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Pathogens
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Molecular Pathogenesis of Staphylococcal Infections
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Molecular Pathogenesis of Staphylococcal Infections

A special issue of Pathogens (ISSN 2076-0817).

Deadline for manuscript submissions: closed (30 August 2018) | Viewed by 36663

Special Issue Editor

Prof. Dr. Tim Foster

E-Mail Website
Guest Editor
Trinity College Dublin, The University of Dublin, College Green, Dublin 2Dublin, Ireland
Interests: Toxins; Superantigens; Immune evasion; Complement evasion; Neutrophil evasion Surface proteins; Invasion; Persisters and small colony variants; Antibiotic resistance; Biofilm Nasal colonization; Invasive infections; Skin infections

Special Issue Information

Dear Colleagus,

Staphylococcus aureus persistently colonizes the nares of about 20% of the population and is a transient resident of the remainder. The bacterium can cause both superficial skin infections and more serious and potentially life-threatening invasive diseases. Treatment has been compromised by the development of resistance to multiple antibiotics. S. aureus expresses a plethora of secreted and surface proteins that promote infection by facilitating adhesion to host cells and tissues, invasion of host cells, and evasion of innate immune responses by interfering with complement and neutrophils. The bacterium can also interfere with adaptive immune responses. Molecular analysis of virulence factors has involved construction of mutants that are defective in a factor and comparing virulence with the wild type in appropriate animal models.

Prof. Dr. Tim Foster
Guest Editor

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Keywords

  • toxins
  • superantigens
  • immune evasion
  • complement evasion
  • neutrophil evasion
  • surface proteins
  • invasion
  • persisters and small colony variants
  • antibiotic resistance
  • biofilm Nasal colonization
  • invasive infections
  • skin infections

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Published Papers (3 papers)

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Research

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8 pages, 629 KiB  
Article
Modulation of the Antibiotic Activity by the Mauritia flexuosa (Buriti) Fixed Oil against Methicillin-Resistant Staphylococcus Aureus (MRSA) and Other Multidrug-Resistant (MDR) Bacterial Strains
by Yara Faustino Pereira, Maria Do Socorro Costa, Saulo Relison Tintino, Janaína Esmeraldo Rocha, Fábio Fernandes Galvão Rodrigues, Maria Karine De Sá Barreto Feitosa, Irwin Rose Alencar De Menezes, Henrique Douglas Melo Coutinho, José Galberto Martins Da Costa and Erlânio Oliveira De Sousa
Pathogens 2018, 7(4), 98; https://doi.org/10.3390/pathogens7040098 - 10 Dec 2018
Cited by 26 | Viewed by 3940
Abstract
Mauritia flexuosa (buriti) is a typical Brazilian palm tree found in swampy regions with many plant forms. The fruit has various purposes with the pulps to the seeds being used for ice creams, sweets, creams, jellies, liqueurs, and vitamin production. A physicochemical characterization [...] Read more.
Mauritia flexuosa (buriti) is a typical Brazilian palm tree found in swampy regions with many plant forms. The fruit has various purposes with the pulps to the seeds being used for ice creams, sweets, creams, jellies, liqueurs, and vitamin production. A physicochemical characterization of the fixed pulp oil and its antibacterial and aminoglycoside antibiotic modifying activity against Gram-positive and Gram-negative multiresistant bacterial strains were performed using broth microdilution assays. Physical properties, such as moisture, pH, acidity, peroxide index, relative density, and refractive index, indicated oil stability and chemical quality. In the GC/MS chemical composition analysis, a high content of unsaturated fatty acids (89.81%) in relation to saturated fatty acids (10.19%) was observed. Oleic acid (89.81%) was the main fatty acid identified. In the antibacterial test, the fixed oil obtained the Minimum Inhibitory Concentration (MIC) ≥ 1024 μg/mL for all standard and multiresistant bacterial strains. The synergic effect of fixed pulp oil combined was observed only in Staphylococcus aureus SA–10, with an MIC reduction of the gentamicin and amikacin by 40.00% and 60.55%, respectively. The data indicates the M. flexuosa fixed oil as a valuable source of oleic acid and modulator of aminoglycoside activity. Full article
(This article belongs to the Special Issue Molecular Pathogenesis of Staphylococcal Infections)
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Review

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23 pages, 2245 KiB  
Review
Manipulation of Innate and Adaptive Immunity by Staphylococcal Superantigens
by Stephen W. Tuffs, S. M. Mansour Haeryfar and John K. McCormick
Pathogens 2018, 7(2), 53; https://doi.org/10.3390/pathogens7020053 - 29 May 2018
Cited by 83 | Viewed by 10831
Abstract
Staphylococcal superantigens (SAgs) constitute a family of potent exotoxins secreted by Staphylococcus aureus and other select staphylococcal species. SAgs function to cross-link major histocompatibility complex (MHC) class II molecules with T cell receptors (TCRs) to stimulate the uncontrolled activation of T lymphocytes, potentially [...] Read more.
Staphylococcal superantigens (SAgs) constitute a family of potent exotoxins secreted by Staphylococcus aureus and other select staphylococcal species. SAgs function to cross-link major histocompatibility complex (MHC) class II molecules with T cell receptors (TCRs) to stimulate the uncontrolled activation of T lymphocytes, potentially leading to severe human illnesses such as toxic shock syndrome. The ubiquity of SAgs in clinical S. aureus isolates suggests that they likely make an important contribution to the evolutionary fitness of S. aureus. Although the apparent redundancy of SAgs in S. aureus has not been explained, the high level of sequence diversity within this toxin family may allow for SAgs to recognize an assorted range of TCR and MHC class II molecules, as well as aid in the avoidance of humoral immunity. Herein, we outline the major diseases associated with the staphylococcal SAgs and how a dysregulated immune system may contribute to pathology. We then highlight recent research that considers the importance of SAgs in the pathogenesis of S. aureus infections, demonstrating that SAgs are more than simply an immunological diversion. We suggest that SAgs can act as targeted modulators that drive the immune response away from an effective response, and thus aid in S. aureus persistence. Full article
(This article belongs to the Special Issue Molecular Pathogenesis of Staphylococcal Infections)
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22 pages, 582 KiB  
Review
The Pathogenesis of Staphylococcus aureus Eye Infections
by Richard J. O’Callaghan
Pathogens 2018, 7(1), 9; https://doi.org/10.3390/pathogens7010009 - 10 Jan 2018
Cited by 93 | Viewed by 21190
Abstract
Staphylococcus aureus is a major pathogen of the eye able to infect the tear duct, eyelid, conjunctiva, cornea, anterior and posterior chambers, and the vitreous chamber. Of these infections, those involving the cornea (keratitis) or the inner chambers of the eye (endophthalmitis) are [...] Read more.
Staphylococcus aureus is a major pathogen of the eye able to infect the tear duct, eyelid, conjunctiva, cornea, anterior and posterior chambers, and the vitreous chamber. Of these infections, those involving the cornea (keratitis) or the inner chambers of the eye (endophthalmitis) are the most threatening because of their potential to cause a loss in visual acuity or even blindness. Each of these ocular sites is protected by the constitutive expression of a variety of antimicrobial factors and these defenses are augmented by a protective host response to the organism. Such infections often involve a predisposing factor that weakens the defenses, such as the use of contact lenses prior to the development of bacterial keratitis or, for endophthalmitis, the trauma caused by cataract surgery or intravitreal injection. The structural carbohydrates of the bacterial surface induce an inflammatory response able to reduce the bacterial load, but contribute to the tissue damage. A variety of bacterial secreted proteins including alpha-toxin, beta-toxin, gamma-toxin, Panton-Valentine leukocidin and other two-component leukocidins mediate tissue damage and contribute to the induction of the inflammatory response. Quantitative animal models of keratitis and endophthalmitis have provided insights into the S. aureus virulence and host factors active in limiting such infections. Full article
(This article belongs to the Special Issue Molecular Pathogenesis of Staphylococcal Infections)
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