Tom 57 (2018): Zeszyt 1 (January 2018)

The human body is believed to be occupied by around 4 × 10¹³ microorganism cells, which is 10 times the number of cells of the human body. Multidisciplinary studies conducted worldwide by microbiologists and physicians suggest that the microorganisms which colonize the human body can more actively influence the state of health than previously thought. The most important role in the regulation of the homeostasis is played by ontocenoses of the intestine. Imbalanced taxonomic composition and number of intestinal microbiota may contribute to the development of numerous infectious (HIV), metabolic (diabetes, obesity) and immunological (allergy, asthma, rheumatoid arthritis) diseases, as well as conditions associated with various organs (kidneys, liver, heart, inflammatory bowel disease, Crohn’s disease), cancer (colon) and the nervous system (autism, sleeping problems, stress, chronic fatigue syndrome, schizophrenia, Alzheimer’s disease). The composition of the intestinal microbiota can be modified by applying a specific type of diet.

1. Introduction. 2. Microbiota in the disorders of the immune system. 3. Microbiota in metabolic diseases. 4. Microbiota in cardiovascular diseases. 5. Microbiota in the disorders of the gastrointestinal tract. 6. Microbiota in renal diseases. 7. Microbiota in central nervous system disorders. 8. Regulation of microbiota through functional foods. 9. Conclusions

The Hfq protein is one of the most important regulatory factors acting at the RNA level. This protein was first discovered as a host factor necessary for Qβ bacteriophage development. Following the discovery, the Hfq role in bacteriophage development was not investigated in depth. In subsequent years, however, many studies revealed various riboregulatory functions of this protein, mainly focused on facilitating sRNA and mRNA pairing, regulating both the degradation and stability of many transcripts. The Hfq protein has the ability to bind to nucleic acids – it binds more efficiently to RNA, but can also attach to DNA. It has been also proved that Hfq is involved in the nucleoid organization. These observations open room for discussion on the potential role of Hfq in the regulation of DNA replication. Since Hfq protein affects many cellular processes, the deletion of the gene encoding this protein has a pleiotropic effect on the cell.

1. Introduction. 2. The history of the Hfq protein discovery and its evolutionary context. 3. Structure of the Hfq protein and its molecular function. 4. Characteristics of cells devoid of the Hfq protein. 5. Hfq interactions with the DNA. 6. Summary

Two Coronaviruses, HCoV-229E and HCoV-OC43, causing generally mild respiratory tract infections in humans, were described in the XX c. Pandemic Coronaviruses were first discovered as late as in the XXI c.: SARS-HCoV in 2002 – causing severe respiratory tract infections (SARS) in China; MERS-HCoV in 2012 – circulating mostly on the Arabian Peninsula. The SARS epidemic ended in 2004 resulting in morbidity of > 8000 and > 770 deaths, while the MERS epidemic is still ongoing (> 2000 ill, > 700 deaths) although its intensity decreased. Both viruses are zoonotic and require at least two “host jumps” for the transmission of the infection to humans: for HCoV-SARS – from bat to palm civet and then to human; for HCoV-MERS – from bats to camels and subsequently to humans. Primary mode of transmission is droplet in close contact (< 1 m), but both viruses remain active in aerosol (up to 24 h), so infection can be also spread by air (ventilation). The ability for human-to-human transmission is higher for HCoV-SARS than for HCoV-MERS (8 generations vs. 4, respectively). Moreover, there are differences in genome structure and pathogenic mechanisms: different receptor, cell entry mechanism, different way of host response modulation (e.g. inhibition of IFNβ cascade), etc. Probably, these differences influence the overall manifestation of the disease in humans. Infection caused by HCoV-MERS might manifest itself as ARDS, a mild-mannered and asymptomatic disease. HCoV-SARS infections seem to be associated with severe disease only. In this paper, a comparison of the structure of these viruses, the mechanisms underlying their ability to cross the interspecies barrier and to multiply in the human body, including modulation of IFNβ cascade, as well as routes of infection transmission and symptoms caused, were presented.

1. Background. 2. Comparison of structure. 3. Transmission of infections. 3.1. Origin of the viruses. 3.2. Interspecies transmission. 4. Infections in humans. 5. Growth of the viruses in the human body. 5.1. Inhibition of interferon cascade. 6. Infections due to MERS- HCoV and SARS-HCoV. 7. Hospital outbreaks. 8. Summary

The HPV virus, belonging to papillomaviruses, causes genital, lung, head and neck cancers. It is currently estimated that there are 190 types of HPV. Over 700 million people worldwide are infected with the virus. In the United States, 14 million new infections occur every year. The most common HPV types responsible for carcinogenesis of head and neck areas are types 16 and 18. The virus infects human epithelial cells, for example during a sexual intercourse. Transmission from mother to child during birth is also possible. There is evidence linking HPV with laryngeal cancer, leukoplakia, tonsil cancer or Bowen’s disease. HPV vaccines are available to help prevent infection by certain types of the virus, e.g. 9-valent HPV vaccine called Gardasil-9.

1. Introduction. 2. Structure of HPV. 3. Taxonomy. 4. Infection. 5. Pathogenicity. 6. Treatment. 7. Vaccines. 8. Summary

Relapsing fevers are considered, on the one hand, emerging or re-emerging diseases, and on the other hand, they still belong to neglected diseases which attract little attention of researchers and the public in developed countries. Genus Borrelia is divided into two large groups. The first of these is Borreli aburgdorferi sensulato– the etiologic agent of Lyme disease, first isolated from the Ixodesdamminitick. The second large group of Borrelia spirochetes contains more than 20 species associated with relapsing fever, which are mainly transmitted by soft ticks, with the exception of B. recurrentis transmitted by lice. Comparision of the DNA of different species within this genus showed that the similarity between them is often small, e.g. the DNA homology between B. miyamotoi and B. burgdorferi s.s. or B. garinii is 13%, and B. afzelii only 8%, whereas the B. miyamotoi DNA has a profile similar to the representatives of the tick-borne relapsing fevers, such as B. hermsii (44%), B. turicatae (41%), B. Parkeri (51%). Symptoms of relapsing fevers transmitted by lice and by ticks are very similar. The following symptoms are characteristic for both types of relapsing fevers: high fever with sudden onset, chills, severe headache, muscle and joint pain, drowsiness, photophobia and cough.

1. Introduction. 2. Systematics – classification. 3. Clinical symptoms. 4. Summary

Fluoroquinolones(FQ) are broad-spectrum antimicrobial agents widely used to treat a range of infections in clinical medicine. However, the surveillance studies demonstrate that fluoroquinolone resistance rates increased in Enterobacteriaceae in the past years. FQ inhibit bacterial DNA synthesis by interfering with the action of two bacterial enzymes - DNA gyrase and topoisomerase IV. There are two categories of quinolone resistance mechanisms: chromosomally encoded and acquired. Mutations in chromosomal genes encoding gyrase and topoisomerase IV are the most common mechanisms responsible for high-level fluoroquinolone resistance. Mutations can occur also in regulatory genes which control the expression of native efflux pumps located in bacterial membrane. Furthermore, three mechanisms of plasmid-mediated quinolone resistance (PMQR) have been discovered so far, including Qnr proteins, the aminoglycoside acetylotransferase variant - AAC(6’)-Ib-cr, and plasmid-mediated efflux pumps - QepA and OqxAB. Although the PMQR mechanisms alone cause only low-level resistance to fluoroquinolone, they can complement other mechanisms of chromosomal resistance and facilitate the selection of higher-level resistance. Moreover, plasmids with PMQR mechanisms often encode additional resistance traits (ESBLs, pAmpC, KPC) contributing to multidrug resistance (MDR). This review is focused on a range of molecular mechanisms which underlie quinolone resistance.

1. Introduction. 2. Mechanisms of fluoroquinolone action. 3. Chromosomally-encoded fluoroquinolone resistance. 3.1. Mutations changing the functions of target enzymes. 3.2. Reduction of drug concentration in the cytoplasm - efflux pump. 4. Plasmid-mediated quinolone resistance. 4.1. Qnr proteins. 4.2. AAC(6’)-Ib-cr enzyme. 4.3. Plasmid-mediated efflux pump: QepA i OqxAB. 4.4. The impact of PMQR on fluoroquinolone susceptibility level. 5. Summary

In the early twentieth century, Francisella tularensis was identified as a pathogenic agent of tularaemia, one of the most dangerous zoonoses. Based on its biochemical properties, infective dose and geographical location, four subspecies have been distinguished within the species F. tularensis: the highly infectious F. tularensis subsp. tularensis (type A) occurring mainly in the United States of America, F. tularensis subsp. holarctica (type B) mainly in Europe, F. tularensis subsp. mediasiatica isolated mostly in Asia and F. tularensis subsp. novicida, non-pathogenic to humans. Due to its ability to infect and variable forms of the disease, the etiological agent of tularaemia is classified by the CDC (Centers for Disease Control and Prevention, USA) as a biological warfare agent with a high danger potential (group A). The majority of data describing incidence of tularaemia in Poland is based on serological tests. However, real-time PCR method and MST analysis of F. tularensis highly variable intergenic regions may be also applicable to detection, differentiation and determination of genetic variation among F. tularensis strains. In addition, the above methods could be successfully used in molecular characterization of tularaemia strains from humans and animals isolated in screening research, and during epizootic and epidemic outbreaks.

1. Historical overview. 2. Characteristics and taxonomy of F. tularensis. 3. Morphology. 4. Culture media and conditions. 5. Biochemical properties. 6. Survivability and persistence of F. tularensis. 7. F. tularensis as a biological weapon agent. 8. Tularaemia vaccines. 9. Pathogenicity of F. tularensis. 10. Tularaemia treatment. 11. Laboratory diagnostics of F. tularensis. 12. Summary

Nocardia spp. bacteria are Gram-positive aerobes occurring worldwide. They cause nocardiosis, of which the most common forms are pulmonary nocardiosis and cutaneous nocardiosis. The pulmonary form progresses as a result of aspiration of pathogens into the respiratory tract, whereas the cutaneous nocardiosis, can spread to other organs (often to CNS) and includes Madura foot, both mycetoma and systemic. Infections usually affect people with immunodeficiency, for example infected with HIV or after immunosupression therapy. Nocardia asteroides is responsible for the majority of infections in humans. Diagnostic methods include cell culture and PCR. The symptoms vary depending on the form of the illness. Cough and hemoptysis are characteristic for pulmonary nocardiosis, while abscesses are typical for the cutaneous form. When the illness spreads, the symptoms vary depending on the organ. The treatment of choice is sulfonamide.

1. Introduction. 2. History. 3. Characteristics of Nocardia spp. 4. Systematics. 5. Pathogenicity. 6. Diagnostics. 7. Treatment. 8. Summary