Computational modeling of microstreaming-induced disruption of Staphylococcus aureus biofilms.

Staphylococcus aureus presents significant challenges in clinical settings due to its ability to form resilient biofilms, which drive persistent infections on medical implants and at wound sites. These bacteria are the leading cause of biomaterial-associated infections, often leading to implant failure. Moreover, S. aureus can form biofilms on cardiovascular implants, further complicating device-related infections. Cavitation microstreaming, generated by ultrasound-activated microbubbles through their oscillations, has emerged as a promising method for disrupting biofilms. However, the underlying biofilm-microstreaming interactions governing bacterial detachment remain poorly understood. In this study, a computational framework integrating coarse-grained molecular dynamics with the lattice Boltzmann method was developed to simulate Staphylococcus aureus biofilm growth and its response to microstreaming. The modeled biofilm morphology closely aligns with experimental confocal microscopy data, with less than 14% deviation in spatial spreading and roughness. To assess biofilm disruption, we applied microstreaming fields with dipole and quadrupole flow patterns at representative speeds of 1, 5, and 10 mm/s. Our results demonstrate that higher flow velocities facilitate greater detachment, with dipole flows inducing gradual erosion and quadrupole flows causing more localized disruption. By integrating computational modeling with experimental validation, this work provides a robust platform to investigate and maximize biofilm-microstreaming interactions. These findings emphasize the potential of ultrasound-activated microbubble-induced microstreaming as a noninvasive strategy for biofilm removal and provide a foundation for future therapeutic approaches.