MRSA compendium of epidemiology, transmission, pathophysiology, treatment, and prevention within one health framework

Abstract

Staphylococcus aureus is recognized as commensal as well as opportunistic pathogen of humans and animals. Methicillin resistant strain of S. aureus (MRSA) has emerged as a major pathogen in hospitals, community and veterinary settings that compromises the public health and livestock production. MRSA basically emerged from MSSA after acquiring SCCmec element through gene transfer containing mecA gene responsible for encoding PBP-2α. This protein renders the MRSA resistant to most of the β-lactam antibiotics. Due to the continuous increasing prevalence and transmission of MRSA in hospitals, community and veterinary settings posing a major threat to public health. Furthermore, high pathogenicity of MRSA due to a number of virulence factors produced by S. aureus along with antibiotic resistance help to breach the immunity of host and responsible for causing severe infections in humans and animals. The clinical manifestations of MRSA consist of skin and soft tissues infection to bacteremia, septicemia, toxic shock, and scalded skin syndrome. Moreover, due to the increasing resistance of MRSA to number of antibiotics, there is need to approach alternatives ways to overcome economic as well as human losses. This review is going to discuss various aspects of MRSA starting from emergence, transmission, epidemiology, pathophysiology, disease patterns in hosts, novel treatment, and control strategies.

Keywords: MRSA; MRSA infections; epidemiology; pathophysiology; prevention; transmission; treatment.

FIGURE 1

Bovine-adapted clonal complexes Staphylococcus aureus (S. aureus CCs) appear to have derived from human CCs and acquired bovine affinities through a series of spill-over events that resulted in the acquisition of various mobile genetic elements (MGEs). Several hosts have a high prevalence of the CC398 lineage. This lineage seems to have started in humans via reverse zoonosis, then it spread to pigs, then it returned to humans via pig zoonosis, and ultimately it spread to other species.

FIGURE 2

Tissue necrosis is caused by Panton-Valentine leukocidin (PVL). The two PVL components secreted by Staphylococcus aureus, LukS-PV, and LukF-PV, collectively form a pore-forming heptamer on the membranes of polymorphonuclear leukocytes (PMNs). Low PVL concentrations cause polymorphonuclear leukocytes (PMN) apoptosis through direct binding to mitochondrial membranes, whereas high PVL concentrations cause PMN lysis (Genestier et al., 2005). From lysed PMNs, reactive oxygen species (ROS) can cause tissue necrosis. Furthermore, the release of granules from PMNs that have been lysed may cause an inflammatory response that leads to tissue necrosis. PVL is unlikely to cause direct necrosis of epithelial cells.

FIGURE 3

Panton-Valentine leukocidin (PVL) producing community-acquired–MRSA (CA-MRSA) model: In MSSA strain, two genes (pvl) encoding the methicillin-resistant phage virus (PVL) are infected and lysed by the phage (phiSLT) (Staphylococcal Leukocytolytic Toxin). Then, a horizontal transfer of a methicillin resistance cassette (SCCmec IV, V, or VT) carrying the mecA gene into the pvl-positive methicillin susceptible Staphylococcus aureus (MSSA) strain allows it to incorporate into the genome somewhere other than the phiSLT (Staphylococcal Leukocytolytic Toxin) integration site.

FIGURE 4

Different tactics used by S. aureus to survive inside mammary glands to cause infection.

FIGURE 5

Antibacterial mechanisms of various phytochemicals against methicillin resistant strain of Staphylococcus aureus (MRSA).

FIGURE 6

Antibacterial mechanisms of action of various nanoparticles against methicillin resistant strain of Staphylococcus aureus (MRSA).

FIGURE 7

General antibacterial mechanism of bacteriophages against methicillin resistant strain of Staphylococcus aureus (MRSA).

FIGURE 8

Antibacterial mechanisms of various probiotics against methicillin resistant strain of Staphylococcus aureus (MRSA).