The bacteria ability to develop community structures known

The gram-positive
bacterium Staphylococcus aureus is a
common human commensal, colonizing the nostrils and skin of ~30% of the
population (Gorwitz et al., 2008; Miller and Diep, 2008). S.
aureus is a versatile pathogen causing
community (CA) and healthcare (HA) skin and soft tissue infections (SSTIs), endovascular infections, pneumonia, septic arthritis,
endocarditis, osteomyelitis, foreign-body infections, and sepsis (Lowy, 1998; Tong et al., 2015).
They range in severity from minor, self-limiting, superficial infections
to life-threatening diseases (Olaniyi et al., 2016). S. aureus is the most commonly isolated
bacteria from such wound infections
and studies involving patients with chronic venous leg ulcers found S. aureus positive cultures in 88–93.5%
of infections.(Archer et al., 2016). Bacteremia caused by S.
aureus is associated with higher morbidity and mortality, compared with
bacteremia caused by other pathogens, with an
annual incidence rate of 20 to 50 cases/100,000 population, and a mortality
rate of 10% and 30%. The highest mortality rates occur in patients with primary
bacteremic pulmonary infections and infective endocarditis, whereas the lowest
rates occur in patients with central or peripheral venous catheter-related
infections. (Van Hal et al., 2012).

One of the reasons the staphylococcal infections are
difficult to eradicate is the bacteria ability to develop community structures
known as biofilms by attaching to different surfaces (tissues, catheters,
medical devices),  and often occur in
areas of the body that are not easily accessible for treatment (del Pozo,
Jacqueline ).

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According to
NIH, as much as 80% of human infections are biofilm-based  (Davies D., 2003)??? Ramane sau schimb cu
altceva

A biofilm is
defined as a sessile microbial community in which cells are attached to a
surface or to other cells and embedded in a protective extracellular polymeric
matrix. This mode of growth exhibits altered physiologies with respect to gene
expression and protein production (Parsek and Singh, 2003;
Archer et al., 2011; Kiedrowski and
Horswill, 2011).

Biofilm formation can be divided into three major stages:
initial attachment, development/maturation of the biofilm and dispersion.

During initial attachment, bacteria adhere to the available
surface and in case of abiotic one its conditioning is important through
various physiochemical parameters:
chemical composition of the material, hydrophobicity, electrostatic charges,
surface energy, surface roughness and in the case of biotic adhesion: serum and
tissue protein adsorption 14, 15. (capitol Staphylococcus aureus Biofilms and their Impact on the on
the Medical Field)

Biofilm
maturation is based on bacterial multiplication and formation of a
multicellular structure.

The final stage of biofilm development is the detachment of
cells from the biofilm colony and their dispersal into the environment which
contributes to biological dispersal, bacterial survival, and disease
transmission. Like other stages of biofilm development, dispersal is a complex
process that involves numerous environmental signals, signal transduction
pathways, and effectors (Karatan and Watnick, 2009 citat de J Dent Res. 2010 Mar; 89(3): 205–218. doi:  10.1177/0022034509359403 MCID: PMC3318030 Biofilm Dispersal Mechanisms,
Clinical Implications, and Potential Therapeutic Uses J.B. Kaplan)

The biofilm matrix is a complex structure that contains
extracellular DNA (eDNA), both from lysed bacteria and potentially from host
neutrophil cell death, (30, 31), proteinaceous adhesins,
directly associated with bacteria in the biofilm, or free in the biofilm matrix
(32), recycled cytoplasmic proteins
that moonlight as components of the extracellular matrix, (Foulston L,
2014), the extracellular polysaccharide intercellular adh                                                                                       
esin (PIA), (34) teichoic acids (35). The
matrix can impede the access of certain types of immune defenses, such as
macrophages. (Scherr et al., 2014). Mai trebuie adaugat legat de
efectul protector

The bacterial attachment is mediated by a serie of
surface-associated adhesins and S. aureus
genome encodes more than twenty adhesins (32, 36, 37
). Staphylococcal adhesion and biofilm accumulation are mediated by covalently
anchored cell wall proteins, non-covalently associated proteins, and
non-protein factors (Microbiol Spectr. 2016 April ; 4(2): .
doi:10.1128/microbiolspec.VMBF-0022-2015. The Staphylococcal Biofilm:
Adhesins, regulation, and host response Alexandra E. Paharik and Alexander R.
Horswill).

Staphylococcal cell wall-anchored (CWA) proteins are
secreted by the Sec system and share a C-terminal cell wall anchoring motif,
hydrophobic domain, and positively-charged domain (40). Foster et al., proposed to classify the
Staphylococcal CWA proteins into four groups based on structural motifs (40): MSCRAMMs
(microbial surface component recognizing adhesive matrix molecules), the NEAT
motif family, the three-helical bundle family, and the G5-E repeat family. All
of these types of CWA proteins are involved in staphylococcal biofilm formation.
 MSCRAMMs
are adhesins that contain at least two IgG-like folds and employ a ligand
binding mechanism called dock, lock, and latch (40). The
Staphylococcal MSCRAMMs are the Clf-Sdr family proteins, including Bbp (bone
sialoprotein-bnding protein), the FnBPs (fibronectin-binding proteins), and CNA
(collagen adhesion). (Alexandra
E. Paharik and Alexander R. Horswill). The Clf-Sdr family consists of Clumping
factor A (ClfA), clumping factor B (ClfB), and the Sdr proteins. ClfA and ClfB
are fibrinogen-binding proteins in S.
aureus (40, 44),
Rot and agr affect bacterial binding
to fibrinogen by regulating clfB but
not clfA (46).  S.
aureus has two fibronectin-binding proteins, FnBPA and FnBPB, encoded by fnbA and fnbB, respectively (103). FnBP binding to fibronectin induces
bacterial invasion into epithelial cells, endothelial cells, and keratinocytes
(107–109). The FnBPs affect biofilm formation by a
self-association mechanism that is distinct from ligand binding and virulence.
(111, 112).

The NEAT motif family consists of the Isd (iron-regulated
surface determinant) proteins who bind heme or hemoglobin, facilitating its
transport into the bacterial cell, and they are up-regulated in iron limiting
conditions (122). S. aureus
IsdA is the most abundant CWA protein in iron starvation conditions, and also
decreases surface hydrophobicity, which makes S. aureus more resistant to bactericidal fatty acids and peptides
in human skin (124). IsdA also is able to bind human fibrinogen and
fibronectin (125).

The sole three-helical bundle cell wall-anchored protein is
Staphylococcal Protein A (SpA), which is present in all strains of S. aureus. SpA allows immune evasion by binding
to the conserved Fc region of immunoglobulin IgG, (129, 130)
and contributes to disruption of the host immune response by promoting
bacterial survival in human blood after being 
released from the cell wall (37, 132). 

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