Staphylococcus aureus Dormancy: Waiting for Insurgency.

Relapse infection usually results from resistance to the antibiotic, acquired genes, or persister cells. Persister cells are formed through mutation, reduced activity or metabolically inactive pathways induced by antibiotics, harassing conditions, low ATP, and malnutrition. These factors provide the ground for bacteria to grow slowly. Such a slow growth rate makes traditional antibiotics ineffective against persister cells. Staphylococcus aureus (S. aureus), in addition to this form, can be observed in Small Colony Variants (SCVs), L-forms, and dormant, all of which are characterized by at least one feature, i.e., slow growth. Despite their slow growth, they are metabolically active in terms of stringent SOS and cell wall stress responses. The stress response involves resistance against harassing conditions, and it survives until it is reactivated later. The present study aims to discuss the mechanisms of all persister cell formations, circumstances involved, gene mutation, and adoptable strategies against it.

Staphylococcus aureus: Biofilm Formation and Strategies Against it.

Formation of Staphylococcus aureus biofilm causes significant infections in the human body. Biofilm forms through the aggregation of bacterial species and brings about many complications. It mediates drug resistance and persistence and facilitates the recurrence of infection at the end of antimicrobial therapy. Biofilm formation is completed in a series of steps, and any interference in these steps can disrupt its formation. Such interference may occur at any stage of biofilm production, including attachment, monolayer formation, and accumulation. Interfering agents can act as quorum sensing inhibitors and interfere in the functionality of quorum sensing receptors, attachment inhibitors, and affect cell hydrophobicity. Among these inhibiting strategies, attachment inhibitors could serve as the best agents against biofilm formation, because in case pathogens abort the attachment, the next stages of biofilm formation, e.g., accumulation and dispersion, will fail to materialize. Inhibition at this stage leads to suppression of virulence factors and invasion. One of the best knowing inhibitors is a chelator that collects metal, Fe+, Zn+, and magnesium critical for biofilm formation. These effective factors in the binding and formation of biofilm are investigated, and the coping strategy is discussed. This review examines the stages of biofilm formation and determines what factors interfere in the continuity of these steps. Finally, the inhibition strategies are investigated, reviewed, and discussed.