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Title: Bacterial Endosymbiosis Does Not Contribute to Mucormycosis Pathogenesis

Author
item IBRAHIM, A - HARBOR-UCLA MED CTR
item GEBREMARIAM, T - HARBOR-UCLA MED CTR
item LIU, M - HARBOR-UCLA MED CTR
item CHAMILOS, G - MD ANDERSON CANCER CTR
item KONTOYIANNIS, D - MD ANDERSON CANCER CTR
item KWON-CHUNG, K - NIH
item FU, Y - HARBOR-UCLA MED CTR
item Skory, Christopher - Chris
item EDWARDS, JR., J - HARBOR-UCLA MED CTR
item SPELLBERG, B - HARBOR-UCLA MED CTR

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 9/20/2007
Publication Date: 9/20/2007
Citation: Ibrahim, A.S., Gebremariam, T., Liu, M., Chamilos, G., Kontoyiannis, D.P., Kwon-Chung, K.J., Fu, Y., Skory, C.D., Edwards, Jr., J.E., Spellberg, B.J. 2007. Bacterial Endosymbiosis does not contribute to Mucormycosis pathogenesis [abstract]. The American Society for Microbiology's 47th Annual Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC). Presentation #B-1443.

Interpretive Summary:

Technical Abstract: Mucormycoses are life-threatening infections caused by molds belonging to order Mucorales of the class Zygomycetes. Recently, it was demonstrated that Rhizopus, the most common genus causing mucormycosis, harbors a bacterial endosymbiont (Burkholderia) that is responsible for producing the mycotoxin, rhizoxin. We sought to define the role of bacterial endosymbionts in the pathogenesis of mucormycosis. Methods: Clinical isolates (n=33) of Rhizopus or Mucor spp. were screened by PCR for the presence of an endosymbiont using specific primers to amplify bacterial 16S rDNA. Molds that harbored bacteria were rendered bacteria-free by ciprofloxacin treatment, as confirmed by lack of amplification of bacterial 16S rDNA. Virulence of bacteria-free molds was compared to their parent strains (bacteria-harboring) in three different models: 1) damage to endothelial cells (EC) using 51Cr-release assay; 2) survival of diabetic ketoacidosis (DKA) mice infected via the tail vein; and 3) survival of Drosophila flies infected intra-abdominally. Results: A 16S rDNA fragment was amplified from 18 isolates (54.5% of the total isolates tested). Sequence alignment of 4 representative bands showed >90% to published Burkholderia 16S rDNA. EC damage caused by bacteria-free molds was not significantly different from damage caused by their parent strains (median damage 12.2% for bacteria-free vs. 15.5% for parent strains, P>0.05). Further, there was no difference in virulence between bacteria-free molds and their corresponding parent strains in either the DKA mouse or fly models (e.g. 8 day mortality, 40% for bacteria-free vs. 44% for parent strain, P=0.4). Conclusions: Bacterial endosymbiosis is widely detected in Mucorales. However, bacterial endosymbionts do not contribute to mucormycosis pathogenesis as judged by three independent infectious models.