Kareem Walid Shehab
- Associate Professor, Pediatrics - (Clinical Scholar Track)
- M.D. Medicine
- University of Arizona, Tucson, Arizona, United States
- University of Arizona, Tucson, Arizona (2012 - Ongoing)
- Palo Alto Medical Foundation (2012)
- Dean's List for Excellence in Teaching
- University of Arizona College of Medicine, Fall 2016
Licensure & Certification
- Board Certification, Pediatrics, American Board of Pediatrics (2009)
- Arizona Medical License, Arizona Medical Board (2012)
- Board Certification, Pediatric Infectious Diseases, American Board of Pediatrics (2013)
Medical student education in medical microbiology, clinical problem-solving, clinical infectious diseases, and pediatrics.
Molecular epidemiology of Clostridium difficile infection and colonization, pediatric coccidioidomycosis.
Independent StudyPED 899 (Fall 2021)
Ped Infectious DiseasesPED 850A (Fall 2021)
Pediatrics ClerkshipPED 813C (Fall 2021)
Ped Infectious DiseasesPED 850A (Spring 2021)
Pediatric Clerkship ClinicalPED 813C2 (Spring 2021)
Pediatrics ClerkshipPED 813C (Spring 2021)
- Shehab, K. W., & Shehab, Z. M. (2018). Coccidioidomycosis. In Feigin and Cherry's Textbook of Pediatric Infectious Diseases. Elsevier.
- Roxas, B. A., Roxas, J. L., Claus-Walker, R., Harishankar, A., Mansoor, A., Anwar, F., Jillella, S., Williams, A., Lindsey, J., Elliott, S. P., Shehab, K. W., Viswanathan, V. K., & Vedantam, G. (2020). Phylogenomic analysis of Clostridioides difficile ribotype 106 strains reveals novel genetic islands and emergent phenotypes. Scientific reports, 10(1), 22135.More infoClostridioides difficile infection (CDI) is a major healthcare-associated diarrheal disease. Consistent with trends across the United States, C. difficile RT106 was the second-most prevalent molecular type in our surveillance in Arizona from 2015 to 2018. A representative RT106 strain displayed robust virulence and 100% lethality in the hamster model of acute CDI. We identified a unique 46 KB genomic island (GI1) in all RT106 strains sequenced to date, including those in public databases. GI1 was not found in its entirety in any other C. difficile clade, or indeed, in any other microbial genome; however, smaller segments were detected in Enterococcus faecium strains. Molecular clock analyses suggested that GI1 was horizontally acquired and sequentially assembled over time. GI1 encodes homologs of VanZ and a SrtB-anchored collagen-binding adhesin, and correspondingly, all tested RT106 strains had increased teicoplanin resistance, and a majority displayed collagen-dependent biofilm formation. Two additional genomic islands (GI2 and GI3) were also present in a subset of RT106 strains. All three islands are predicted to encode mobile genetic elements as well as virulence factors. Emergent phenotypes associated with these genetic islands may have contributed to the relatively rapid expansion of RT106 in US healthcare and community settings.
- Katsanis, E., Shehab, K. W., Meyer, R., & Riley, G. (2017). Successful resolution of hyperammonemia following hematopoietic cell transplantation with directed treatment of Ureaplasma parvum infection. Transplant Infectious Disease.
- Cramer, N., & Shehab, K. W. (2016, October 2016). Pediatric Infectious Diseases 2 Go!. American Academy of Pediatrics National Conference and Exhibition. San Francisco, CA.
- Mansoor, A., Shehab, K. W., Anwar, F., Viswanathan, V., & Vedantam, G. (2016, July 2016). Active Clostridium difficile Infection Surveillance in a Large Tertiary Medical Center Reveals Significant Strain Variation. Anaerobe Society of the Americas Biennial Meeting. Nashville, TN.