SPECIFIC AND NONSPECIFIC RESISTANCE 



(Marcus, Esplin and Donaldson, 1954), it seems unlikely that the 

 properdin system is contributing much to the natural defenses of the 

 mouse (Miya, Marcus, and Perkins, 1960). 



Results of our experiments indicate that mice chronically ex- 

 posed to cold are able to form agglutinin antibody. Trapani (1960) 

 reported that cold exposed rabbits were able to form antibody al- 

 most as rapidly as rabbits kept at room temperature. In contrast, 

 Ipsen (1952) reported that antibody formation is impaired in mice 

 exposed to 4° C, We have not attempted to determine if antibody 

 formation is impaired by acute exposure to cold. 



Although the results of the Coxsackie virus experiments suggest 

 that acclimatization will result in a normal degree of host resistance 

 of nonimmune animals against challenge with this agent, the results 

 of others are not in agreement. Walker and Boring (1958) reported 

 on experiments using a Connecticut 5 strain of Type B-1 Coxsackie 

 virus. They observed that acute limited exposure to 4 C was in- 

 sufficient to change the viral infection from an asymptomatic into a 

 lethal process, but that continued exposure for several days did 

 accomplish conversion to disseminated lethal disease. They re- 

 ported on experiments in which adapted (14 days) animals were em- 

 ployed, and found that this period of adaptation at 4° C did not 

 counteract the lethal effects of the virus disease at 4° C, Mice 

 challenged at 4*^ C, following acclimatization and then placed at 

 25° C, did not die. Therefore, Walker and Boring concluded that 

 exposure to 4° C caused a decrease in resistance of the challenged 

 animals. 



In our experiments we have shown that acclimatization for 40 

 days at 2° C is sufficient for the adult mice to overcome a challenge 

 dose that is lethal for virus challenged unacclimatized mice re- 

 placed in the cold box. Since the adrenal activity does initially in- 

 crease upon cold exposure (Her oux and Hart, 19 54 ;Schonbaum, 1960), 

 and since the Coxsackie disease process resembled that due to 

 cortisone effects. Walker and Boring (1958) attempted to reproduce 

 the disease in mice at room temperature by ACTH injections follow- 

 ing challenge with Coxsackie virus. They were unable to detect any 

 decrease in resistance in mice treated inthis manner. Although the 

 increased mortality correlates will with increased corticosteroid 



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