Infection and Immunity, February 2000, p. 953-955, Vol. 68, No. 2
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Unidad de Investigación, Hospital Universitario de Son Dureta,1 and Área de Microbiología, Departamento de Biología, Universidad de las Islas Baleares and IMEDEA (CSIC-UIB),2 Palma de Mallorca, and Departamento de Microbiología, Universidad de Barcelona, Barcelona,3 Spain
Received 27 August 1999/Accepted 9 November 1999
We have previously demonstrated the existence of Klebsiella pneumoniae clinical isolates deficient in the lipopolysaccharide O side chain, the major factor for resistance to complement-mediated killing in this bacterial species. These isolates are complement resistant, and their mechanisms to resist complement were investigated by selecting transposon-generated complement-sensitive mutants. One mutant with a drastically reduced capacity to grow in nonimmune human serum carried the transposon inserted in an open reading frame of a gene cluster involved in capsule synthesis. This mutant produced less capsule, bound more molecules of the complement component C3, and was more sensitive to complement-mediated and opsonophagocytic killings than was the parent strain. Four additional clinical isolates representing four different K serotypes were studied, and results showed that capsular polysaccharide is a major complement resistance factor in these O side chain-deficient isolates.
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