Where is staphylococcus albus found

Sun, D. Inhibition of biofilm formation by monoclonal antibodies against Staphylococcus epidermidis RP62A accumulation-associated protein. Conlon, K. Inactivations of rsbU and sarA by IS represent novel mechanisms of biofilm phenotypic variation in Staphylococcus epidermidis. Chaignon, P. Susceptibility of staphylococcal biofilms to enzymatic treatments depends on their chemical composition. Increased colonization of indwelling medical devices by quorum-sensing mutants of Staphylococcus epidermidis in vivo.

This manuscript shows the role of the S. Yarwood, J. Quorum sensing in Staphylococcus aureus biofilms. Boles, B. Agr-mediated dispersal of Staphylococcus aureus biofilms. Teufel, P. Characterization of an extracellular metalloprotease with elastase activity from Staphylococcus epidermidis. Dubin, G. Molecular cloning and biochemical characterisation of proteases from Staphylococcus epidermidis.

Ohara-Nemoto, Y. Characterization and molecular cloning of a glutamyl endopeptidase from Staphylococcus epidermidis.

Kaplan, J. Genes involved in the synthesis and degradation of matrix polysaccharide in Actinobacillus actinomycetemcomitans and Actinobacillus pleuropneumoniae biofilms. Kong, K. Staphylococcus quorum sensing in biofilm formation and infection. Regulated expression of pathogen-associated molecular pattern molecules in Staphylococcus epidermidis : quorum-sensing determines pro-inflammatory capacity and production of phenol-soluble modulins.

Characterization of the Staphylococcus epidermidis accessory-gene regulator response: quorum-sensing regulation of resistance to human innate host defence. Article PubMed Google Scholar. Kocianova, S. Little, S. Molecular pathogenesis of Bacillus anthracis infection.

Oppermann-Sanio, F. Occurrence, functions and biosynthesis of polyamides in microorganisms and biotechnological production. Naturwissenschaften 89 , 11—22 Kristian, S. Biofilm formation induces C3a release and protects Staphylococcus epidermidis from IgG and complement deposition and from neutrophil-dependent killing.

Polysaccharide intercellular adhesin PIA protects Staphylococcus epidermidis against major components of the human innate immune system. This study shows the important role of PNAG in immune evasion. Begun, J. Staphylococcal biofilm exopolysaccharide protects against Caenorhabditis elegans immune defences. Mah, T. A genetic basis for Pseudomonas aeruginosa biofilm antibiotic resistance. Heine, H. Recognition of bacterial products by Toll-like receptors.

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Lipoproteins are critical TLR2 activating toxins in group B streptococcal sepsis. Li, H. Commercial peptidoglycan preparations are contaminated with superantigen-like activity that stimulates IL production. Hashimoto, M. Not lipoteichoic acid but lipoproteins appear to be the dominant immunobiologically active compounds in Staphylococcus aureus.

Mehlin, C. An inflammatory polypeptide complex from Staphylococcus epidermidis : isolation and characterization. This article describes the identification and pro-inflammatory properties of the main S. Wang, R. Identification of novel cytolytic peptides as key virulence determinants for community-associated MRSA. Nature Med. Hajjar, A. Lambert, P. Lipid S, a novel Staphylococcus epidermidis exocellular antigen with potential for the serodiagnosis of infections.

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The antimicrobial peptide-sensing system aps of Staphylococcus aureus. Bader, M. Recognition of antimicrobial peptides by a bacterial sensor kinase. Marin, M. Enterotoxigenicity of Staphylococcus strains isolated from Spanish dry-cured hams.

Bautista, L. A quantitative study of enterotoxin production by sheep milk staphylococci. Klingenberg, C. Persistent strains of coagulase-negative staphylococci in a neonatal intensive care unit: virulence factors and invasiveness. Scheifele, D. Delta-like toxin produced by coagulase-negative staphylococci is associated with neonatal necrotizing enterocolitis.

Detection of virulence-associated genes not useful for discriminating between invasive and commensal Staphylococcus epidermidis strains from a bone marrow transplant unit. Modulation of the polysaccharide intercellular adhesin PIA expression in biofilm forming Staphylococcus epidermidis. Analysis of genetic mechanisms. The presence of icaADBC is detrimental to the colonization of human skin by Staphylococcus epidermidis. Lai, Y. The human anionic antimicrobial peptide dermcidin induces proteolytic defence mechanisms in staphylococci.

Diekema, D. Vos, M. Successful search-and-destroy policy for methicillin-resistant Staphylococcus aureus in The Netherlands. Strict infection control measures do not prevent clonal spread of coagulase negative staphylococci colonizing central venous catheters in neutropenic hemato-oncologic patients. Chambers, H. Increased amounts of a novel penicillin-binding protein in a strain of methicillin-resistant Staphylococcus aureus exposed to nafcillin.

Ma, X. Novel type of staphylococcal cassette chromosome mec identified in community-acquired methicillin-resistant Staphylococcus aureus strains. Drug Resist. Diep, B. The arginine catabolic mobile element and staphylococcal chromosomal cassette mec linkage: convergence of virulence and resistance in the USA clone of methicillin-resistant Staphylococcus aureus.

Molecular characterization of methicillin-resistant Staphylococcus epidermidis clones: evidence of geographic dissemination. Raad, I. Intravascular catheter-related infections: advances in diagnosis, prevention, and management. Lancet Infect. Schwalbe, R.

Emergence of vancomycin resistance in coagulase-negative staphylococci. Gagnon, R. Vancomycin therapy of experimental peritoneal catheter-associated infection Staphylococcus epidermidis in a mouse model. Richards, G. Antibiotic activity against Staphylococcus epidermidis biofilms in dialysis fluids. Comparative activities of daptomycin, linezolid, and tigecycline against catheter-related methicillin-resistant Staphylococcus bacteremic isolates embedded in biofilm.

Hanssen, A. Local variants of staphylococcal cassette chromosome mec in sporadic methicillin-resistant Staphylococcus aureus and methicillin-resistant coagulase-negative staphylococci: evidence of horizontal gene transfer? These late-developing infections may be linked to the sub-acute nature of S. This differs from the acute and often obvious nature of S. The diagnosis of ODRI is based on the combination of clinical presentation, biopsy culture, histological analysis and clinical diagnostic criteria, such as high C-reactive protein Metsemakers et al.

Diagnosis may be particularly challenging for sub-acute infections due to the lack of obvious clinical signs of infection. Therefore, microbiological culture results are often the most critical diagnostic criteria.

Since the microbes grow in biofilms on the foreign material and in necrotic bone tissue, cultivation and identification of the disease-causing pathogens may require the culture of several intraoperative tissue samples and removal of the implant for appropriate sampling Costerton et al.

To increase the yield of positive cultures, it is advised to terminate antibiotic therapy before sampling, acquire at least three tissue biopsies, and to perform sonication of removed hardware to remove biofilm-associated bacteria from the surface Trampuz and Zimmerli, ; Trampuz et al. In suspected S. In contrast, in virulent species such as S. The treatment of S. Despite such prolonged and comprehensive therapy, infection recurs in approximately one third of the cases and up to one fifth of cases cannot achieve a cure with restoration of limb function Salgado et al.

Morgenstern et al. This data therefore supports clinical beliefs that S. As a commensal microorganism, S. In a surgical wound, the bacterium utilizes these adhesion mechanisms in order to adhere to the deeper tissues and to the implanted device, or more specifically, the conditioning layer of host proteins deposited upon the device.

Initial adhesion of bacteria to implant surfaces is mediated by non-specific interactions such as hydrophobic interactions Gristina, , and then as shown schematically in Figure 1 , by specific adhesins such as autolysin AtlE Heilmann et al.

In the context of medical devices, the surface of the device becomes coated with host-derived plasma proteins, extracellular matrix ECM proteins and coagulation products platelets and thrombin immediately following implantation Baier et al. Peptidoglycan-bound wall teichoic acids WTA are an essential part of the S. WTA enhances the initial adhesion of S. Figure 1. Biofilm formation scheme with scanning electron micrographs of S. Image adapted with permission from Moriarty et al. Figure 2.

Scheme of the main S. The most well described adhesins involved in adhesion to native surfaces or protein-coated surfaces are shown in the upper part molecules also involved in biofilm formation shown in purple. See text for further details. The ability to adhere to a surface represents the first step in biofilm formation, commonly believed to be the most important virulence factor possessed by S.

Biofilm development facilitates resistance against host defense mechanisms Myrvik et al. Biofilm formation also complicates medical and surgical treatment protocols because implant removal is often required to remove the biofilm. Biofilms are defined as complex communities of adherent bacteria encased in a matrix of self-produced extracellular polymeric substances EPS Costerton et al.

The accumulation and maturation of the S. This was endorsed by the observation that the ica operon was absent in most commensal S. However, not all S. The aap gene has been observed in both pathogenic and commensal isolates, more frequently than the ica operon Gill et al.

Interestingly, Rohde et al. WTA have also been linked with S. TagO encodes the first enzymatic step in WTA biosynthesis and a tagO mutant has been shown to have a biofilm negative phenotype. This is partly attributed to an increase in cell surface hydrophobicity, impairing its initial adhesion to the surface, and a decreased production of PIA by activating the icaADBC repressor, icaR Holland et al.

Further information on regulation of biofilm in S. As already mentioned, biofilms play a role in immune evasion, primarily by providing a barrier to immune cells.

PIA may contribute to innate immune system evasion by promoting generation of complement C5a fragment Satorius et al. Recently, other studies have reported slightly opposite findings, with PIA-producing bacteria inducing greater inflammatory responses and enhanced phagocytosis Spiliopoulou et al.

Synthesized by the gene products of the cap locus, PGA is important in mediating S. It has yet to be elucidated if WTA has a direct role in S. However, like S. Although the majority of S. Methicillin resistance in S. It is carried on the mobile genetic element, staphylococcal cassette chromosome mec SCC mec , of which several types have been identified for S.

The specific causes of the increased prevalence of resistant isolates in the hospital environment is unknown, although is likely associated with high antibiotic exposure and direct or indirect interpersonal transmission. It remains unclear whether infection with resistant organisms results in a worse clinical outcome in comparison with susceptible counterparts.

In a recent study of patients with S. In any case, clear therapeutic guidelines are available for the treatment of both MRSE and MSSE, with a high likelihood of treatment success in both cases when guidelines are followed closely. Until relatively recently it was thought that S.

However, the identification and characterization of the PSMs have now changed that concept Mehlin et al. They are specifically associated with the formation of channels observed between the biofilm layers, which are considered important for nutrient uptake Wang et al. However, S. As growing conditions are likely to have an influence on PSM production, the role of S. Finally, certain S. PSM-mec has cytolytic potential against neutrophils in vitro and its presence has been associated with decreased bacterial clearance and higher mortality rates in a murine model of sepsis Qin et al.

Small colony variants SCVs , a colony phenotype characterized by small size, slow growth and downregulation of virulence genes, are recognized as a pathogenic mechanism for several bacterial species, including S.

SCVs seem to be less susceptible to antibiotics and to the immune system, potentially by being able to survive intracellularly and inducing a more anti-inflammatory environment due to increased secretion of IL Magrys et al. The topic has been extensively reviewed recently Kahl et al. Finally, internalization and intracellular persistence in non-professional phagocytes e.

A few internalization mechanisms have been described for S. This represents a potentially new pathogenic mechanism for S. The interaction between S. That is, to induce immune responses in the host which control aberrant inflammatory responses to non-pathogenic molecules such as those found in food but also in commensal bacteria. This question was assessed in recent murine studies with the topical application of S.

Scharschmidt et al. Mice that were not colonized during the neonatal period presented with higher inflammation and neutrophil recruitment compared to colonized mice, when challenged with the same strain of S. The use of the sphingosinephosphate receptor antagonist FTY during neonatal period, which blocked the egression of Tregs into skin, suppressed the tolerogenic effect indicating that there may exist a critical period when Treg mediated tolerance can be acquired Scharschmidt et al.

On the other hand, Naik et al. This was mediated through the action of a skin-resident dendritic cell subset and was not associated with the induction of inflammation Naik et al. More importantly, when an epicutaneous infection model with Candida albicans was used, the application of the fungus in mice pretreated with topical S. The effect was lost when either anti-CD8 or anti-ILA antibodies were co-administered, which highlights the relevance of the adaptive immune responses generated.

Altogether, the study suggested that resident bacteria in the skin S. The effect seemed to be tissue-specific, since S. In two other studies, S. However, the true nature of these observations needs to be clarified, as LTA purity even from commercial preparations has been questioned Nguyen et al.

The capacity of S. Nevertheless, this idea can be somewhat supported by in vitro findings, whereby human monocytes, monocyte-derived dendritic cells moDC and T lymphocytes stimulated with S. Further in vivo and human microbiome studies may provide a deeper understanding of the complex nature of this microorganism-host interaction.

Innate immune responses are triggered by the detection of microbial structures through pattern-recognition receptors PRRs on immune and tissue cells. Secreted components can also be recognized and activate the immune system, as it was shown for S. Figure 3. Summary of S. Recognition of S. Other receptors recognizing S. Upon recognition, downstream signaling and effector mechanisms are triggered, including secretion of AMPs, phagocytosis by neutrophils and macrophages and secretion of cytokines and chemokines from numerous cell types, which will orchestrate additional innate and adaptive immune responses.

Furthermore, in preclinical models of S. The use of TLR-2 knock-out KO in bacteremia models with neonatal and adult mice resulted in delayed clearance, especially at early time-points after infection Strunk et al. These data suggest that TLR-2 is involved in the early responses to S. Responses toward S. Other PRRs that may potentially be involved in S. CD14, expressed mostly in monocytes and macrophages, is a TLR-2 co-receptor which may contribute to S. PSMs produced by S.

To date, the contribution of these receptors in vivo has not been addressed. Human AMPs are a heterogeneous group of amphipathic peptides, which may be subdivided depending on their structure and function. In vitro experiments with keratinocytes or skin explants have shown that S. This AMP induction may be beneficial under healthy conditions to counteract more pathogenic species Lai et al. Nevertheless, the studies mentioned above showed some discrepancies in terms of AMP killing capacity, which could be explained by differences in strains used, as some of them may possess mechanisms against AMP.

More relevant in the context of S. These AMPs will often be located in the phagolysosomes, where they can contribute to bacteria killing.

The mechanisms of action is currently unknown, although for hBD-3 a decrease in icaA and icaD expression and increase of icaR were associated with the observations Zhu et al. Phagocytosis by neutrophils is one of the most important mechanisms for elimination of contaminating or infecting bacteria. Neutrophils migrate to the site of infection, following host signals e. At the infection site, neutrophils will internalize opsonized bacteria forming a phagosome and, finally, bacteria will be destroyed in the phagolysosome by the action of reactive oxygen species ROS , proteases and AMPs.

An additional mechanism to kill bacteria has been described for neutrophils: the generation of neutrophil extracellular traps NETs or NETosis. Nuclear and mitochondrial DNA is released to the extracellular space to form NETs, which contain high local concentrations of intracellular antimicrobial proteins. Although literature is still limited, S. Macrophages are also able to phagocytose and destroy S. Phagocytosis of S. Phagocytes will also act against biofilms.

It has been shown that neutrophils can bind to opsonized but also non-opsonized biofilms, partly by recognizing EPS Meyle et al. Nevertheless, it is generally accepted that the biofilm mode of growth will protect bacteria from phagocytosis, despite some discrepancies in the literature that have been discussed elsewhere Nguyen et al. Furthermore, biofilm mode of growth, most often studied in PIA-producing strains, has been shown to decrease killing efficiency in macrophages and neutrophils Vuong et al.

Interesting observations were made when comparing the phagocytosis of S. However, although S. In fact S. However, some strains are killed less efficiently, potentially by having a low capacity to prime the oxidative response of neutrophils Nilsdotter-Augustinsson et al.

These observations, together with lower induction of neutrophil apoptosis, may lead to intracellular survival and could partially explain the low inflammatory nature and chronicity often associated with S. Cytokines are a broad group of secreted proteins that play a role in intercellular communication, with a broad range of functions within the immune system as cell recruitment, differentiation and activation. Interleukins and other factors play an essential role in leukocyte communication and differentiation, while chemokines are mainly involved in cell recruitment.

Of note, S. The regulatory cytokine IL is also present in vivo Ferreirinha et al. Interestingly, bacterial counts were the same in both wild-type and KO strains, suggesting that IL does not impact bacterial clearance Gutierrez-Murgas et al.

Overall, despite differences due to different S. Multiple chemokines are also released upon S. Secretion of IL-8, important for neutrophil recruitment, has been described in vitro and in the first hours post-infection in in vivo studies Wakabayashi et al.

Additionally, a murine peritonitis model revealed increasing levels of numerous chemokines upon challenge with S. The aggregation and activation of platelets in the presence of bacteria was first described over 25 years ago Usui et al. Platelets and bacteria can interact in three ways: the indirect binding of bacteria to a plasma protein which is a ligand of a platelet receptor , the direct recognition of bacteria by platelet receptors and the binding of secreted bacterial products to platelets Hamzeh-Cognasse et al.

Only the first type has been described for S. Future studies will be required to elucidate if S. Adaptive immunity refers to antigen-specific and long-lasting immune responses that are mediated by lymphocytes. Adaptive immunity can be broadly divided in cellular responses, represented by T helper Th and cytotoxic T lymphocytes, and humoral responses, represented by B lymphocytes and antibodies.

Classically, extracellular bacterial infections have been shown to trigger mostly Th1 cell responses, but more recently Th17 responses have also been linked to the clearance of bacterial infections.

Of relevance, an in vivo model using immunocompromised mice have shown a higher susceptibility for S. Arising from its status as a commensal microorganism, S. This has been proposed to be largely triggered by a pattern of transient self-resolving infections due to micro-invasions, rather than resulting from local response due to colonization Brown et al.

These life-long interactions will lead to the generation of an antibody repertoire and a set of memory T and B cells that may confer partial protection from infection. Generation of adaptive immune responses require the presentation of antigens to T cells by antigen presenting cells APCs , primarily dendritic cells DC , which will also contribute to T cell polarization.

Upon infection, it can also be expected that certain DC subtypes, already present in the tissue or that will migrate there, will shape adaptive immune responses. Data available for S. Studies describing cytokine secretion by DC stimulated with S. The inconsistency between these reports may be due to the different sources of DC and stimuli used, which can lead to different outcomes by activating distinct pathways. The relevance of the stimuli is further highlighted in a series of experiments from Durantez et al.

Further experiments are required to clarify the exact role of APCs and different DC subsets in priming and polarizing the T cell response. With regards to humoral responses, antibodies against S. Antibodies against biofilm components and cytoplasmic proteins have been found to be predominant Carvalhais et al. To assess the potential use of antibody titers in diagnosis of infection, serum antibody titters against Staphylococcal proteins have been measured in patients with S.

Recently, a multiplex antibody detection-based immunoassay was evaluated for the diagnosis of peri prosthetic joint infections PJI. The assay included protein antigens from several strains: diverse Staphylococci, Streptococcus agalactiae and P. Studies employing 2D protein electrophoresis or phage display technology with the aim of identifying S. Sera of rabbits immunized with live S. Other proposed immunogenic proteins include AtlE, Staphylococcal conserved antigen B ScaB , and GehD lipase, which elicited higher antibody titers in infected patients compared to non-infected subjects.

Active immunization of mice with these antigens resulted in production of specific antibodies with in vitro opsonization capacity against S. An anti-SdrG antibody was shown to reduce mortality in a neonate bacteremia rat model and to decrease bacterial counts in a DRI endocarditis rabbit model Vernachio et al.

More recently it was shown that immunization with staphylococcal Major amidase Atl-AM , a cell wall hydrolase present in some S. In the same study, immunized animals challenged with a lethal intraperitoneal dose of S. Additionally, immunized mice also presented higher levels of Th1 and Th2 cells, although it did not elucidate which responses were the most relevant for the increased survival. Immunizations with Aap or with antibodies against surface proteins have also been shown to reduce colonization in a murine DRI model by ultimately inhibiting biofilm formation Shahrooei et al.

Despite the fact that their efficacy against S. A recent study focused on staphylococcal adhesion proteins, which contain long stretches of Sdr and are key virulence factors for S. The study led to the discovery of two novel bacterial glycosyltransferases, SdgA and SdgB, which can modify all Sdr-proteins to protect them from cleavage by cathepsin G a neutrophil protein.

Neutralization of these enzymes may be the next opportunity for an effective anti-staphylococcal approach Hazenbos et al. To date, all anti-staphylococcal antibodies tested against S. Although there is still much work to be done to fully understand effective immune responses against S. Additionally, there are also T cell-mediated immune responses to S. Based on in vitro studies, it has been suggested that S.

Based on cytokines induced by S. This goes in line with the findings of Ferreirinha et al. Also, as mentioned above, immunization of mice with Atl-AM led to an increase in Th1 and Th2 cells Th17 cells were not evaluated on that study.

Immunization also led to a higher survival; however, direct effect of T cell responses in that finding was not further addressed Nair et al. The usual chronic nature of S. Bone as an organ is particularly sensitive to chronic inflammation, due to its continuous remodeling process that is influenced by different components of the immune system and inflammatory pathways Redlich and Smolen, Therefore, persistently elevated levels of pro-inflammatory cytokines in the local bone microenvironment frequently result in marked osteolysis, driven by enhanced osteoclast activity at the site of infection Figure 4 ; Nair et al.

Figure 4. Despite the importance of S. A recent study has shown the induction in vitro of IL-6 by primary human osteoblasts stimulated with S. Interestingly, the authors also demonstrated that osteoblasts were activated not only by the planktonic form of S.

This suggests that, rather than the relatively simplistic view of the osteoblast for producing bone matrix and regulating osteoclast activity, osteoblasts may also serve an important role as sensors and initiators of immune responses directed against bacteria resident in the local bone microenvironment.

Additionally, in vitro studies have observed a decrease in osteoblast viability when co-cultured with S. This is in stark contrast to S. For example, S. Furthermore, specific bacterial proteins have been identified as responsible for some of these effects on osteoblasts such as S.

Regarding the effects of bacterial infection on osteoclasts, a number of studies have reported the effects of inactivated S.

Such conflicting data strongly argues for the use of preferably live intact bacteria in such osteoclastogenesis assays rather than purified bacterial components. When the effect of intact bacteria on osteoclastogenesis was recently investigated, S. By inducing activation of macrophages and thereby stimulating the production of pro-inflammatory cytokines, S. Additionally, S. Much less is known regarding direct interaction of S.

Given the multitude of different effects of S. Lastly, the interaction of S. Both S. This is supported by the findings of a recent study that reported SdrG mediates the binding of S. However, this immune evasion mechanism may be of more importance for S. This is reinforced by a recent in vitro study demonstrating that S. Osteoclasts are also able to internalize, at least, S. Given the inherent phagocytic capacity of osteoclasts, it may be that internalization of S.

This raises the possibility that S. Together with the previously stated ability of S. Taken together, this suggests that while the persistence of orthopedic implant-associated S.

Finally, the integration of immune responses within the bone system in the context of S. The number of models described for S. Most of the data available is based on S. The observation that anti-ILp40 conferred protection in S. This observation, however, could be due to a decrease in myeloid-derived suppressor cells MDSC that otherwise would impair immune responses in the vicinity of an implant, as described by Heim et al. Concluding remarks and future directions Together, these findings demonstrate the variable physiology and contextual control of S.

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Sci Transl Med. Exploring Staphylococcus epidermidis in atopic eczema: friend or foe? Clin Exp Dermatol. The germ can also enter the body through the hands, blood, cough secretion, wound secretion and skin contact, as well as through contact with contaminated objects and surfaces.

Staphylococcus epidermidis can cause wound infections, boils, sinus infections, endocarditis and other inflammations. The bacterium can reside for a long period of time in "hiding places" in the body, where it is not noticed by the immune system, and therefore also not fought. As soon as the conditions for a new infection are favourable for the bacterium, for example, if the human has a weak immune system, the bacterium can reignite centres of inflammation that can become chronic and — if the pathogen is multi-resistant — are difficult to fight.