Antimicrobial Resistance and Food Animals: Influence of Livestock Environment on the Emergence and Dissemination of Antimicrobial Resistance

Abstract

The emergence and dissemination of antimicrobial resistance among human, animal and zoonotic pathogens pose an enormous threat to human health worldwide. The use of antibiotics in human and veterinary medicine, and especially the use of large quantities of antibiotics in livestock for the purpose of growth promotion of food animals is believed to be contributing to the modern trend of the emergence and spread of bacteria with antibiotic resistant traits. To better control the emergence and spread of antimicrobial resistance several countries from Western Europe implemented a ban for antibiotic use in livestock, specifically the use of antibiotics for growth promotion of food animals. This review article summarizes the recent knowledge of molecular acquisition of antimicrobial resistance and the effects of implementation of antibiotic growth promoter bans on the spread of antimicrobial resistant bacteria in animals and humans. In this article, we also discuss the main zoonotic transmission routes of antimicrobial resistance and novel approaches designed to prevent or slow down the emergence and spread of antimicrobial resistance worldwide. Finally, we provide future perspectives associated with the control and management of the emergence and spread of antimicrobial resistant bacteria.

Keywords: antimicrobial resistance; emerging infectious diseases; growth promotions; livestock; selective pressure.

Figure 1

Overview of Zn NPs mediated toxicity against a Gram-negative organism. ZnO and ZN-CuO NPs release high concentrations of reactive oxygen species (ROS) and Zn²⁺, followed by Zn²⁺ entrance into the periplasmic space via porins and the outer membrane lipid peroxidation caused by ROS (i.e., OH, O₂, and O₂⁻). The process of lipid peroxidation leads to an increase the outer membrane permeability, resulting in an enhanced influx of Zn²⁺ into the periplasm milieu. Transport of highly concentrated Zn²⁺ across the inner membrane remains largely unknown. It can be hypothesized that Zn²⁺ enters the cytoplasm through a permeabilized inner membrane, caused by an ongoing process of lipid peroxidation and also via MFS transporters, as they can facilitate symport, antiport and uniport transfer in response to chemiosmotic ion gradients. Once penetrated, the intracellular Zn²⁺ reacts with a wide range of proteins leading to down-regulation and inhibition of enzymes and proteins involved in translation, the ATP cycle and the amino acid biosynthesis, all key metabolic processes. Disruption of these central metabolic processes leads to serious metabolic imbalances and finally to cellular death. OM, outer membrane; P, periplasmic space; IM, inner membrane.