Immune evasion by staphylococci

Abstract

Staphylococcus aureus can cause superficial skin infections and, occasionally, deep-seated infections that entail spread through the blood stream. The organism expresses several factors that compromise the effectiveness of neutrophils and macrophages, the first line of defence against infection. S. aureus secretes proteins that inhibit complement activation and neutrophil chemotaxis or that lyse neutrophils, neutralizes antimicrobial defensin peptides, and its cell surface is modified to reduce their effectiveness. The organism can survive in phagosomes, express polysaccharides and proteins that inhibit opsonization by antibody and complement, and its cell wall is resistant to lysozyme. Furthermore, S. aureus expresses several types of superantigen that corrupt the normal humoral immune response, resulting in anergy and immunosuppression. In contrast, Staphylococcus epidermidis must rely primarily on cell-surface polymers and the ability to form a biolfilm to survive in the host.

The bacterial flora in the teat duct of ewes can protect against and can cause mastitis

“…Occupation of the host's epithelial surfaces by bacterial flora and thus, prevention of pathogen adherence on these cells [5,6], can be particularly important, given that adherence on mammary epithelial cells by M. haemolytica is necessary for leucotoxin production [55]. Since staphylococci adhere to mammary epithelial cells forming biofilms [13,42], one may postulate this as the primary mechanism by which the protective effects took place in the present experiments.…”

Hypoxic regulation of neutrophil function and consequences for Staphylococcus aureus infection

“…aureus has evolved extensive virulence mechanisms, which aim to evade neutrophil killing, including inhibition of neutrophil chemotaxis and extravasation, strategies to evade phagocytosis, disarmament of antimicrobial peptides and proteases, removal of anti-oxidants, degradation of NETs and direct lysis of neutrophils by secreted leukotoxins. This subject has been extensively reviewed [80], and further details are beyond the scope of this review. Despite being considered classically an extracellular pathogen, S. aureus has been shown to survive within the phagosome, and transfer of neutrophils containing viable intracellular bacteria to a naïve animal can institute infection [81].…”

Bacterial endophthalmitis: Therapeutic challenges and host–pathogen interactions

“…The ability of S. epidermidis to form biofilms on IOL materials contributes not only to colonization, but also to circumvention of an immune response designed to eliminate bacteria, and to limitation in the effectiveness of antibiotics (Baillif, et al, 2006). Although S. epidermidis produces few toxins, this organism can readily evade the immune system by biofilm formation, a process mediated by surface proteins such as autolysin, polysaccharide intercellular adhesin, fibrinogen-binding proteins, and accumulation-associated protein (Foster, 2005). The role of these specific adhesins in the formation of intraocular biofilms or the pathogenicity of S. epidermidis endophthalmitis has yet to be determined.…”