All posts by Postępy Mikrobiologii

Molekularne podłoże oddziaływań pomiędzy Borrelia burgdorferi, kleszczem i kręgowcem

Molecular interactions between Borrelia burgdorferi ticks and mammals
D. Lewandowski, A. Urbanowicz, M. Figlerowicz

1. Wprowadzenie. 2. Borrelia burgdorferi – podstawowe informacje. 3. Kleszcz jako pasożyt. 4. Kolonizacja kleszcza przez B. burgdorferi. 5. Białka kleszcza wykorzystywane przez B. burgdorferi podczas zakażania organizmu gospodarza. 6. Podsumowanie

Abstract: Over the last decade, the incidence of tick-borne diseases has been rapidly increasing in Poland. Lyme disease cases are especially frequent. They disease in caused by Borrelia burgdorferi spirochetes. The enzootic cycle of the Lyme disease pathogen involves both a mammalian host and an Ixodes tick vector. B. burgdorferi enters the tick during its feeding on an infected vertebrate. To survive in the vector and to enter the host, spirochetes utilize their lipoproteins anchored in the external bacterial membrane and tick-encoded proteins. B. burgdorferi is so well adapted to the vector that it is also capable of employing tick strategies to more effectively infect mammalian hosts.
Tick-Borrelia interaction is a very interesting and complex example of parasitism. Better understanding of the mechanisms underlying this phenomenon is indispensable for the development effective strategies of Lyme disease prophylactics and treatment. Here, we describe how B. burgdorferi alters gene expression depending on the tick or vertebrate environment. We also characterize the key bacterial and vector proteins necessary for spirochete for effective colonization of the tick.

1. Introduction. 2. B. burgdorferi characteristics. 3. Ticks as a parasites. 4. Tick colonization by B. burgdorferi. 5. Tick proteins exploited by B. burgdorferi during host infestation. 6. Summary

Wirus cytomegalii – problem zakażeń wrodzonych

Cytomegalovirus – problems due to congenital infection
M. Dunal, A. Trzcińska, J. Siennicka

1. Wstęp. 2. Budowa wirusa cytomegalii. 3. Replikacja CMV. 4. Latencja. 5. Patogeneza i formy kliniczne zakażenia. 6. Epidemiologia. 7. Zakażenie wrodzone CMV. 8. Diagnostyka zakażeń wrodzonych. 8.1. Oznaczenia serologiczne u matki. 8.2. Badanie płynu owodniowego. 8.3. USG. 8.4. Diagnostyka zakażenia wrodzonego u noworodka. 9. Profilaktyka i leczenie. 9.1. Szczepionka. 9.2. Bierna immunizacja. 9.3. Leki przeciwwirusowe. 9.4. Zapobieganie zakażeniom CMV. 10. Podsumowanie

Abstract: Human cytomegalovirus (CMV) is the most common cause of perinatal viral infections in the developed world and the leading cause of congenital infections. About 30–40% infected pregnant women transmit the infection to their fetus. The consequences of CMV infection on pregnant women are very diverse, however, due to their universality, are a serious public health problem. Therefore, the development of prevention in the form of an effective vaccine is one of the priorities of the World Health Organization. Until the vaccine is implemented, it seems very important to raise awareness about the risks associated with CMV infection. The epidemiology, clinical manifestations, prevention, diagnosis and treatment of CMV congenital infection are reviewed.

1. Introduction. 2. The structure of cytomegalovirus. 3. CMV replication. 4. Latency. 5. Pathogenesis and clinical forms of infection. 6. Epidemiology. 7. Congenital CMV infection. 8. Diagnosis of congenital infection. 8.1. Serological tests for mothers. 8.2. Examination of amniotic fluid. 8.3. USG. 8.4. Diagnosis of congenital infection in a newborn. 9. Prevention and treatment. 9.1. The vaccine. 9.2. Passive immunization. 9.3. Antivirals. 9.4. Prevention of CMV infection. 10. Summary

Mikrobiologiczne ogniwa paliwowe: podstawy technologii, jej ograniczenia i potencjalne zastosowania

Microbial fuel cells: rationale, limitations and potential applications of the technology
K. Markowska, A. M. Grudniak, K. I. Wolska

1. Wstęp. 2. Zasada działania i rodzaje MFC. 3. Mikroorganizmy wytwarzające elektryczność. 4. Transfer elektronów na anodę. 5. Wydajność pracy MFC. 6. Optymalizacja pracy ogniwa. 7. Wykorzystanie ogniw mikrobiologicznych. 8. Podsumowanie

Abstract: Microbial fuel cells (MFC) are devices which use electrochemically active microorganisms to generate an electrical current from a wide range of substrates. Because of the promise of sustainable energy production from organic wastes and wastewaters, this technology is of interest to many scientists. This article deseribes to rationale and limitations of this technology. The performance of MFC depends on a complex system of parameters. Apart from technical variables like the fuel cell design, mechanisms of the bioelectrochemical energy conversion decisively determine the MFC power and energy output. Current limitations make this technology inefficient in electricity generation. Therefore some researchers focus ori the ability of electrochemically active microorganisms to degrade wastes and toxic chemicals as their greatest value. Still continuous efforts are exerted to optimize performance. This article presents the most interesting
current and potential applications of microbial fuel cells are highlighted.

1. Introduction. 2. The principle of operation and types of MFC. 3. Microorganisms that produce electricity. 4. Electron transfer to the anode. 5. MFC work efficiency. 6. Optimization of the fuel cells. 7. Application of MFC. 8. Summary

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

Najnowszy numer

Najnowszy numer

POSTĘPY MIKROBIOLOGII
2017, 56, 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.