An epidemic of infections due to group A Streptococcus haemolyticus type 12 originated in an infant with bronchiectasis, and involved children and nurses. Some of the children spread contagion; the nurses did not spread contagion. The children who spread contagion had few or no recognizable type 12 organisms in their throats; most of the nurses had type 12 predominant in their throat flora.
Two children who spread contagion had non-hemolytic streptococci in their throat flora, which became hemolytic on cultivation and proved to be type 12. Four children had in their throat flora hemolytic type 12 streptococci which became non-hemolytic when grown in fluid media containing serum. These infants appeared to act as disseminating hosts in which the pathogen developed communicability and at the same time became morphologically and physiologically labile.
The labile streptococci gave rise to atypical forms whose requirements for rapid reproduction (as tested in vitro) were similar to those existing in the human host.
The hypothesis presented is that the genesis of communicability depends on the coexistence of two conditions: a transmitting host lacking in restraining influences, permitting the acquisition of physiological lability by the microorganism; and the development of adaptive mechanisms in the bacterial cell, facilitating survival under atmospheric conditions and subsequent colonization in the environment of human tissues.