International Conference on Microbial Pathogenesis,Infectious Diseases & Control August 23-24 , 2017 Toronto, Canada
Avail Upto 11 CME Credits

Yung-Hua Li received his Doctorate in Molecular Microbiology at University of Manitoba. Following his Post-doctoral fellowships in the University of British Columbia and University of Rochester, NY, he worked as a Scientist in the University of Toronto, with his research focus on molecular dissection of microbial biofilms. In 2004, he joined the Faculties of Dentistry and Medicine at Dalhousie University, where he has been directing a research team on genetic analyses of bacterial biofilms, biofilm ecology and pathogenesis.

Streptococcus mutans is a primary etiological agent of dental caries worldwide. Natural life of S. mutans in dental biofilms often faces life-threatening insults, such as killing by antibiotics or innate defense molecules produced by competing species or by the host. How such insults affect physiology and virulence of S. mutans is poorly understood. In this study, we explored this question by analyzing the effects of sub-MIC concentrations of bacitracin and -defensin 3 on S. mutans. Microarray analysis showed that both bacitracin and -defensin 3 induced differential expression of subsets of genes that were largely regulated by the BceABRS four-component system. The results were further confirmed by examining gene expression profiles of selected genes or genetic loci using qRT-PCR. We then examined the effects of gene deletion of bceRS on the peptide antibiotics and virulence. The results showed that a deletion of bceRS resulted in a mutant that was sensitive to bacitracin or -defensin 3. Introduction of a wild copy of becRS in trans (complementation) restored the wild type phenotype of the mutant. In particular, both peptide antibiotics at a sub-MIC induced biofilm formation in the parent but not in the mutant. A competitive fitness analysis showed that the mutant was unable to compete with the parent for co-existence in duel-strain mixed cultures in the presence of bacitracin. In conclusion, the BceABRS four-component system controls a regulon that is required for sensing, response and resistance to bacitracin and -defensin. This system may play an important role in adaptation and virulence expression of S. mutans in dental biofilms.

Xiao-Lin Tian has received her MD from Shanghai Medical University. Since 1993, she worked as a Research Technician in Novopharm Biotech Inc. in Winnepeg for six years. She then worked in the Mount Sinai Hospital Lunenfeld Research Institute, Toronto, for another six years. Since 2006, she has been working as a Researcher at Dalhousie University, with expertise in Moleculr Biology, Bacterial Biofilms and Pathogenesis.

Streptococcus mutans is a leading cariogenic pathogen of dental caries worldwide. Clinically, eliminating S. mutans from dental biofilms using antibiotics is not practical, because these agents indiscriminately kill other members of the resident microflora, leading to ecological disruption and other negative clinical consequences. To develop target-specific antimicrobials, we evaluated several fusion peptides and identified a new peptide HP30 that showed a high selectivity for targeted killing of S. mutans. In the dual-species cultures, 80% of S. mutans cells were killed, but only 20% of S. sanguinis were killed following exposure to HP30 (5.0 M) for 15 min. Similarly, 80% of S. mutans cells were killed but only 5% of Actinomyces naeuslundii were killed following the same exposure. The peptide-guided killing was also confirmed in the dual-species biofilms and the killing increased with increasing concentrations of HP30. However, a combination of low concentrations of HP30 with EDTA well maintained the killing activity against S. mutans in the biofilms. A S. mutans mutant lacking the ComD receptor only showed 20% of killing, while a ComD overexpression strain showed 90% of killing, suggesting that HP30 predominantly binds to the ComD receptor before triggering the selective killing. New peptide HP30 displays a high selectivity for targeted killing of S. mutans due to an improved binding of the peptide to the ComD receptor.

Vinay Kumar Pathak has completed his MSc Biotechnology from Guru Nanak Dev University. Currently, he is pursuing his PhD at Stanley Browne Laboratory, The Leprosy Mission Community Hospital, Delhi. He is working as Senior Research fellow and has published one paper in a reputed journal.

Several attempts have been made to establish a diagnostic test for leprosy since decades. None of these assays could diagnose more than 60% of PB cases or early cases of leprosy. The present study was attempted to develop a diagnostic test using M. leprae specific PCR in clinical samples. The study was aimed to detect M. leprae genomic DNA by using two different gene targets. Standardization for sensitivity of PCR for two genes was performed with standard genomic DNA of M. leprae strain NHDP-63. The standard DNA was serially diluted in 1:10 ratio up to 12 dilutions in decreasing concentrations. The DNA concentration of first dilution was 1x10-1 µg/µl or 100 ng/µl to 12th dilution 1x10-12 µg/µl or 1 αg/µl. PCR amplification using two gene targets of M. leprae namely repetitive element rlep and 16S rRNA were performed with the same. PCR amplification for rlep gene was positive up to concentration of 1x10 -9 µg/µl or 1 fg/µl, similarly it was 1x10-10 µg/µl or 100 αg/µl for 16S rRNA gene target. The sensitivity has been tested with clinical samples of leprosy patients and positivity of result was found 66.0% in case of rlep whereas it was 82.0% for 16S rRNA gene. In present study, PCR positivity for rlep and 16S rRNA gene were found efficient in the clinical samples and these gene targets can be further considered to develop a diagnostic tool for detection of sub clinical leprosy.

Sara Abolghasemi is an Infectious Diseases Specialist and completed her Fellowship of Infectious Diseases in Immunocompromised patients from Shahd Beheshti University of Medical Sciences, Tehran. She has published few papers about infectious diseases in ISI and PubMed journals and is currently working as an Assistant Professor in Shahid Beheshti University of Medical Sciences.

Background: Considering heavy economic burden of influenza, various efforts have been done for better prevention and different vaccination methods employed for expediting immune response. Up to our knowledge, no study has been conducted in patients undergoing routine hemodialysis, so the goal of this study is to evaluate difference between the immunogenicity caused by two different routes of influenza vaccine injection (i.e. intradermal versus intramuscular), and evaluating whether pretreatment with imiquimod could augment and expedite the immune response. Method: In this prospective randomized, double blind, controlled trial, 120 patents undergoing routine hemodialysis (i.e. for more than 1 month, at least 2 times a week) entered the study and randomly assigned into 3 groups: one experimental, and two controls. For the experimental group (INT-I), 250 mg imiquimod 5% cream (Aldara) was rubbed on deltoid region of right arm, and after 15 minutes, 0.25 cc of trivalent influenza vaccine was injected intradermal. The individuals in the first control group (INT-A), received 0.25 cc trivalent influenza vaccine via intradermal route after rubbing 250 mg aqueous cream in the same region with the same prior interval. For the second control group (IM-A), 0.5 cc trivalent influenza vaccine was injected intramuscular after using 250 mg aqueous topical cream on the same area. The immunogenicity was then measured by serum antibody titers using hemagglutination-inhibition (HI) assays, against two influenza strains: A (H1N1) and B. For comparing antibody titers two blood samples were obtained: the first immediately before and the second 14-21 days after vaccination. The increase in antibody levels against each strain then analyzed for significance. Results: Among initial 120 participants, 117 persons completed the study. The antibody titers before and after vaccination were measured by hemagglutination inhibition assay. Both increase in antibody titers and means of the antibody increases in intradermal with imiquimod cream (INT-I), intradermal with placebo (INT-A) and intramuscular group (IM-A) were determined. Then the differences between the mean titers of INT-A and IM groups and between INT-I and INT-A groups were analyzed by covariance method (Acova). This study revealed significant response among strain A (H1N1) in intramuscular group (IM-A) comparing with the intradermal with aquas cream (INT-A) (P, 0.05). The subsequent immunogenicity in other groups and for different strains did not show any significant difference (i.e. INTA and IM-A for B strain and INT-A and INT-I for both A and B strains). Conclusion: Although some previous studies among elderly and healthy people showed intradermal route of influenza vaccination more efficacious comparing with intramuscular route, and imiquimod pretreatment expediting and augmenting the subsequent immunogenicity comparing with non-imiquimod pretreated people, this study did not reveal the superiority of intradermal injection over intramuscular route, and also the benefit of imiquimod as premedication. Finally, regarding the acceptable immunogenicity among individuals in intradermal groups (both INT-I and INT-A), we conclude that intradermal route would be an alternative for intramuscular injections.

Mohammad Moradi completed his Ph. D in Medical Microbiology, University of Manchester. He is currently working as a Assistance Professor of Medical Microbiology in the Department of Medical Microbiology Medical School, Kerman University of Medical Sciences, Kerman, Iran. He has published numerous research papers and articles in reputed journals and has various other achievements in Molecular diagnosis and anti-microbial resistance patterns. He has extended his valuable service towards the scientific community with his extensive research work.

Introduction: The non-toxin production variant C. difficile A-/B-/CDT- are prevalent in clinical samples. But the reason for their high prevalence of these strains in the clinical diarrhea specimens has not yet been performed. Materials & Methods: Minimum inhibitory concentration bacteria were performed by micro- dilution technique. About ~106 bacteria from 18-hour culture were inoculated to pre-reduced media containing ½×MIC of each antibiotic. After 24, 48 and 96 hours, 1/mL of culture was excluded and heated to killing vegetative forms and pre-activated the spores. The 100 of appropriate dilution are cultured on Columbia blood agar in the form of triplicates. After 72 hours the number of spore were counted based on the colony forming unit. Results: The results showed that non-toxigenic isolates and historically strain of C. difficile (ATCC 9689) and the clinically isolates A+/B+/CDT- produced spore in free antibiotic and ½×MIC media. The spore production non-toxigenic isolates in free antibiotic media was like toxigenic (clinically and ATCC 9689 strain). The VAN, CLI and CAZ inhibited spore production in toxigenic as the same as non-toxigenic isolates (A-/B-/CDT-) of C. difficile in the similar manner. Discussion: Since non-toxigenic isolates are common in the clinical samples. Our research showed these isolates capable to produce spore in absence and the presence of antibiotic in similar manner to toxigenic strain. In total, they have lost toxin production ability but they kept the power sporulation and survival in the hospitalized patients who receive antibiotics.