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HOBART A. REIMANN, M.D.

Arch Intern Med. 1960;106(3):341-344.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Staphylococcus now exceeds other Grampositive cocci as an important cause of disease and death, yet basic information of its ecology, pathogenesis, and immune relationships is incomplete.¹ Intensive studies of its dissociative pattern had not been made in contrast with those of Pneumococcus and Streptococcus whose main colonial variant forms are known as mucoid (M), smooth (S), and rough (R). Besides, transformation from one serologic type to another, each with its M, S, and R forms, can be induced among pneumococci and takes place spontaneously in tetragena.² However, there is little evidence of the implication of these changes in the origin or recovery from infection.

Because Staphylococcus is unique among pathogenic cocci in its ability to become resistant to antimicrobials, this study was made to fill in missing data about its dissociative behavior and to see if microbic variation plays a role in the development of drug-resistance and in . . . [Full Text PDF of this Article]

Author Affiliations
Philadelphia

Footnotes
Submitted for publication July 2, 1959.

The Hahnemann Medical College and Hospital.

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