Biography:

Maurizio Provenzano graduated as MD from La Sapienza University of Rome and obtained his specialization in Medical Oncology at the University of Milan and his PhD in Virology at the University of Padua. He is the Head of Research at the Department of Urology, University Hospital of Zurich and Lecturer at the Faculty of Medicine, University of Zurich. Since 2007 he has been member of the Cancer Network of Zurich. He has published more than 50 papers and has been serving as an editorial board member of reputed journals. He has received several acknowledgments for his efforts in cancer virology

Abstract:

Several studies associating BK polyomavirus (BKPyV) and prostate cancer (PCa) suggested that this virus may exert its oncogenic activity at early stages of cancer development. The BKPyV oncogene, the large T antigen (LTag), has frequently been detected in areas of proliferative inflammatory atrophy, which is considered a precursor lesion leading to prostatic intraepithelial neoplasia and overt PCa. In a recently updated systematic review, the presence of BKPyV was significantly higher in PCa tissues than in healthy control tissues, providing evidence for a link between BKPyV infection and cancer risk. In addition, recent original investigations highlighted an association between expression of the virus and the clinical course of PCa. For example, by studying immune responses elicited against BKPyV LTag, a significant association between LTag positive cancer lesions and a peculiar regulatory profiling has been observed in PCa patients with evidence of disease recurrence after surgical radical prostatectomy. Lastly, a study carried out in a larger cohort of patients undergoing radical prostatectomy revealed the IgG response against LTag as an independent predictor of disease recurrence. Although a full picture of the mechanisms potentially responsible for the involvement of BKPyV in PCa is not available yet, continuing work on this topic should help to refine the potential role of BKPyV in PCa patients, perhaps revealing unsuspected associations with the clinical course of this disease.

Biography:

Malgorzata G. Norton (nee. Mikolajczyk) received her M.S. degree in Veterinary Medical Sciences/Immunology from Louisiana State University, School of Veterinary Medicine studying Cat Scratch Disease. She is currently a Biologist at the U.S. Food and Drug Administration in the Laboratory of Plasma Derivatives, a position she’s held for over 10 years. She is involved in both regulatory review and research involving plasma-derived polyclonal immune globulin. Her current research involves protein-protein and protein-carbohydrate interactions using Surface Plasmon Resonance (SPR). Her collaborations span the fields of virology, bacteriology, immunology, and hematology.

Abstract:

Avian influenza continues to be a public health problem.  Vaccination may prevent or ameliorate the disease; however, it may not always be feasible to match the timing of the vaccine administration to the time of exposure, or additional therapeutics may be needed in the case of severe disease. Passive antibody therapy with polyclonal anti-influenza immune (hyperimmune) globulins may be an effective complementary therapy. Hyperimmune globulin therapy is already in place for several infectious agents and an anti-H5N1 Equine F(ab’)2 product has recently obtained EMA Orphan Drug status. In order to screen individual plasma donations for high neutralizing titers to pool into a hyperimmune product, a fast and reliable neutralizing antibody assay is needed. Currently, the hemagluttination inhibition (HAI) and microneutralization (MN) assays are used to detect neutralizing antibodies against Influenza viruses; however, each assay requires the use of live virus. We developed a Surface Plasmon Resonance (SPR) assay to measure anti-H5 HA antibodies for neutralizing activity which has no requirement for live virus. Briefly, biotinylated multimeric glycans containing sialic acid moieties were captured on a streptavidin-coated surface, acting as a model for influenza cell-surface receptors. Multimeric H5 HA recombinant protein micelles preincubated with a dilution sequence of antibodies or serum were then injected over the glycans.  The results of the antibody dilutions preincubated with H5 HA were compared to H5 HA only, and an IC50 was calculated. Using the IC50 measurement we could rank the mAb and polyclonal sera in order of neutralizing activity. The SPR assay may also be adapted to measure the neutralizing antibody against other infectious agents where the host receptor is known.

Biography:

A molecular virologist for over 30 years, and Professor in the Department of Cell and Tissue Biology at the University of California San Francisco Lenore Pereira has focused the last 16 years on the biology of human cytomegalovirus replication and pathogenesis at the uterine-placental interface. Dr. Pereira has published over 120 papers and invited reviews. Recently, her group in collaborative studies with Dr. Eva Harris at the University of California Berkeley identified ZIKV target cells and immune mechanisms that protect the placenta.

Abstract:

The Zika epidemic that began in Braziland has spread throughout the Americas has beenreported as definitively linked to severe birth defects – microcephaly, miscarriage and stillbirth.Detection of ZIKV RNA in the placenta and fetus and frequent intrauterine growth restriction suggestsinfection of the placenta leading to pathology.Our studies in primary cells from 14 placentas reveal that prototype and recently iso¬lated Nicaraguan ZIKV 2016 strains infect cells that express Axl, Tyro3 and TIM1 tyrosine kinase receptors, which modulate innate immune responses and mediate infection by ZIKV and the closely related dengue virus (DENV) infection in skin. Infected placental cells, including fetal-derivedamniotic epithelial cells (AmEpC), trophoblast progenitor cells (TBPC),placental fibroblasts (HPF),umbilical veinendothelial cells (HUVEC)and differentiating cytotrophoblasts(CTBs) showed cytopathic effects, expressed ZIKV envelope and non¬structural NS3 proteins, and titers of infectious progeny depended on cell type, receptors expressed,individual donors and gestational age.Indicative of infection route, the decidua (decidual cells, invasive CTBs), chorionic villi (HPF, Hofbauer cells, blood vessels) and amniochorionicmembranes (AmEpC,TBPC) expressed the receptors. Nonetheless, differential expression was foundin 26 biopsy specimens, in particular TIM1 was detected throughout pregnancy, but Axl was absent in late gestation. In summary, the results suggest that ZIKV could infect the pregnantuterus and spread to the placenta, fetus and amniochorionic membranes. The models of placental infection we have developed can be used to understand molecular mechanisms of ZIKV infection and assess the therapeutic potential of antibodies and small molecule inhibitors to block infection in the placental-fetal unit.

Biography:

Annika C Karlsson completed her PhD at the Karolinska Institutet in December 2000 and continued her postdoctoral studies at the Gladstone Institute of Virology and Immunology, University of California San Francisco. In 2005 she returned to Karolinska Institutet working as an independent research scientist, senior researcher and group leader. Dr Karlsson has published 38 original articles (12 as last author) in peer reviewed journals.

Abstract:

During chronic HIV-1 infection, CD8+ T cells display a loss of effector functions. These dysfunctiona CD8+ T cells also up-regulate inhibitory molecules, such as PD-1, 2B4, CD160, a process referred to as T cell exhaustion. Recently a new inhibitory molecule, T cell immunoglobulin and ITIM domain (TIGIT), expressed on T cells was shown to inhibit their function. In addition its co-stimulatory receptor CD226 and ligan PVR is severely altered in in chronic viral infections and human cancers. However, it remains to be identified if the TIGIT/ CD226/PVR axis is dysregulated during HIV infection and linked to CD8+ T cell exhaustion. We found an increased expression of TIGIT on bulk and HIV-specific CD8+ T cells that was linked to expression of PD-1, CD160 and 2B4. On HIV-specific cells the increase in TIGIT expression was coupled to a decreased expression of CD226. Furthermore, TIGIThi cells was less common in elite controller subjects, compared to treatment naïve and long-term treated subjects and the TIGIThi cells were linked to a decreased functional capacity (IFN-γ, TNF, granzyme B & CD107a). As TIGIT needs to bind its ligand, PVR, in order to inhibit T cell function, we next measured PVR expression on CD4+ T cells in blood and lymph node. PVR expression was elevated on CD4+ T cells, especially T follicular helper (Tfh) cells which is a major reservoir for HIV-1. In summary, the TIGIT/CD226/PVR axis is altered in HIV-infected subjects, a process which was linked to a decreased functional capacity as well as an upregulation of PVR on Tfh cells. These findings highlight the importance of the TIGIT/CD226/PVR axis in the context of HIV-infection and demonstrate an immune checkpoint barrier that potentially could hinder future cure approaches mediating cellular killing of HIV-1 infected Tfh cells.

Biography:

Fiona McPhee completed her D.Phil. in Organic Chemistry from Oxford University and postdoctoral studies on coxsackieviruses at the Max-Planck Institute (Martinsreid, Germany) and on HIV at the University of San Francisco (United States). She is the Discovery Head for Clinical Virology at Bristol-Myers Squibb where her current research focus includes HBV and HCV drug resistance. She has published more than 80 papers in peer-reviewed journals, over 80 communications at international scientific meetings, and has 7 patents.

Abstract:

The most prevalent Hepatitis C virus (HCV) genotype (GT) globally is GT-1 (46%) with GT-1b being the most common subtype (22%). In Europe, GT-1b accounts for approximately 50% of all HCV cases. Daclatasvir (DCV)-based regimens are approved in many countries globally, including Europe, United States and Asia, for the treatment of HCV. In patients infected with HCV, response rates to DCV-based regimens can depend on the regimen, GT, and pre-treatment nonstructural 5A (NS5A) resistance-associated polymorphisms (RAPs) to DCV. The effects of NS5A RAPs at L31 or Y93H on sustained virologic response (SVR) to treatment with DCV+asunaprevir (ASV; NS3 protease inhibitor) for 24 weeks or treatment with DCV+sofosbuvir (SOF; NS5B inhibitor) for 12 weeks were explored using pooled data from clinical studies in HCV GT-1b-infected patients. SVR with versus without baseline NS5A RAPs was compared by age (<65 vs.>65 years), cirrhosis status, and baseline viral load. Baseline NS5A sequences were available for 1224 GT-1b patients treated with DCV+ASV and 28 GT-1b patients treated with DCV+SOF. NS5A RAPs at L31 or Y93H were observed pretreatment in 4% or 11% of patients, respectively. The overall SVR rate in DCV+ASV-treated patients without NS5A RAPs at L31 or Y93H was 95% compared to 40% with these RAPs. SVR rates in DCV+ASV treated patients without RAPs was high irrespective of cirrhosis, age, or baseline viral load. The overall SVR rate in DCV+SOF-treated patients was 100%. These results will be discussed.

Biography:

Sheldon Stone is a Stroke Physician and Acute Care of the Edlerly Specialist with a research interest in infection control. He has been funded to carry out several national studies on evaluating the national hand hygiene campaign(doi: 10.1136/bmj.e3005), universal MRSA screening (DOI: http://dx.doi.org/10.1016/S1473-3099(15)00417-X), and the national RCT of the behaviourally designed Feedback Intervention Trial (FIT) for hand hygiene (PLoS ONE 7(10): e41617. doi:10.1371/journal.pone.0041617). Lead author of the ORION statement (www.idrn.org/php) and was secretary to the working party for national guidelines for prevention and control of Clostridium difficile infection . One wife, 3 children, 2 cats , 1 football team (Tottenham).

Abstract:

Background: Sepsis has a mortality rate of 40 %. This is halved if the evidence-based “Sepsis-Six” care bundle is implemented within 1h. UK audit shows low implementation rates. Interventions to improve this, often designed using plan-do-study-act (P-D-S-A) cycles, have had suboptimal effects. The aim of this presentation is to show how behavioural science tools were used to modify such an intervention that had achieved 60% implementation of Sepsis-Six with a view to increasing implementation to the hospital’s target of 95%. Methods: Factors influencing implementation were investigated using the TDF (Theoretical Domains Framework) to analyse interviews with 34 health professionals. The data was used to select modifications using the Behaviour Change Technique (BCT) Taxonomy and the APEASE criteria. Results: Five themes were identified as influencing implementation and guided intervention modification (1) “knowing what to do and why” (2) “risks and benefits” e.g. fear of harming patients through fluid overload versus belief in “Sepsis-Six”’seffectiveness (3) “working together” e.g. team collaboration versus doctor/nurse conflict (4) “empowerment and support” e.g lack of confidence of staff to challenge colleagues’ decisions not to implement (5) “staffing levels” e.g. shortages of doctors at night preventing implementation. The modified intervention consisted of two additional components (Sepsis-Six training for the Hospital at Night Co-ordinator; partnership agreement endorsing staff-engagement and collegial challenge) and modifications to two existing educational components Conclusions:This work demonstrates the feasibility of using the TDF and BCT Taxonomy to modify an existing Sepsis-Six implementation intervention and their compatibility with P-D-S-A cycle approaches to quality improvement.

Biography:

Jae Woong has completed his Mater at the age of 30 years from Jun-Nam Universityin Korea. He is working at Catholic-University in Korea at PhD course. His major is Molecular-biology and Viology.

Abstract:

Noroviruses (NoVs) is the dominant etiological agent of acute gastroenteritis in humans and recognized as a major ethiologic agent of nonbacterial acute gastroenteritis in all age groups worldwide. Furthermore, variants and recombinant strains of this virus are continuously emerging worldwide. These variants could be related to antigenic variations that alter viral transmission and immune systems in human bodies, thus influencing the patterns of viral activities. Therefore, studies of the genetic diversity and evolution of human NoV could provide important information that may prove useful for controlling human NoV infection. And the full genome sequence analysis of NoVs is important to be able to pursue of sporadic gastroenteritis in the world by NoV.

Here, we determined the full-length sequences of a recombinant NoV strain and uniqe NoV strain isolated from clinical samples in South Korea. Because these strains may result in hazardous NoV outbreaks in Korea, this information should prove to be valuable. The results from this study highlight the many challenges in the identification of new recombination strains and suggest that guidelines be applied for identifying newly emerging recombinant strains of NoV.

Biography:

Giada Frascaroli is part of Ulm University Medical Center, Germany

Abstract:

Human cytomegalovirus (HCMV) is an enveloped double stranded DNA virus member of the Herpesvirus family. HCMV has a very high seroprevalence among the human population and infects 50% to 100% of individuals depending on the socio-economic conditions. Although the course of infection is mainly asymptomatic in normally healthy individuals, HCMV infection in immunocompromised persons can lead to life-threatening complications, like gastrointestinal disease, hepatitis, or pneumonia. Importantly, HCMV is also the most frequent viral cause of malformations in newborns, leading to deafness or mental retardation. HCMV can infect a broad spectrum of cells in the human body including central cells of the immune system such as monocytes, dendritic cells and macrophages (Mφ). Despite their broad equipment of pathogen sensing and scavenging molecules, Mφ are susceptible to HCMV infection and support viral persistence and dissemination in the human body. Since Mφ are also a first line of defense against pathogens and key modulators of the innate and adaptive immune responses, these cells represent an essential switch between protection or viral persistence and pathogenesis. In this talk I will provide an overview about the manipulative strategies used by HCMV to escape the immune response explaining the viral proteins and mechanisms that impact 1) antigen presentation, 2) cell migration and 3) cytokine secretion. I will present several examples of the immunoevasive strategies used by HCMV to manipulate the immunological properties and functions of Mφ. Moreover, by introducing newly developed experimental systems and approaches, I will provide the last data showing the cross-talk existing between Mφ and essential cells of the innate immune system such as natural killer (NK) cells as well as cells of the adaptive immune system such as T lymphocytes.

Biography:

Qamar Gulzar is a part of Avalon University School of Medicine, Curaçao

Abstract:

Herpes simplex viral (HSV) keratitis is a common and serious external ocular infection leading to unilateral blindness primarily because of its recurrent nature. Despite considerable progress in understanding of the virus at cellular and molecular levels, the proper management of the disease in its different stages is still a dilemma particularly whether to use antiviral or steroids or both. The risk of using steroids with its attendant complications has to be weighed against the risk of progression of the disease if avoiding the use of steroids. This dilemma can be reduced to a considerable extent if basic principles of virology and pathogenesis are kept in mind. This article reviews current concepts of virological and clinical aspects of HSV keratitis to enable a broad understanding of the disease process. It is recognized several influential host factors including the fact that HSK is more common in men than women.It is observed that the ability of HSV to establish latent infection in sensory neurons and possibly cornea, but have as yet been unable to use this knowledge to prevent the disease limitations. Acknowledging limitations may further stimulate application of laboratory knowledge in coping with HSK which constitutes to present major challenge in terms of management.

Biography:

LuminiÅ£a Smaranda Iancu has completed his PhD at the age of 35 years from UMP “Gr. T. Popa” Iasi, Romania and postdoctoral studies from: Royal Free Hospital, London, University Hospital Groningen, The Netherland, and Biological Molecular Laboratory Innere Medizin II, Universt-sklinikum Freiburg, Deutschland. She is the head of Regional Center of Public Health Iasi, and of Microbiology Discipline from Faculty of Medicine and Vice rector of UMF “Gr. T. Popa” Iasi. She has published more than 50 papers, 11 of them in reputed journals.

Abstract:

Since 2009 in the Virology Laboratory of Microbiology Discipline we run Human Papilloma Viruses (HPV) genotyping tests by Linear Array HPV Genotyping test. In the first step we obtained WHO proficiency for our laboratory, after best results that we obtained for a panel with HPV samples. In a country in which the prevalence of endocol cancer is in the first place in Europe (23.9/100.000) we tested more than 500 woman for HPV genotype and our results show that 192/514 (37.4%) patients were positive for HPV (infected with single and with multiple HPV types). Most frequent types were: 16 (10.5%), 53 (5.44%), 51 (5.05%), 52 (4.08%) 18 (2.91%) and 31 (2.73%) (Virol J, 2011). In an other study we test HPV and HIV coinfection: DNA/HPV was detected in 18/40 (45%) of the HIV+ patients, and in 350/992 (35.2%) of the HIV- patients. We detect HIV being a risk factor for acquiring multiple HPV type infections. The eight most common HPV types for women below age 30, HIV+/- were: HPV 16, 18, 31, 51, 58, 68, 6 and 82 respectively (PLOS ONE, 2015). In the last years we were focused to test HPV infection related with different neck and head cancers; till know, even we tested more than 200 samples, we do not find a significant association between HPV and these types of cancers. An interesting cases was related with squamous cell carcinoma of conjunctiva, in which we find that 52 HPV type was involved (Indian J Ophthalmology, 2015).

Biography:

Sominina Anna has completed her PhD at the age of 29 years from the Institute of Experimental Medicine and postdoctoral studies from the Research Institute of Influenza. She was awarded the academic title of professor in1992. She is the head of WHO National Influenza Center and of the Laboratory of Biotechnology of the Research Institute of Influenza. She has published more than 120 papers in reputed journals.

Abstract:

The unusalrapid growth of influenza activity caused by A(H1N1)pdm09 viruses was registered simultaneously in number of geographically remote areas of Russia during the season 2015-2016.Intensity of epidemic was much higher in comparison with previous four years. Significant increase of incidence rate,hospitalization and number of lethal cases observed since week 3,2016.peak of epidemic registered already on the week 5.Such a rapid speard of the epidemic indicated high transmission level of the virus. Many factors can influence this process including changes in the antigenic properties of virus HA, certain changes in internal genes, as well as decrease of population immunity . Antigenic analysis of viruses circulated showed that all A(H1N1)pdm09 viruses were antigenically related to A/California/07/09. The contribution of the rest influenza and B viruses last season was insignificant: proportion of isolated influenza A(H1N1)pdm09, A(H3N2) and B viruses estimated as 93.2%, 2.2% and 4.5%. According to sequencing and phylogenetic analysis HA gene of all A(H1N1)pdm09 viruses belonged to 6B clade (A/South Africa/3626/2013-like), sub-clade 6B1 with substitutions S84N, S162N, I216T located outside of known antigenic sites. Substitution D222G revealed in HA of some H1N1pdm09 sequences from autopsy samples. Whole-genome sequencing of influenza A(H1N1)pdm09 viruses revealed specific mutations in internal genes NEP,NS1,NP,M1 and PA-X common to most of the strains (A. Komissarov et al.,2016). Decrease of population immunity level in pre-epidemic period (October 2015) registered in number of cities of Russia by determination of the GMT of antibiotics and percent of people seropositive to A(H1N1)pdm09 virus.

Biography:

Gavin Screaton is the Dean of Faculty of Medicine at Imperial College London. After completing his first degree from Cambridge he went on to Oxford to complete his medical studies and DPhil in General Medicine. He is a member of the MRC Strategy Board, Academy of Medical Sciences, Association of Physicians, a Fellow of the Royal College of Physicians and sits on funding committees at the Wellcome Trust and MRC.

Abstract:

Dengue is a rapidly emerging, mosquito-borne viral infection, with an estimated 400 million infections occurring annually. Of these approximately one quarter are clinically apparent or symptomatic. The majority of these result in a self-limited, but none the less unpleasant febrile illness, dengue fever. 1-5% of infections lead to a more severe disease, dengue haemorrhagic fever, which is characterized by a severe vascular leak, hypovolaemia and in extreme cases shock and haemorrhage. Dengue exists as four highly divergent serotypes differing in sequence by some 30-35%; infection with one serotype does not provide protection against the other three. In endemic areas serotypes frequently co-circulate and repeat infections are common. Interestingly, severe disease is much more common in secondary as opposed to primary infections, implying a role of the acquired immune system in disease pathogenesis. Understanding this immune enhancement of disease is crucial for the design of safe and effective vaccines. Through clinical collaborations in Thailand and Vietnam, we have been studying the immune response to dengue in cohorts of infected children. We have characterized 145 human monoclonal antibodies (mAbs) and identified a previously unknown epitope, the envelope dimer epitope (EDE) that bridges two envelope protein subunits that make up the 90 repeating dimers on the mature virion. We will describe the antibody response to the two virion surface glycoproteins prM and E and discuss the E dimer epitope (EDE), a novel site bridging the 90 basic head to tail envelope dimers making up the virion surface. The antibodies directed to the EDE are both potent and broadly neutralizing across the dengue serocomplex suggesting the EDE could be a target for a new generation of subunit vaccines against dengue.

Biography:

Maria Rita Gismondo is part of CLIMVIB – L.Sacco Fatebenefratelli University Hospital, Italy

Abstract:

On March 29, 2016, WHO Director-General declared the end of the Public Health Emergency of International Concern regarding the Ebola virus disease outbreak in West Africa. A total of 28 610 confirmed, probable, and suspected cases have been reported in Guinea, Liberia, and Sierra Leone, with 11 308 deaths since the onset of the Ebola outbreak (WHO) . The majority of these cases and deaths were reported between August and December 2014, after which case incidence began to decline as a result of the rapid scale-up of treatment, isolation, and safe burial capacity in the three countries. Seven countries (Italy, Mali, Nigeria, Senegal, Spain, the United Kingdom, and the United States of America) have previously reported a case or cases imported from a country with widespread and intense transmission. In order to effectively interrupt remaining transmission chains and manage the residual risks posed by viral persistence, WHO, as lead agency within the Interagency Collaboration on Ebola and in coordination with national and international partners, designed the phase 3 Ebola response framework. The first appeared in 1976 in 2 simultaneous outbreaks, one in what is now, Nzara, South Sudan, and the other in the Ebola virus causes an acute, serious illness which is often fatal if untreated. Ebola virus disease (EVD) Yambuku, Democratic Republic of Congo. The latter occurred in a village near the Ebola River, from which the disease takes its name. The diagnosis of VHF is based on 3 components: 1. History of exposure 2. Detailed clinical assessment 3. Laboratory investigations. Evidence from outbreaks strongly indicates that the main routes of transmission of VHF infection are direct contact (through broken skin or mucous membrane) with blood or body fluids, and indirect contact with environments contaminated with splashes or droplets of blood or body fluids. Avoiding transmission dictates strict adherence to standard precautions as well as droplet and contact precautions for health care, environmental, and laboratory workers. Moreover, while epidemiology during VHF outbreaks does not suggest airborne transmission, precautions should be taken to avoid procedures or protect health workers, family members and other patients during procedures that might aerosolize virus. The Ebola epidemic showed the need to be better prepared in order to face efficiently the next major health emergency. Elements such as coordination, risk assessment processes and intersectoral cooperation are paramount for a good preparedness planning. The Ebola outbreak also highlighted the need for action in areas which usually do not always get sufficient attention, such as border issues (exit and entry screening), medical evacuation, the mobilisation of specific expertise for EU and the affected countries, transport facilities for big amount of waste related to the laboratory and clinical activities in the EU, the sample sharing and contact tracing. A. shows international and Italian experience.

Biography:

Silvia Angeletti obtained the Degree in Biological Science at the University “La Sapienza” of Rome. She was specialist in Microbiology and Virology on November 1998. On October 2008 she obtained the Degree in Medicine and Surgery at the University Campus Bio-Medico of Rome, Italy. She is the Director of the Clinical Pathology and Microbiology Division at the University Hopsital Campus Bio-Medico and the Director of the Reaserch Unit of Clinical Pathology and Microbiology at the University Campus Bio-Medico of Rome, Italy. He has published more than 60 scientific papers in international journals and has been serving as a reviewer and an editorial board in reputed journal as Disease markers or PlosOne. Area of research interest are the following: epidemiology and diagnosis of infectious disease; phylogenetic analysis applied to viral and bacterial infections; Multidrug resistant (MDR) pathogens analysis in nosocomial settings; diagnostic and prognostic markers associated to infectious and chronic diseases; key indicators of laboratory quality.

Abstract:

Migrant populations are represented by group of people forced to migrate by the difficult conditions of life experimented in their Country of origin as a consequence of civil wars and political instability. The onset of civil war can led to the complete deterioration of the health infrastructure through the destruction of facilities, the shortage in health care personnel and medicines other than a lack of secure routes and transportation. These conditions joined with the deterioration of immunization programs induced the spread of communicable diseases like measles, poliomyelitis, meningitis through the migrant populations creating a fertile condition for the epidemic spread of unsual infections also within the refugee camps of the hosting Country. The refugees camps are a sort of community where almost 900 migrants and refugees stay for a medium of 15 months and for this reason the monitoring by a sentinel surveillance the people arriving so as their health status before and after the entrance in the camps it is noteworthy. At this aim we present data from the microbiological surveillance of migrants coming from Syria and Eritrea at their arrival in an asylum seekers Centre in Italy to define their health status and to evidence the need for strategic policy of assistance to people that have to travel within Europe facing many kilometers again. In conclusion the microbiological surveillance represents a useful action to understand refugees health status and to trace unusual microorganisms movement even carriers of antimicrobial resistance during migrants travelling.

Biography:

Niels Høiby MD DMSc a Professor of Medical Microbiology at the University of Copenhagen and at department of Clinical Microbiology at Rigshospitalet in Denmark. Prof. Høiby was the first president of the European Cystic Fibrosis Society and was the founder and Chairman of multiple societies, including the Scandinavian Society for Antimicrobial Chemotherapy, the ESCMID study group of Biofilms and the Biofilm Study Group of the Danish Society for Clinical Microbiology. He has published extensively in the area of chronic lung infection in CF and other biofilm infections. Prof. Høiby has won multiple awards and honors throughout his career.

Abstract:

Cystic fibrosis (CF) patients suffer from recurrent and chronic sinus- and lung infections due to the basic defect of the CFTR protein, which is a chloride channel. This leads to decreased volume of the paraciliary fluid in the airways and impaired mucus detachment which interfere with the mucociliary transport and the consequence is therefore defective host defense against bacterial infections. P. aeruginosa is causing the most important chronic lung infection in CF and it was the first biofilm infection which was described in human beings and the most well studied biofilm infection. The inflammatory response - dominated by polymorphonuclear leukocytes - to the chronic infection is the main cause of the lung tissue damage. The antibody response against the sinus biofilm infections is mainly s-IgA which reduce the inflammation, whereas IgG dominates against the lung biofilm infection and aggrevates the inflammation. The antibody response is used diagnostically. The current treatment is early aggressive eradication therapy of intermittent P. aeruginosa colonization to prevent chronic biofilm infection which is treated by chronic suppressive ’maintenance’ therapy to maintain the lung function for decades. Both systemic and inhaled antibiotics are used.

Biography:

Iolanda Francolini has obtained a degree in Industrial Chemistry in 2000 from the Sapienza University of Rome. In 2003, she was a visiting scientist at the Center for Biofilm Engineering, Montana, USA. In 2005, she obtained a Ph.D. degree in Chemical and Industrial Processes at the Sapienza University of Rome. She currently serves as a Lecturer in the Science and Technologies of Polymers at the Sapienza University of Rome and performs research on antimicrobial polymers. She has published more than 45 papers in reputed journals and has been serving as an editorial board member for International Journal of Molecular Science.

Abstract:

The impact for public health of medical device-related infections has received considerable attention over the last decade. Clinical signs of most of these infections clearly suggest that they are caused by microbes colonizing the implant surface and nearby tissues. The subsequent microbial biofilm formation aids the development of antibiotic resistant microrganisms and compromises the device functionality. A revision surgery is therefore frequently required adding healthcare costs to those already required for taking care of the infection. The enormous advances achieved in the last decades in polymer sciences together with therapeutic innovations hold the promise to meet the need of improving patient experience associated with device implants. Particularly, novel, high-performance polymer systems with antimicrobial or antifouling properties have been lately developed. The application of these materials as coatings for medical devices has demonstrated in some cases to offer a protection towards microbial colonization and biofilm formation. In this talk, an overview of innovative materials and technologies facing with biofilm-based medical device-related infections will be provided and how our group is addressing this issue will be presented.

Biography:

Trine Rolighed Thomsen has completed her PhD at the age of 32 years from Aalborg University and was appointed Associate Professor in Medical Microbiology in January 2012. She is affiliated to Aalborg University and the Danish Technological Institute and heads a research group. Main interests and research grants are on diagnosis, prevention and treatment of human infections, with a special focus on biofilm. She has published more than 40 peer-reviewed original papers and is active member of several danish and international boards and sicentific societies.

Abstract:

Recent evidence suggests that the microbial community, its spatial distribution and activity play an important role in the prolongation of treatment and healing of chronic infections. Standard bacterial cultures often underestimate the microbial diversity present in chronic infections. This lack of growth is often due to a combination of inadequate growth conditions, prior usage of antibiotics and presence of slow-growing, fastidious, anaerobic or unculturable bacteria living in biofilms. Thus, diagnosis of chronic infections is challenged by lack of appropriate sampling strategies and by limitations in microbiological testing methods. The purpose of this study was to improve sampling and diagnosis of chronic infections, especially considering the biofilm issue. Systematic and optimized sampling of various specimen types was performed. Extended culture, optimized DNA extraction, quantitative PCR, cloning, next generation sequencing and PNA FISH were applied on different types of specimens for optimized diagnosis. For further investigation of the microbial pathogenesis, in situ transcriptomics and metabolomics were applied. Molecular techniques detected a larger diversity of microorganisms than culture methods in several patients and a heterogeneous distribution of bacteria in various specimens from the same patient was evident. Data from a 2-year prospective study on prosthetic joint infections including 164 patient cases will be presented. Transcriptomic and metabolomic analyses indicated the important virulence genes and nutrient acquisition mechanisms of Staphylococcus aureus in situ. Our studies show that diagnosis of chronic biofilm related infections required multiple specimen types, standardized sampling, extended culture and molecular analysis.

Biography:

Claudia Vuotto has obtained her PhD in Biomedical sciences, Medicine and Public Health at Marche Polytechnic University Medical School. She won a fellowship at the Italian National Institute of Health and she is currently researcher at the Microbial Biofilm Laboratory of the Fondazione Santa Lucia in Rome. She has published 18 articles on international peer reviewed journals and 2 book chapters for Springer. She was in the Local Organizing Committee in the International Congress "Eurobiofilms 2009" and in the Scientific Committee of "Eurobiofilms 2015" as well as Scientific Secretary of the ESGB Meeting "Biofilm-based Healthcare-associated Infections: from Microbiology to Clinics"(2015).

Abstract:

The increasing number of anaerobic bacteria isolated from different clinical samples has led to a growing awareness of their contribution in acute and chronic infections. These bacteria, in fact, are able to become opportunistic pathogens after that a permissive environment within the host have been created or in presence of other predisposing factors. In these conditions, infections in which are involved anaerobic bacteria, often together with aerobes, arise. However, despite the increasingly frequent isolation of anaerobic species during infectious processes and the demonstrated ability of some of them to form biofilms, their involvement in the establishment of healthcare-associated infections (HAI) is still undervalued and thus little studied. The current knowledge about the implication of biofilm-forming anaerobic bacteria in some human infections will be examined, and the data acquired in our laboratory by means of Quantitative Biofilm Production Assay, Field Emission Scanning Electron Microscopy and Confocal Laser Scanning Microscopy will be presented. In particular, data obtained on the synergistic and/or competitive interactions within multi-species biofilms among different anaerobic species, including Clostridium difficile, Veillonella spp, Peptostreptococcus magnus, Porphyromonas gengivalis, will be summarized and discussed. Information on the involvement of some anaerobic species in causing difficult-to-treat infections as part of polimicrobial biofilms and on the ability of commensal microorganisms, including Lactobacilli, to antagonistically operate against anaerobic pathogens will be provided.

Biography:

Claus Moser is part of University of Copenhagen, Denmark

Abstract:

Biofilm infections are significant clinical challenges. They are frequent,can be related to foreign bodies or be tissue related, and are recalcitrant to host responses and antibiotic treatments. Furthermore, they can be primary focus for systemic spread, they are persistent and characterized for recurrent infections, especially since timing of termination of antibiotic treatment can be exceedingly difficult. The biofilm mode of growth can also render low virulent microorganisms into virulent strains due to the induced inflammation, which generates tissue damage.Microbiologically, biofilms are defined by a selfproduced matrix containing extrapolysaccharides, eDNA and proteins. Therefore, biofilms can be considered as independent compartments with distinct antibiotic PK/PD parameters. Adding to this, physiological gradients are observed in biofilms with significantly different nutrition and oxygen conditions in different zones of the biofilms.Diagnostically, biofilm growing microorganisms can be challenging to demonstrate by traditional culturing due to adherent and/or extremely slowly growing microorganisms (persisters/dormant types/viable but non-culturable microorganisms).Finally, susceptibility testing is only indirectly representative for the responsiveness of the biofilm to antibiotic treatments. Therefore, the first clinical guidelines for diagnosing, prevention and treatment of biofilm infections have been published in 2015. The present abstract aims at presenting novel therapeutic regimens published since the guidelines became available last year. The focus of the presentation will be on consequences of the biofilm as a distinct compartment, hyperbaric oxygen treatment, IgY gargling and human autologous leucopatches. The presented therapeutic possibilities are involved in ongoing clinical trials or used as adjuntive treatment of other medical syndromes.

Biography:

PalinaVyhouskaya has a master degree in LaboratoryMedicine, and currently she is a PhDstudent at the Jagiellonian University, Poland. She is anactive member of The Scientific Students Association of Laboratory Diagnosticians and Clinical Microbiology, where she experiences and practices modern research techniques in Medicine. She has been involved in various research programs, and her work was published in international journals.

Abstract:

Background
In therapeutic context, glycolytic pathway is an interesting field of research also for studying dental diseases. Metabolism of biofilm-forming Streptococcus mutans––main factor of caries progression––is based on glycolysis even in the presence of oxygen. In a such condition, an increase in the expression of genes coding key glycolytic enzymes, pyruvate kinase (PK) and phosphofructokinase (PFK), is observed. Modification of enzyme activity of PK and PFK gives an ability to inhibit bacterial growth and biofilm formation––a potential approach for caries prevention and therapy.

Material and methods

Activity of PK and PFK from double- and mixed-species biofilm was estimated spectrophotometrically. Biofilm assay was carried out according to Current Protocols in Microbiology using ATCC and clinical strains (Streptococcus mutans,Streptococcus sobrinus, Lactobacillus acidophilus,and Actinomycesviscosus). In this study, we measured the activity of PK and PFK in various pH values and formation time of double and mixed-species biofilms.

Results

The activity of PK and PFK increased after 6 and 12 hours of a double-species biofilm formation (1.43 mU/mg of protein vs. 1.52 mU/mg of protein) compared to 18 and 24 hourswhen we observed a slight decrease in the activity of the glycolytic enzymes (1.37 mU/mg of protein vs. 1.48 mU/mg of protein). In case offorming the mixed-cariogenic biofilm, the activity of glycolytic enzymes also grew after 18 and 24 hours of mixed-species biofilm formation and the differences were statistically significant (p<0.001).

Conclusions

The increase in the activity of glycolytic enzymes (PK and PFK) during the biofilm formation (due to the effect of low pH), can be explained by the need to overcome the inhibitory effect of acidification on the metabolic activity of the microorganisms in the biofilm. Bacterial cells adapt to new conditions better in mixed-species biofilm than in the mono- or double-species biofilms––the increase of theglycolysis rate associated with increased activity of glycolytic enzymes reflects this phenomenon very well.

Therefore, inhibition of glycolytic enzymes might be an essential step in the reduction of mixed-species cariogenic biofilm, what could be a useful tool in prevention of caries.