The production of pyrogenic exotoxins by group A streptococci

Hallas, Gillian

doi:10.1017/s0022172400062276

Cited by 43 publications

(13 citation statements)

References 8 publications

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“…In contrast, other wild-type strains tested expressed neither speB mRNA nor enzymatically or immunologically detectable SpeB at any time. These findings are consistent with the knowledge that, while all strains of GAS are endowed with the gene for SpeB, not all strains produce the toxin, and even among strains that do, the quantity produced varies greatly from strain to strain (6,15,16,22,31).…”

Section: Discussionsupporting

confidence: 89%

“…SpeB is also found on the surfaces of the bacteria and possesses glycoprotein and laminin binding activities (19). While all strains of GAS are endowed with the gene for SpeB, not all strains produce the toxin in vitro, and even among strains that do, the quantity produced varies greatly from strain to strain (6,15,16,22,31). Other environmental factors, such as acidic pH, concentration of NaCl, the availability of nutrients, the presence of kanamycin, etc., also affect speB expression (7, 9, 39).…”

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confidence: 99%

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Identification and Characterization of BicistronicspeBandprsAGene Expression in the Group A Streptococcus

Ma¹,

Bryant²,

Salmi³

et al. 2006

J Bacteriol

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Severe, invasive group A streptococcal infections have reemerged worldwide, and extracellular toxins, including streptococcal pyrogenic exotoxin B (SpeB), have been implicated in pathogenesis. The genetic regulation of SpeB is not fully understood, and the mechanisms involved in the processing of the protoxin to its enzymatically active form have not been definitively established. The present work demonstrated that the genes encoding SpeB (speB) and a peptidyl-prolyl isomerase (prsA) constitute an operon with transcription initiated from two promoters upstream of speB. Further, the speB-prsA operon was transcribed as a bicistronic mRNA. This finding is in contrast to the generally accepted notion that speB is transcribed only as a monocistronic gene. In addition, prsA has its own promoter, and transcription from this promoter starts in early log phase, prior to the transcription of speB. Genomic disruption of prsA decreased the production of enzymatically active SpeB but not the level of the pro-SpeB zymogen. Taken together, these results demonstrate that prsA is required for production of fully mature, enzymatically active SpeB.Group A streptococcus (GAS) causes many diseases in humans, ranging in severity from milder infections such as pharyngitis, simple cellulitis, erysipelas, and scarlet fever to life-threatening necrotizing fasciitis, septicemia, and toxic shock syndrome. One of the many potentially important virulent factors produced by this organism is streptococcal pyrogenic exotoxin B (SpeB). As a potent cysteine proteinase, SpeB cleaves multiple streptococcal virulence factors, including M protein (3), as well as many host factors controlling inflammation (18,20).The gene for SpeB (speB) is chromosomally located on every GAS strain studied and consists of a 1,196-base pair (bp) open reading frame yielding a 371-amino-acid polypeptide with a predicted molecular weight of 40,000 (16). SpeB is secreted strictly in the late log/early stationary phase of growth as a proteinase precursor that must be proteolytically cleaved to the mature active form having a calculated molecular mass of approximately 28 kDa. SpeB is also found on the surfaces of the bacteria and possesses glycoprotein and laminin binding activities (19). While all strains of GAS are endowed with the gene for SpeB, not all strains produce the toxin in vitro, and even among strains that do, the quantity produced varies greatly from strain to strain (6,15,16,22,31). Other environmental factors, such as acidic pH, concentration of NaCl, the availability of nutrients, the presence of kanamycin, etc., also affect speB expression (7, 9, 39).Current knowledge regarding SpeB's transcriptional regulation and maturation is derived from many labs around the world. At the transcriptional level, rgg (also known as ropB) positively regulates SpeB expression and production (5), as does the global regulator mga (35). In addition, inactivation of both oligopeptide and dipeptide transport systems diminished speB mRNA levels (33, 34). At the posttranscriptiona...

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Section: Discussionsupporting

confidence: 89%

mentioning

confidence: 99%

Identification and Characterization of BicistronicspeBandprsAGene Expression in the Group A Streptococcus

Ma¹,

Bryant²,

Salmi³

et al. 2006

J Bacteriol

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“…Distinguishing streptococcal myositis from spontaneous gas injury observed in patients with StrepTSS [1]. Pyrogenic exotoxin C has been associated with mild cases of scarlet fever in gangrene due to C. perfringens or C. septicum [46] may be difficult, although crepitus or demonstration of gas in the tissue the United States (unpublished data) and in England [50]. The roles of two newly described pyrogenic exotoxins, SSA and strongly favors clostridial infection [44].…”

Section: Adams Et Al [42] Documented Only 21 Reported Cases Ofmentioning

confidence: 99%

The Flesh‐Eating Bacterium: What's Next?

1999

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Since the 1980s, there has been a marked increase in the recognition and reporting of highly invasive group A streptococcal (GAS) infections associated with shock and organ failure, with or without necrotizing fasciitis. Such dramatic cases have been defined as streptococcal toxic shock syndrome (StrepTSS). Strains of GAS isolated from patients with invasive disease have been predominantly M types 1 and 3, which produce either pyrogenic exotoxin A or B or both. The clinical and demographic features of streptococcal bacteremia, myositis, and necrotizing fasciitis are presented and compared with those of StrepTSS. Current concepts in the pathogenesis of invasive streptococcal infection will be presented, with emphasis on the interaction between GAS virulence factors and host defense mechanisms. Finally, new concepts in the treatment of StrepTSS will be discussed.

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“…Streptococcal pyrogenic exotoxins A and B induce human mononuclear cells to synthesize not only tumor necrosis factor-α (TNFα) (44) but also interleukin-1β (IL-1β) (45) and interleukin-6 (IL-6) (45), suggesting that TNF could mediate the fever, shock, and tissue injury observed in patients with streptococcal TSS (8). Pyrogenic exotoxin C has been associated with mild cases of scarlet fever in the United States (author's observations) and in England (46). The roles of two newly described pyrogenic exotoxins, SSA and MF (see section on "Clinical Isolates"), in streptococcal TSS have not been elucidated.…”

Section: Current Hypotheses Regarding Mechanisms Of Shock and Tissue mentioning

confidence: 99%

Streptococcal Toxic Shock Syndrome: Synthesis of Tumor Necrosis Factor and Interleukin-1 by Monocytes Stimulated with Pyrogenic Exotoxin A and Streptolysin O

Hackett

Stevens²

1992

Journal of Infectious Diseases

183

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The production of pyrogenic exotoxins by group A streptococci

Cited by 43 publications

References 8 publications

Identification and Characterization of BicistronicspeBandprsAGene Expression in the Group A Streptococcus

Identification and Characterization of BicistronicspeBandprsAGene Expression in the Group A Streptococcus

The Flesh‐Eating Bacterium: What's Next?

Streptococcal Toxic Shock Syndrome: Synthesis of Tumor Necrosis Factor and Interleukin-1 by Monocytes Stimulated with Pyrogenic Exotoxin A and Streptolysin O

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