Dr. David Bruce Haslam MD
Infectious Disease Specialist (Pediatric) | Pediatric Infectious Diseases
3333 BURNET AVE CINCINNATI OH, 45229About
Dr. David Haslam is a pediatric infectious disease specialist practicing in Saint Louis, MO. Dr. Haslam specializes in recurring or persistent diseases caused by bacteria, parasites or fungus in infants, children and adolescents. Pediatric infectious disease specialists also provide consultation to other health care professionals dealing with complex cases.
Education and Training
University of Calgary / Faculty of Medicine 1987
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Characterization of the human Forssman synthetase gene. An evolving association between glycolipid synthesis and host-microbial interactions.
- HEDJ, an Hsp40 co-chaperone localized to the endoplasmic reticulum of human cells.
- Expression cloning of human globoside synthase cDNAs. Identification of beta 3Gal-T3 as UDP-N-acetylgalactosamine:globotriaosylceramide beta 1,3-N-acetylgalactosaminyltransferase.
- Managing the child with fever and neutropenia in an era of increasing microbial resistance.
- Forssman synthetase expression results in diminished shiga toxin susceptibility: a role for glycolipids in determining host-microbe interactions.
- Shiga toxin is transported from the endoplasmic reticulum following interaction with the luminal chaperone HEDJ/ERdj3.
- A quantitative and highly sensitive luciferase-based assay for bacterial toxins that inhibit protein synthesis.
- Identification and characterization of small molecules that inhibit intracellular toxin transport.
- Contribution of the HEDJ/ERdj3 cysteine-rich domain to substrate interactions.
- Golgicide A reveals essential roles for GBF1 in Golgi assembly and function.
- The MAP kinase-activated protein kinase 2 (MK2) contributes to the Shiga toxin-induced inflammatory response.
- Structural and functional interactions between the cholera toxin A1 subunit and ERdj3/HEDJ, a chaperone of the endoplasmic reticulum.
- MAPK-activated protein kinase 2 contributes to Clostridium difficile-associated inflammation.
- Markers of intestinal inflammation, not bacterial burden, correlate with clinical outcomes in Clostridium difficile infection.
- Viral co-infections are common and are associated with higher bacterial burden in children with clostridium difficile infection.
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