This is a narrative (non-systematic) review from South Asian University published 21 August 2018 in the Indian Journal of Microbiology. It covers: (1) the four-stage biofilm lifecycle (attachment, QS-governed sessile growth, EPS-driven maturation, dispersal); (2) EPS compositionβexopolysaccharides, proteins, eDNA, and structural amyloids such as curli in Enterobacteriaceae and TasA in Bacillus subtilis; (3) three QS modes (Gram-negative AHL, Gram-positive peptides, universal AI-2); and (4) control strategies including quorum-quenching molecules (furanone C30, meta-bromothiolactone), EPS-disrupting enzymes (DNase I, dispersin B), and antimicrobial peptides . The authors also cite a food-industry figure that ~60% of outbreaks involve biofilm-associated infections .
The review treats EPS as a broadly protective barrier. Subsequent primary research complicates this: in Salmonella enterica, increased csgD-driven matrix production thickened per-cell EPS envelopes and shifted architecture from dense isotropic to sparse nematic, and biofilm survival after 500 Β΅g/mL cefotaxime decreased with increasing matrix productionβcontrary to the passive-barrier view; architecture combined with metabolic-cost-adjusted sink strength predicted survival best (RΒ² = 0.98) . Environment and substratum also shape community structure independent of QS: marine biofilms on four substrata showed Proteobacteria dominance varying from 35β44% and differential mussel settlement (>80% on glass/steel vs. lower on hydrophobic glass) . Clinically, fungal biofilms follow the same refractory pattern the review describes for bacteria: mature Candida auris biofilms are up to 100-fold more fluconazole-resistant than planktonic cells .
Strengths: clear organization, broad coverage, appropriate citation density, and a useful conceptual figure (Fig. 1) linking persister cells, QQ molecules, and EPS-disrupting enzymes. Weaknesses: no systematic search methodology (selection/citation bias risk); the passive-barrier framing of EPS protection is now partially overturned by reaction-diffusion work; the 60% foodborne outbreak figure is cited secondhand without primary verification; dispersal is acknowledged as weakly understood but receives no new data; no quantitative effect sizes, no meta-analytic synthesis, and no discussion of dry-surface biofilms relevant to hospital decontamination, where standardized models now exist . Confidence: the review's descriptive claims are well-supported; its mechanistic framing of EPS as a diffusion barrier should be updated. What would change this assessment: evidence that increased matrix production consistently raises survival across multiple antimicrobials and species would restore the barrier model.
Reported relative abundances (16S V4βV5, n=4 substrata, 7-day marine biofilms); illustrates the environmental contingency of biofilm architecture that the 2018 review underweights.
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