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EDITORIAL  
Year : 2015  |  Volume : 7  |  Issue : 3  |  Page : 95-96
State of the globe: Toxin and toxic genes associated with Staphylococcus aureus and clinical implication


Department of Medicine, King George's Medical University, Lucknow, Uttar Pradesh, India

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Date of Web Publication18-Aug-2015
 

How to cite this article:
Agrawal A. State of the globe: Toxin and toxic genes associated with Staphylococcus aureus and clinical implication. J Global Infect Dis 2015;7:95-6

How to cite this URL:
Agrawal A. State of the globe: Toxin and toxic genes associated with Staphylococcus aureus and clinical implication. J Global Infect Dis [serial online] 2015 [cited 2019 Jun 16];7:95-6. Available from: http://www.jgid.org/text.asp?2015/7/3/95/163076


Staphylococcus aureus , a gram positive coccal bacterium, is either commensal colonizing healthy nasal mucosa [1] or a pathogen of humans. The bacteria cause a variety of community and hospital acquired diseases including skin abscess, pneumonitis, food poisoning, sepsis, and toxic shock syndrome. [2]

It produces virulent factors including adhesins (colonization factors), toxic proteins/enzymes (e.g., DNase for bacterial spread, coagulase, and catalase for escaping host immunity) and exotoxins including exfoliative toxins (ExTs), enterotoxins (SEs), and toxic shock syndrome toxin-1 (TSST-1). Patients infected with the S. aureus producing ExT may develop scalded-skin syndrome. [3] The SEs and TSST-1, cause food poisoning, but are also super antigens (SAg) that can stimulate a relatively large fraction of peripheral blood T cells to release massive amounts of pro inflammatory cytokines and T-cell stimulating factors leading to toxic shock syndrome which can cause fatality. [4] The enterotoxicity and super antigenicity are distinct properties of this toxin molecule. [2]

Despite appropriate treatment, these complications are associated with high morbidity and mortality and they cause a significant financial burden. In SENTRY - An Antimicrobial Surveillance Program done during the period 1997-2002, it was found that S. aureus was the most common cause of nosocomial bacteremia in North America (prevalence 26%) and the second most common cause of nosocomial bacteremia in Europe. [5]

There are about 21 known SAgs including the TSST-1, enterotoxins (SEA-E and SEI), enterotoxin like toxin (SelG, H, and J-U) [6] and not less than 15 exotoxins (SET1-SET15). The staphylococcal enterotoxin F (SEF) lacks emetic activity but it is associated with toxic shock syndrome thus it is presently called toxic shock syndrome toxin-1 (TSST-1). [6] The SEs and the TSST-1 as well as the property of bacterial resistance to drugs are encoded by genes lying on the mobile genetic elements including prophages, plasmids, pathogenicity islands, genomic islands, and antibiotic resistance cassette; [7] therefore they are transmitted horizontally easily. In addition, S. aureus produces several virulence factors such as teichoic acids, microbial surface components recognizing adhesive matrix molecules (MSCRAMMs), and capsular polysaccharides which enable it's adhesion to host mucosal surfaces or implanted devices and secreted virulence factors such as hemolysins, leukocidins, enterotoxins, and exfoliative toxins aid in invasion and spread of infection. [7] Toxins, such as TSST-1 and enterotoxins, are actually super antigens (SAgs) that trigger massive release of pro inflammatory cytokines thereby producing an over the top inflammatory response which results in endotoxin-like shock including endothelial leakage, hemodynamic shock, multiorgan failure, and death. During growth of bacteria expression of S. aureus virulence factors and metabolism are regulated by a quorum sensing operon named accessory gene regulator (AGR). [7] Based on the polymorphisms of amino acid sequence, the AGR-encoding auto inducing peptides and their responding receptors, S. aureus strains can be divided into four major AGR groups (Groups 1-4). [8]

In the past five decades, methicillin resistant S. aureus clones (methicillin-resistant S. aureus, MRSA) have spread and posed public health problems worldwide. [9] These MRSA strains are resistant to methicillin, they are also resistant to all other β-lactams, such as cephalosporin's. [9] Community-acquired MRSA (CA-MRSA) commonly causes skin/soft tissue infections and necrotizing pneumonias. In comparison to hospital-acquired (HA-MRSA) they are more susceptible to non-beta-lactam antibiotics like trimethoprim-sulfamethoxazole and quinolones. The strain producing Panton-Valentine leukocidins (PVL) gene was described in 1932, it is known to cause necrotizing pneumonias among the young, immunocompetent individuals, the risk factors being from overcrowding, colonization. [10] One of the major risk factors for MRSA infection is the colonization with MRSA and a previously done study reports identical nasal isolates in 82% of patients having MRSA bacteremia. [11] Other common risk factors for HA-MRSA infection are prior hospitalization, presence of prosthetic devices, antibiotic use and open/surgical wounds. Comorbid conditions like diabetes mellitus, malignancy, and nasal colonization; presence of prosthetic device; drug etc. are the major risk factors for community acquired SAB. [11]

 
   References Top

1.
Williams RE. Healthy carriage of Staphylococcus aureus: Its prevalence and importance. Bacteriol Rev 1963;27:56-71.  Back to cited text no. 1
[PUBMED]    
2.
Proft T, Fraser JD. Bacterial superantigens. Clin Exp Immunol 2003;133:299-306.  Back to cited text no. 2
    
3.
Dinges MM, Orwin PM, Schlievert PM. Exotoxins of Staphylococcus aureus. Clin Microbiol Rev 2000;13:16-34.  Back to cited text no. 3
    
4.
Balaban N, Rasooly A. Staphylococcal enterotoxins. Int J Food Microbiol 2000;61:1-10.  Back to cited text no. 4
    
5.
Biedenbach DJ, Moet GJ, Jones RN. Occurrence and antimicrobial resistance pattern comparisons among bloodstream infection isolates from the SENTRY antimicrobial surveillance program (1997-2002). Diagn Microbiol Infect Dis 2004;50:59-69.  Back to cited text no. 5
    
6.
Fitzgerald JR, Reid SD, Ruotsalainen E, Tripp TJ, Liu M, Cole R, et al. Genome diversification in Staphylococcus aureus: Molecular evolution of a highly variable chromosomal region encoding the staphylococcal exotoxin-like family of proteins. Infect Immun 2003;71:2827-38.  Back to cited text no. 6
    
7.
Holtfreter S, Grumann D, Schmudde M, Nguyen HT, Eichler P, Strommenger B, et al. Clonal distribution of superantigen genes in clinical Staphylococcus aureus isolates. J Clin Microbiol 2007;45:2669-80.  Back to cited text no. 7
    
8.
Gilot P, Lina G, Cochard T, Poutrel B. Analysis of the genetic variability of genes encoding the RNA III-activating components Agr and TRAP in a population of Staphylococcus aureus strains isolated from cows with mastitis. J Clin Microbiol 2002;40:4060-7.  Back to cited text no. 8
    
9.
Lowy FD. Antimicrobial resistance: The example of Staphylococcus aureus. J Clin Invest 2003;111:1265-73.  Back to cited text no. 9
    
10.
Panton P, Valentine F. Staphylococcal toxin. Lancet 1932;219:506-8.  Back to cited text no. 10
    
11.
Gordon RJ, Lowy FD. Pathogenesis of methicillin-resistant Staphylococcus aureus infection. Clin Infect Dis 2008;46 Suppl 5:S350-9.  Back to cited text no. 11
    

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Correspondence Address:
Avinash Agrawal
Department of Medicine, King George's Medical University, Lucknow, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-777X.163076

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2008 Journal of Global Infectious Diseases | Published by Wolters Kluwer - Medknow
Online since 10th December, 2008