Changes in the phage typing patterns of strains of staphylococci of the 80/81-52/52A/80/ 81 complex and of phage group III were produced by lysogenization with temperate phages derived from selected strains of Staphylococcus aureus. The phages used were of the serological groups A, B, and F. Certain changes of phage pattern were related to serologically specific prophage immunity; others were nonspecific, or resulted from the conversion of a strain from partial resistance to full sensitivity to certain typing phages. In addition to an alteration of their phage typing pattern, the lysogenization of certain strains by appropriate phages effected a reversal of their susceptibility to penicillin. The capacity to produce toxin was conferred upon certain nontoxigenic strains by lysogenization with a phage derived from a toxigenic strain.
The phage typing patterns of 194 typable strains of Staphylococcus aureus isolated in the years 1927 through 1947 and preserved as stock cultures revealed that 43 strains were of phage type 80/81. The occurrence of other typable strains in the broad phage groups I, II, and III corresponded closely to the frequency distribution of staphylococci reported in 1945 by Wilson and Atkinson.
Summary
A large proportion of cultures of coagulase-positive Staphylococcus aureus are susceptible to penicillin. Some strains of definitely high natural resistance may be encountered. Staphylococci may be made resistant to penicillin by growth in progressively increasing concentrations in broth. Their metabolic activity is retarded, and their pathogenicity is reduced or lost. The coagulase reaction is unaffected. This in vitro resistance is temporary; restoration to sensitivity, but only partial return to pathogenicity, may be effected by serial transfer in broth. Staphylococci may acquire resistance during penicillin therapy. Their metabolic activity is retarded, but their pathogenicity is often unaltered. The coagulase reaction is unaffected. This resistance appears to be permanent. Penicillin has no effect on the coagulase reaction. It occurs even in the presence of concentrations of penicillin which are ultimately bactericidal. Penicillin has no effect on the formation of staphylococcal alpha-toxin, and neither enhances or destroys pre-formed toxin. The implication of resistance acquired by staphylococci during penicillin therapy is discussed.
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