NUNGESTER 



better in vitro at 30° C than at 37° C, yet in vivo they do very well 

 at 37° C. 



If we accept the evidence currently available, we must conclude 

 that cold does lower animal host resistance to many infectious a- 

 gents.The question with which we must concern ourselves is, "How?" 



Host resistance to infectious agents involves anatomical, physio- 

 logical, biochemical, and immunological factors, and most of these 

 have been touched upon by the various participants here. 



Anatomical. Any break in the skin resulting from frost bite or 

 cold sensitization obviously increases the chances of infection. Some 

 of the most serious infections of man result from such losses of 

 mechanical protection of the skin, as can be seen in the infection 

 which can complicate burns. Much more subtle anatomical factors 

 such as the bloodsupply of theskin,the nasal mucosa, and the arch- 

 itecture of the upper respiratory tract may be concerned with this 

 problem. 



Physiological. The physiological changes in the host resulting 

 from sudden or prolonged exposure to cold are even more subtle. 

 Changes of this type have been called to our attention by Dr. Blair 

 and Dr. Miya. The latter has shown that there is an increased re- 

 sistance to bacterial endotoxins in the cooled animal, while Dr. Blair 

 and Col. Moncrief have described their use of hypothermy to treat 

 bacterial shock in man. Probably the increased resistance of chilled 

 animals and man to endotoxin is based on some physiological mech- 

 anism which has not yetbeen defined. As Sir Christopher pointed out, 

 disease production and mechanisms related to it are important as- 

 pects of this story. And the report of Washburn (1962) on the changes 

 in blood circulation in frost bitten skin is pertinent to the lowering 

 of skin resistance by cold. 



My own experience in this area relates to the mucus secretions in 

 the upper respiratory tract. It is recognized that sterile hog gastric 

 mucin (Nungester et al., 1936; Olitzki, 1948) and human respiratory 

 tract mucin (Nungester et al., 1951) lowers host resistance to bac- 

 terial infections. Experimental pneumonia can be produced readily 

 by injecting a suspension of bacteria and mucin deep into the res- 



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