Department of Pathology, Microbiology, and Immunology


  James E. Cassat, M.D., Ph.D.a     



Assistant Professor

Dept. of Pediatrics, Pediatric Infectious Diseases

Dept. of Pathology, Microbiology and Immunology



  Contact Information



Office Location:

Light Hall /1035H MRB IV

Phone: 615-322-2250

E-mail:  jim.cassat@vanderbilt.edu


Campus Mail Address:

Dept of Pediatrics, Pediatric Infectious Disease

MCN D-7235 (2581)


Mailing Address:

Vanderbilt University School of Medicine

Dept of Pediatrics, Pediatric Infectious Disease 

MCN D76235

Nashville, TN 37232-2581







Fellowship, Vanderbilt University Medical Center, Nashville, TN
Residency, Vanderbilt University Medical Center, Nashville, TN
Ph.D., University of Arkansas for Medical Sciences, Little Rock, AR
M.D., University of Arkansas for Medical Sciences, Little Rock, AR
B.S., University of Arkansas, Fayetteville, AR



Research Keywords



Staphylococcus aureus; Osteomyelitis; Bacterial pathogenesis; Bone biology; Host-pathogen interactions



Research Description



The major focus of my research is to understand the interaction between host and pathogen during invasive bacterial infections. Specifically, we seek to define the bacterial virulence mechanisms and host defenses employed during osteomyelitis, an invasive infection of bone common in both children and adults. Risk factors and protective immune responses for osteomyelitis are poorly defined, and bone infections are notoriously recalcitrant to antimicrobial therapy due to both pathogen-induced bone destruction and the emergence of multi-drug resistant pathogens. Therefore, we have created new tools to investigate the host-pathogen interface during osteomyelitis. As Staphylococcus aureus is by far the most common cause of osteomyelitis, we have focused our efforts on identifying the mechanisms by which S. aureus causes bone infection and resulting bone destruction, as well as the host defenses that protect against staphylococcal infection. Using a combination of bone cell culture models, proteomic analyses of bacterial virulence factors, and a new quantitative in vivo model of staphylococcal osteomyelitis, we have uncovered specific bacterial factors that contribute to the pathogenesis of osteomyelitis by triggering osteoblast cell death and bone destruction in vivo. We have also identified staphylococcal genes necessary for survival within the bone. By further defining the mechanisms by which S. aureus survives within bone and ultimately triggers bone destruction, we hope to identify new therapeutic targets to treat osteomyelitis and to limit the morbidity associated with this invasive infection. Moreover, by characterizing the host responses to bacterial pathogens in the bone, we seek to define protective correlates of innate immunity in bone and potentially uncover risk factors for the development of osteomyelitis in otherwise healthy children. Finally, by investigating how bacterial pathogens perturb bone cell physiology, we wish to enhance an understanding of changes in bone remodeling in the face of infectious and inflammatory insults.






Cassat, JE, Smeltzer, MS, Lee, CY. Investigation of biofilm formation in clinical isolates of Staphylococcus aureus. Methods Mol Biol, 1085, 195-211, 2014

Hammer, ND*, Cassat, JE*, Noto, MJ, Lojek, LJ, Chadha, AD, Schmitz, JE, Creech, CB, Skaar, EP. Inter- and Intraspecies Metabolite Exchange Promotes Virulence of Antibiotic-Resistant Staphylococcus aureus. Cell Host Microbe, 16(4), 531-7, 2014

Gillon, JE, Cassat, JE, Di Pentima, MC. Validation of two vancomycin nomograms in patients 10 years of age and older. J Clin Pharmacol, 54(1), 35-8, 2014

Cassat, JE, Hammer, ND, Campbell, JP, Benson, MA, Perrien, DS, Mrak, LN, Smeltzer, MS, Torres, VJ, Skaar, EP. A secreted bacterial protease tailors the Staphylococcus aureus virulence repertoire to modulate bone remodeling during osteomyelitis. Cell Host Microbe, 13(6), 759-72, 2013

Attia, AS*, Cassat, JE*, Aranmolate, SO, Zimmerman, LJ, Boyd, KL, Skaar, EP. Analysis of the Staphylococcus aureus abscess proteome identifies antimicrobial host proteins and bacterial stress responses at the host-pathogen interface. Pathog Dis, 2013

Hammer, ND, Reniere, ML, Cassat, JE, Zhang, Y, Hirsch, AO, Indriati Hood, M, Skaar, EP. Two heme-dependent terminal oxidases power Staphylococcus aureus organ-specific colonization of the vertebrate host. MBio, 4(4), 2013

Cassat, JE, Skaar, EP. Recent advances in experimental models of osteomyelitis. Expert Rev Anti Infect Ther, 11(12), 1263-5, 2013

Cassat, JE, Skaar, EP. Iron in infection and immunity. Cell Host Microbe, 13(5), 509-19, 2013

Cassat, JE, Skaar, EP. Metal ion acquisition in Staphylococcus aureus: overcoming nutritional immunity. Semin Immunopathol, 34(2), 215-35, 2012

Tsang, LH*, Cassat, JE*, Shaw, LN, Beenken, KE, Smeltzer, MS. Factors contributing to the biofilm-deficient phenotype of Staphylococcus aureus sarA mutants. PLoS One, 3(10), e3361, 2008

Stenz, L, Fran??ois, P, Fischer, A, Huyghe, A, Tangomo, M, Hernandez, D, Cassat, J, Linder, P, Schrenzel, J. Impact of oleic acid (cis-9-octadecenoic acid) on bacterial viability and biofilm production in Staphylococcus aureus. FEMS Microbiol Lett, 287(2), 149-55, 2008

Cassat, JE, Lee, CY, Smeltzer, MS. Investigation of biofilm formation in clinical isolates of Staphylococcus aureus. Methods Mol Biol, 391, 127-44, 2007

Rice, KC, Mann, EE, Endres, JL, Weiss, EC, Cassat, JE, Smeltzer, MS, Bayles, KW. The cidA murein hydrolase regulator contributes to DNA release and biofilm development in Staphylococcus aureus. Proc Natl Acad Sci U S A, 104(19), 8113-8, 2007

Cassat, J, Dunman, PM, Murphy, E, Projan, SJ, Beenken, KE, Palm, KJ, Yang, SJ, Rice, KC, Bayles, KW, Smeltzer, MS. Transcriptional profiling of a Staphylococcus aureus clinical isolate and its isogenic agr and sarA mutants reveals global differences in comparison to the laboratory strain RN6390. Microbiology, 152(Pt 10), 3075-90, 2006

Cassat, JE, Dunman, PM, McAleese, F, Murphy, E, Projan, SJ, Smeltzer, MS. Comparative genomics of Staphylococcus aureus musculoskeletal isolates. J Bacteriol, 187(2), 576-92, 2005

Kaiser, JR, Cassat, JE, Lewno, MJ. Should antibiotics be discontinued at 48 hours for negative late-onset sepsis evaluations in the neonatal intensive care unit. J Perinatol, 22(6), 445-7, 2002