The bacteriophage infection cycle has been extensively studied, yet little is known about the nanostructure and mechanical changes that lead to bacterial lysis. Here, atomic force microscopy was used to study in real time and in situ the impact of the canonical phage T4 on the nanotopography and biomechanics of irreversibly attached, biofilm-forming E. coli cells. The results show that in contrast to the lytic cycle in planktonic cells, which ends explosively, anchored cells that are in the process of forming a biofilm undergo a more gradual lysis, developing distinct nanoscale lesions (~300 nm in diameter) within the cell envelope. Furthermore, it is shown that the envelope rigidity and cell elasticity decrease (>50% and >40%, respectively) following T4 infection, a process likely linked to changes in the nanostructure of infected cells. These insights show that the well-established lytic pathway of planktonic cells may be significantly different from that of biofilm-forming cells. Elucidating the lysis paradigm of these cells may advance biofilm removal and phage therapeutics.

噬菌体感染周期已被广泛研究，但对导致细菌裂解的纳米结构和机械变化知之甚少。在这里，原子力显微镜被用来实时、原位研究典型噬菌体 T4 对不可逆附着、形成生物膜的大肠杆菌细胞的纳米形貌和生物力学的影响。结果表明，与浮游细胞中爆炸性结束的裂解周期相反，正在形成生物膜的锚定细胞经历更渐进的裂解，在细胞包膜内形成明显的纳米级损伤（直径约 300 nm） 。此外，结果表明，T4 感染后包膜刚性和细胞弹性降低（分别为 >50% 和 >40%），这一过程可能与受感染细胞纳米结构的变化有关。这些见解表明，浮游细胞成熟的裂解途径可能与生物膜形成细胞的裂解途径显着不同。阐明这些细胞的裂解模式可能会促进生物膜去除和噬菌体治疗。