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A total of 95 K1 Escherichia coli strains of the O (lipopolysaccharide) serotypes O1, O7, or O18 had been analyzed previously for the ability to cause bacteremia after colonizing the gut of newborn rats. In this study, these strains were tested for their resistance to the bactericidal activity of rat serum. All strains that had caused bacteremia in a high percentage of the inoculated rats were able to survive for several hours in 90% adult rat serum. With only a few exceptions, O7:K1 and O18:K1 strains were serum resistant and virulent, whereas O1:K1 strains were serum sensitive and avirulent. Serum sensitivity was due to the classical complement pathway. K1 strains of all three O serotypes were resistant to the alternative complement pathway. O7:K1 and O18:K1 cells were killed efficiently after the classical pathway was triggered by specific antilipopolysaccharide antibodies. However, killing of O1:K1 bacteria by the classical pathway system did not require antibodies. Isolated O1-lipopolysaccharide fixed complement more efficiently than did isolated O7- or O18-lipopolysaccharide, suggesting that the differences in the chemical structure of the O antigens are responsible for the observed differences in complement sensitivity. In combination with epidemiological data, the results indicate that antibody-independent classical pathway activation provides an important defense mechanism for newborns against certain gram-negative infections.

infection and immunity

Degree of antibody-independent activation of the classical complement pathway by K1 Escherichia coli differs with O antigen type and correlates with virulence of meningitis in newborns