Abstract
An emergent clone of Haemophilus influenzae biogroup aegyptius (Hae) is responsible for outbreaks of Brazilian purpuric fever (BPF). First recorded in Brazil in 1984, the so-called BPF clone of Hae caused a fulminant disease that started with conjunctivitis but developed into septicemic shock; mortality rates were as high as 70%. To identify virulence determinants, we conducted a pan-genomic analysis. Sequencing of the genomes of the BPF clone strain F3031 and a noninvasive conjunctivitis strain, F3047, and comparison of these sequences with 5 other complete H. influenzae genomes showed that >77% of the F3031 genome is shared among all H. influenzae strains. Delineation of the Hae accessory genome enabled characterization of 163 predicted protein-coding genes; identified differences in established autotransporter adhesins; and revealed a suite of novel adhesins unique to Hae, including novel trimeric autotransporter adhesins and 4 new fimbrial operons. These novel adhesins might play a critical role in host-pathogen interactions.
Highlights
An emergent clone of Haemophilus influenzae biogroup aegyptius (Hae) is responsible for outbreaks of Brazilian purpuric fever (BPF)
Farley et al [13] identified duplication of fimbrial genes, with sequences differing from H. influenzae type b pilin, but could find no systematic difference in binding of HaeBPF and conventional Hae strains to human epithelial cells and could not conclusively implicate this locus in virulence
HaeBPF has a copy of the Haemophilus insertion element IS1016 [16], which has been implicated in acquisition of capsulation genes and other unspecified virulence factors in other H. influenzae strains [17,18], but its role has not been defined
Summary
An emergent clone of Haemophilus influenzae biogroup aegyptius (Hae) is responsible for outbreaks of Brazilian purpuric fever (BPF). Delineation of the Hae accessory genome enabled characterization of 163 predicted protein-coding genes; identified differences in established autotransporter adhesins; and revealed a suite of novel adhesins unique to Hae, including novel trimeric autotransporter adhesins and 4 new fimbrial operons. These novel adhesins might play a critical role in host–pathogen interactions. HaeBPF (but not other Hae strains) has a copy of the Haemophilus insertion element IS1016 [16], which has been implicated in acquisition of capsulation genes and other unspecified virulence factors in other H. influenzae strains [17,18], but its role has not been defined
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