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Over the past decade, there has been a rising interest in Achromobacter sp., an emerging opportunistic pathogen responsible for nosocomial and cystic fibrosis lung infections. Species of this genus are ubiquitous in the environment, can outcompete resident microbiota, and are resistant to commonly used disinfectants as well as antibiotics. Nevertheless, the Achromobacter genus suffers from difficulties in diagnosis, unresolved taxonomy and limited understanding of how it adapts to the cystic fibrosis lung, not to mention other host environments. The goals of this first genus-wide comparative genomics study were to clarify the taxonomy of this genus and identify genomic features associated with pathogenicity and host adaptation. This was done with a widely applicable approach based on pan-genome analysis. First, using all publicly available genomes, a combination of phylogenetic analysis based on 1,780 conserved genes with average nucleotide identity and accessory genome composition allowed the identification of a largely clinical lineage composed of Achromobacter xylosoxidans, Achromobacter insuavis, Achromobacter dolens, and Achromobacter ruhlandii. Within this lineage, we identified 35 positively selected genes involved in metabolism, regulation and efflux-mediated antibiotic resistance. Second, resistome analysis showed that this clinical lineage carried additional antibiotic resistance genes compared with other isolates. Finally, we identified putative mobile elements that contribute 53% of the genus’s resistome and support horizontal gene transfer between Achromobacter and other ecologically similar genera. This study provides strong phylogenetic and pan-genomic bases to motivate further research on Achromobacter, and contributes to the understanding of opportunistic pathogen evolution.

Background and methods Achromobacter species leads to chronic infection in an increasing number of CF patients. We report 2 cases of Achromobacter ruhlandii cross-infection between patients after well-described indirect contact. Results Both cases were young, stable, CF patients without chronic infections and with normal FEV 1 , but experienced clinical deterioration after visits to the home of a CF patient with A. ruhlandii infection and after sharing facilities with an A. ruhlandii infected CF patient on a skiing vacation, respectively. Both cases became positive for A. ruhlandii in airway secretions and were colonized with A. ruhlandii in their sinuses. Aggressive, long-term antibiotic treatment led to clinical stability. One of the cases developed chronic A. ruhlandii infection. Conclusion A. species can cause cross-infection even after a short period of indirect contact between infected and non-infected CF patients. Patients should be followed closely for several months before the possibility of cross-infection is ruled out.

Background We recently described a multilocus sequence typing scheme for Achromobacter that identified several novel species in this genus. Methods We assessed the ability of nrdA sequence analysis to differentiate Achromobacter species, including the seven previously named species and 14 recently described genogroups. Confirmation of distinctness between groups was confirmed using the k parameter. Using this single locus sequence to differentiate species, we analyzed Achromobacter isolates obtained from 341 CF patients in the U.S. Results We found that Achromobacter xylosoxidans accounts for 42% of Achromobacter infections, while Achromobacter ruhlandii accounted for 23.5% of infections. Isolates from 17% of patients were members of the novel genogroup 14. The remaining 17.5% of strains belonged to 11 other species/genogroups. Conclusion The use of nrdA sequence analysis allows differentiation of the several Achromobacter species that can infect persons with CF. Achromobacter species other than A. xylosoxidans account for the majority of Achromobacter infection in CF patients in the U.S.

that hypermutation play an important role during diversification and adaptation of Achromobacter sp. Methods: The mutation frequency of Achromobacter sp. isolates is estimated by plating isolates onto LB agar and LB agar containing rifampicin. Mutation frequency values are reported as the number of rifampicin-resistant colonies in proportion to the total viable count. Genes of the MMR-system of Achromobacter will be amplified by PCR and subsequently sequenced. Results: In this study we investigate the prevalence of hypermutator strains of Achromobacter sp. among patients affiliated with the CF Centre at Aarhus University Hospital. MMR gene sequences of potential hypermutators and normomutators will be compared in order to decipher the genetics of hypermutation in Achromobacter sp. Conclusion: Hypermutation might be a key element of genetic adaptation of Achromobacter sp. in the CF lung. Adaptation of Achromobacter sp. to changing environments is essential for persistence in the CF lung.