146 BIOLOGY OF PNEUMOCOCCUS 



the necropsy of animals that had died as a result of the develop- 

 ment of pneumococcal lesions in the heart or other organs, exhib- 

 ited attenuation of virulence, loss of capsule formation, antigenic 

 power and type-specificity, and changed susceptibility to phagocy- 

 tosis. In the case of some of these variants the specific characters 

 of the original type from which they were derived were quickly re- 

 stored by one or two mouse passages. In other instances, the or- 

 ganism remained atypical. 



Sickles, 1279 in a later study (1932) of pneumococcal strains that 

 had become atypical in the tissues of horses undergoing immuniza- 

 tion, in comparison with the typical cultures from which they were 

 derived and with various other typical and atypical strains, found 

 that all the organisms were bile-soluble. The maximal limits of 

 growth, along with the other characters, such as limiting hydrogen 

 ion concentration and peroxide and hemoglobin formation, were 

 similar for the same type culture whether original, degenerated, or 

 reverted. Sickles found only one strain which departed from the 

 general rule and that organism grew at 42°, and survived even 

 after incubation at 43.5°. No other pneumococcal strains studied 

 were alive after twenty to twenty-four hours at 42°. 



That Pneumococcus may, however, retain its specific type char- 

 acters when growing in the animal body was proved by Megrail 

 and Ecker 888 in 1924, who injected mice and rats with suspensions 

 of gum tragacanth followed by a saline suspension of pneumo- 

 cocci. In these fixation abscesses the strains displayed no variation 

 and no change in agglutinability. Here the conditions differed from 

 those in the horses harboring pneumococci, as reported by Sic- 

 kles, 1279 since the rats and mice had not been subjected to any im- 

 munizing treatment, and their tissues, therefore, presumably con- 

 tained no antibodies which might favor variation. 



Reimann 1128 found that R forms occurred in vivo but could dis- 

 cover in his experiments no positive evidence that recovery from 

 pneumococcal infection depended upon the degradation of virulent 



