All posts by Postępy Mikrobiologii

Wystepowanie i chorobotwórczość dla człowieka potencjalnie toksynotwórczych maczugowców – Corynebacterium diphtheriae, Corynebacterium ulcerans i Corynebacterium pseudotuberculosis

The occurrence and pathogenicity of potentially toxinogenic corynebacteria – Corynebacterium diphtheriae, Corynebacterium ulcerans i Corynebacterium pseudotuberculosis
A. A. Zasada

1. Charakterystyka rodzaju. 2. Występowanie w środowisku. 3. Zakażenia człowieka. 4. Czynniki zjadliwości. 4.1. Toksyna błonicza. 4.2. Inne czynniki zjadliwości. 4.2.1. Czynniki adhezji. 4.2.2. Pobieranie żelaza. 4.2.3. Fosfolipaza D (Pld). 4.2.4. Proteazy serynowe. 4.2.5. Neuraminidaza H (NanH). 5. Podsumowanie

Abstract: C. diphtheriae, C. ulcerans and C. pseudotuberculosis are closely related species possessing the ability to produce the lethal diphtheria toxin. The toxin is considered as the main virulence factor, but these species express also other virulence factors so nontoxigenic strains of the species are also able to cause serious infections. The interest in the virulence factors other then diphtheria toxin has been increasing and new factors and virulence mechanisms have been investigated. This paper is an overview of C. diphtheriae, C. ulcerans and C. pseudotuberculosis infections in humans, presenting the mechanism of action of diphtheria toxin adhesive factors, iron uptake systems and other putative virulence factors.

1. Description of the genus. 2. Occurrence in the environment. 3. Human infections. 4. Virulence factors. 4.1. Diphtheria toxin. 4.2.  Other virulence factors. 4.2.1. Adhesive factors. 4.2.2. Iron utilization. 4.2.3. Phospholipase D (Pld). 4.2.4. Serine proteases. 4.2.5. Neuraminidase H (NanH). 5. Summary

Molekularne metody identyfikacji bakterii z rodzaju Staphylococcus

Molecular methods for the identification of bacteria from the genus Staphylococcus
E. Szczuka, N. Makowska, A. Kaznowski

1. Wprowadzenie. 2.1. Różnicowanie gatunków na postawie sekwencji 16S rDNA. 2.2. Wykorzystanie polimorfizmu międzygenowego 16S rRNA i 23S rRNA do identyfikacji gronkowców. 2.3. Identyfikacja gronkowców na podstawie sekwencji oraz analizy restrykcyjnej genu gap. 2.4. Sekwencja genu hsp60 jako marker genetyczny stosowany w klasyfikacji i identyfikacji gronkowców. 2.5. Polimorfizm genu dnaJ wykorzystany w identyfikacji Staphylococcus spp. 2.6. Różnicowanie gatunków gronkowców na podstawie sekwencji genu tuf. 2.7. Diagnostyka gatunków gronkowców w oparciu o polimorfizm genu sodA. 2.8. Identyfikacja na postawie sekwencji genu rpoB. 3. Zastosowanie reakcji PCR w czasie rzeczywistym w diagnostyce gronkowców. 4. Wykorzystanie spektrometrii mas w identyfikacji gronkowców. 5. Podsumowanie

Abstract: Staphylococci are increasingly recognized as etiological agent of many opportunistic human and animal infections, indicating the need for rapid and accurate identification of these bacteria. In recent years, a significant progress in the identification and phylogenetic studies of Staphylococcus species has been made. In this paper we describe several molecular methods used in taxonomy and identification of staphylococci. The analysis of 16S rRNA gene, gap gene (coding for glyceraldehyde-3-phosphate dehydrogenase), hsp60 gene (encoding heat shock protein Hsp60), dnaJ gene (encoding heat shock protein Hsp40), tuf gene (encoding elongation factor Tu), sodA gene (encoding superoxide dismutase), ropB gene (encoding the beta subunit of RNA polymerase) has been used as tool for the identification of Staphylococcus isolates. Besides the sequence analysis, the PCR-restriction fragment length polymorphism (PCR-RFLP) analysis of core genes (16S rRNA, gap, hsp60, dnaJ, tuf) has been described. Attention is also paid to new molecular methods such as real-time PCR and mass spectrometry.

1. Introduction. 2.1. Differentiation of staphylococcal species based on 16S rRNA gene sequence. 2.2. Use of the polymorphism of the 16S-23S rRNA spacer for staphylococci identification. 2.3. Identification of staphylococci using the sequence and restriction fragment length polymorphism analysis of gap gene. 2.4. The sequence of the hsp60 gene as a marker for classification and identification of staphylococci. 2.5. Use of polymorphism of dnaJ gene for the identification of Staphylococcus spp. 2.6. Differentiation of staphylococcal species based on tuf gene sequence. 2.7. Use of the polymorphism of sodA gene in diagnostics of staphylococcal species. 2.8. Identification based on ropB gene sequence. 3. Application of real-time PCR in diagnostics of staphylococci. 4. Application of mass spectrometry in the identification of staphylococcal isolates. 5. Summary

Epidemiologia zakażeń Streptococcus pyogenes, struktura klonalna populacji i antybiotykooporność

Epidemiology of Streptococcus pyogenes infections, clonal structure population and antibiotic resistance
K. Szczypa, J. Wilemska, W. Hryniewicz, I. Sitkiewicz

1. Wstęp. 2. Zakażenia wywoływane przez S. pyogenes. 3. Nosicielstwo i drogi szerzenia się zakażeń S. pyogenes. 4. Ustalanie pokrewieństwa genetycznego pomiędzy szczepami S. pyogenes. 5. Oporność S. pyogenes na antybiotyki. 6. Profilaktyka zakażeń S. pyogenes. 7. Podsumowanie

Abstract: Streptococcus pyogenes (GAS) is one of the major human pathogens responsible for infections worldwide. It may cause mild infections of the skin and mucosal surfaces, as well as severe invasive infections. It has been estimated that S. pyogenes is responsible for half a million deaths a year, and is considered as one of the most important pathogens.
Many clinical investigations on S. pyogenes focus on characterization of pathogenic strains, heterogeneity/homogeneity of the population clonal spread, transfer between patients and tracing sources of antibiotic resistance. Advanced studies on vaccines that prevent GAS infections are in progress.

1. Introduction. 2. S. pyogenes infections. 3. Carrier state and epidemiology of infections. 4. S. pyogenes strains genetic affinity. 5. S. pyogenes resistance to antibiotics. 6. The prophylactics of S. pyogenes infections. 7. Summary

Immobilizacja komórek – znaczenie biomedyczne

Cell immobilization - biomedical significance
Z. Bakuła, R. Stachowiak, J. Wiśniewski, L. Granicka, J. Bielecki

1. Wprowadzenie. 2. Metody immobilizacji komórek. 2.1. Unieruchomienie bez nośnika. 2.2. Unieruchomienie na powierzchni nośnika. 2.3. Unieruchomienie wewnątrz nośnika. 2.3.1. pułapkowanie. 2.3.2. Kapsułkowanie. 2.3.3. Nanoopłaszczanie. 3.  Historia zastosowania nośników do immobilizacji materiału biologicznego. 4. Immobilizacja w zastosowaniach biomedycznych. 4.1. Drogi podawania terapeutyków przy użyciu unieruchomionych komórek. 4.2. Właściwości kapsułek wykorzystywanych we wszczepieniach. 4.2.1. Struktura materiału nośnika. 4.2.2. Biozgodność. 4.2.3. Wytrzymałość. 4.2.4. Właściwości chemiczne. 4.3. Właściwości kapsułek wykorzystywanych w terapii doustnej. 4.4. Immobilizowany materiał biologiczny. 4.5. Biomedyczne zastosowania immobilizowanych komórek. 4.5.1. Wykorzystanie unieruchomionych komórek eukariotycznych. 4.5.2. Wykorzystanie unieruchomionych drobnoustrojów. 5. Podsumowanie

Abstract: Cell encapsulation, which aims to entrap viable cells within the confines of semi-permeable membranes, represents one of the current leading methodologies aimed at the delivery of biological factors to patients for the treatment of multiple diseases. The pores of the membrane are suitably sized to allow the entry of small molecules such as oxygen, nutrients and electrolytes into the capsule and egress of metabolites and small bioactive molecules from the capsule. Entrapment of cells in physical membranes has been practiced since the early 1930s. Numerous encapsulation techniques have been developed over the years and they are classified as entrapment, microencapsulation (usually small spherical devices), macroencapsulation (hollow fiber membranes) and nanocoating. Cell encapsulation technologies were initially directed towards the transplantation of cells across an immunological barrier without the use of immunosuppressant drugs. Some encapsulated microorganisms may carry a transfected human gene, and thus become a source of valuable regulatory factors or anti-tumor factors. Such factors released in strategic locations may direct or modify the biological processes in the eukaryotic organism in biomedical applications. Membranes with immobilized cells can be also used as a novel method for oral drug delivery.

1. Introduction. 2. Methods of cell immobilization. 2.1. Immobilization without carrier. 2.2. Immobilization on carrier. 2.3. Immobilization in carrier. 2.3.1. Entrapment. 2.3.2. Encapsulation. 2.3.3. Nanocoating. 3. The history of using membranes for immobilization. 4. Encapsulation in biomedical applications. 4.1. Methods of drug delivery using encapsulated cells. 4.2. Membrane properties important for implantation. 4.2.1. Structure of carrier material. 4.2.2. Biocompatibility. 4.2.3. Durability. 4.2.4. Chemical properties. 4.3. Membrane properties for oral drug delivery. 4.4. Immobilized biological material. 4.5. Biomedical applications of encapsulated cells. 4.5.1. Use of encapsulated eukaryotic cells. 4.5.2. Use of encapsulated microorganisms. 5. Summary

Choroba niedokrwienna serca a zakażenia bakteryjne Helicobacter pylori i Chlamydophila pneumoniae – rola białek szoku cieplnego i zjawisko mimikry antygenowej

Coronary heart disease versus Helicobacter pylori and Chlamydophila pneumoniae bacterial infections – the role of heat shock proteins and the phenomenon of antigenic mimicry
A. Matusiak, M. Chmiela

1. Patogeneza choroby niedokrwiennej serca. 2. Choroba niedokrwienna serca jako proces zapalny. 3. Markery reakcji zapalnej w chorobie niedokrwiennej serca. 4. Czynniki bakteryjne a choroba niedokrwienna serca. 5. Podłoże autoimmunizacyjne choroby niedokrwiennej serca. 6. Białka szoku cieplnego (Hsp) – bodźce i tarcze w procesach z autoimmunizacji w chorobie niedokrwiennej serca.  7. Prozapalne działanie białek Hsp w chorobie niedokrwiennej serca. 8. Hipoteza cytotoksycznego działania przeciwciał przeciwko bakteryjnym białkom szoku cieplnego o masie cząsteczkowej 60 i 65 kDa w chorobie niedokrwiennej serca. 9. Podsumowanie

Abstract: The end of the previous century brought new findings concerning the role of inflammation and the infectious agents in the development of atherosclerosis. However, it is still not clear whether and how the infectious agents participate in the formation and the development of the atherosclerotic plaque. This article discusses the findings which to confirm the hypothesis that the bacterial Hsp proteins are factors promoting the autoimmune reactions and pathological processes leading to coronary heart disease. The involvement of bacterial Hsp proteins in the atherosclerotic processes is probably based on the upregulation of anti-Hsp60 autoantibodies produced in response to infection with a pathogen which produces Hsp60. Since the Hsp proteins are very conservative, the antibodies produced in response to bacterial Hsp60 may react with the human analogue Hsp60 exposed on the surface of endothelium. The complexes of autoantibodies and human Hsp60 proteins may induce the complement dependent cytotoxicity and promote inflammatory damage of the vessels.

1. Pathogenesis of coronary heart disease. 2. Coronary heart disease as an inflammatory process. 3. Markers of inflammation in coronary heart disease. 4. Bacterial factors and coronary heart disease. 5. Autoimmune background of coronary heart disease. 6. Heat shock proteins (Hsp) – the stimuli and the targets of autoimmune processes in coronary heart disease 7. Proinflammatory action of Hsp proteins in coronary heart disease. 8. The hypothesis of the cytotoxic effect of antibodies against bacterial Hsp60 and Hsp65 proteins in coronary heart disease. 9. Summary