EXCESS RISK OF STAPHYLOCCUS INFECTION AND DISEASE
IN NEWBORN MALES¹

By

DONOVAN J. THOMPSON,² HORACE M. GEZON,³ KENNETH D. ROGERS,⁴
ROBERT B. YEE,⁵ AND THEODORE F. HATCH^6,7

(Received for publication December 27, 1965)

SUMMARY

Colonization by S. aureus during the hospital stay and staphylococcal disease during the first month of life of newborn infants were both shown to be related to the sex of the infant, males being at greater risk. This excess risk begins at birth and continues throughout the neonatal period. Colonization excess in males was present in the nose, umbilicus, groin, and rectum. Males became positive earlier and in more body sites and with greater intensity than females. In roughly equivalent positivity classes of infants, males developed disease at a greater rate. This excess disease risk was not limited to a single or a few phage types but appeared to be present for all. The males with disease tended to have more lesions than their female counterparts and the anterior abdomen and groin were the most frequent sites of the excess lesions. Possible explanations for the difference in the two sexes are suggested.

[CIRP Comment: This long and careful report investigated the higher incidence of Staphylococcus aureus infection and disease in newborn males as compared with females. Much of the information is not relevant to circumcision and will not be presented here. In this study, which was carried out in five Pittsburgh hospital nurseries from 1959 through 1965, 97 percent of the newborn boys were circumcised. The small size of the non-circumcised group limited the statistical comparison of the circumcised boys with the non-circumcised boys. The authors, however, reported that the infection rate among the circumcised boys was 26 percent as compared with 13 percent among the non-circumcised intact boys. (p.323)]

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    ¹From the Graduate School of Public Health and the School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania.
    ²Professor of Biometry, Graduate School of Public Health.
    ³Professor of Epidemiology and Microbiology, Graduate School of Public Health.
    ⁴Professor of Preventive Medicine, School of Medicine.
    ⁵Assistant Research Professor of Microbiology, Graduate School of Public Health.
    ⁶Professor of Industrial Health Engineering, Graduate School of Public Health.
    ⁷This investigation was supported in whole by Public Health Service Research Grant EF-00060-05 from the Division of Environmental Engineering and Food Protection.
    It is a pleasure to acknowledge the assistance of Joyce Lego, Doris Evans, Kathryn Rogulin and Catherine Brosky.