928. Comparative Profile of Iron Acquisition Genes in Nontypeable Haemophilus influenzae in Colonization and Disease
Session: Poster Abstract Session: Bacterial Pathogenesis
Saturday, October 22, 2011
Room: Poster Hall B1
Background: Nontypeable Haemophilus influenzae (NTHi) are small gram negative bacteria that colonize the human nasopharynx, and can also cause respiratory tract infections. Since NTHi has an absolute requirement for iron from its host for aerobic growth, comparing the profile of iron acquisition genes between disease isolates from the middle ears of children with acute otitis media and commensal isolates from the throats of healthy children may elucidate their role in determining virulence.

Methods: Fluorescein-labeled probes for iron acquisition genes hxuC, hemR, and hup were prepared using strain 86-028NP as the template. Microarray slides containing NTHi DNA from middle ear (522) and throat (315) isolates were probed with a mixture of seven multilocus sequence typing gene fragments as a DNA concentration control, followed by probes for the iron acquisition genes. The bacterial DNA samples were also probed with iga and lgtC genes to differentiate NTHi from H. haemolyticus, a closely related commensal of the pharyngeal cavity.

Results: Among 315 specimens from the throat, 32 did not meet the criteria to be categorized as H. influenzae and were excluded from further analysis. Of 522 NTHi specimens from the middle ear, hxuC was present in 89.3%, hemR in 87.7%, and hup in 86.2%. Of 283 NTHi specimens from the throat, the percentages were 76%, 69.6%, and 78.8% for hxuC, hemR, and hup respectively. The prevalence ratio of middle ear specimens compared to throat specimens was 1.18 for hxuC (p < 0.001), 1.26 for hemR (p < 0.001), and 1.09 for hup (p = 0.009).

Conclusion: The higher prevalence of iron acquisition genes in NTHi isolated from infected middle ears suggests that these genes have been preserved by natural selection for survival in the middle ear space.


Subject Category: B. Bacterial pathogenesis, studies in animal models, molecular pathogenicity

Nurul Hariadi, MD1, Sara Sandstedt, PhD2, Mayuri Patel2, Lixin Zhang, PhD2, Nathan LaCross2, William Nance2, Gregg Davis2, Carl Marrs, PhD2 and Janet Gilsdorf, MD1,2, (1)Pediatric Infectious Diseases, University of Michigan, Ann Arbor, MI, (2)Epidemiology, University of Michigan School of Public Health, Ann Arbor, MI

Disclosures:

N. Hariadi, None

S. Sandstedt, None

M. Patel, None

L. Zhang, None

N. LaCross, None

W. Nance, None

G. Davis, None

C. Marrs, None

J. Gilsdorf, None

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