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Andreas Pikis, Joseph M. Campos, William J. Rodriguez, Jerry M. Keith, Optochin Resistance in Streptococcus pneumoniae: Mechanism, Significance, and Clinical Implications, The Journal of Infectious Diseases, Volume 184, Issue 5, 1 September 2001, Pages 582–590, https://doi.org/10.1086/322803
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Abstract
Traditionally, Streptococcus pneumoniae is identified in the laboratory by demonstrating susceptibility to optochin. Between 1992 and 1998, 4 pneumococcal isolates exhibiting optochin resistance were recovered from patients at Children’s National Medical Center. Three of the 4 isolates consisted of mixed populations of optochin-resistant and -susceptible organisms. Both subpopulations had identical antibiograms, serotypes, and restriction fragment profiles. The other isolate was uniformly resistant to optochin. Resistant strains had MICs of optochin 4–30-fold higher than susceptible strains, belonged to different serotypes, and had dissimilar restriction fragment profiles, indicating clonal unrelatedness. Resistance arose from single point mutations in either the a-subunit (W206S) or the c-subunit (G20S, M23I, and A49T) of H+-ATPase. There is speculation of a possible association between exposure to antimalarial drugs and evolution of optochin resistance. α-Hemolytic streptococci resistant to optochin, particularly invasive isolates, should be tested for bile solubility or with an S. pneumoniae DNA probe before identification as viridans streptococci