Staphylococcus aureusSecreted Toxins and Extracellular Enzymes

Abstract

S. aureus is a formidable pathogen capable of causing infections in different sites of the body in a variety of vertebrate animals, including humans and livestock. A major contribution to the success of S. aureus as a pathogen is the plethora of virulence factors that manipulate the host's innate and adaptive immune responses. Many of these immune modulating virulence factors are secreted toxins, cofactors for activating host zymogens, and exoenzymes. Secreted toxins, such as poreforming toxins and superantigens are highly inflammatory and can cause leukocyte cell death by cytolysis and clonal deletion, respectively. Coagulases and staphylokinases are cofactors that hijack the host's coagulation system. Exoenzymes, including nucleases and proteases, cleave and inactivate various immune defense and surveillance molecules, such as complement factors, antimicrobial peptides, and surface receptors important for leukocyte chemotaxis. Additionally, some of these secreted toxins and exoenzymes can cause disruption of endothelial and epithelial barriers through cell lysis and cleavage of junction proteins. A unique feature when examining the repertoire of S. aureus secreted virulence factors is the apparent functional redundancy exhibited by the majority of the toxins and exoenzymes. However, closer examination of each virulence factor revealed that each has unique properties that have important functional consequences. This chapter will provide a brief overview of the current understanding on the major secreted virulence factors critical for S. aureus pathogenesis.

Phenotypic and Molecular Detection of Biofilm Formation in Staphylococcus aureus Isolated from Different Sources in Algeria

“…Staphylococcus (S.) aureus is a bacterium that can cause a wide range of diseases in humans and animals. The capacity of S. aureus to colonize and infect different sites of the body is related to the presence of a variety of virulence factors [1]. Among the virulence factors responsible for the pathogenicity of S. aureus, adhesion proteins and the ability to form biofilms on biotic and abiotic surfaces are of importance [2,3].…”

The evolution of virulence inPseudomonas aeruginosaduring chronic wound infection

“…Host immunity and mixedspecies interactions cannot be ruled out as variables in our experiment, as they are not entirely standardized even in laboratory mice, who may have small genetic variations and unique flora. Furthermore, given all of these considerations, caution must be exercised when extrapolating experimental results from a laboratory mouse model to a vastly more complex human infection, as virulence factors can be host specific [69,70].…”

Critical Parameters for the Development of Novel Therapies for Severe and Resistant Infections—A Case Study on CAL02, a Non-Traditional Broad-Spectrum Anti-Virulence Drug

“…The tremendous impact of virulence effectors on disease severity was originally demonstrated using transgenic or knock-out mouse strains. For instance, loss of the expression of pore-forming toxins causes pathogenic bacteria to be less virulent or completely avirulent, while transgenic expression of virulence effectors in harmless bacteria turn them into aggressive pathogens [2,8]. With CAL02, the role of virulence effectors was also studied, using bacterial culture supernatant, which comprises the entire secretome of the pathogen with its panoply of virulence effectors.…”