HOST SPECIFICITY 131 



The significance of this omission was demonstrated by Roun- 

 tree (1949b) in an investigation of the serological relationships of 

 a number of staphylococcal phages. She found that typing 

 phages 42C and 42D were serologically unrelated to phage 42B 

 although all were supposed to have been derived from a common 

 source, strain 42. Strain 42 had been adapted to host strain 36 

 to give phage strain 42A ; 42A was adapted to host strain 1 307 

 to give 42C, which on adaptation to host strain 1363 became 

 42D. On investigation Rountree found that host strain 36 was 

 lysogenic, carrying a latent phage which was capable of lysing 

 host strain 1307. This latent phage from host strain 36 proved 

 to be serologically related to phage strain 42C and 42D. There- 

 fore the phage strains 42 C and 42D were derived from a con- 

 taminating phage from a lysogenic host strain used for passage 

 and were not host range mutants of strain 42. Since the fre- 

 quency of lysogenic strains is high in many bacterial species, 

 this source of confusion must be kept in mind. Serological rela- 

 tionship is the minimum evidence required to demonstrate 

 derivation by mutation, and resemblance in other properties 

 should be looked for as well. These requirements were clearly 

 stated by Craigie and Felix (1947) in discussing the standardiza- 

 tion of the Vi typing phages for S. typhi. 



Luria (1945a) in a detailed study of host range variants of 

 phages Tl and T2 applied the fluctuation test to demonstrate 

 the spontaneous mutational origin of these variants. The mutant 

 phage particles proved to be indistinguishable from their parents 

 in serological specificity and in growth characteristics on the 

 common host strain B of E. coli. They appeared to differ only in 

 host range. The frequency of these host range mutant virus 

 particles in small independent culture lysates was of the order of 

 10-8. 



Hershey (1946b) demonstrated the existence of sev^eral inde- 

 pendent host range mutations of phage T2 and that in mixed 

 infection experiments genetic recombination between host range 

 and plaque type mutants could occur (Hershey and Rotman, 

 1949). In further studies Hershey and Davidson (1951) found 



