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McHugh, T. D.

Publications and source records attributed to McHugh, T. D..

8 recordsLinked to original sources

Characterising the microbial and antimicrobial resistance signatures of hospital-acquired pneumonia using nanopore metagenomic sequencing

Hospital-acquired pneumonia (HAP) is a significant burden in nosocomial settings, yet its microbial underpinnings remain poorly understood. Here, we leverage shotgun nanopore sequencing to characterise the respiratory microbiomes of 250 HAP patients in a UK multi-site cohort, validating these using paired PCR and culture assays. Sequencing identified the dominant microbes implicated in HAP, including detection of probable pathogens in 49 PCR- and culture-negative cases. We found a high prevalence of fungi in 81/239 (34%) in HAP patients, of whom 26/81 (32%) were PCR/culture-negative, suggesting that fungi may represent an under-investigated component of HAP, whether as colonists or pathogens. Although HAP is clinically sub-categorised based on the use and duration of ventilation before disease onset, we found that the microbial profiles of these sub-groups were indistinguishable. We also found a concerningly high proportion of multi-drug-resistant microbes in HAP patients, with 21% of assembled bacterial genomes harbouring acquired antimicrobial resistance (AMR) genes that confer resistance to at least three classes of antimicrobials. This included high AMR gene carriage associated to Staphylococcus epidermidis, which may be an important reservoir of AMR, though typically viewed as a commensal. Our work provides extensive metagenomic characterisation of HAP, underscores the value of metagenomics in describing its complex aetiology, and further prompts its potential role for pathogen detection, resistance profiling and treatment.

microbiology↗

A metagenomic approach to One Health surveillance of antimicrobial resistance in a UK veterinary centre

IntroductionThere are currently no standardised guidelines for genomic surveillance of One Health (OH) antimicrobial resistance (AMR). This project aimed to utilise metagenomics to identify AMR genes present in a companion animal hospital and compare these with phenotypic results from bacterial isolates from clinical specimens from the same veterinary hospital. MethodsSamples were collected from sites around a primary companion animal veterinary hospital in North London. Metagenomic DNA was sequenced using Oxford Nanopore Technologies (ONT) MinION. The sequencing data were analysed for AMR genes, plasmids and clinically relevant pathogen species. These data were compared to phenotypic speciation and antibiotic susceptibility tests (ASTs) of bacteria isolates from patients. ResultsThe most common resistance genes identified were aph (n=101 times genes were isolated across 48 metagenomic samples), sul (84), blaCARB (63), tet (58) and blaTEM (46). In clinical isolates, a high proportion of phenotypic resistance to the {beta}-lactams was identified. Rooms with the greatest mean number of resistance genes identified per swab site were the medical preparation room, dog ward and surgical preparation room. Twenty-four Gram-positive and four enterobacterial plasmids were identified. Sequencing reads matched with 14/22 (64%) of the phenotypically isolated bacterial species. DiscussionMetagenomics identified AMR genes, plasmids and species of relevance to human and animal medicine. Communal animal-handling areas harboured more AMR genes than areas animals did not frequent. When considering infection prevention and control (IPC) measures, adherence to, and frequency of, cleaning schedules, alongside potentially more comprehensive disinfection of animal-handling areas may reduce the number of potentially harmful bacteria present. PubMed "veterinary" or "companion" AND "AMR" or "resistan*" NOT (Review[Publication Type]) (2018-2023) "veterinary" or "companion" AND "AMR" or "resist*" AND "sequencing" or "metagenomic*" "veterinary" or "companion" AND "AMR" or "resistan*" NOT (Review[Publication Type]) (2018-2023) https://www.iscaid.org/clinical-practice

genomics↗

Quinoline synergy and reduced use: a study of pharmacodynamic interactions

SynopsisO_ST_ABSBackgroundC_ST_ABSMeropenem, gentamicin and ciprofloxacin have been used as empiric broad-spectrum combination therapy in different combinations. Recent restrictions on the use of quinolones jeopardises the rational of administering this combination to increase the spectrum of coverage for this particular case. A mechanistic understanding of pharmacodynamic interaction for these combinations is lacking but can provide insight in the necessity of using the different moieties. ObjectivesTo study pharmacodynamic drug-drug interaction between meropenem, gentamicin and ciprofloxacin against Escherichia coli. MethodsStatic time kill curve experiments were conducted with Escherichia coli (NCTC(R) 12241) at 0.25 - 16 x MIC for a duration of 24 hours with samples being collected at 0, 2, 4, 6, 8, and 24 hour. Meropenem, gentamicin and ciprofloxacin were tested alone, in two- and three-way combinations. Bacterial load time series data were enumerated on Meuller Hinton plates and Colony Forming Unit data was modelled using nonlinear mixed-effects models in nlmixr. ResultsMeropenem, gentamicin and ciprofloxacin two- and three-way combinations prevented regrowth, but did not when these moieties were studied alone. Gentamicin and meropenem were synergistic by decreasing ciprofloxacin IC50 and the combination effects of meropenem and gentamicin and the addition of meropenem on top of a gentamicin and ciprofloxacin combination were indifferent. ConclusionsOur findings emphasize the added value of a quinolone in the drug combination. In light of the recent move towards reduced use of quinolones, a quinolone free combination still prevented regrowth, it just did not display further synergy on IC50 and was indifferent in initial killing.

pharmacology and toxicology↗

The impact of physiological state and environmental stress on bacterial load estimation methodologies for Mycobacterium tuberculosis

SynopsisO_ST_ABSBackgroundC_ST_ABSSolid and liquid medium cultures from patient samples recover different proportions of a heterogenous bacterial community over the duration of treatment. In vitro experiments were designed to study the population composition at early-logarithmic and stationary phases of growth as well as under drug pressure. ObjectivesTo derive a relationship between methodologies for bacterial load determination and assess the effect of the growth phase of the parent culture and its exposure to stress on the results. MethodsMycobacterium tuberculosis H37Rv was grown with and without drug (isoniazid or rifampicin) and sampled on day 0, 3, 11 and 21 of growth in broth culture. The bacterial load was estimated by colony counts and the BD BACTEC MGIT automated mycobacterial detection system. Linear and nonlinear mixed-effects models were used to describe the relationship between time-to-positivity (TTP) and time-to-growth (TTG) vs colony forming units (CFU), and growth units (GU) vs time. ResultsFor samples with the same CFU, drug-treated and stationary phase cells had a shorter TTP than the drug-free control and early-logarithmic phase cells respectively. Similarly, stationary phase samples reached higher GUs and had shorter time to start growing than early-log phase ones. ConclusionsThe growth phase affects the relationship between CFU-TTP/TTG and previous exposure to drugs affects only the relationship between CFU-TTP. This suggests that there is a population of bacterial cells that can be differentially recovered in liquid medium giving us an insight into the physiological states of the original culture which aids in the interpretation of clinical trial outputs.

microbiology↗

The emergence of goblet inflammatory or ITGB6hi nasal progenitor cells determines age-associated SARS-CoV-2 pathogenesis

Children infected with SARS-CoV-2 rarely progress to respiratory failure, but the risk of mortality in infected people over 85 years of age remains high, despite vaccination and improving treatment options. Here, we take a comprehensive, multidisciplinary approach to investigate differences in the cellular landscape and function of paediatric (<11y), adult (30- 50y) and elderly (>70y) nasal epithelial cells experimentally infected with SARS-CoV-2. Our data reveal that nasal epithelial cell subtypes show different tropism to SARS-CoV-2, correlating with age, ACE2 and TMPRSS2 expression. Ciliated cells are a viral replication centre across all age groups, but a distinct goblet inflammatory subtype emerges in infected paediatric cultures, identifiable by high expression of interferon stimulated genes and truncated viral genomes. In contrast, infected elderly cultures show a proportional increase in ITGB6hi progenitors, which facilitate viral spread and are associated with dysfunctional epithelial repair pathways. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=155 SRC="FIGDIR/small/524211v2_ufig1.gif" ALT="Figure 1"> View larger version (61K): org.highwire.dtl.DTLVardef@dab12aorg.highwire.dtl.DTLVardef@1a57334org.highwire.dtl.DTLVardef@12e7983org.highwire.dtl.DTLVardef@2bbe6e_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

Understanding emergence of antimycobacterial dose dependent resistance.

Concentration dependency of phenotypic and genotypic isoniazid-rifampicin resistance emergence was investigated to obtain a mechanistic understanding on how anti-mycobacterial drugs facilitate the emergence of bacterial populations that survive throughout treatment. Using static kill curve experiments, observing two evolution cycles, it was demonstrated that rifampicin resistance was the result of non-specific mechanisms and not associated with accumulation of drug resistance encoding SNPs. Whereas, part of isoniazid resistance could be accounted for by accumulation of specific SNPs, which was concentration dependent. Using a Hollow Fibre Infection Model it was demonstrated that emergence of genotypic resistance only occurs when antibiotic levels fall below MIC although MICs are typically maintained following clinical dosing provided that adherence to the regimen is good. This study showed that disentangling and quantifying concentration dependent emergence of resistance provides improved rational for drug and dose selection although further work on understanding underlying mechanisms is needed to improve the drug development pipeline. One Sentence SummaryDisentangling and quantifying concentration dependent emergence of resistance will contribute to better informed drug and dose selection for anti-mycobacterial combination therapy.

pharmacology and toxicology↗

Improving diagnosis and monitoring of treatment response in pulmonary tuberculosis using the molecular bacterial load assay (MBLA)

ObjectivesBetter outcomes in tuberculosis require new diagnostic and treatment monitoring tools. In this paper we evaluated the utility of a marker of M. tuberculosis viable count, the Molecular Bacterial Load assay (MBLA) for diagnosis and treatment monitoring of tuberculosis in a high burden setting. MethodsPatients with smear positive pulmonary tuberculosis from two sites in Tanzania and one each in Malawi and Mozambique. Sputum samples were taken weekly for the first 12 weeks of treatment and evaluated by MBLA and mycobacterial growth indicator tube method (MGIT). ResultsThe results of high and low positive control samples confirmed inter site reproducibility. Over the 12 weeks of treatment there was a steady decline in the viable bacterial load as measured by the MBLA that corresponds to rise in time to a positive result (TTP) in the Mycobacterial Growth Indicator Tube. Both MBLA and MGIT provided similar time to test negativity. Importantly, as treatment progressed samples in MGIT were increasingly likely to be contaminated, which compromised the acquisition of results but did not affect MBLA samples. ConclusionsMBLA produces a reproducible measure of Mtb viable count comparable to that of MGIT that is not compromised by contamination in a real-world setting. As a molecular test, the results can be available in as little as four hours and could allow health care professionals to identify rapidly patients who are failing therapy.

microbiology↗

Cell-wall synthesis and ribosome maturation are co-regulated by an RNA switch in Mycobacterium tuberculosis

The success of Mycobacterium tuberculosis as a pathogen relies on the ability to switch between active growth and non-replicating persistence, associated with latent TB infection. Resuscitation promoting factors (Rpfs) are essential for the transition of M. tuberculosis to dormancy and for emergence from the non-replicating persistent state. But these enzymes are double-edged swords, as their ability to degrade the cell wall, is potentially lethal to the bacterium itself. Hence, Rpf expression is tightly regulated. We have identified a novel regulatory element in the 5 untranslated region (UTR) of rpfB. We demonstrate that this element is a transcriptionally regulated RNA switch/riboswitch candidate, which is restricted to pathogenic mycobacteria, suggesting a role in virulence. Moreover, we have used translation start site mapping to re-annotate the RpfB start codon and identified and validated a ribosome binding site that is likely to be targeted by an RpfB antisense RNA. Finally, we show that rpfB is co-transcribed with downstream genes, ksgA and ispE. ksgA encodes a universally conserved methyl transferase involved in ribosome maturation and ispE encodes an essential ATP-dependent kinase involved in cell wall synthesis. This arrangement implies co-regulation of resuscitation, cell wall synthesis and ribosome maturation via the RNA switch. We propose that deregulation of this switch, associated with cell wall synthesis and ribosome function, presents a new target for anti-tuberculosis drug development.\n\nImportanceThis work describes the identification and characterisation of a novel regulatory RNA element/attenuator that controls cell wall synthesis and ribosome function in Mycobacterium tuberculosis, the causative agent of human tuberculosis (TB). By switching between two different conformations, this RNA switch can either enable or inhibit transcription of a tri-cistronic mRNA that encodes a cell-wall remodelling enzyme crucial for activation of latent TB, an RNA methytransferase that is important for ribosome function and a protein kinase essential for early steps in cell wall synthesis. This RNA switch is only present in a subset of pathogenic mycobacteria, and by regulating the expression of three genes associated with classical antimicrobial targets we believe that it offers a novel important target for future anti-tuberculosis drugs.

molecular biology↗