All posts by Postępy Mikrobiologii

Bacteroides spp. – znaczenie kliniczne, lekooporność i metody jej oznaczania

Bacteroides spp. – clinical significance, antibiotic resistance and identification methods
S. Niestępski, M. Harnisz E. Korzeniewska, A. Osińska, B. Dziuba

1. Wstęp. 2. Systematyka bakterii z rodzaju Bacteroides. 3. Znaczenie kliniczne Bacteroides spp. 4. Oporność na leki u Bacteroides spp.
4.1. Bakterie z rodzaju Bacteroides jako rezerwuar determinantów oporności. 4.2. Oporność na środki przeciwdrobnoustrojowe. 5. Metody określania lekowrażliwości. 6. Podsumowanie

Abstract: Anaerobic Bacteroides species are dominant microbiota of the digestive tract of mammals. Along with other symbiotic bacteria located in the gastrointestinal tract, they contribute to the proper functioning of the organism. Some Bacteroides species are highly pathogenic. Virulence of these bacteria is related to their polysaccharide capsule, lipopolysaccharide and a variety of enzymes and enterotoxin. In recent years, an increase of antibiotic resistance in Bacteroides spp. has been noted, therefore the changes to the antibiotic resistance patterns in these bacteria should be monitored. This study summarizes the current knowledge about the bacteria of Bacteroides species.

1. Introduction. 2. Taxonomy of Bacteroides species. 3. Clinical significance of Bacteroides spp. 4. Antibiotic resistance. 4.1. Bacteroides species as a reservoir of antimicrobial resistance determinants. 4.2. Antimicrobial resistance. 5. Methods of drug resistance determination. 6. Summary

Amyloidy, białka powszechne wśród drobnoustrojów

Amyloids, common proteins among microorganisms
B.K. Pawłowska, B.M. Sobieszczańska

1. Wprowadzenie. 2. Amyloidy bakteryjne. 2.1. Fimbrie spiralne. 2.1.1. Synteza fimbrii spiralnych. 2.1.2. Regulacja ekspresji operonu csg. 2.1.3. Udział fimbrii spiralnych w wirulencji bakterii. 2.1.4. Rola fimbrii spiralnych w patogenezie zakażeń człowieka. 2.2. Inne amyloidy bakteryjne. 2.3. Amyloidy grzybicze. 3. Podsumowanie

Abstract: Historically, the term amyloid was used strictly with reference to human neurodegenerative diseases. Nowadays, it is known that many proteins have the potential to conformational changes into β-sheet structures with tendency to form insoluble amyloid fibrils. Moreover, amyloid proteins are widespread among microorganisms. Bacteria and fungi produce functional amyloids which exhibit all characteristics of amyloid proteins, but in contrast to a numerous group of human toxic amyloids, they play important physiological functions in microorganisms. There is growing evidence that functional amyloids are important in bacterial adhesion and invasion. Furthermore, amyloids make biofilms thicker, rougher, and more resistant to drying out. The increasing interest in better understanding of the nature of these unusual microbial proteins and their role in pathogenesis are likely to contribute to the effective treatment or prevention of infectious diseases in humans.

1. Introduction. 2. Bacterial amyloids. 2.1. Curli fibers. 2.1.1. Curli biogenesis. 2.1.2. Regulation of csg operon. 2.1.3. Participation of curli in bacterial virulence. 2.1.4. Role of curli in pathogenesis. 2.2. Other bacterial amyloids. 2.3. Fungal amyloids. 3. Recapitulation

Mechanizmy toksyczności i transportu arsenu u mikroorganizmów

Mechanisms of arsenic toxicity and transport in microorganisms
S. Mucha, M. Berezowski, K. Markowska

1. Wstęp. 2. Właściwości chemiczne i występowanie arsenu w środowisku. 3. Sposoby wnikania arsenu do komórek. 4. Mechanizmy toksycznego działania arsenu trójwartościowego. 4.1. Stres oksydacyjny. 4.2. Wiązanie z białkami. 4.3. Agregacja białek. 5. Toksyczność pięciowartościowego arsenu. 6. Mechanizmy detoksykacji komórek ze związków arsenu. 6.1. Operony ars. 6.2. Geny ACR. 6.3. Usuwanie koniugatów arsenu przez pierwotne transportery ABC. 6.4. Dwukierunkowy transport arsenu. 7. Podsumowanie

Abstract: Arsenic is an ubiquitous element present in the environment either through geological or anthropogenic activities. Millions of people all over the world are exposed to arsenic mainly via air, drinking water and food sources, which results in higher incidence of cancer. Several mechanisms by which arsenic compounds induce tumorigenesis have been proposed. Arsenic mediates its toxicity by generating oxidative stress, inducing protein misfolding, promoting genotoxicity, hampering DNA repair and disrupting signal transduction. Thus, all organisms have developed multiple pathways for arsenic detoxification. In this article, we review recent advances in the understanding of arsenic toxicity and its transport routes in prokaryotes and eukaryotes, including a dual role of aquaglyceroporins in the uptake and efflux, active transport out of the cell via secondary ion pumps and sequestration of metalloid-thiol conjugates into vacuoles by primary ABC transporters. We believe that such studies are of high importance due to the increasing usage of arsenic-based drugs in the treatment of certain types of cancer and diseases caused by protozoan parasites as well as for the development of bio- and phytoremediation strategies for metalloid-polluted areas.

1. Introduction. 2. The chemical properties and the presence of arsenic in the environment. 3. Pathways for arsenic uptake. 4. Mechanism of trivalent arsenic toxicity. 4.1. Oxidative stress. 4.2. Arsenic binding to proteins. 4.3. Protein aggregation. 5. Pentavalent arsenic toxicity. 6. Cellular detoxification mechanisms of arsenic compounds. 6.1. ars operons. 6.2. ACR genes. 6.3. Removal of arsenic conjugates by the ABC transporters. 6.4. Bi-directional transport of arsenic. 7. Summary

Czynniki odpowiedzialne za rozwój Lyme carditis

Factors responsible for the development of Lyme carditis
T. Chmielewski, S. Tylewska-Wierzbanowska

1. Wstęp. 2. Lyme carditis – objawy, rozpoznanie i leczenie. 3. Patomechanizm zapalenia serca. 3.1. Ruch krętków. 3.2. Chemotaksja i adhezja. 3.3. Reakcje autoimmunologiczne. 4. Podsumowanie

Abstract: Borrelia burgdorferi sensu lato spirochetes are unique in many aspects. They are the etiological agents of Lyme borreliosis, meta-zoonotic, tick-borne disease of mammals, including humans. Ixodes spp. ticks are the vector. With the exception of erythema chronicum migrant (EM), manifestations of the disease may vary depending on the genospecies of Borrelia burgdorferi sensu lato. One of the symptoms is Lyme carditis. To date, the causative factors and the mechanisms of pathogenesis have not been well-described.
Borrelia burgdorferi spirochetes are considered as one of the most invasive mammalian pathogen. They are able to move through the skin, as well as break into and out of blood vessels, easily crossing the blood-brain barrier. Genes encoding various motility forms are bound with chemotaxis signaling system which leads and coordinates motion functions. The attachment of bacteria to host cells or extracellular matrix may promote colonization and disease development. Lyme disease spirochetes encode several surface proteins including decorin binding adhesion (DbpA), which varies among strains contributing to strain-specific differences in tissue tropism. The strains demonstrating the greatest decorin-binding activity promote the greatest colonization of heart and cause the most severe carditis. Moreover, the manifestation of Lyme carditis in certain hosts may be a result of an autoimmunological reaction due to molecular mimicry between B. burgdorferi and host self-components. In mammals, infection with B. burgdorferi induces the development of antibodies which may cross-react with myosin and neural tissue.

1. Introduction. 2. Lyme carditis – symptoms, recognition and treatment. 3. Patho-mechanism of Lyme carditis. 3.1. Spirochetes motility. 3.2. Chemotaxis and adhesion. 3.3. Autoimmunological reactions. 4. Summary

Pełzaki wolno żyjące o właściwościach patogenicznych dla człowieka

Pathogenic free-living amoeba
N. Łanocha-Arendarczyk, D. Kosik-Bogacka, K. Galant, W. Zaorski, K. Kot, A. Łanocha

1. Wstęp. 2. Budowa morfologiczna i rozwój pasożytów. 3. Występowanie pełzaków wolno żyjących w środowisku. 4. Chorobotwórczość pełzaków z „grupy limax”. 4.1. Przewlekłe ziarniniakowe zapalenie mózgu (GAE). 4.2. Pełzakowe zapalenie rogówki oka (AK). 4.3. Pierwotne zapalenie mózgu i opon mózgowo-rdzeniowych (PAM). 5. Podstawy diagnostyki zarażeń wywołanych przez pełzaki wolno żyjące. 5.1. Badania bezpośrednie. 5.2. Badanie płynu mózgowo-rdzeniowego. 5.3. Badania wymazu lub bioptatu pobranego ze zmian w narządach. 5.4. Metody hodowlane. 5.5. Diagnostyka molekularna. 6. Leczenie. 7. Pełzaki jako wektory chorobotwórczych drobnoustrojów. 8. Podsumowanie

Abstract: Invasions caused by free-living and parasitic limax amoeba can pose a major threat to human health and life. The amoeba from the genera Acanthamoeba and Naegleria as well as the following species: Sappina diploidea, S. pedata, Balamuthia mandrillaris, and probably Hartmannella vermiformis, are the major cause of primary amoebic meningoencephalitis (PAM), granulomatous amebic encephalitis (GAE) and amoebic keratitis (AK). Furthermore, free-living amoeba can be vectors of bacteria, including Legionella pneumophila, Pseudomonas aeruginosa, Acinetobacter baumannii, Stenotrophomonas maltophila, Klebsiella pneumoniae, Serratia marcescens and Mycobacterium tuberculosis. There is a need for more research on free-living amoeba invasions in humans, particularly on the methods of diagnosis and appropriate forms of pharmacological therapy. Despite the undeniable role of free-living amoeba in the transmission of pathogenic bacteria, there is still insufficient amount of research and optimal diagnostic methods to identify the mechanisms of penetration, proliferation and exocytosis of many pathogenic microorganisms.

1. Introduction. 2. Morphology and growth of parasites. 3. Presence of free-living amoeba in the environment. 4. Pathogenicity of limax amoeba 4.1. Granulomatous amebic encephalitis (GAE). 4.2. Acanthamoeba keratitis (AK). 4.3. Primary amoebic meningoencephalitis (PAM). 5. Basic diagnosis of infections caused by free-living amoeba. 5.1. Direct testing. 5.2. Cerebral spinal fluid analysis. 5.3. Smear test or biopsy of abnormal tissue. 5.4. Proliferation methods. 5.5. Molecular diagnostics. 6. Treatment. 7. Amoeba as vectors of pathogenic microorganisms. 8. Summary

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POSTĘPY MIKROBIOLOGII
2018, 57, 4

O Towarzystwie

PTM

Celem Polskiego Towarzystwa
Mikrobiologów jest propagowanie rozwoju nauk mikrobiologicznych

i popularyzowanie osiągnięć
mikrobiologii wśród członków Towarzystwa oraz szerokich kręgów społeczeństwa. Formami działalności jest organizowanie zjazdów, posiedzeń naukowych, kursów, wykładów
i odczytów oraz konkursów prac naukowych; wydawanie i popieranie wydawania czasopism naukowych, książek
i innych publikacji
z dziedziny mikrobiologii; opiniowanie o stanie i potrzebach mikrobiologii polskiej

i występowanie w jej sprawach wobec
władz państwowych; współpraca
z pokrewnymi stowarzyszeniami
w kraju i za granicą.