Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 4th Clinical Microbiology and Microbial Genomics Conference Philadelphia, USA.

Day 1 :

Keynote Forum

John G Thomas

West Virginia University, USA

Keynote: One health: Animals, humans and our globe, our mega-organism

Time : 10:00-10:30

Conference Series Clinical Microbiology 2015 International Conference Keynote Speaker John G Thomas photo

Professor John G. Thomas is recognized as an “International Educator and Global Microbiologist “ ( having lectured in more than 43 countries while a clinical microbiologist in pathology, dentistry and medicine for 51 years, his research emphasizing biofilms and medical devices including endo-trachs and the connection between oral diseases, VAP and wound infections (“Intellectual Design”) with the recent integration of micro 3-D- bio Printing using bio-plastics and unique Prebiotics (Therapeutic Bacteria ) for intervention. He has over 50 publications, multiple book chapters, significant grant support, pending patents and over 100 posters/abstracts at national and international meetings. His sabbatical at Cardiff University, Wales, UK (2007) was a driving influence. He has been a member of the ADA Scientific Advisory Committee for the last 8years.As Faculty at 6 Universities during his career , he has received Alumni and University awards for research and International Student Mentoring ; retiring from WVU in 2013 after 23 years as Professor Emeritus , he presently is expanding his research/teaching utilizing the advanced resources of the Allegheny Health Network in Pittsburgh, PA, Carnegie–Mellon University and Mass. Gen. Hospital, Boston, MA.


We evolved to conquer and emerged with a concept that we were the focus of our environment, our world. The concept was doomed from the start and our disruption of the world we live in has forced us to re-evaluate or position, recognizing that there are 3 parts (Humans, Earth/Environment and Animals) and we collectively address Newton’s third law of Motion: For every action there is an equal and opposite reaction. Thus, balance or one health and its intrinsic buffering capacity is the key and humans have been collectively “Multi- Disruptive”, particularly the untoward consequences of antibiotics. Human population will approach 9 billion shortly and with it an increase in low socio-economic habitat (Global Slums) with increased potential for disease transmission, so evident in the most recent Ebola episode in Africa. Old and new routes of emerging pathogens will be unmasked, perhaps 2-4 new ones per year. Animal diseases, zoonosis, particularly viral, will predominate as we realize that most global recent diseases have had an animal vector; over the last 3 decades approximately 75% of human diseases and have come from or through wildlife. Perhaps most significant will be the unpredictable impact of global warming , climate change and the subsequent increased range of vector-borne diseases and the pollution of water, a potential for wars. Microbes are central to all three and the unbalance now provides the opportunity for the “Perfect Microbial Storm”. There is ‘No Health Sanctuaries’ as humans have “collapsed their space” with animals and the environment/earth. Fungi offer a unique view as they encompass more animals/plants in a deadly fashion. Proactive surveillance is key-based on global collaboration using tools like Google Earth and GIDEON to maximize rapid computer inter-face and global diversity. New laboratory tools, like BARDOT, laser light scatter identification need incorporation to link international microbial libraries and unmask the other threatening potential, Bioterrorism.

Conference Series Clinical Microbiology 2015 International Conference Keynote Speaker Giovanni Matera photo

Giovanni Matera obtained his M.D at University of Messina, Italy, in 1982 and PhD in Microbiology in 1987. Specialist in Infectious Diseases in 1994. From 1985 to 1986 Postdoctoral Fellow at the Medical University of South Carolina, Charleston, USA. From 1986 to 1988 Research Associate at the Dept. of Microbiology, University of Saskatchewan, Saskatoon, Canada. Instructor from 1990 to 2000 at the Chair of Microbiology, University of Catanzaro. From 2000 to 2006 Assistant Professor and since 2006 Associate Professor of Microbiology and Clinical Microbiology at the same University. Since 2008 Head of Simple Unit \"Parasitology\" at O.U. Clinical Microbiology, University of Catanzaro. Main lines of research: 1. Biological effects of bacterial endotoxins; 2. Physiopathology of sepsis and markers of systemic infections and endocarditis. 3. The mechanisms of antibacterial drugs; 4. Laboratory diagnosis of infectious diseases; 5.Clinical Parasitology. Author of over 80 articles published in reputed international journals of Microbiology and Infectious Diseases.


Parasitic diseases are very often chronic and during such long-lasting infections, host inflammatory and immune cells are quite unresponsive to stimulation by products from the infecting organism and other pathogens. Leishmania are hemoflagellate protozoa, which cause three types of illness (cutaneous, muco-cutaneous and often fatal visceral leishmaniasis) exhibiting a high prevalence and incidence worldwide. More informations are needed to explain the role of different branches of immune response in leishmaniasis pathogenesis, as well as to get a timely diagnosis, an accurate prognosis and a more effective therapy.rnOur contribution to understanding mechanism of Leishmania disease included in vitro model with live protozoa infecting human peripheral blood mononuclear cells, as well as the dosage of serum mediators in infected humans. In our approach with clinical specimens, both conventional and molecular tests were able to verify the presence of Leishmania spp. in cutaneous and mucous biopsies of suspected tegumentary leishmaniasis patients. In these subjects, levels of Th2, Treg cytokines, MCP-1 chemokine and CD25+ cells were statistically more elevated than in Leishmania-negative patients and healthy controls; on the other hand a decrease of TNFα, VEGF and EGF were found among samples obtained from Leishmania-positive group. We noticed the absence of allergic pathologies among parasitized patients.rnMoreover we sought to reproduce in vitro the early phase of the natural infection. Therefore human PBMC were challenged by Leishmania infantum or Leishmania major infective metacyclic promastigotes. Following 4 hours from L. major infection, differently from L. infantum, TNFα , IL-1β, IL-6 levels were significantly higher than controls. However, after 24 hours, promastigotes of both species stimulated significantly higher TNFα , IL-1β, IL-6 levels. A negative correlation was observed between the parasite concentration and the cytokine levels. Regarding MCP-1 release, at 24 hours, but not at 4 hours, an interesting dose-dependent effect was observed for both species. Nitric oxide levels, at 4 and 24 hours, were increased when lower parasite burden of both species was used; interestingly the higher promastigote concentration of L. major or L. infantum fails to stimulate nitric oxide levels. rnThe protozoal infection studied seems to reduce major Th1 response cytokines, while increasing both immune cells and mediators with regulatory/inhibitory effect, in both in vitro and in the clinical approaches used. Host might take advantage in reducing re-infections, as well as immunopathology/allergies. Leishmania species may exploit immunoregulatory mechanisms in early steps of infection in order to evade the host immune system and in the chronic phase to protect the earned host niche against other invaders. The clinical impact of our findings consists in the relevant number of mediators which could be proposed as potential diagnostic and prognostic biomarkers helpful to integrate clinical management of leishmaniasis.rnrnrn

Conference Series Clinical Microbiology 2015 International Conference Keynote Speaker Joanna S Brooke photo

Joanna S. Brooke is an Associate Professor in the Department of Biology at DePaul University. She holds doctorate and masters degrees in Microbiology and Immunology from the University of Western Ontario, with focus on bacterial lipopolysaccharide assembly and bacterial cell ultrastructure, respectively. Her postdoctoral research at the University of Texas Southwestern Medical Center investigated the interactions of diphtheria toxin with its receptor. Her current research examines S. maltophilia and its biofilms. She also studies other potential bacterial pathogens. She has published 18 papers in peer-reviewed journals. She is a Guest Associate Editor for a Frontiers Research Topic on S. maltophilia


Stenotrophomonas maltophilia is a drug-resistant Gram-negative bacterial opportunistic pathogen found in moist environments in and outside the clinical setting. The World Health Organization has named S. maltophilia as a leading global drug-resistant pathogen in hospitals. Infections of S. maltophilia are of significant concern and associated with high mortality rates in the immunocompromised patient population. Various infections in humans are associated with S. maltophilia, most commonly those of the respiratory tract, and this bacterium forms biofilms on medical devices and living tissues. S. maltophilia can be a co-colonizer in polymicrobial biofilms found in cystic fibrosis patients. Our studies and others have shown that the biofilm is influenced by cell ultrastructure and culture growth conditions. Genome sequencing and analysis have revealed considerable genetic diversity among S. maltophilia strains and multiple molecular mechanisms used to thwart antimicrobial treatment. The rise in antibiotic resistance of S. maltophilia worldwide emphasizes the need to develop new strategies and therapies to combat this emerging opportunistic pathogen. Studying the colonization, biofilm formation, and virulence of S. maltophilia may help to identify suitable targets for pharmaceutical therapy. We will discuss the clinical challenges presented by this pathogen and new approaches being used to identify and treat S. maltophilia infections. rnrn