Polymorphism of ftsI gene in Haemophilus influenzae and emergence of cefotaxime resistance in two Tunisian hospitals.

Abstract Objectives The decreased affinity to β-lactams in Haemophilus influenzae is usually caused by specific alterations in penicillin binding protein 3 due to varieties of substitutions in ftsI gene. This study aimed to characterize the polymorphism of ftsI gene in 19 H. influenza strains, isolated between 2014 and 2016 [different resistance phenotypes to β-lactams (n=9) and susceptible strains (n=10) used for comparative purposes]. Methods All strains were characterized for capsular type by PCR and agglutination tests and for β-lactam resistance by amplification and sequencing of ftsI. Biotyping and clonality were done by API-NH and pulsed field gel electrophoresis, respectively. Results Four strains were β-lactamase negative ampicillin resistant (BLNAR) and 5 were β-lactamase positive acid-clavulanic resistant (BLPACR). One strain from each group was resistant to cefotaxime. Our isolates belonged mainly to biotype IV and I and were non-typeable and genetically unrelated. According to mutation profiles of their ftsI, strains were classified as group I (n=3), group II (n=4), group III like (n=1) and group III (n=1). All group II strains were further classified as subgroup IIb, except one strain which harbored a new mutation (N422I). Ampicillin MICs of BLNAR strains were 6 to 12 times the MICs of susceptible strains. Only blaTEM-1 was detected in BLPACR strains, and was responsible of high MICs for ampicillin (>256μg/mL), whatever the ftsI mutational resistance group. Conclusion The emergence of cefotaxime resistant isolates in our country is a matter of concern and requires strict surveillance and rationalization of antibiotic use in order to preserve these molecules.