Browsing tag: czynniki wirulencji


Patogenicity mechanisms of Streptococcus pyogenes
K. Szczypa, J. Wilemska, W. Hryniewicz, I. Sitkiewicz

1. Wstęp. 2. Charakterystyka zakażeń powodowanych przez S. pyogenes. 3. Czynniki wirulencji S. pyogenes. 3.1. Adhezyny. 3.2. Czynniki sprzyjające rozprzestrzenianiu się infekcji w organizmie gospodarza. 3.3. Toksyny. 4. Regulacja ekspresji czynników wirulencji. 5. Podsumowanie

1. Introduction. 2. Infections caused by S. pyogenes. 3. Virulence factors of S. pyogenes. 3.1. Adhesins. 3.2. Factors of infections in host organism. 3.3. Toxins. 4. Regulation of virulence factors expression. 5. Summary

Abstract: The group A Streptococcus (Streptococcus pyogenes, GAS) is responsible for over 600 million infections and over half million deaths a year. GAS is a major human pathogen which causes diseases ranging from mild superficial infections of the throat or skin, up to severe systemic and invasive diseases such as necrotizing fasciitis and streptococcal toxic shock syndrome. Nowadays, post-infection sequelae such as glomerulonephritis and rheumatic fever are also alarming medical problems worldwide. Molecular analyses of streptococcal virulence carried by multiple centers worldwide, suggest the presence of a complex mechanism that coordinates pathogenesis. It involves a broad range of unique protein virulence factors, as M protein, superantigens, proteases and DNases, affecting tissues and the host’s immune system. Detailed analyses of individual virulence factors as well as regulatory systems that coordinate expression of virulence factors are the first steps on the way to develop innovative strategies for diagnostics and treatment. This review aims to highlight the epidemiology of S. pyogenes and summarize the current state of knowledge about the mechanisms of its virulence.

Budowa, regulacja i znaczenie czynników wirulencji szczepów Streptococcus agalactiae

The structure, regulation and the importance of S. agalactiae virulence factors
M. Łysakowska, M. Bigos, M. Wasiela

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

Sekrecja pęcherzyków błonowych jako mechanizm promujący infekcje H. pylori

Secretion of outer membrane vesicles as a mechanism promoting H. pylori infections
P. Krzyżek

1. Wstęp. 2. Sekrecja pęcherzyków błonowych u H. pylori. 3. Proteom pęcherzyków błonowych H. pylori. 4. Transport czynników wirulencji poprzez OMV. 4.1. Toksyna VacA. 4.2. Onkoproteina CagA. 4.3. Inne substancje. 5. Udział OMV w formowaniu biofilmu. 5.1. Funkcje biofilmu. 5.2. Zaangażowanie OMV w tworzenie biofilmu u bakterii. 5.3. Zaangażowanie OMV w tworzenie biofilmu u H. pylori. 5.4. Funkcja strukturalna zewnątrzkomórkowego DNA H. pylori. 6. Zewnątrzkomórkowe DNA jako nośnik informacji. 6.1. Wpływ na wirulencję. 6.2. Transformacja. 6.3. Naturalna kompetencja H. pylori. 7. Podsumowanie

Abstract: Helicobacter pylori commonly colonizes the human gastric mucosa. Infections with this microorganism can contribute to serious health consequences, such as peptic ulceration, gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue lymphoma. Chronic persistence of this bacteria in the host organism is probably strongly dependent on the secretion of outer membrane vesicles (OMV). These organelles are small, electron-dense, extracellular structures which are secreted in large amounts during stressful conditions, among others. H. pylori OMV mediate transfer of virulence factors such as toxins and immunomodulatory compounds. They contribute to avoiding a response from the host immune system and inducing chronic gastritis. OMV secretion also affects the formation of cell aggregates, microcolonies and biofilm matrix. Enhanced OMV production is connected to maintenance of direct contact through cell-cell and
cell-surface interactions. A key component of OMV, which determines their structural function, is extracellular DNA (eDNA) anchored to the surface of these organelles. eDNA associated with OMV additionally determines the genetic recombination in the process of horizontal gene transfer. H. pylori is naturally competent for genetic transformation and is constantly capable of DNA uptake from the environment. The natural competence state promotes the assimilation of eDNA anchored to the OMV surface. This is probably dependent on ComB and ComEC components, which are involved in the transformation process. For this reason, the OMV secretion mediates intensive exchange of genetic material, promotes adaptation to changing environmental conditions and enables persistent infecting of the gastric mucosa by H. pylori.

1. Introduction. 2. Secretion of outer membrane vesicles by H. pylori. 3. Proteome of H. pylori outer membrane vesicles. 4. Transport of virulence factors through OMV. 4.1. Toxin VacA. 4.2. Oncoprotein CagA. 4.3. Other substances. 5. OMV involvement in biofilm formation. 5.1. Functions of biofilm. 5.2. OMV influence on bacterial biofilm formation. 5.3. OMV influence on biofilm formation by H. pylori. 5.4. Structural function of H. pylori extracellular DNA. 6. Extracellular DNA as an information carrier. 6.1. Influence on virulence. 6.2. Transformation. 6.3. Natural competence of H. pylori. 7. Conclusions

Patogeneza i leczenie zakażeń Candida spp.

Pathogenesis and treatment of fungal infections by Candida spp.
M. Staniszewska, M. Bondaryk, M. Kowalska, U. Magda, M. Łuka, Z. Ochal, W. Kurzątkowski

1. Wprowadzenie. 2. Epidemiologia kandydoz. 3. Czynniki zjadliwości Candida albicans. 3.1. Adhezja. 3.2. Proteazy aspartylowe. 3.3. Pleomorfizm. 4. Leczenie zakażeń o etiologii Candida spp. 5. Nowe trendy w poszukiwaniu antymikotyków. 6. Podsumowanie

Abstract: Candida albicans normally exists as harmless commensal inhabiting mucosal surfaces of healthy individuals. Yet, this opportunistic pathogen in immunocompromised hosts causes superficial or invasive life treating infections with high mortality rate. The incidence of candidiasis appeared to have several predisposing factors such as immunosuppressant or steroids treatments, long-term catheterization, invasive medical procedures, treatment with broad-spectrum antibiotic, destruction of skin by deep skin burns, local disorders of the gastrointestinal tract, diabetes mellitus, premature very low birth weight infants, immunologically compromised individuals, spread of HIV infection. This serious problem causes a need for better understanding of C. albicans virulence and antifungal treatment. This review features characterization of chosen virulence factors i.e.: adhesion, pleomorphism and enzymatic activity. Currently natural antifungal substances as well as synthetic derivatives are used at broad scale in candidiasis treatment. Recently, an increase of resistance to antifungal agents commonly used in fungal infection management has been observed. This world-scale problem generated a need for a search for novel antifungals.

1. Introduction. 2. Epidemiology of candidiasis. 3. Virulence factors of Candida albicans. 3.1. Adhesion. 3.2. Secreted aspartyl proteases. 3.3. Pleomorphism. 4. Candidiasis management. 5. New trends in the search for novel antifungal agents. 6. Summary

Antygeny powierzchniowe i czynniki wirulencji Escherichia coli O157

Cell-surface antigens and virulence factors of Escherichia coli O157
J. Kutkowska, M. Michalska-Szymaszek, R. Matuszewska, E. Chmiel, T. Urbanik-Sypniewska

1. Wstęp. 2. Występowanie w środowisku i źródła zakażenia bakteriami EHEC E. coli O157. 3. Patogeneza. 3.1. Objawy kliniczne zakażenia E. coli EHEC. 4. Czynniki wirulencji kodowane na plazmidach. 5. Antygen O; struktura, biosynteza, znaczenie w chorobotwórczości i jako markera w diagnostyce. 6. Antygeny H serotypu O157. 7. Identyfikacja E. coli O157. 8. Epidemie EHEC E. coli przenoszące się drogą wodną. 9. Zapobieganie. 10. Podsumowanie

Abstract: Shiga toxin-producing Escherichia coli (STEC) strains are commensal bacteria in cattle with high potential for transmission to humans. The serotype E. coli O157:H7 is the main cause of hemorrhagic colitis and hemolytic-uremic syndrome. E. coli O157 synthesizes an O-antigen containing a repeating tetrasaccharide with the structure (4-N-acetyl-perosamine →3-fucose →3-glucose →3-N-acetyl-galactosmine). The presence of a common epitope consisting of 2-substituted N-acyl-perosamine is responsible for the serological cross-reactions with Yersinia enterocolitica O9 or Vibrio cholerae O1. The sequence homology indicates that the O157:H7 rfbE gene encoding perosamine synthetase may have originated in a species other than E. coli. The peculiarity of O157 repeat unit biosynthesis is a new pathway performed by epimerase Gnu that catalyses the reversible epimerization of N-acetyl-glucosamine-P-P-undecaprenol to N-acetyl-galactosmine-P-P-undecaprenol. The potential of the bacterial epimerase as a new target for antimicrobial agents is discussed. O157 and H7 antigens seem to be accessory virulence factors implicated in the pathogenesis of human diseases. The O157 antigen is important in the animal and plant host immune response and plays a role in the adherence of this organism to epithelial cells. One of the sources of epidemic outbreaks is water from the municipal water supply and other reservoirs. Survival of O157 bacteria in water environments has been recorded. The comparative analysis of nucleotide sequences within the rfb O antigen gene cluster and of other genes in the genome among STEC strains will elucidate the genetic basis of the evolution and virulence of these enteric pathogens.

1. Introduction. 2. Environmental occurrence and sources of EHEC E. coli O157 infections. 3. Pathogenesis. 3.1. Clinical symptoms of E. coli EHEC infection. 4. Plasmid-encoded virulence factors. 5. The O-antigen; the structure, biosynthesis and the role in pathogenesis and as a diagnostic marker. 6. H antigens of the O157 serotype. 7. E. coli O157 identification. 8. Waterborne EHEC outbreakes. 9. Prevention. 10. Summary