (34/82) of those from Askøy, Bergen and Os, carried S. Typhimurium 4,5,12:i:1,2. The PFGE profile of isolates from hedgehogs and human beings were identical within each of the two outbreak areas. A significantly higher carrier rate of S. Typhimurium occurred among hedgehogs sampled at feeding places, compared to those caught elsewhere. The salmonella-infected hedgehog populations most likely constituted the primary source of infection during both of the human disease outbreaks, and the Norwegian hedgehog is suggested as a reservoir host of S. Typhimurium 4,5,12:i:1,2.

Experiments were carried out to determine the infectivity, clinical course of disease, and lethality of aerosols of Legionella pneumophila for guinea pigs. The median infectious dose was less than 129 organisms; the 50% lethal dose was 1.4 x 10(5) organisms. In addition, the intraperitoneal 50% lethal dose was 3.0 x 10(6) cells, a value indicating that the organisms were less virulent by the intraperitoneal route than by aerosol. Nonfatal disease always included fever and weight loss. These signs were accompanied by sporadic bacteremia and dyspnea. Leukocyte counts were uninformative. In general, the severity of fever and extent of serologic (microagglutination titer) response were dose-related. The guinea pig may be used as a model for Legionnaires' disease, but the only dependable clinical criteria of infection after airborne challenge are weight loss, fever, and seroconversion.

Five cyclic nitrosamines, four containing oxygen in the ring, were administered by gavage to groups of 20 male Syrian golden hamsters. After administration of very similar doses, nitrosomorpholine, nitroso-2-methylmorpholine and nitroso-5-methyl-1,3-oxazolidine caused the animals to die with tumors after similar times, but nitrosomorpholine induced mainly tumors of the nasal cavity (and a few of the trachea), whereas the 2-methyl derivative induced tumors of the nasal cavity and liver. While nitroso-1,3-oxazolidine and its 5-methyl derivative both induced liver tumors (but no tumors in the nasal cavity) those induced by the former compound took much longer to kill the animals. Nitrosoazetidine, a liver carcinogen in rats, but which had been reported to be inactive in hamsters, did induce tumors of the liver in 30% of hamsters after a much larger dose than the other cyclic nitrosamines.

The effect of subsequent administration of chloroform or phenobarbital on the incidence of ethylnitrosourea (ENU) initiated liver and lung tumors was investigated. Fifteen day old Swiss mice were administered ENU, and at weaning they started to receive either 1800 p.p.m. chloroform or 500 p.p.m. sodium phenobarbital in their drinking water. The mice continued to receive either chloroform or phenobarbital until 51 weeks of age. They were sacrificed at 52 weeks of age. ENU at 5 and 20 mg/kg, caused a dose-dependent increase in liver and lung tumors. The male mice were more sensitive to the induction of liver tumors, while no sex preference was observed for the induction of lung tumors. In male mice chloroform inhibited, while in female and male mice phenobarbital promoted spontaneous and ENU-induced liver tumors. Subsequent treatment with either chloroform or phenobarbital did not affect the incidence of ENU-induced lung tumors. In conclusion, when administered in the drinking water, chloroform inhibited while phenobarbital promoted hepatocarcinogenesis in mice.

Squirrel monkeys were inoculated by the intratracheal inoculation of 700 Klebsiella pneumoniae organisms and developed lobar pneumonia in about 24 h. Characteristic clinical findings were fever, anorexia, and coughing. Laboratory findings included leukocytosis or leukopenia (with the latter more prominent in ultimately fatal infections), bacteremia, and shedding of bacteria into the pharynx. Infected monkeys showed increased plasma lysozyme activity as well as increased plasma ceruloplasmin, haptoglobin and alpha1-antitrypsin. The mortality rate was 60%, and the mean time of death was 50.5 h. Pathologically, the disease spread by means of Kohn's pores and other pathways that generally did not involve airways as a means of dissemination until about 30 h. Squirrel monkeys seem to be better models for human respiratory K. pneumoniae infection than rats or mice.