STAGES IN PHAGE MULTIPLICATION 165 



It will be recalled that infection with large numbers of T2 

 (but not of many other phages) is abortive and causes prompt 

 "lysis from without." Smaller numbers of T2 ghosts (Barlow 

 and Herriott, 1954) or of phage particles inactivated by ultra- 

 violet light (Watson, 1950) produce the same effect, as do also 

 phage particles inactivated by X-rays until bacteria-killing ability 

 is lost (Watson, 1950). These facts may be summarized by say- 

 ing that phage particles can damage cells severely at the time of 

 infection, and that this damage is independent of injection of 

 DNA, appearing, in fact, to be especially severe when one or 

 another early step in the normal sequence of events is blocked. 

 Thus sensitivity to lysis from without is also increased in the 

 presence of metabolic inhibitors or by deprivation of food 

 (Heagy, 1950; Watson, 1950), but is greatly reduced in the 

 presence of high concentrations of magnesium that do not pre- 

 vent infection (Barlow and Herriott, 1954). Many of these 

 facts can now be partly understood in terms of two competing 

 processes, one lytic and one antilytic, set in train by the normal 

 process of infection. 



Doermann (1948a) first noticed that normal infection pro- 

 duces a rapid change in cellular properties. He observed a 

 sudden fall in turbidity of bacterial cultures following infection. 

 The turbidity passed through a minimum at about 10 minutes 

 after infection, and then rose again. The initial drop was caused 

 by T2, T4, T6, and T5, but not by Tl, T3, or T7. It was seen 

 also following infection with T5 in the absence of calcium (no 

 injection), in which case there was no subsequent rise. The 

 effect was independent of multiplicity of infection in the range 

 between 3 and 10 or 15, above which lysis from without was ob- 

 served. Doermann suggested a spreading alteration of the bac- 

 terial surface followed by "recovery." Subsequent experiments 

 confirm his interpretation, except that his "recovery" is much 

 too slow to reflect the development of resistance to superinfection 

 and probably should be ascribed to the general biosyntheses 

 accompanying phage growth. 



Two phenomena, the chemical breakdown of superinfecting 



