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SERUM ANTIBODIES IN STAPHYLOCOCCAL DISEASE

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Serum antibody titers to the staphylococcal Muller factor and alpha-hemolysin were determined in population groups of various ages and in maternal-cord serum pairs. There was evidence for placental transmission of antibodies and after 2 years of age most persons demonstrated antibody to both of these staphylococcal extracellular products. Antibody titers in patients with staphylococcal lesions were usually in the upper range of those found in the normal population of similar age, but no striking or consistent elevation of titers was observed in association with or following staphylococcal disease. Exceptions, due in part perhaps to age, were found in patients with staphylococcal pneumonia whose sera often contained no measurable antibody and in certain patients with recurrent skin infection whose sera contained alpha-hemolysin antibodies but failed to demonstrate Muller factor antibodies. The general similarity of antibody titers in patients with staphylococcal lesions to those in normal persons suggests that the antibody response to staphylococcal Muller factor and to alpha-hemolysin is little different after a staphylococcal lesion than after nasal or cutaneous colonization. These findings emphasize that, in addition to antibodies to toxins, presently ill-defined cellular bactericidal mechanisms are necessary for complete defense against staphylococcal disease.
American Academy of Pediatrics (AAP)
Title: SERUM ANTIBODIES IN STAPHYLOCOCCAL DISEASE
Description:
Serum antibody titers to the staphylococcal Muller factor and alpha-hemolysin were determined in population groups of various ages and in maternal-cord serum pairs.
There was evidence for placental transmission of antibodies and after 2 years of age most persons demonstrated antibody to both of these staphylococcal extracellular products.
Antibody titers in patients with staphylococcal lesions were usually in the upper range of those found in the normal population of similar age, but no striking or consistent elevation of titers was observed in association with or following staphylococcal disease.
Exceptions, due in part perhaps to age, were found in patients with staphylococcal pneumonia whose sera often contained no measurable antibody and in certain patients with recurrent skin infection whose sera contained alpha-hemolysin antibodies but failed to demonstrate Muller factor antibodies.
The general similarity of antibody titers in patients with staphylococcal lesions to those in normal persons suggests that the antibody response to staphylococcal Muller factor and to alpha-hemolysin is little different after a staphylococcal lesion than after nasal or cutaneous colonization.
These findings emphasize that, in addition to antibodies to toxins, presently ill-defined cellular bactericidal mechanisms are necessary for complete defense against staphylococcal disease.

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