1. Wstęp. 2. Czynniki wirulencji szczepów S. agalactiae. 3. Toksyny GBS. 3.1. β-hemolizyna/cytolizyna. 3.2. Czynnik CAMP. 4. Czynniki umożliwiające unikanie odpowiedzi układu odporności. 4.1. Otoczka. 4.2. Dysmutaza nadtlenkowa. 4.3. Peptydaza C5a. 4.4. Proteinaza serynowa. 5. Oporność na peptydy przeciwbakteryjne. 5.1. Białka wiążące penicyliny. 5.2. Fimbrie. 5.3. Antygen b. 6. Adhezja i wnikanie. 6.1. Białka wiążące fibrinogen. 6.2. Białko wiążące lamininę. 6.3. Białka bogate w powtórzenia seryny. 6.4. Immunogenna adhezyna GBS. 6.5. Białko αC (APC). 6.6. Białko IagA. 6.7. Białko powierzchniowe Rib. 7. Inne czynniki uczestniczące w patogenezie GBS. 7.1. Hialuronidaza. 7.2. Regulator transportu metioniny (MtaR). 7.3. Zdolność do wykorzystania hemu. 8. Podsumowanie
Abstract: The course of the disease caused by S. agalactiae seems to depend greatly on the presence of its diverse virulence factors. To the most important virulence factors belong: capsule, C5a peptidase, which inhibits the action of neutrophils, α-C protein, laminin binding protein, and β hemolysin typical for invasive strains. Additionally, GBS strains may present FbsA protein which protects bacteria from opsonization and fagocytosis as well as takes part in adhesion. FbsB protein facilitates invasion to epithelial cells. Some GBS strains are able to produce surface protein inactivatng chemokine, CspA. S. agalactiae strains naturally inhabit genital and digestive tract, but in certain circumstances may be responsible for varions infections, both in neonates and adults. It suggests that these bacteria are able to adapt to diffwrent environments in infected individual and proper expression of virulence factors, in response to diverse niches, makes their survival possible. The goal of this work is to present the current knowledge concerning the virulence factors of S. agalactiae and, at the same time, possible reasons why these pathogens are still causing life threatening infections, especially in neonates.
1. Introduction. 2. Virulence factors S. agalactiae strains. 3. GBS toxins. 3.1. β-haemolisin/cytolisin. 3.2. CAMP factor. 4. Factors make possible escape answer of immunity system. 4.1. Capsule. 4.2. Peroxide dysmutase. 4.3. C5a peptidase. 4.4. Serine peptidase. 5. Resistance to antibacterial peptides. 5.1. Penicilin binding proteins. 5.2. Fimbries. 5.3. Antigen b. 6. Adhesion and penetration. 6.1. Fibrinogen binding proteins. 6.2. Laminin binding proteins. 6.3. Serine reports wich proteins. 6.4. Immunogenic GBS adhesin. 6.5. αC (APC) protein. 6.6. IagA protein. 6.7. Surface Rib protein. 7. Other patogenic GBS factors. 7.1. Hialuronidase. 7.2. Metionine transport regulator (MtaR). 7.3. Heme use ability. 8. Summary
