Ghassan M. Matar is currently a Professor in the Department of Experimental Pathology, Immunology & Microbiology and Laboratory Director of the Center for Infectious Diseases Research at the Faculty of Medicine, American University of Beirut (AUB). Professor Matar received his PhD in Basic Medical Sciences (Microbiology) from AUB and was a post-doctoral fellow (Fulbright) at the Centers for Disease Control Prevention (CDC) and Department of Microbiology and Immunology, Emory University in Atlanta, Georgia, USA. He was then appointed as Research Microbiologist at the Division of Bacterial and Mycotic Diseases, CDC. Professor Matar was also appointed as Assistant Dean at the Faculty of Health Science, AUB. In addition, he currently serves in WHO as advisor in the Advisory Group on Integrated Surveillance of Antimicrobial Agents (AGISAR), and as American Society for Microbiology (ASM) Ambassador to Lebanon. Professor Matar’s Laboratory is a PulseNet Laboratory certified by CDC. To present he published 90 articles in peer reviewed international journals and presented 115 papers in international, regional and local conferences. He received funding from various extramural sources such as: CDC, U.S. Department of Defense (DOD), WHO/AGISAR, PulseNet (CDC, WHO, MOPH) and others. His research interests include: 1) Molecular mechanisms of resistance to antimicrobial agents in pathogenic bacteria, 2) Potential Treatment of E. coli O157:H7 and O104:H4 infections, 3) Biofilm production in P. aeruginosa and potential inhibition of biofilm formation, 4) Expression levels of virulence factors in bacterial agents in relation to disease production, 5) Molecular epidemiology of foodborne diseases and nosocomial infections.


The effect of different regimens of rifampicin and gentamicin were evaluated to determine possible treatment modes for the novel Escherichia coli O104:H4 pathotype and evaluate the effect of the SOS response on shiga-toxin 2 (Stx2) release. Pulsed field gel electrophoresis (PFGE) was performed on the novel E. coli O104:H4 pathotype and two pre-outbreak E. coli O104:H4 CDC strains. Transcription levels of the stx2 and recA gene (SOS response inducer) were evaluated by RT-qPCR using different regimens of rifampicin and gentamicin. Reverse passive latex agglutination (RPLA) determined the Stx2 titers in these samples. Western blotting detected the LexA levels (SOS response repressor).The efficacy of treatment with antimicrobial agents was assessed in BALB/c mice. PFGE analysis showed that the outbreak and pre-outbreak strains are genomically closely related. The transcription level of the stx2 gene in the new pathotype was 1.41 and 1.75 fold that of the 2 pre-outbreak strains respectively. Different combinations of the antimicrobial agents concentrations led to a significant reduction in the transcription level of the stx2 gene. RPLA data were in accordance with the RT-qPCR results. E.coli O104:H4 exposed to gentamicin led to high transcription levels of the recA gene and lack of expression of the LexA protein, implying activation of the SOS response. In vivo, the highest survival rate in BALB/c mice was observed with treatment by MBC of gentamicin. In conclusion, the use of antimicrobial agents in E. coli O104:H4 infection seems to be effective. This provides a promising ground for treatment of E. coli O104:H4 infections.