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Webb, J. R.

Publications and source records attributed to Webb, J. R..

5 recordsLinked to original sources

Modified defence peptides from horseshoe crab target and kill bacteria inside host cells

Bacteria that occupy an intracellular niche can evade extracellular host immune responses and antimicrobial molecules. In addition to classic intracellular pathogens, other bacteria including uropathogenic Escherichia coli (UPEC) can adopt both extracellular and intracellular lifestyles. UPEC intracellular survival and replication complicates treatment, as many therapeutic molecules do not effectively reach all components of the infection cycle. In this study, we explored cell penetrating antimicrobial peptides from distinct structural classes as alternative molecules for targeting bacteria. We identified two {beta}-hairpin peptides from the horseshoe crab, tachyplesin I and polyphemusin I, with broad antimicrobial activity toward a panel of pathogenic and non-pathogenic bacteria in planktonic form. Peptide analogues [I11A]tachyplesin I and [I11S]tachyplesin I maintained activity toward bacteria, but were less toxic to mammalian cells than native tachyplesin I. This important increase in therapeutic window allowed treatment with higher concentrations of [I11A]tachyplesin I and [I11S]tachyplesin I, to significantly reduce intramacrophage survival of UPEC in an in vitro infection model. Mechanistic studies using bacterial cells, model membranes and cell membrane extracts, suggest that tachyplesin I and polyphemusin I peptides kill UPEC by selectively binding and disrupting bacterial cell membranes. Moreover, treatment of UPEC with sublethal peptide concentrations increased zinc toxicity and enhanced innate macrophage antimicrobial pathways. In summary, our combined data show that cell penetrating peptides are attractive alternatives to traditional small molecule antibiotics for treating UPEC infection, and that optimization of native peptide sequences can deliver effective antimicrobials for targeting bacteria in extracellular and intracellular environments.

microbiology↗

Drug susceptibility profiling of Australian Burkholderia species as models for developing melioidosis therapeutics

SynopsisO_ST_ABSBackgroundC_ST_ABSMelioidosis is a neglected tropical disease caused by the Gram-negative soil bacterium Burkholderia pseudomallei. Current treatment regimens are prolonged and costly, and acquired antimicrobial resistance has been reported for all currently used antibiotics. ObjectivesEfforts to develop new treatments for melioidosis are hampered by the risks associated with handling pathogenic B. pseudomallei, which restricts research to facilities with Biosafety Level (BSL) 3 containment. Closely related Burkholderia species that are less pathogenic can be investigated under less stringent BSL 2 containment. We hypothesized that near-neighbour Burkholderia species could be used as model organisms for developing therapies that would also be effective against B. pseudomallei. MethodsWe used microbroth dilution assays to compare the susceptibility of three Australian B. pseudomallei isolates and five near-neighbour Burkholderia species - B. humptydooensis, B. thailandensis, B. oklahomensis, B territorii and B. stagnalis - to antibiotics currently used to treat melioidosis, and general-use antibacterial agents. We also established the susceptibility profiles of B. humptydooensis and B. territorii to 400 compounds from the Medicines for Malaria Venture Pathogen Box. ResultsFrom these comparisons, we observed a high degree of similarity in the susceptibility profiles of B. pseudomallei and near-neighbour species B. humptydooensis, B. thailandensis, B. oklahomensis and B. territorii. ConclusionsLess pathogenic Australian Burkholderia species B. humptydooensis, B. thailandensis, B. oklahomensis and B. territorii are excellent model organisms for developing potential new therapies for melioidosis.

microbiology↗

Taking the next-gen step: comprehensive antimicrobial resistance detection from Burkholderia pseudomallei genomes

BackgroundAntimicrobial resistance (AMR) poses a major threat to human health. Whole-genome sequencing holds great potential for AMR identification; however, there remain major gaps in comprehensively detecting AMR across the spectrum of AMR-conferring determinants and pathogens. MethodsUsing 16 wild-type Burkholderia pseudomallei and 25 with acquired AMR, we first assessed the performance of existing AMR software (ARIBA and CARD) for detecting clinically relevant AMR in this pathogen. B. pseudomallei was chosen due to limited treatment options, high fatality rate, and AMR caused exclusively by chromosomal mutation (i.e. single-nucleotide polymorphisms [SNPs], insertions-deletions [indels], copy-number variations [CNVs], and functional gene loss). Due to poor performance with existing tools, we developed ARDaP (Antimicrobial Resistance Detection and Prediction) to identify the spectrum of AMR-conferring determinants in B. pseudomallei. ResultsCARD failed to identify any clinically-relevant AMR in B. pseudomallei, ARIBA cannot differentiate AMR determinants from natural genetic variation, and neither CARD or ARIBA can identify CNV or gene loss determinants. In contrast, ARDaP accurately detected all SNP, indel, CNV, and gene loss AMR determinants described in B. pseudomallei (n{approx}50). Additionally, ARDaP accurately predicted three previously undescribed determinants. In mixed strain data, ARDaP identified AMR to as low as ~5% allelic frequency. ConclusionsWe demonstrate that existing AMR software are inadequate for comprehensive AMR detection; ARDaP overcomes the shortcomings of existing tools. Further, ARDaP enables AMR prediction from mixed sequence data down to 5% allelic frequency. ARDaP databases can be constructed for any microbial species of interest for comprehensive AMR detection.

genomics↗

Development and validation of a triplex qPCR assay to detect efflux pump-mediated antibiotic resistance in Burkholderia pseudomallei

Burkholderia pseudomallei, the causative agent of the deadly tropical disease melioidosis, is intrinsically resistant to many antibiotics, leaving few effective treatment options. Trimethoprim-sulfamethoxazole (SXT), meropenem (MEM) and doxycycline (DOX) are valuable antibiotics for melioidosis treatment due to inherently low or no primary resistance. Although considered rare, upregulation of one or more resistance-nodulation-division (RND) efflux pumps is now known to lead to acquired resistance towards these drugs in B. pseudomallei. Here, we developed a triplex quantitative PCR assay to detect upregulation of the three clinically relevant RND efflux systems: AmrAB-OprA, BpeB-OprB and BpeEF-OprC. The triplex assay was tested on seven clinically-derived B. pseudomallei isogenic pairs, where the latter strain of each pair had altered regulator activity and exhibited reduced susceptibility to SXT, MEM or DOX. The triplex assay accurately detected efflux pump upregulation between isogenic pairs, which corresponded with decreased antibiotic susceptibility. We further verified assay performance on eight laboratory-generated B. pseudomallei mutants encoding efflux pump regulator mutations. Targeting antibiotic resistance in B. pseudomallei using molecular genotyping provides clinicians with a rapid tool to identify potential treatment failure in near real-time, enabling informed alteration of treatment during an infection and improved patient outcomes.\n\nIMPORTANCEThe melioidosis bacterium Burkholderia pseudomallei is intrinsically resistant to many antibiotics, limiting treatment options to a handful of drugs including meropenem, doxycycline and trimethoprim-sulfamethoxazole. Although rare, there have now been several documented melioidosis cases where resistance to these antibiotics has developed during an infection, leading to treatment failure and increased mortality rates. Interestingly, all strains resistant to these drugs exhibit increased efflux pump expression, representing a shared molecular signature that can be exploited for rapid diagnostic purposes. Here, we developed and validated a single-tube real-time qPCR assay to detect clinically relevant efflux pump upregulation in B. pseudomallei, an important first step towards high-level resistance. This triplex assay offers a drastically reduced turn-around-time compared to current methodology, enabling earlier detection of resistance emergence. Implementation of this new diagnostic will aid clinicians in the selection of appropriate therapy, thereby minimizing resistance development and treatment failure for this high-mortality disease.

microbiology↗

Raising the stakes: Loss of efflux-pump regulation decreases meropenem susceptibility in Burkholderia pseudomallei

Burkholderia pseudomallei, the causative agent of the high-mortality disease melioidosis, is a Gram-negative bacterium that is naturally resistant to many antibiotics. There is no vaccine for melioidosis, and effective eradication is reliant on biphasic and prolonged antibiotic administration. The carbapenem drug, meropenem, is the current gold-standard option for treating severe melioidosis. Intrinsic B. pseudomallei resistance towards meropenem has not yet been documented; however, resistance could conceivably develop over the course of infection, leading to prolonged sepsis and treatment failure. Here, we document 11 melioidosis cases in which B. pseudomallei isolates developed decreased susceptibility towards meropenem during treatment, including two cases not treated with this antibiotic. Meropenem minimum inhibitory concentrations increased over time from 0.5-0.75 to 3-8 g/mL. Using comparative genomics, we identified multiple mutations affecting multidrug resistance-nodulation-division (RND) efflux pump regulators, leading to over-expression of their corresponding pumps. The most commonly affected pump was AmrAB-OprA, although alterations in the local regulators of BpeEF-OprC or BpeAB-OprB were observed in three cases. This study confirms the role of RND efflux pumps in decreased meropenem susceptibility in B. pseudomallei. Further, we document two concerning examples of severe melioidosis where the reduced treatment efficacy of meropenem was associated with a fatal outcome.\n\nSignificance StatementThe bacterium Burkholderia pseudomallei, which causes the often-fatal tropical disease melioidosis, is difficult to eradicate. Due to high levels of intrinsic antibiotic resistance, only a handful of antibiotics are effective against this pathogen. One of these, meropenem, is commonly used in the treatment of melioidosis patients who are unresponsive to other treatments or are critically ill. Here, we describe 11 melioidosis cases whereby patients exhibited prolonged or repeated infections that were associated with the development of decreased meropenem susceptibility. We identified the molecular basis for this decreased susceptibility in latter B. pseudomallei isolates obtained from these patients, and functionally confirmed the mechanism conferring this phenotype. Our findings have important ramifications for the diagnosis, treatment and management of life-threatening melioidosis cases.

microbiology↗