Abstract
Although antibiotics have been indispensable in the advancement of modern medicine, there are downsides to their use. Growing resistance to broad-spectrum antibiotics is leading to an epidemic of infections untreatable by first-line therapies. Resistance is exacerbated by antibiotics used as growth factors in livestock, over-prescribing by doctors, and poor treatment adherence by patients. This generates populations of resistant bacteria that can then spread resistance genes horizontally to other bacterial species, including commensals. Furthermore, even when antibiotics are used appropriately, they harm commensal bacteria leading to increased secondary infection risk. Effective antibiotic treatment can induce bacterial survival tactics, such as toxin release and increasing resistance gene transfer. These problems highlight the need for new approaches to treating bacterial infection. Current solutions include combination therapies, narrow-spectrum therapeutics, and antibiotic stewardship programs. These mediate the issues but do not address their root cause. One emerging solution to these problems is anti-virulence treatment: preventing bacterial pathogenesis instead of using bactericidal agents. In this review, we discuss select examples of potential anti-virulence targets and strategies that could be developed into bacterial infection treatments: the bacterial type III secretion system, quorum sensing, and liposomes.
Highlights
Maisetta, Giovanna Batoni and Before the serendipitous discovery of penicillin in 1929, the three leading causes of death in the United States were all infectious diseases: influenza, pneumonia, and tuberculosis [1,2]
Humans infected with Shiga toxin (Stx)-producing bacteria manifest in hemolytic uremic syndrome (HUS), a disease characterized by a triad of symptoms that all stem from the apoptotic mechanism of Stx: reduced serum platelet levels, hemolytic anemia, and renal damage [132,133,134]
Every year in the US there are approximately 17,000 shigellosis and 18,500 Shiga toxin-producing E. coli (STEC)-caused deaths [2]. The majority of these deaths occur after the patient and 18,500 STEC-caused deaths [2]. The majority of these deaths occur after the patient has undergone treatment which lends to the question: Were the deaths caused by the has undergone treatment which lends to the question: Were the deaths caused by the ininfection or by complications induced by antibiotic treatment, such as toxins released fection or bacterial by complications induced by antibiotic treatment, such as toxins released through through bacterial SOS responses?
Summary
Giovanna Batoni and Before the serendipitous discovery of penicillin in 1929, the three leading causes of death in the United States were all infectious diseases: influenza, pneumonia, and tuberculosis [1,2]. The observance of resistance to each new antibiotic is never far behind the commercial release of the drug [6]. Antibiotics can destroy commensal bacterial colonies, leading to an increased risk of infection and other health complications [8,9,10]. They may induce bacterial SOS tactics, which can include toxin release and increased transfer of resistance genes [11,12]. Anti-virulence therapies target the pathogenic mechanisms of bacteria rather than killing bacteria outright. These targets and strategies include the bacterial type III secretion system [13,14,15], quorum sensing [16,17,18], and liposomes [19,20,21]
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