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Gram Pos S. pyogenes
S. pyogenes
| Question | Answer |
|---|---|
| How many cases of pharyngitis are caused per year by S. pyogenes? | over 600 million |
| Is S. pyogenes an obligate human pathogen? | yes |
| Why is S. pyogenes considered an emerging and re-emerging pathogen? | Emerging - streptococcal toxic shock and necrotizing fasciitis (1980s - present) reemerging - scarlet fever, rheumatic fever, and puerperal fever (1830-1900) |
| How are M protein, Sda1, SpeA2, Phospholipase SlaA, and Hyaluronidase involved in the pathogeneisis of S. pyogenes? | Virulence factors! |
| What is the inolvement of Mga and CovR/CovS in S. pyogenes virulence? | Regulate virulence |
| What kind of hemolysis does S. pyogenes have? | Beta-hemolysis |
| How did S. pyogenes become so hypervirulent and invasive? | virulence factors were acquired on a phage |
| S. pyogenes Protein F: | the primary adhesin in the throat that binds to fibronectin. Upon attachment, change in cytoskeleton - forces non phagocytic cells to phagocyze bacterium. |
| How is S. pyogenes infection aquired? | aerosilized droplets or topical insertion |
| Adherence of S. pyogenes to keratinocytes induces synthesis of? | IL-1, IL-6, IL-8, prostaglandin E2 |
| S. pyogenes non specific adherence: | Initial step is adherence to epithelial tissue by non-specific interaction from Lipoteichoic acid. |
| What extracellular matrix proteins do MSCRAMMs bind to in S. pyogenes infections? | fibronectin, fibrinogen & collagen |
| S. pyogenes specific adherence: | Specific interactions occur when MSCRAMMs bind to extracellular matrix proteins. "moonlighting proteins"- Anchorless adhesins (GAPDH, SpeB) and Hyluronic Acid binds to CD44. |
| What protein is the primary adhesin for skin epithelium in S. pyogenes? | M protein |
| What functions as the receptor for the hyaluronic capsule with S. pyogenes? | CD44 |
| What must attach before membrane "ruffling" occurs? (S. pyogenes) | M protein |
| When was "ruffling" of S. pyogenes first observed and by whom? | 1994 LaPenta et al |
| Fibronectin-binding protein (PrtF1/SfbI) binds to fibronectin in what type of cells? What does it cause? (S. pyogenes) | Pharyngeal cells. Stimulates host cell signaling cascade that leads to rearrangement of cytoskeletal proteins |
| What protein functions in non-pharyngeal cells the same way fibronectin-binding protein (PrtF1/SfbI) does in pharyngeal cells? (S. pyogenes) | M protein |
| S. pyogenes M protein: | Cell wall associated - different variants between strains. Involved in attachment to various host tissues, and evasion of host immune response. |
| S. pyogenes Sda1: | Involved in protection against neutrophil entrapment traps (NETs)--highly virulent strains have mutated Sda1, mildly virulent strains do not |
| S. pyogenes pyrogenic exotoxin SpeA2: | prime suspect for increased virulence. Not present in strains isolated between 1920-1980. Activates T-cells in non-antigen specific manner. Involved in disruption of immune response that causes increased inflammation |
| S. pyogenes Phospholipase SlaA: | Involved in severe invasive infections. Expression results in increased adherence to host and decreased host cell viability |
| S. pyogenes Hyaluronidase: | Extracellular enzyme hydrolyzes hyaluronic acid |
| What strains of bacteria is hyaluronidase found in? | Staphylococcus aureus, Propionibacterium acnes, Clostridium perfringens, Streptococcus pneumoniae - also found in spider, bee, and snake venom as well as human sperm |
| How is virulence regulated in S. pyogenes? | Carbon dioxide levels regulate the Multiple gene regulator in group A streptococci (Mga). Also regulated by 13 component regulatory system or 2 component (CovR/CovS). |
| How does CovR/CovS regulate virulence of S. pyogenes? | regulates hyaluronic acid production, streptolysin, and streptokinase production (early virulence components) |
| What type of enzyme is Sda1? (S. pyogenes) | DNase |
| What bacteria is a "humdinger of a pathogen"? | S. pyogenes! |
| can SpeB be an adhesion? (S. pyogenes) | yes |
| How does S. pyogenes evade the immune response? | CAPSULE (Hyaluronic acid) - Needed to survive in the blood |
| Why are vaccines against S. pyogenes difficult to do? | different M-types and surface antigens for each organism, |
| some people do not have all of the necessary components needed to become infected with | S. pyogenes |
| What is the pathogenesis for pharyngeal cells | increase proteins and enzymes, start to secrete anti-immune components (DNase, capsule), produces toxins to destroy cells (like blood) |
| What component varies between strains of S. pyogenes? | M protein |
| What mediates attachment to epithelial cells in S. pyogenes? | fibrillae protein |
| Sda1 is found in which types of S. pyogenes strains? | hypervirulent/hyperinfective strains |
| Streptodornase: | Sda1 - DNase |
| Mutated forms of S. pyogenes Sda1 are found with what disease? | necrotizing fasciitis |
| SpeA2 is associated with what strains? | shock like causing strains (scarlett fever, necrotizing fasciitis) |
| True or False: SpeA2 is a superantigen? | True |
| How did S. pyogenes acquire SpeA2? | phage associated mutated forms |
| What virulence factor is associated with Streptococcal Toxic Shock Syndrome? | SpaA2. Toxin and bacteria are both found throughout the body. |
| What leads to the appearance of "chewed meat" in the body? | SlaA - Phospholipase. causes the destruction of phospholipids. |
| What effects can SlaA (Phospholipase) have on the body? | increase attachment to host, can disrupt membrane, block intracellular signalling which can result in apoptosis. |
| What does hylauronidase do? | breaks down hyaluronic acid for nutrients and helps allow pockets of growth for the bacteria. Also allows for spreading of toxin. |
| How many forms of hylauronidase can S. pyogenes have? | 3 - two from phages, one chromosomally encoded. the super invasive strains have all 3 |
| What is streptokinase? | anticoagulant |
| What does Mga do? | turns on different adhesion factors triggered by the presence of carbon dioxide |
Created by:
arsenicgerbil
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