Department of Infectious Diseases
Athletic Association Professor of Infectious Diseases, Department Head, Professor
Expertise
Bacteriology | Immunology and Infectious Disease | Infectious Diseases | Microbiology | Vaccinology
Biography
Frederick D. Quinn, Ph.D., is Athletic Association Professor of Infectious Diseases, Head of the Department of Infectious Diseases and Interim Director of the Center for Vaccines and Immunology in the College of Veterinary Medicine at the University of Georgia.
Dr. Quinn received his BS from Marquette University, PhD in Microbiology and Biochemistry from Indiana University, Bloomington and completed a postdoctoral fellowship at Stanford University. Subsequently, Dr. Quinn oversaw several laboratory groups at the Centers for Disease Control and Prevention in Atlanta investigating bacterial disease outbreaks including Brazilian Purpuric Fever, Cat Scratch Disease, meningococcal meningitis, Buruli ulcer, and ultimately tuberculosis. Prior to accepting the position at UGA, Dr. Quinn completed a Fullbright Fellowship studying novel imaging technologies for tuberculosis at the University of Bristol in Great Britain.
Dr. Quinn’s current research focuses on understanding the pathogenesis and transmission of Mycobacterium tuberculosis and M. bovis, with the ultimate goal of developing improved vaccines and diagnostic tests for human and animal tuberculosis. Collaborative projects include: tuberculosis vaccine animal efficacy testing; ferret, badger and ultimately bovine and camel infection model development for studying tuberculosis pathogenesis, disease transmission, carriage and early infection; tuberculosis transmission patterns via human social networks in Uganda, and zoonotic animal to human transmission studies in Morocco, Mozambique, San Diego/Baja California, the Republic of Georgia and China.
The mission of this laboratory is to identify, isolate and analyze virulence factors from Mycobacterium tuberculosis, M. shottsii, and other pathogenic mycobacteria of humans and animals. The primary focus is currently on examining a number of mycobacterial genes for the purpose of understanding their regulation and control of the host-pathogen interaction. Ultimately, these genes, gene products or associated factors could be used as targets for (the causative agent of tuberculosis) and their genetic coding regions for potential use as vaccine and diagnostic candidates and perhaps as guides for novel disease treatments. An example of one of our studies involves a gene product only expressed during the latent stage of tuberculosis (the most common and most difficult phase to treat). The currently available diagnostic test for tuberculosis, the tuberculin skin test, is not always accurate, does not reflect active disease or latent disease, and most unfortunately, once a person is vaccinated with the currently available BCG vaccine, the skin reaction is positive for at least seven years. Additionally, since the BCG vaccine is not effective in a large fraction of the population, and as previously mentioned causes a positive tuberculin skin reaction, this vaccine is not recommended for use in the United States. We are currently attempting to define the role of this protein in disease and are engaged in an international field trial using this protein as a diagnostic for latent infection.
With the number of cases of tuberculosis and particularly multi-drug resistant tuberculosis at its highest level in decades, this project is extremely relevant to not only the goals of our laboratory but also public health agencies. Identifying and working with virulence-associated genes and gene products are not only attainable goals with current technologies but vitally necessary if we are to deal with the prevention of emerging infectious diseases such as the Mycobacteria. We anticipate that the genes and gene products analyzed in this project ultimately will be a useful beginning in the search for accurate diagnostic tests for latent disease (and perhaps active disease), more effective vaccines and more basic knowledge about the bacterial factors involved in the overall pathogenesis of tuberculosis.
Research Interests
- Identification and analysis of virulence factors from Mycobacterium tuberculosis and other mycobacteria
Educational Background
- MS (1982) Indiana University
- PhD (1982) Indiana University
Activities
The mission of this laboratory is to identify, isolate and analyze virulence factors from Mycobacterium tuberculosis, M. shottsii, and other pathogenic mycobacteria of humans and animals. The primary focus is currently on examining a number of mycobacterial genes for the purpose of understanding their regulation and control of the host-pathogen interaction. Ultimately, these genes, gene products or associated factors could be used as targets for (the causative agent of tuberculosis) and their genetic coding regions for potential use as vaccine and diagnostic candidates and perhaps as guides for novel disease treatments. An example of one of our studies involves a gene product only expressed during the latent stage of tuberculosis (the most common and most difficult phase to treat). The currently available diagnostic test for tuberculosis, the tuberculin skin test, is not always accurate, does not reflect active disease or latent disease, and most unfortunately, once a person is vaccinated with the currently available BCG vaccine, the skin reaction is positive for at least seven years. Additionally, since the BCG vaccine is not effective in a large fraction of the population, and as previously mentioned causes a positive tuberculin skin reaction, this vaccine is not recommended for use in the United States. We are currently attempting to define the role of this protein in disease and are engaged in an international field trial using this protein as a diagnostic for latent infection.
With the number of cases of tuberculosis and particularly multi-drug resistant tuberculosis at its highest level in decades, this project is extremely relevant to not only the goals of our laboratory but also public health agencies. Identifying and working with virulence-associated genes and gene products are not only attainable goals with current technologies but vitally necessary if we are to deal with the prevention of emerging infectious diseases such as the Mycobacteria. We anticipate that the genes and gene products analyzed in this project ultimately will be a useful beginning in the search for accurate diagnostic tests for latent disease (and perhaps active disease), more effective vaccines and more basic knowledge about the bacterial factors involved in the overall pathogenesis of tuberculosis.
Selected Publications
- Vargas-Villarreal, J., B. D. Mata, M. Deslauriers, F. D. Quinn, J. Castro-Garza, H. G. Martinez-Rodriguez, and S. Said-Fernandez. 2004. Identification of acidic, alkaline, and neutral sphingomyelinase activities in Mycobacterium tuberculosis. Med. Sci. Monit. 9: BR224-229.
- Swords, W.E., P.C. Guenthner, K.A. Birkness, R.B. Lal, C.S. Dezzutti, and F.D. Quinn. 2006. Mycobacterium xenopi multiplies within human macrophages and enhances HIV replication during co-infection in human PBMC. Microb. Path. 40: 41-47.
- Mehta, P.K., R.K. Karls, E.H. White, E.W. Ades and F.D. Quinn. 2006. Entry and intracellular replication of Mycobacterium tuberculosis in cultured human microvascular endothelial cells. Microb. Path. 41:119-124.
- Birkness, K.A., J. Guarner, S.B. Sable, R.A. Tripp, K.L. Kellar, J. Bartlett and F.D. Quinn. 2006. An in vitro model of the leukocyte interactions associated with granuloma formation in M. tuberculosis infection. Immunol. Cell Biol. 85:160-168.
- Posey, J.E., T.M. Shinnick and F.D. Quinn. 2006. Characterization of the twin arginine translocase (TAT) secretion system of Mycobacterium smegmatis. J. Bacteriol. 188: 1332-1340.
- Schueller, C., F.D. Quinn and A. Haas. 2009. The Afipia toolbox and its use to isolate flagella mutants. FEMS Microbiol. Lett. 302:203-210.
- Creevy, K.E. and F.D. Quinn. 2010. Updating our knowledge of mycobacterial infections of fish.Vet J. 180(1):5-6.
- Fine, K.L., M. Metcalfe, E. White, M. Virji, R.K. Karls, and F.D. Quinn. 2012. Involvement of the autophagy pathway in trafficking of Mycobacterium tuberculosis bacilli in alveolar epithelial cells. Cell. Microbiol.
- Castro-Garza, J., W. E. Swords, R. K. Karls and F. D. Quinn. 2012. Dual mechanism for Mycobacterium tuberculosis cytotoxicity on lung epithelial cells. Can. J. Microbiol., 58:909-916.
- Fine-Coulson, K.L., R.K. Karls and F.D. Quinn. 2012. The role of lipid raft aggregation in the infection of type II pneumocytes by Mycobacterium tuberculosis. PLoS One, 7(9):e45028.
