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Abstract
The present study was conducted with the aim to find the prevalence of biofilm formation ability among methicillin resistant Staphylococcus aureus (MRSA) isolates and to assess the activities of commonly used drugs against biofilm producing MRSA. Evaluation of prevalence of genes involved in MRSA biofilm production and their gene expression was also studied. Of 55 MRSA, 47 isolates were biofilm producers and 8 isolates were non-biofilm producers. Of 47 biofilm producers, 24 (51.0%), 14 (29.8%) and 9 (19.1%) produced strong (OD570 ≥ 0.5), medium (OD570 ≥ 0.2 to linezolid (128 to 256 μg/ml) >daptomycin, clindamycin and teicoplanin (256 to 512 μg/ml). Biofilms eradication rate was also observed in the same order with Vancoplus (87%) >linezolid (51.8%) >clindamycin (31.9%) >daptomycin (27.5%) >teicoplanin (26.5%). Our results showed that the percentage of finbA, hla, eno, clfA and fib genes expressions down-regulation after Vancoplus treatment was 64.0 ± 5.9, 63.8 ± 5.8, 73.0 ± 7.4, 72.8 ± 7.8 and 71.9 ± 7.8%, respectively as compared to the control among strong biofilm producing MRSA whereas teicoplanin produced only 30.3 ± 2.7 to 34.5 ± 3.8% down regulation in fnbA, hla, eno, clfA and fib genes expression. The other comparator drugs, vancomycin, linezolid and daptomycin, demonstrated variable effects on these genes varying from 4.9 ± 3.9 to 30.3 ± 2.7%. Our data showed that Vancoplus has significantly enhanced activity against MRSA biofilm producing isolates as compared to other drugs. Therefore, use of this antibiotic should be considered to treat the infections caused by biofilm producing MRSA.
Highlights
Staphylococcus aureus is among the 5 most common pathogens that constitutes normal skin and nasal flora in at least 25 to 30% of healthy humans and is associated with large proportions of hospitalacquired and community acquired infections ranging from superficial wound infections to life-threatening deep infections such as septicemia, endocarditis and toxic shock syndrome [1,2,3]
Our results showed that the percentage of finbA, hla, eno, clfA and fib genes expression down-regulation after Vancoplus treatment was 64.0 ± 5.9, 63.8 ± 5.8, 73.0 ± 7.4, 72.8 ± 7.8 and 71.9 ± 7.8%, respectively as compared to the control among strong biofilm producers methicillin-resistant S. aureus (MRSA) whereas teicoplanin produced only 34.5 ± 3.8, 25.09 ± 2.3, 25.6 ± 2.5, 28.9 ± 2.5 and 30.3 ± 2.7% down regulation in fnbA, hla, eno, clfA and fib genes expression
Our results revealed that among the tested drugs, Vancoplus was found to be more active against planktonic bacteria (MIC 0.125 to 4 μg/ml) as well as bacteria embedded in biofilm (MBECs 0.5 to 16 μg/ml)
Summary
Staphylococcus aureus is among the 5 most common pathogens that constitutes normal skin and nasal flora in at least 25 to 30% of healthy humans and is associated with large proportions of hospitalacquired and community acquired infections ranging from superficial wound infections to life-threatening deep infections such as septicemia, endocarditis and toxic shock syndrome [1,2,3]. The S. aureus with biofilm forming ability is capable of causing a number of diseases, including infective endocarditis, osteomyelitis, foreign body–related infections, catheters associated Urinary Tract Infections (UTIs), and ventilator associated pneumonia and blood stream infections closely related to intravascular devices [5,6,7,8]. In addition to a large number of cell surface associated proteins, secreted proteins, Polysaccharide Intercellular Adhesin (PIA) and intracellular adhesin A, D, B and C (icaA, icaD, icaB and icaC) which are synthesized by products of the intercellular adhesin A, D, B and C (icaA, icaD, icaB and icaC) operon are required for biofilm formation in staphylococci [5,6,7,8]
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