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ANTONIO J. GONZAGA, M.D.; CHARLES H. RAMMELKAMP, JR., M.D.

Arch Intern Med. 1962;110(5):615-618.

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

The presence of diphosphopyridine nucleotidase (DPNase) in filtrates of cultures of hemolytic streptococci was first described in 1956.^1,2 Among several bacterial species studied, only streptococci of Groups A, C, and G produced this extracellular enzyme. The capacity to release DPNase during growth of different types of Group A strains varied markedly; many strains produced no enzyme, while others elaborated large amounts. In general, DPNase production appeared to be restricted to those serological types of Group A streptococci now known to be associated with acute glomerulonephritis.^3,4

DPNase destroys the coenzyme, diphosphopyridine nucleotide (DPN), thus interfering with the oxidative metabolism of mitochondria in vitor.¹ In addition, Wilson⁴ has observed a close association between the capacity of Group A streptococci to kill leukocytes in vitro after phagocytosis and the capacity of the strain to produce DPNase. Ayoub and Wannamaker⁵ have observed higher titers of neutralizing antibodies against DPNase . . . [Full Text PDF of this Article]

Author Affiliations
CLEVELAND

Trainee, United States Public Health Service (Grant Number 2E-180) (Dr. Gonzaga).; From the Research Laboratories, Cleveland Metropolitan General Hospital, and the Departments of Medicine and Preventive Medicine, Western Reserve University School of Medicine.

Footnotes
This investigation was conducted under the sponsorship of the Commission on Streptococcal and Staphylococcal Diseases, Armed Forces Epidemiological Board, and was supported by the Office of the Surgeon General, Department of the Army, Washington, D.C.

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