The disparate effects of bacteriophages on antibiotic-resistant bacteria

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Term Occurence Count Dictionary
infectious disease 2 infectiousdiseases
streptomycin 1 infectiousdiseasesdrugs
toxic shock syndrome 2 infectiousdiseases
dysentery 1 infectiousdiseases
diphtheria 1 infectiousdiseases
ofloxacin 1 infectiousdiseasesdrugs
chloramphenicol 1 infectiousdiseasesdrugs
bacterial infectious disease 2 infectiousdiseases
cholera 6 infectiousdiseases
erythromycin 1 infectiousdiseasesdrugs
scarlet fever 2 infectiousdiseases
AIDS 1 infectiousdiseases
botulism 1 infectiousdiseases
ciprofloxacin 1 infectiousdiseasesdrugs
pneumonia 3 infectiousdiseases
tetracycline 2 infectiousdiseasesdrugs
vancomycin 1 infectiousdiseasesdrugs
ampicillin 1 infectiousdiseasesdrugs

Graph of close proximity drug and disease terms (within 200 characters).

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Select Drug Character Offset Drug Term Instance
ampicillin 20598 and β-lactamase genes in the viral f7raction[27].In a second study, the authors treated mice with ampicillin or ciprofloxacin and sequenced viromes from the collected fecal samples[28]. Relative to control samples
chloramphenicol 11427 generalized transduction frequencies. In separate experiments, the transduction of tetracycline or chloramphenicol resistance was determined to occur at a rate between 10−8 and 10−9 transductants/pfu (Table 1)[5],[8].
ciprofloxacin 20612 β-lactamase genes in the viral f7raction[27].In a second study, the authors treated mice with ampicillin or ciprofloxacin and sequenced viromes from the collected fecal samples[28]. Relative to control samples from untreated
erythromycin 14549 whether they could be mobilized by phages was never established[17]. Goh et al. recently showed that erythromycin resistance codified on a transposon is transferred by generalized transduction at an average frequency
ofloxacin 20616 genes in the viral f7raction[27].In a second study, the authors treated mice with ampicillin or cipr ofloxacin and sequenced viromes from the collected fecal samples[28]. Relative to control samples from untreated
streptomycin 17583 observed to be abundant in the assayed microbiota, specifically those encoding E. coli resistance to streptomycin , sulfamethazine, aminoglycosides, and β-lactams. The quantity of ARGs in the phage fraction did not
tetracycline 11411 their extremely low generalized transduction frequencies. In separate experiments, the transduction of tetracycline or chloramphenicol resistance was determined to occur at a rate between 10−8 and 10−9 transductants/pfu
tetracycline 11854 Staphylococcus aureus transduction, including by phages φ80α and φJB, which transfer penicillinase and tetracycline resistance plasmids at moderate frequencies (10−5–10−6 transductants/pfu) (Table 1)[6],[9]. A
vancomycin 38750 bacteriaAnti-staphylococcal treatments are dwindling due to the selection of methicillin-resistant and vancomycin -resistant strains, which were last resort antibiotics. Fortunately, old and new clinical evidence exists
Select Disease Character Offset Disease Term Instance
AIDS 36046 therapeutic targets to combat bacterial pathogens[64]. This approach is behind a promising strategy to cure AIDS using a recombinase that efficiently removes the integrated HIV virus from infected eukaryotic cells
bacterial infectious disease 1560 for virulence. Foremost among these treatments is phage therapy, which could be used to treat many bacterial infectious disease s and confront the pressing problem of antibiotic resistance in pathogenic bacteria. This review discusses
bacterial infectious disease 49642 knowledge and molecular tools enable an accurate therapeutic approach.The golden age for medicine to treat bacterial infectious disease s has passed. Virulent phages, natural killers of bacteria, can fill the gap left by antibiotics. The
botulism 28500 bacteria are encoded by phages in toxin-mediated diseases, such as diphtheria, cholera, dysentery, botulism , scarlet fever, and some food poisoning diseases[35]. However, not all of these prophages behave in
cholera 28480 many toxins produced by bacteria are encoded by phages in toxin-mediated diseases, such as diphtheria, cholera , dysentery, botulism, scarlet fever, and some food poisoning diseases[35]. However, not all of these
cholera 28680 of these prophages behave in a similar manner. For example, the deadly CTX toxin produced by Vibrio cholera e is also encoded by a phage that can be integrated into the chromosome or behave as a plasmid, although
cholera 29267 filamentous coliphages) reproduces and is secreted, it does not lyse the host cells[45]. In severe cases of cholera , antibiotic treatment is a good practice that improves patient outcome. With respect to phage-bacterial
cholera 45632 loss and modified cell surface properties[101],[102]. Even more indisputable is the example of the cholera -causing bacterium V. cholerae sampled from human patient stools from Haiti and Bangladesh[103]. This
cholera 45661 surface properties[101],[102]. Even more indisputable is the example of the cholera-causing bacterium V. cholera e sampled from human patient stools from Haiti and Bangladesh[103]. This in vivo study showed that the
cholera 45972 and transmissibility of the pathogen. Genetic analyses revealed that the less virulent strains of V. cholera e had mutations in ompU, which encodes the outer membrane porin and phage receptor. It is expected that
diphtheria 28468 general, many toxins produced by bacteria are encoded by phages in toxin-mediated diseases, such as diphtheria , cholera, dysentery, botulism, scarlet fever, and some food poisoning diseases[35]. However, not all
dysentery 28489 produced by bacteria are encoded by phages in toxin-mediated diseases, such as diphtheria, cholera, dysentery , botulism, scarlet fever, and some food poisoning diseases[35]. However, not all of these prophages
infectious disease 1570 virulence. Foremost among these treatments is phage therapy, which could be used to treat many bacterial infectious disease s and confront the pressing problem of antibiotic resistance in pathogenic bacteria. This review discusses
infectious disease 49652 molecular tools enable an accurate therapeutic approach.The golden age for medicine to treat bacterial infectious disease s has passed. Virulent phages, natural killers of bacteria, can fill the gap left by antibiotics. The
pneumonia 32159 phage-derived protein was suggested to lead to increased mortality in patients with an invasive S. pneumonia e infection, which may be explained by enhanced platelet activation[53]. In addition, a filamentous phage
pneumonia 32788 increased incidence of S. aureus-related acute otitis[55]. It was later discovered that the targeted S. pneumonia e normally out-competes S. aureus in the nasopharynx. Phages have a role in this clinical issue because
pneumonia 32927 aureus in the nasopharynx. Phages have a role in this clinical issue because the mechanism by which S. pneumonia e controlled S. aureus was through the production of hydrogen peroxide, a stress factor that induces
scarlet fever 28510 are encoded by phages in toxin-mediated diseases, such as diphtheria, cholera, dysentery, botulism, scarlet fever , and some food poisoning diseases[35]. However, not all of these prophages behave in a similar manner.
scarlet fever 31329 numerous prophages encode virulence factors, such as a pyrogenic exotoxin (responsible for the rash in scarlet fever and many of the symptoms of streptococcal toxic shock syndrome), an extracellular phospholipase (responsible
toxic shock syndrome 29700 with phages are the S. aureus SaPIs, which are implicated in the production of the toxin that causes toxic shock syndrome associated with menstrual tampon use, which caused the death of healthy young women in the early 1980s,
toxic shock syndrome 31385 pyrogenic exotoxin (responsible for the rash in scarlet fever and many of the symptoms of streptococcal toxic shock syndrome ), an extracellular phospholipase (responsible for the destabilization of membranes and cell lysis) and

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