1. Wstęp. 2. Budowa, sposób działania i autoregulacja dwuskładnikowych systemów regulacyjnych (TCS). 3. TCS a biofilm. 3.1. Biofilm paciorkowców. 3.1.1. System VicRK S. mutans. 3.1.2. System ComDE S. mutans. 3.1.3. System HK11/RR11 (LiaSR) S. mutans. 3.1.4. System CiaRH S. mutans. 3.1.5. System CovRS (CsrRS) paciorkowców grup A, B, C. 3.1.6. System BfrAB S. gordonii. 3.2. Biofilm gronkowców. 3.2.1. System ArlRS S. aureus. 3.2.2. System GraRS S. aureus. 3.2.3. System WalKR S. aureus. 3.2.4. System LytSR S. aureus. 3.2.5. System SaeRS S. aureus oraz S. epidermidis. 3.3. Biofilm enterokoków. 3.3.1. System FsrABC E. faecalis. 3.3.2. System EtaSR E. faecalis. 4. Podsumowanie
Browsing tag: biofilm
1. Wstęp. 2. Patogeneza zakażenia okołowszczepowego. 3. Klasyfikacja zakażeń okołowszczepowych. 4. Diagnostyka. 5. Profilaktyka zakażeń. 6. Leczenie zakażeń. 6. Podsumowanie
Abstract: Bacterial infections accompanying implanted medical devices create serious clinical problems. Using titanium implants may reduce the rate of there infections. Physicochemical properties of titanium allow using it as implantable biomaterial to maintain osseointegration, phenomenon described as “biological and functional connection of the implant with the living bone”. One of the most important factors which can affect osseointegration is bacterial colonization of the implant surface and development of Biomaterial Associated Infection (BAI). Impaired osseointegration can increase the risk of subsequent loosening due to micromotion. BAI’s in orthopaedics and maxillofacial surgery are serious complications, which ultimately lead to osteomyelitis with consequent devastating effects on bone and surrounding soft tissues. Implant associated infections are caused by microorganisms which adhere to the implant surface and then live clustered together in a highly hydrated extracellular matrix attached to the surface, known as bacterial biofilm. Simple debridement procedures with retention of prosthesis and chemotherapy with antimicrobial agents are the treatments not always effective against infections already established.
1. Introduction. 2. Pathogenesis of biomaterial associated infection. 3. Classification. 4. Diagnostics. 5. Prophylaxis. 6. Treatment. 6. Summary
1. Zakażenia układu moczowego. 2. Proteus mirabilis – charakterystyka ogólna. 3. Biofilm – definicja, opis. 4. Biofilm na cewniku urologicznym i jego inkrustacja. 5. Zapobieganie i leczenie CAUTI u osób poddanych cewnikowaniu. 6. Podsumowanie
Abstract: Urinary tract infection (UTI) is one of the most common nosocomial infections. Proteus mirabilis is important Gram-negative, dimorphic and motile pathogen (Enterobacteriaceae family), causing UTI – especially in catheterized patients. Key elements leading to CAUTI are: catheter colonization, mono- or multi-species biofilm formation and the long period of the catherization. Biofilm is microorganisms’ protective and dynamic community, attached to surface and embedded in extracellular matrix (mainly polysaccharides). P. mirabilis can easily adhere to catheter surface and cause it’s encrustation and blockage (due to urine alkalization by urease, leading to struvite and apatite crystals precipitation). Struvite contains magnesium ammonium phosphate and apatite – calcium phosphate. Urine flow obstruction can elicit pyelonephritis. Other uropathogens, producing urease e.g. Morganella morganii, Providencia stuartii, Escherichia coli (some strains), Klebsiella pneumoniae rather rarely cause catheter blockage. There have been proposed many solutions, preventing catheter biofilm colonization or disrupting formed consortium. However by this time there is no high-effective and broadly used remedy. One of the solutions is the impregnation of the catheters with silver, EDTA, antiseptics (e.g. triclosan, chlorohexidine), antibiotics, heparin or lactoferrin – short-term and insufficient-concentration release, risk of the resistance onset, sometimes non-wide spectrum activity. This solutions are generally moderately effective and postpones the emergence of bacteruria. Another approach (experimental) for example is to inhibit urease or the quorum sensing. The surface of the catheter also could be more hydrophilic and smooth, to inhibit the bacterial attachment.
1. Urinary tract infections. 2. Proteus mirabilis – general description. 3. Biofilm – definition, characterization. 4. Biofilm on urinary catheter and it’s encrustation. 5. Prophylaxis and treatment of CAUTI in catheterized patients. 6. Summary
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
1. Wstęp. 2. Leczenie zakażeń S. maltophilia. 3. Oporność na związki przeciwbakteryjne. 3.1. Oporność na antybiotyki i chemioterapeutyki. 3.2. Oporność na środki dezynfekcyjne. 3.3. Oporność na jony metali. 4. Systemy pomp. 4.1. Rodzina RND. 4.2. Rodzina MFS. 4.3. Rodzina ABC. 4.4. Pompa FuaABC. 5. Biofilm bakteryjny i system quorum sensing. 6. Podsumowanie
Abstract: Stenotrophomonas maltophilia is a non-fermentative Gram-negative rod, which can cause many infections, including pneumonia and bacteremia, especially in immunocompromised or long-term hospitalized patients. The infections are difficult in therapy, because clinical isolates are usually highly resistant to many classes of antimicrobial agents, moreover, they are able to colonize medical devices and epithelial cells and form biofilm. The several resistance mechanisms of S. maltophilia to antibacterial agents have been described, among them: β-lactamases production, production of other enzymes modifying antibiotics structure and activity of multidrug efflux pumps (MDR). Up to date, eight MDR efflux pumps have been identified in S. maltophilia strains. These pumps belong to three different families of MDR pumps and RND family plays the most important role in multidrug resistance.
1. Introduction. 2. Treatment of S. maltophilia infections. 3. Resistance to antibacterial substances. 3.1. Resistance to antibiotics and chemotherapeutics. 3.2. Resistance to disinfectants. 3.3. Resistance to metals. 4. Efflux systems. 4.1. RND family. 4.2. MFS family. 4.3. ABC family. 4.4. The FuaABC efflux pump. 5. Biofilm and quorum sensing system. 6. Summary