Robert Daum, M.D.

APPOINTMENTS

  • Professor, Department of Pediatrics - Section of Infectious Diseases, Committee on Microbiology

CONTACT INFORMATION

The University of Chicago
Wyler C634, (MC 6054)
5841 South Maryland Avenue
Chicago, Illinois 60637

rdaum@peds.bsd.uchicago.edu

Phone:  (773) 702-6176

RESEARCH SUMMARY

Bacterial Pathogenesis and Antibiotic Resistance

Dr. Daum’s NIH funded laboratory studies the pathogenesis of staphylococcal infections and molecular mechanisms of antimicrobial resistance. Specifically, the laboratory focuses on understanding the changes in the biochemistry of the cell wall of vancomycin-resistant Staphylococcus aureus strains. The first change occurring after exposure to vancomycin is resistance to endogenous endopeptidases, also called autolysins, enzymes intended to assist in cell division and replication. These enzymes are unable to lyse walls from at least some vancomycin-resistant cells. Paradoxically, these autolysins are produced in excessive quantities in these resistant strains. Taken together, these data suggest that cytoplasmic proteins are unable to anchor in the bacterial cell surface in these resistant strains. Genes up-regulated or down-regulated by vancomycin and related stress are also under study using microarray technology.

A separate project has begun to address the molecular biology of methicillin-resistant S. aureus (MRSA) strains now known to be circulating in the community. Until recently, these strains had been confined to the hospital environment. Initial data from the laboratory suggests that these isolates differed from their hospital circulating counterparts in that they are most often resistant only to methicillin alone and not to multiple antibiotics like hospital MRSA strains frequently are. These MRSA strains circulating in the community represent unique molecular clones inserted into the genome of classic "methicillin-susceptible backgrounds." Further work is in progress to further characterize the molecular epidemiology of these strains and to understand the molecular origins of this new resistant clone.

Research Papers on PubMed