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C. V. Sundar-Raj, N. A. Stella, P. P. Thompson, R. P. Kowaski, R. M. Shanks; Atypical Mycobacterium Biofilm Formation Is Inhibited by Fluoroquinolone and Macrolide Antibiotics. Invest. Ophthalmol. Vis. Sci. 2008;49(13):4852.
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Atypical Mycobacterium cause a number of ocular infections and may possibly be an overlooked agent of contact lens associated keratitis. First, the ability of a keratitis isolate of M. chelonae and M. fortuitum to form biofilms on contact lens cases from different sources was determined. Second, the ability of different antimicrobials to inhibit biofilm formation by these organisms was assayed.
Mycobacterial strains were grown in Brain Heart Infusion broth (BHI) overnight, diluted to normalized optical density (A600=0.01), and incubated with contact lens cases for 48 hours at 30°C. Attached cells were washed and stained with 0.1% crystal violet. Biofilms were quantified by spectrophotometric analysis of crystal violet levels. Tested contact lens cases were from Bausch and Lomb (provided by company), Alcon (provided by company), or a X-Cel (purchased). For the antimicrobial studies, cultures were untreated or treated with a concentration gradient of sodium citrate, moxifloxacin, erythromycin, or saline at the time of inoculation.
The M. fortuitum isolate forms a robust biofilm on all tested contact lens cases, whereas the M. chelonae isolate forms a relatively weak biofilm. A statistically significant (p<0.02) 30% reduction in M. fortuitum biofilm was detected on the X-Cel cases compared to both the Alcon and Bausch and Lomb contact lens cases. Biofilm formation by both organisms was completely inhibited by addition of moxifloxacin or higher concentrations of erythromycin, while sodium citrate and saline did not inhibit biofilm formation.
The tested contact lens cases were largely equivalent for colonization by atypical Mycobacteria, although there was a significant reduction on the X-Cel cases compared to those from Alcon and Bausch and Lomb. Fluoroquinolone and macrolide antibiotics can prevent the formation of biofilms, but it remains to be seen whether they can disrupt existing biofilms. This work establishes a model for testing the efficacy of antimicrobial agents against mycobacterial biofilms.
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