Biofilm Formation In Clinical Isolates Research Articles

Inhibitory effects of lactoferrin on biofilm formation in clinical isolates of Pseudomonas aeruginosa

Lactoferrin, a multifunctional protein with antimicrobial activity, is a component of the innate immune system. It may possibly prevent clinical isolates of Pseudomonas aeruginosa from developing biofilm, but this hypothesis is yet to be widely accepted. We evaluated the in vitro effects of lactoferrin on biofilm formation by various clinical isolates of P. aeruginosa using a modified method of the microtiter plate biofilm assay. Lactoferrin significantly inhibited biofilm formation in these isolates. The effect was the most marked at 2 mg/ml, which suggested that an optimal concentration of lactoferrin might exist. Lactoferrin inhibited biofilm formation in eight of nine clinical isolates after 1 day of incubation; however, the inhibitory effects were maintained until 7 days of incubation in only two of those eight strains. Suppression of biofilm formation may be caused by a mechanism that is independent of the bactericidal effects of lactoferrin because the number of viable bacteria was not influenced by lactoferrin under the experimental conditions. Supplementation of lactoferrin to preformed biofilm demonstrated a reduction in biofilm, which suggests that lactoferrin may have a destructive effect on biofilm. Pretreatment with ferric chloride partially restored biofilm formation, suggesting an iron-chelating action may be involved in the inhibitory mechanism of lactoferrin. These results suggest that lactoferrin provides inhibitory effects on biofilm formation in many clinical isolates of P. aeruginosa and that it may also have destructive effects on preformed biofilm, but further research using multiple clinical strains should be undertaken to clarify if those effects are universal.

Biofilm Formation and Detection of IcaAB Genes in Clinical Isolates of Methicillin Resistant Staphylococcus aureus

Objective(s) Methicillin-resistant Staphylococcus aureus (MRSA) is an important cause of nosocomial and community infections. Biofilm formation, mediated by a polysaccharide intercellular adhesin (PIA) and encoded by the ica operon, is considered to be an important virulence factor in both S. epidermidis and S. aureus. However, the clinical impact of the ica locus and PIA production is less well described in S. aureus. We studied biofilm formation in clinical isolates of MRSA in relation to the presence of the ica operon. Materials and Methods Forty five MRSA were studied for biofilm formation by colony morphology on Congo red agar (CRA) and the microtitre plate assay (MtP). Presence of the ica genes was detected by PCR and specific primers. Results The results showed that 53.3% of the isolates had the potential to form biofilm by colony morphology of which, 75% carried the ica operon. Weak biofilm production was observed in the MtP assay by 57.8%, of which 53.8% harbored the ica operon. However, about 70% of biofilm non-producers also carried the ica operon. Conclusion Overall, there was no agreement between the icaAB gene carriage and biofilm phenotype by either of the two phenotypic methods. However, 91% of biofilm formers on CRA also produced biofilm in the MtP assay.

Biofilm formation in clinical isolates of group B streptococci from north India

Many bacterial species are capable of living as biofilm, thought to be the predominant growth mode for bacteria in natural environments. Increasing evidence implicates biofilm as the cause of various human infections. In this study, biofilm formation was demonstrated in group B streptococci (GBS) isolated from different sources in the north Indian community at various pH ranges as well as sugar concentrations and correlated it with different serotypes and surface gene ( c alpha) profiles. The capability to form biofilm was better demonstrated in strains from asymptomatic carriers (pregnant women) compared to symptomatic patients. Quantitatively bacterial adherence with host cells was greater in isolates that produced biofilm under neutral conditions. This study assessed the biofilm formation in clinical isolates of GBS, which is a step towards understanding its role in pathogenesis.

Agr RNAIII divergently regulates glucose-induced biofilm formation in clinical isolates of Staphylococcus aureus

Staphylococcus aureus is an important nosocomial and community-acquired pathogen. Hospital infections are frequently complicated by the ability of bacteria to form biofilms on different surfaces. The development of bacterial films on medical indwelling devices, such as prostheses, often requires surgical procedures to remove the contaminated implant. Indeed, biofilm formation on central endovenous catheters is a major cause of primary bacteraemia in hospitals. The modulation of virulence factors in S. aureus is orchestrated by a number of global regulators including agr RNAIII. To improve our understanding of the role of the agr quorum-sensing system in biofilm formation by S. aureus, we constructed a number of agr-null mutants, derived from contemporary clinical isolates. Analysis of these mutants indicates that agr has a significant impact on biofilm development for most of the isolates tested. Our data show that RNAIII can control both biofilm formation and accumulation. The agr effect included both up- and downregulation of biofilms, even for isolates within the same lineage, corroborating the hypothesis that the mechanisms involved in S. aureus biofilms are complex and probably multifactorial.

Effects of a topical essential oil-containing formulation on biofilm-forming coagulase-negative staphylococci

To evaluate the antimicrobial effects of Polytoxinol (PT), a topical essential oil-based formulation, against biofilm positive strains of coagulase-negative staphylococci. Using a microtitre plate assay we measured inhibitory effects for PT against a selection of biofilm-forming clinical isolates of coagulase-negative staphylococci. Susceptibility varied considerably (MIC = 0.6-20 000 ppm). For the most tolerant clinical isolate (Staphylococcus warneri) biofilm growth was inhibited by a 32-fold lower PT concentration than planktonic growth. This inhibition of biofilm development, which was not observed with the other test isolates, was related to an inhibition of the initial phase of S. warneri cell adherence to the polystyrene surface. The antimicrobial efficacy of PT was verified against clinical isolates of coagulase-negative staphylococci in vitro. PT was able to inhibit biofilm formation in the most tolerant isolate at sub-inhibitory concentrations. These observations indicate that an ability to prevent biofilm formation, independently of effects on cell viability may contribute to the in vivo topical efficacy of essential oils.