278 /. /, Christian 



In earlier experiments it had been shown that either cortisone or ACTH 

 increased the invasiveness of Trichinella larvae by suppressing the defen- 

 sive inflammatory response of the host's intestinal wall and possibly by 

 prolonging the sojourn of the adult females in the gut by suppressmg im- 

 mune responses to the worms (Stoner and Godwin, 1953). Thus, these 

 hormones decreased the resistance of mice to invasion by the larvae of 

 Trichinella spiralis by inhibiting inflammation and possibly antibody 

 formation. Grouping evidently stimulated a sufficient increase in the secre- 

 tion of adrenal corticoids to produce similar effects. This conclusion is sup- 

 ported by the demonstration that grouping was sufficient stimulus to 

 pituitary-adrenocortical activity to diminish granuloma formation appreci- 

 ably. These experiments with trichinosis in house mice have been repeated 

 with albino mice with similar results, confirming the original results and 

 demonstrating that albino and wild-strain house mice react similarly (Davis 

 and Read, unpublished) .- 



The effects of crowding on trichinosis in mice is presumably primarily due 

 to the effects of increased adrenocortical secretion on the inflammatory 

 response to the worms. Therefore a similar series of experiments were per- 

 formed which were more specificaUy designed to demonstrate the effects of 

 grouping on antibody formation (Davis and Prudovsky, 1959). In this case 

 mice were injected with tetanus toxoid and challenged 10 days later with 

 13 mouse MLD of tetanus toxin. The dosage of toxin was selected to cause 

 death in 50% of segregated mice. Mice were placed in groups either 5 or 3 

 days prior to giving the toxoid and left in groups until 5 days after the 

 toxoid. Control mice were left segregated in individual cages throughout 

 the experimental period but otherwise were treated identically to the experi- 

 mental animals. Grouping appreciably decreased resistance and increased 

 mortality of mice to the challenge dose over the control levels. This effect 

 was less marked when the mice were grouped 3 days before administering 

 the toxoid. The effects of grouping resembled the effects of injected corti- 

 sone at the appropriate times and in appropriate doses. These results indi- 



^ A report was published recently which implied that cortisone or ACTH are without 

 effect on the course of trichinosis in mice, but which showed that cortisone markedl}' 

 increased mortality (Lord, 1958). These experiments require some critical comment. 

 The procedure used to infect the mice was similar to that used by Davis and Read 

 (1958), but injections of cortisone and ACTH were not begun until 6 days after infection. 

 One would not anticipate that these hormones would affect the course of trichinosis at 

 that late date, as invasion by the larval worms, the inflammatorj' response to them in 

 the intestinal wall, and immune responses to them are fairly well accomplished facts 

 by that time. Therefore one would not anticipate an alteration in the resistance to 

 invasion by the worms. The doses of cortisone used in these experiments were extremely 

 high pharmacologic doses: 76 mg. in 39 days, beginning with 3 mg. a day per mouse. 

 It is not surprising that cortisone increased mortality. 



