IMMUNOLOGICAL RELATIONSHIPS 347 



peculiar reactivity of the blood vessels of the organs treated with 

 active bacterial fdtrates has been clearly demonstrated by ob- 

 ser\ations reported so far by various authors. For these reasons 

 he considers tiie phenomenon of local skin reactivity as a con- 

 dition of vasctdar allergy wiiich must be clearly distinguished 

 from anaphylaxis. 



Inasmuch as the essential prerecpusite of the phenomenon is 

 tliat the provocative injection be made by way of the blood 

 stream, attempts ^vere made to determine whether there are elab- 

 orated in the blood stream any hemorrhagic-inducing principles. 

 P. Bordet injected 1 c.c. of B. coli into the skin of rabbits. 

 T^\'enty-fot^" horns later the rabbits received an intravenous in- 

 jection of the filtrate and w^ere bled from the carotid artery tAvo 

 to three hours later. Large amotnits of citrated blood thus ob- 

 tained and transfused into rabbits prepared t^venty-foiu' horns 

 previously by intradermal injection of B. coli failed to elicit 

 reactions in these rabbits. 



THE RELATION OF TOXIN HVPERSUSCEPTIBILITY 

 TO THE PHENOMENON 



Von Behring (1893) observed that animals ^vhich are being 

 actively immunized with tetanus and diphtheria toxins develop 

 a high degree of stisceptibility to these poisons ^vhich is greater 

 than in normal animals. Further sttidies made later by von 

 Behring and Kitashima (1901), and Knorr (1895) show^ed that 

 guinea pigs repeatedly treated ^vith small doses of toxin may 

 sometimes not only fail to sho^v innnimity but develop a stis- 

 ceptibility whereby the sensitized guinea pigs are killed by small 

 doses innocuous to normal guinea pigs. Similar obser\'ations ^vere 

 made on horses by Salomonsen and Madsen (1897) "^'^^^ ^^Y K^retz 

 (1902). It ^vas early indicated by Friedemann (1911) that little 

 similarity exists between anaj)hylaxis and this toxin hypersensi- 

 tiveness. In the case of the latter, there de\elops hypersensiti\e- 

 ness to a primary injurious substance which expresses itself not 

 in symptoms of anaphylactic intoxication but in a picture specific 

 for tiie toxin to which this hypersensitiveness develops. Further 

 differences exist also in fail tire of passive transfer of toxin hyper- 

 sensitiveness. This hypersensitiveness is quite apart from the abil- 

 ity of exotoxic antigens to act as anaphylactogens, i.e., induce 

 symptoms typical of anaphylactic shock (Neill, Fleming and 

 Gasparri, 1927; also Neill, Sugg and Richardson) . It becomes 



