210 /. /. Christian 



haus, 1953; Bullough, 1955; Dougherty and Schneebeli, 1955; Kass et al., 

 1955; Irving, 1957) . The effects on inflammation result from a failure of the 

 usual inflammatory cells, lymphocytes and fibroblasts, to appear at the site 

 of injury (Dougherty, 1953; Dougherty and Schneebeli, 1955). The lack of 

 an adecjuate inflammatory response together with the failure of adetiuate 

 granulation to take place markedly delays wound healing (Dougherty, 

 1953; Dougherty and Schneebeli, 1955) . These effects, coupled with inhibi- 

 tion of phagocytosis and antibod}^ formation, result in a marked decrease 

 in resistance to infections, so that an animal may be rapidly overwhelmed 

 by an infection (Thomas, 1953). There is ample experimental evidence to 

 show that cortisone and hydrocortisone decrease host resistance to infection 

 by a wide variety of pathogenic viruses, bacteria, protozoan and metazoan 

 parasites (Thomas, 1953; Shwartzman and Aronson, 1953; LeMaistre^ia/., 

 1953; Kass et al. 1953b; Robinson and Smith, 1953; Whitney and Anigstein, 

 1953; Pollard and Wilson, 1955) . Animals resistant to particular organisms 

 may be made nonresistant by these steroids, and usually mild infections 

 may become highly virulent. 



High physiological doses of cortisone or hydrocortisone in the pregnant 

 mammal may result in the development of malformations, especially cleft 

 palate, in the fetus, the particular anomaly apparently depending on the 

 stage of development of the fetus when it is subjected to the actions of the 

 hormone (Glaubach, 1952; Fraser et al, 1953; Davis and Plotz, 1954; Kal- 

 ter, 1954; Moss, 1955). Cortisone and hydrocortisone both produce cleft 

 palates and other congenital defects in the fetus when injected into pregnant 

 mice, the incidence of these anomalies being greater when the injections 

 were made on the tenth day than when later ( Fraser et al., 1953) . The tera- 

 togenic effects of cortisone in mice have been shown to be decreased with 

 increased maternal body weight and to be affected by maternal genotype 

 (Kalter, 1954; 1956). Treatment of pregnant rats with high physiologic 

 doses of cortisone results in a significant increase in intra-uterine mortalit3\ 

 occurring minly at mid-term, and later (Seifter et al., 1951 ; Davis and Plotz, 

 1954) . High doses of cortisone administered to nursing mice 9-12 days after 

 parturition depress the growth of progeny, whereas ACTH and low doses 

 of cortisone were without effect on the offspring, except to abolish the 

 difference in growth rate normally seen between male and female mice 

 (Glaubach, 1952). Cortisone, and to a lesser degree ACTH, depresses the 

 growth of infant rats, stimulates the eruption of teeth, opening of the eyes, 

 and development of the gingivae (Parmer et al, 1951) . Cortisone in a total 

 dose of 0.5 mg. given to newborn rats during the first week produced long- 

 term damage, as indicated by the failure of the animals to attain normal 

 body weight after three months (Parmer et al., 1951). Corticosterone and 

 pregneninolone were without effect in these experiments. Cortisone treat- 



