Antimicrobial resistance three ways: healthcare crisis, major concepts and the relevance of biofilms

Abstract

Worldwide, infections are resuming their role as highly effective killing diseases, as current treatments are failing to respond to the growing problem of antimicrobial resistance (AMR). The social and economic burden of AMR seems ever rising, with health- and research-related organizations rushing to collaborate on a worldwide scale to find effective solutions. Resistant bacteria are spreading even in first-world nations, being found not only in healthcare-related settings, but also in food and in the environment. In this minireview, the impact of AMR in healthcare systems and the major bacteria behind it are highlighted. Ecological aspects of AMR evolution and the complexity of its molecular mechanisms are explained. Major concepts, such as intrinsic, acquired and adaptive resistance, as well as tolerance and heteroresistance, are also clarified. More importantly, the problematic of biofilms and their role in AMR, namely their main resistance and tolerance mechanisms, are elucidated. Finally, some of the most promising anti-biofilm strategies being investigated are reviewed. Much is still to be done regarding the study of AMR and the discovery of new anti-biofilm strategies. Gladly, considerable research on this topic is generated every day and increasingly concerted actions are being engaged globally to try and tackle this problem.

Entrapment of a phage cocktail and cinnamaldehyde on sodium alginate emulsion-based films to fight food contamination by Escherichia coli and Salmonella Enteritidis

“…The ability of these pathogens to grow on food matrices often leads to the establishment of microbial communities embedded on a self-produced extracellular matrix, known as biofilms, which confers them protection to antimicrobial agents (Galié, García-Gutiérrez, Miguélez, Villar, & Lombó, 2018). Furthermore, the inappropriate use of antibiotics in both humans and animals (livestock industry) has led to an acceleration of microbial resistance (Jorge et al, 2019).…”

Pseudomonas aeruginosa and Staphylococcus aureus communication in biofilm infections: insights through network and database construction

“…The latter phenomenon is also controlled by the LasI/LasR system by downregulation the expression of PEL, a major biofilm matrix component (Ueda and Wood 2009). QS also influences swarming motility, which has been linked to early stages of biofilm formation (Shrout et al 2006) and is also related to the antibiotic tolerance found in P. aeruginosa biofilms but not in planktonic cells (Ciofu et al 2015;Jorge et al 2019).…”

“…b-lactamase) (Pang et al 2019). P. aeruginosa can also acquire resistance genes from other microorganisms by horizontal gene transfer, while also being able to experience adaptive resistance, as is the case of biofilm formation (Jorge et al 2019).…”

“…Because of this, S. aureus is very often associated with nosocomial infections, since it is commonly transmitted by colonised healthcare staff through direct contact or invasive medical procedures (Bhattacharya et al 2015). Its ability to evolve and adapt to multiple settings has led MRSA to rapid disperse over the globe, being considered a high threat according to the WHO (WHO 2017b; Jorge et al 2019). Additionally, MRSA has been developing resistance to virtually all antibiotics classes that are used to treat it, either by making use of its intrinsic resistance factors or by acquiring more through mutations or horizontal gene transfer from other microorganisms (Watkins et al 2019).…”

Fostering Innovation in the Treatment of Chronic Polymicrobial Cystic Fibrosis-Associated Infections Exploring Aspartic Acid and Succinic Acid as Ciprofloxacin Adjuvants

“…However, these therapies are often unsuccessful, mostly due to biofilms that are microbial communities encased in a self-produced matrix that provide to the resident organisms augmented tolerance to antibiotics (Lopez et al, 2010). Their impressive high level of antimicrobial tolerance results from the combination of several mechanisms, including restricted penetration of antibiotics through the matrix, slow growth of bacteria within biofilms due to nutritional constraints and restricted oxygen penetration, quorum-sensing, expression of biofilm-specific genes, and the presence of persister cells (Mah, 2012;Jorge et al, 2019).…”