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18,535 results for “Infections”
Data from : Metabolic footprint of Vero E6 cells highlights the key metabolic routes associated with SARS-CoV-2 infection and response to drug combinations
<p>This dataset contains representative 1D 1H NMR spectra and data used in the manuscript " Metabolic footprint of Vero E6 cells highlights the key metabolic routes associated with SARS-CoV-2 infection and response to drug combinations " . </p><p> </p><p>The present study used Nuclear Magnetic Resonance-based metabolic footprinting to characterize the secreted cellular metabolite levels (exometabolomes) of Vero E6 cells in response to SARS-CoV-2 infection and to two candidate drugs (Remdesivir, RDV and Azithromycin, AZI). </p><p> </p><p><strong>Supplementary File 1.zip = </strong>Representative 1D 1H NMR profiles of examined VE6 esometabolomes, </p><p> </p><p><strong>Supplementary File 2.xlsx</strong> = Average Mean ± Standard Deviations of NMR relative quantified data (integrals, a.u.) from examined VE6 esometabolomes. </p><p> </p><p><strong>Supplementary File 3.csv = </strong>p–values and associated False Discover Rate (FDR) derived from univariate ANOVA with Fischer's LDS post-hoc test comparisons carried out on NMR relative quantified data.</p><p> </p><p><strong>List of Supplementary Files derived from Metabolite Set Enrichment Analysis (MSEA) : </strong></p><p> </p><p><strong>Supplementary File 4.csv </strong>= Tabular Results from MSEA performed on VE6+ VE6- comparison.</p><p><strong>Supplementary File 5.csv </strong>= Tabular Results from MSEA performed on VE6+ RDV vs. VE6+ comparison.</p><p><strong>Supplementary File 6.csv </strong>= Tabular Results from MSEA performed on VE6+ AZI vs. VE6+ comparison.</p><p><strong>Supplementary File 7.csv</strong> = Tabular Results from MSEA performed on VE6+ R+A vs. VE6+ comparison.</p><p> </p>
Bacterial pathogens dynamic during multi-species infections
<p>Illumina gapA sequences of synthetic communities of plant bacterial pathogens: Pectobacterium and Dickeya genus. Sequencing was performed after growth on TSB synthetic medium (2 days post inoculation) or growth on potato tubers (5 days post infection).</p> <p> </p> <p>The following files are available:</p> <p>PT_table.txt: description of the potato tubers samples</p> <p>TSB_table.txt: description of samples in synthetic medium (TSB)</p> <p>gapA_PT.fasta.gz: Illumina fasta sequences after potato tubers infection (35,000 reads)</p> <p>gapA_TSB.fasta.gz: Illumina fasta sequences after synthetic medium inoculation (35,000 reads)</p> <p>gapA_without_primers.fasta: gapA sequences (without primers) of Pectobacterium and Dickeya strains used in this study (27 strains)</p> <p>species.txt: list of bacterial species used in this study (9 species)</p> <p>strains.txt: list of bacterial strains used in this study (27 strains)</p> <p>count.py: python3 script used to analyse the output of blastn</p> <p>R_script_FigureS1.R: R script for statistical analysis</p> <p>R_script_Figure2b.R: R script for statistical analysis</p> <p>R_script_Figure2a.R: R script for statistical analysis</p> <p> </p> <p>Method (examplified with the gapA_TSB sequences at the species level):</p> <p>• gapA sequences were blasted (blastn) against gapA sequences of Pectobacterium and Dickeya strains used in this study:</p> <p>makeblastdb -in gapA_without_primers.fasta -dbtype nucl -out dbblastn</p> <p>blastn -db dbblastn -query gapA_TSB.fasta -outfmt 6 -out blast.blastn -num_threads 12 -evalue 0.00001 -num_alignments 1</p> <p>• Reads count. Reads matching (100% identity) with gapA sequences of Pectobacterium and Dickeya strains used in this study were counted using the count.py python script. The output is a tab-separated values (.tsv) file:</p> <p>python3 count.py species.txt blast.blastn</p>
The effect of Israeli acute paralysis infection on honey bee brood care behavior
<p>To protect themselves from communicable diseases, social insects utilize social immunity—behavioral, phsyiological, and organizational means to combat disease transmission and severity. Within a honey bee colony, larvae are visited thousands of times by nurse bees, representing a prime environment for pathogen transmission. We investigated a potential social immune response to Israeli acute paralysis virus (IAPV) infection in brood care, testing the hypotheses that bees will respond with behaviors that result in reduced brood care, or that infection results in elevated brood care as a virus-driven mechanism to increase transmission. We tested for group-level effects by comparing three different social environments in which 0%, 50%, or 100% of bees were experimentally infected with IAPV. We investigated individual-level effects by comparing exposed bees to unexposed bees within the mixed-exposure treatment group. We found no evidence for a social immune response at the group level; however, individually, exposed bees interacted with the larva more frequently than their unexposed nestmates. While this could increase virus transmission from adults to larvae, it could also represent a hygienic response to increase grooming when an infection is detected. Together, our findings underline the complexity of disease dynamics in complex social animal systems.</p>
Low sex drive and choosy females: Fungal infections are a reproductive downfall for male house flies
<p>Many entomopathogenic fungi cause infections that kill their insect host. Little is understood about changes in the reproductive investment that occur during an infection by a lethal disease over the waning life of an insect. Life history theory suggests the host will respond by investing resources into fighting the disease or increasing reproduction. Here, we investigate how the reproductive life of adult house flies, <em>Musca domestica</em>, is impacted by its host-specific fungal pathogen, <em>Entomophthora muscae</em>. Specifically, we test how the week-long infection alters the mating behavior of virgin adult male house flies. We find that the pathogen significantly decreases male libido; an effect which grows stronger over the course of the infection. Furthermore, females were significantly less likely to choose an infected male, reducing male mating success. Additionally, we assessed sperm viability to understand the reproductive costs for monandrous females to mate with infected males. Analyses revealed that sperm quality decreases as early as three days post-infection. These results show that <em>E. muscae</em>, which can have a prevalence near 100% in wild populations, causes severe lifetime reproductive costs to male house flies. Understanding how host-pathogen interactions affect host life history is crucial for elucidating all the negative effects pathogen virulence exerts on hosts.</p>
R scripts, input and output data for: Season of death, pathogen persistence and wildlife behaviour alter number of anthrax secondary infections from environmental reservoirs
<p>An important part of infectious disease management is predicting factors that influence disease outbreaks, such as <em>R</em>, the number of secondary infections arising from an infected individual. Estimating <em>R</em> is particularly challenging for environmentally transmitted pathogens given time lags between cases and subsequent infections. Here, we calculated <em>R</em> for <em>Bacillus anthracis</em> infections arising from anthrax carcass sites in Etosha National Park, Namibia. Combining host behavioural data, pathogen concentrations, and simulation models, we show that <em>R</em> is spatially and temporally variable, driven by spore concentrations at death, host visitation rates and early preference for foraging at infectious sites. While spores were detected up to a decade after death, most secondary infections occurred within two years. Transmission simulations under scenarios combining site infectiousness and host exposure risk under different environmental conditions led to dramatically different outbreak dynamics, from pathogen extinction (<em>R</em><1) to explosive outbreaks (<em>R</em>>10). These transmission heterogeneities may explain variation in anthrax outbreak dynamics observed globally, and more generally, the critical importance of environmental variation underlying host-pathogens interactions. Notably, our approach allowed us to estimate the lethal dose of a highly virulent pathogen non-invasively from observational studies and epidemiological data, useful when experiments on wildlife are undesirable or impractical.</p>
Figs. 7–9. Paraharmotrema karinganiense Dutton & Bullard n in Paraharmotrema karinganiense n. gen., n. sp. (Digenea: Liolopidae) infecting the intestine of serrated hinged terrapin (Pelusios sinuatus), east African black mud turtle (Pelusios subniger), and South African helmeted turtle (Pelomedusa galeata) and a phylogenetic hypothesis for liolopid genera
Figs. 7–9. Paraharmotrema karinganiense Dutton & Bullard n. sp. (Digenea: Liolopidae) from the intestine of the intestine of the serrated hinged terrapin, Pelusios sinuatus (Smith 1838) (Pleurodira: Pelomedusidae). (7) Tegumental scales in antero-dextral ventral body surface, ventral view, light micrograph. (8) Tegumental scales on ventral body surface posterior to oral sucker, ventral view, light micrograph. (9) Tegumental scales in same position as in Fig. 8 (showing exposed tips of scales only), ventral view, scanning electron micrograph.
Figs. 5–6. Paraharmotrema karinganiense Dutton & Bullard n in Paraharmotrema karinganiense n. gen., n. sp. (Digenea: Liolopidae) infecting the intestine of serrated hinged terrapin (Pelusios sinuatus), east African black mud turtle (Pelusios subniger), and South African helmeted turtle (Pelomedusa galeata) and a phylogenetic hypothesis for liolopid genera
Figs. 5–6. Paraharmotrema karinganiense Dutton & Bullard n. sp. (Digenea: Liolopidae) from intestine of serrated hinged terrapin, Pelusios sinuatus (Smith 1838) (Pleurodira: Pelomedusidae). (5) Ventral sucker, ventral view, scanning electron micrograph. (6) Ventral sucker, ventral view, light micrograph.
Figs. 1–2. Paraharmotrema karinganiense Dutton & Bullard n in Paraharmotrema karinganiense n. gen., n. sp. (Digenea: Liolopidae) infecting the intestine of serrated hinged terrapin (Pelusios sinuatus), east African black mud turtle (Pelusios subniger), and South African helmeted turtle (Pelomedusa galeata) and a phylogenetic hypothesis for liolopid genera
Figs. 1–2. Paraharmotrema karinganiense Dutton & Bullard n. sp. (Digenea: Liolopidae). (1) Body of adult (holotype, USNM No. 1659278) from intestine of serrated hinged terrapin, Pelusios sinuatus (Smith 1838) (Pleurodira: Pelomedusidae), ventral view. (2) Body of juvenile (paratype, USNM No. 1659285) from intestine of east African black mud turtle, Pelusios subniger (Bonnaterre, 1789) (Pleurodira: Pelomedusidae), dorsal view. Oral sucker (os), pharynx (ph), nerve commissure (nc), excretory system (es), sinistral caecum (sc), ventral sucker (vs), vitellarium (vr), cirrus sac (cs), metraterm (m), vas deferens (vd), anterior vas efferens (ave), anterior testis (at), uterus (u), posterior vas efferens (pve), ovary (o), posterior testis (pt), and excretory pore (ep).
Figs. 3–4. Paraharmotrema karinganiense Dutton & Bullard n in Paraharmotrema karinganiense n. gen., n. sp. (Digenea: Liolopidae) infecting the intestine of serrated hinged terrapin (Pelusios sinuatus), east African black mud turtle (Pelusios subniger), and South African helmeted turtle (Pelomedusa galeata) and a phylogenetic hypothesis for liolopid genera
Figs. 3–4. Paraharmotrema karinganiense Dutton & Bullard n. sp. (Digenea: Liolopidae) from intestine of serrated hinged terrapin, Pelusios sinuatus (Smith 1838) (Pleurodira: Pelomedusidae). (3) Female genitalia (holotype, USNM No. 1659278), ventral view. (4) Male genitalia (holotype, USNM No. 1659278), ventral view. Egg (e), ovary (o), oviduct (ov), ootype (oo), uterus (u), primary vitelline reservoir (pvr), dextral caecum (dc), transverse vitelline duct (tvd), sinistral caecum (sc), dextral excretory branch (deb), posterior vas efferens (pve), sinistral excretory branch (seb), posterior testis (pt), cirrus sac (cs), pars prostatica (pp), secondary bipartite internal seminal vesicle (sbisv), cirrus (c), initial bipartite internal seminal vesicle (ibisv), common genital pore (cgp), metraterm (m), vitellarium (vr), and vas deferens (vd).
Fat oxidation rates and cardiorespiratory responses during exercise in different subject populations with post-acute sequelae of SARS-CoV-2 infection: a comparison with normative percentile values
<p>INTRODUCTION: Post-acute sequelae of SARS-CoV-2 infection (PASC) presents a spectrum of symptoms following acute COVID-19, with exercise intolerance being a prevalent manifestation likely linked to disrupted oxygen metabolism and mitochondrial function. This study aims to assess maximal fat oxidation (MFO) and exercise intensity at MFO (FATmax) in distinct PASC subject groups and compare these findings with normative data.</p> <p>METHODS: Eight male subjects with PASC were involved in this study. The participants were divided in two groups: “endurance-trained” subjects (V̇O<sub>2</sub>max > 55 ml/min/kg) and “recreationally-active” subjects (V̇O<sub>2</sub>max < 55 ml/min/kg). Each subject performed a graded exercise test until maximal oxygen consumption (V̇O<sub>2</sub>max) to measure fat oxidation. Subsequently, MFO was assessed and FATmax calculated as the ratio between V̇O<sub>2 </sub>at MFO and V̇O<sub>2</sub>max.</p> <p>RESULTS: The MFO and FATmax of “endurance-trained” subjects were 0.85, 0.89, 0.71 and 0.42, and 68%, 69%, 64% and 53%, respectively. Three out of four subjects showed both MFO and FATmax values placed over the 80<sup>th</sup> percentile of normative data. The MFO and FATmax of “recreationally-active” subjects were 0.34, 0.27, 0.35 and 0.38, and 47%, 39%, 43% and 41%, respectively. All MFO and FATmax values of those subjects placed below the 20<sup>th</sup> percentile or between the 20<sup>th</sup> and 40<sup>th</sup> percentile.</p> <p>DISCUSSION: Significant differences in MFO and FATmax values between 'endurance-trained' and “recreationally-active” subjects suggest that specific endurance training, rather than simply an active lifestyle, may provide protective effects against alterations in mitochondrial function during exercise in subjects with PASC.</p>
When does antimicrobial resistance increase bacterial fitness? Effects of dosing, social interactions and frequency dependence on the benefits of AmpC β-lactamases in broth, biofilms and a gut infection model.
<p><span>One of the longstanding puzzles of antimicrobial resistance is why the frequency of resistance persists at intermediate levels.<span> </span>Theoretical explanations for the lack of fixation of resistance include cryptic costs of resistance or negative frequency-dependence but are seldom explored experimentally. <span> </span><em>β</em>-lactamases, which detoxify penicillin-related antibiotics, have well-characterized frequency-dependent dynamics driven by cheating and cooperation.<span> </span>However, bacterial physiology determines whether <em>β</em>-lactamases are cooperative and we know little about the sociality or fitness of <em>β</em>-lactamase producers in infections.<span> </span>Moreover, media-based experiments constrain how we measure fitness, and ignore important parameters such as infectivity and transmission among hosts.<span> </span>Here, we investigated the fitness effects of broad-spectrum AmpC <em>β</em>-lactamases in <em>Enterobacter cloacae</em> in broth, biofilms and gut infections in a model insect. <span> </span>We quantified frequency- and dose-dependent fitness using cefotaxime, a third-generation cephalosporin.<span> </span>We predicted that infection dynamics would be similar to those observed in biofilms, with social protection extending over a wide dose range.<span> </span>We found evidence for the sociality of <em>β</em>-lactamases in all contexts with negative frequency-dependent selection ensuring the persistence of wild-type bacteria although cooperation was less prevalent in biofilms, contrary to predictions.<span> </span>While competitive fitness in gut infections and broth had similar dynamics, incorporating infectivity into measurements of fitness in infections<em> </em>significantly affected conclusions. <span> </span>Resistant bacteria had reduced infectivity which limited the fitness benefits of resistance to infections challenged with low antibiotic doses and having low initial frequencies of resistance. <span> </span>The fitness of resistant bacteria in more physiologically tolerant states (in biofilms, in infections) could be constrained by the presence of wild-type bacteria, high antibiotic doses and limited availability of <em>β</em>-lactamases.<span> </span>One conclusion is that increased tolerance of <em>β</em> -lactams does not necessarily increase selection pressure for resistance.<span> </span>Overall, both cryptic fitness costs and frequency-dependence curtailed the fitness benefits of resistance in this study.<span> </span></span></p> <p><span> </span></p>
PI3Kg inhibition circumvents inflammation and mortality in SARS-CoV-2 and other infections
<p>Virulent infectious agents such as SARS-CoV-2 and Methicillin Resistant <em>Staphylococcus Aureus</em> (MRSA) induce tissue damage that recruits neutrophils and monocyte/macrophages that promote T cell exhaustion, fibrosis, vascular leak, epithelial cell depletion, and fatal organ damage. Neutrophils and macrophages recruited to pathogen infected lungs, including SARS-CoV-2 infected lungs, express phosphatidylinositol 3-kinase gamma (PI3Kg), a signaling protein that coordinately controls granulocyte and monocyte trafficking to diseased tissues and immune suppressive, pro-fibrotic transcription in myeloid cells. PI3Kg deletion and inhibition with the clinical PI3Kg inhibitor eganelisib promoted survival in models of infectious diseases, including SARS-CoV-2 and MRSA, by suppressing inflammation, vascular leak, organ damage and cytokine storm. These results demonstrate essential roles for PI3Kg in inflammatory lung disease and support the potential use of PI3Kg inhibitors to suppress inflammation in severe infectious diseases.</p>
Figure 1 in Exposure of the snail Potamopyrgus antipodarum to herbicide boosts output and survival of parasite infective stages
Figure 1. Mean (±SE) number of cercariae emerging per day from individual snails, P. antipodarum, exposed to either control water, low, medium or high concentrations of the herbicide glyphosate. Data are shown separately for the trematodes C. parvum (N = 6 snails for each treatment), Apatemon sp. (N = 3), and an undescribed renicolid species from two localities (Tomahawk Lagoon, N = 12; Lake Waihola, N = 9). In each case, different letters on the bars indicate mean values that are significantly different (Tukey–Kramer tests, P <0.05).
Fig. 4 in Sexual differences in prevalence of a new species of trypanosome infecting túngara frogs
Fig. 4. Phylogeny of the aquatic clade, and PTP species delimitation results. Best maximum likelihood tree of the18S rRNA gene of member of the aquatic clade and selected outgroups. Numbers on the branches represent support values corresponding to ±70% bootstrap replicates (left) and ±0.9 Bayesian posterior probabilities (right). Subclades are highlighted with colored boxes to indicate host associations. Color of the branches indicate the PTP species delimitation results; monophyletic groups in red indicate members of a single species, blue terminal branches indicate that only one sample is included in such species. Names of the terminals indicate the GenBank accession numbers, scientific name, and sample or isolate code. Star indicates the position of T. tungarae n. sp. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
Fig. 3 in Sexual differences in prevalence of a new species of trypanosome infecting túngara frogs
Fig. 3. Light microscopy of Trypanosoma tungarae n. sp. (Giemasa-staining). (a e) Trypomastigotes stained using Hemacolor ® Giemsa stain kit (Voigt Global Distribution Inc, USA); ‾ (f‾i) Trypomastigotes stained using Giemsa stain following Mohr (1981). Scale bars: 10 µm.
Fig. 1 in Sexual differences in prevalence of a new species of trypanosome infecting túngara frogs
Fig. 1. Photographs of túngara frogs (Engystomops pustulosus) and frog-biting midges (Corethrella spp). (a) Calling male túngara frog preyed upon by frog-biting midges; (b) female (bottom) in amplexus with a male (top) covered with biting midges; (c) female (bottom) with a biting midge on her nostril that was passed from the male during amplexus. Túngara frogs are about 30 mm long while the frog-biting midges are only about 1.5 mm. Photos taken by Alexander Baugh (a) and Ximena E Bernal (b,c).
Fig. 2 in Sexual differences in prevalence of a new species of trypanosome infecting túngara frogs
Fig. 2. Map of the Republic of Panaḿa indicating with a star the location of Gamboa, the type locality of Trypanosoma tungarae n. sp. Insert shows the location of Panamáin the New World.
Fig. 1 in Identification of freshwater snail species and survey of their trematode infections in Ordos, China
Fig. 1. Morphological characteristics of major freshwater snails in the Ordos area. a: Bellamya aeruginosa; b, c: Radix plicatula; d: Gyraulus convexiusculus; e, f: Galba pervia.
Fig. 2 in Investigation of Ichthyophthirius multifiliis infection in fish from natural water bodies in the Lhasa and Nagqu regions of Tibet
Fig. 2. Pairwise comparisons of locality. Localities: BZ, Boqu Zangbo (river); CEL, Cuoe lake; CNL, Cuona lake; CW, Chabalang Wetland; LR, Lhasa River; LW, Lalu Wetland; SL, Selincuo Lake ZZ, Za'gya Zangbo (river). *: Indicates a significant difference between location 1 and location 2.
Fig. 3 in First case of Trichinella spiralis infection in beavers (Castor fiber) in Poland and Europe
Fig. 3. The Neighbor-Joining tree of Trichinella species inferred from 5S rDNA inter-gene spacer region sequences. Phylogeny Test - Bootstrap method, No. of Bootstrap Replications - 10000 Jukes Cantor model.
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Allen Brain Atlas
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OpenNeuro
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