From seven tropical fruits, 55 LAB strains were isolated; 11 inhibited F. oxysporum, and two Ficus racemosa isolates maintained >15 mm inhibition zones after 10 days. 16S rDNA identified them as Lpb. plantarum MYSVCF3 (OL347999) and Lpb. argentoratensis MYSVCF5 (OR435844) . Probiotic screening: both tolerated pH 2, 0.3% bile, and 0.6% phenol (Lpb. plantarum >90% viable); hydrophobicity 27% vs 42%; auto-aggregation 57% vs 52% at 24 h; non-hemolytic, vancomycin-resistant (typical for lactobacilli) .
Viable MYSVCF5 cells completely suppressed mycelial biomass from day 1 (control reached 0.9 g dry weight by day 14); 10% CFS cut biomass 94% (1.1 β <0.1 g), 20% gave >98% inhibition, and 0.4β0.6 mg/mL CFS prevented visible growth and conidial germ-tube formation . Activity survived 100 Β°C/15 min and 8 months of storage, but was abolished by pH neutralization and proteinase K β authors infer organic acids plus a heat-stable proteinaceous component, the latter unconfirmed. Citric acid (34.9 Β΅g/mL, 67% of acid pool) was proposed as the key antifungal compound; notably, the authors do not test purified citric acid alone against F. oxysporum, so citric causality remains correlational .
The first report of Lpb. argentoratensis antifungal activity is genuinely novel; fruit-derived LAB biocontrol is consistent with prior honey- and rhizosphere-derived L. plantarum work showing neutralized CFS loses activity, implicating organic acids . Blindspots: (1) n = 3 replicates, single dry-season sampling, t-tests only with no multiple-testing correction; (2) conidial germination "complete inhibition" measured microscopically without supporting viability assays; (3) no whole-genome sequencing, bacteriocin gene screening, or purified-compound MIC confirmation; (4) no in vivo plant or animal models β the authors themselves flag scalability and delivery as unaddressed . Falsification would require showing CFS effects persist after acid-neutralization plus protease, or that field application fails to suppress Fusarium wilt.
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