Macrolides and Lincosamides

Canu, Annie; Leclercq, Roland

doi:10.1007/978-1-59745-180-2_18

Cited by 7 publications

(7 citation statements)

References 53 publications

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“…One of the mechanisms of resistance to clindamycin involves acquisition of an erm gene (erythromycin ribosome methylase) usually carried on plasmids or transposons in pathogenic bacteria ( 19 ). Comparison of antimicrobial resistance levels in strains isolated 30 years apart (1970s and 2000) showed that Gram-negative Bacteroides species have acquired an ermB gene that originated in Gram-positive bacteria— Clostridium perfringens , Streptococcus pneumoniae , and Enterococcus faecalis ( 32 ).…”

Section: Discussionmentioning

confidence: 99%

“…These included four different antibiotic classes with different modes of action, antimicrobial spectra, and pharmacokinetic properties—a lincosamide (clindamycin), a quinolone (ciprofloxacin), a tetracycline (minocycline), and a penicillin (amoxicillin). Lincosamides inhibit bacterial protein synthesis by binding to the 50S ribosomal subunit and hence ultimately inhibit microbial growth ( 19 ). The lincosamide clindamycin has a broad spectrum of antimicrobial activity, including Gram-positive aerobes and anaerobes, Gram-negative anaerobes, and selected protozoa and fungi ( 20 ).…”

Section: Introductionmentioning

confidence: 99%

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Same Exposure but Two Radically Different Responses to Antibiotics: Resilience of the Salivary Microbiome versus Long-Term Microbial Shifts in Feces

Zaura

Brandt

Mattos

et al. 2015

mBio

363

324

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Due to the spread of resistance, antibiotic exposure receives increasing attention. Ecological consequences for the different niches of individual microbiomes are, however, largely ignored. Here, we report the effects of widely used antibiotics (clindamycin, ciprofloxacin, amoxicillin, and minocycline) with different modes of action on the ecology of both the gut and the oral microbiomes in 66 healthy adults from the United Kingdom and Sweden in a two-center randomized placebo-controlled clinical trial. Feces and saliva were collected at baseline, immediately after exposure, and 1, 2, 4, and 12 months after administration of antibiotics or placebo. Sequences of 16S rRNA gene amplicons from all samples and metagenomic shotgun sequences from selected baseline and post-antibiotic-treatment sample pairs were analyzed. Additionally, metagenomic predictions based on 16S rRNA gene amplicon data were performed using PICRUSt. The salivary microbiome was found to be significantly more robust, whereas the antibiotics negatively affected the fecal microbiome: in particular, health-associated butyrate-producing species became strongly underrepresented. Additionally, exposure to different antibiotics enriched genes associated with antibiotic resistance. In conclusion, healthy individuals, exposed to a single antibiotic treatment, undergo considerable microbial shifts and enrichment in antibiotic resistance in their feces, while their salivary microbiome composition remains unexpectedly stable. The health-related consequences for the gut microbiome should increase the awareness of the individual risks involved with antibiotic use, especially in a (diseased) population with an already dysregulated microbiome. On the other hand, understanding the mechanisms behind the resilience of the oral microbiome toward ecological collapse might prove useful in combating microbial dysbiosis elsewhere in the body.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Same Exposure but Two Radically Different Responses to Antibiotics: Resilience of the Salivary Microbiome versus Long-Term Microbial Shifts in Feces

Zaura

Brandt

Mattos

et al. 2015

mBio

363

324

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“…To date, 34 erm alleles have been identified and all but two have been reported in Gram-positive pathogens [18]. The classes of erm genes, erm(A) , erm(B) and erm(C ) are the most widely distributed in Gram-positive pathogens (Table 1) [19]. Distinctions between each erm class are based on bacterial host range and the MLS B resistance phenotype that is conferred.…”

Section: Induction Of Antibiotic Resistance Mediated By Ribosome-assomentioning

confidence: 99%

“…Distinctions between each erm class are based on bacterial host range and the MLS B resistance phenotype that is conferred. Each erm is predominantly associated with, but not limited to, one or two genera [18,19,201]; erm(A) is often associated with Staphylococcus , but has been reported in four other Gram-positive genera including Streptococcus and Enterococcus [20,21]; erm(B) is the prevalent determinant of MLS B resistance in streptococci but has been observed in 17 additional Gram-positive genera [18,201]. The most widely disseminated and clinically important determinant of MLS B resistance in Gram-positive pathogens is erm(C) , which has been identified in at least 13 Gram-positive genera, and is the predominant determinant of MLS B resistance in staphylococci [18].…”

Section: Induction Of Antibiotic Resistance Mediated By Ribosome-assomentioning

confidence: 99%

Acquired Inducible Antimicrobial Resistance in Gram-Positive Bacteria

2012

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A major contributor to the emergence of antibiotic resistance in Gram-positive bacterial pathogens is the expansion of acquired, inducible genetic elements. Although acquired, inducible antibiotic resistance is not new, the interest in its molecular basis has been accelerated by the widening distribution and often ‘silent’ spread of the elements responsible, the diagnostic challenges of such resistance and the mounting limitations of available agents to treat Gram-positive infections. Acquired, inducible antibiotic resistance elements belong to the accessory genome of a species and are horizontally acquired by transformation/recombination or through the transfer of mobile DNA elements. The two key, but mechanistically very different, induction mechanisms are: ribosome-sensed induction, characteristic of the macrolide–lincosamide–streptogramin B antibiotics and tetracycline resistance, leading to ribosomal modifications or efflux pump activation; and resistance by cell surface-associated sensing of β-lactams (e.g., oxacillin), glycopeptides (e.g., vancomycin) and the polypeptide bacitracin, leading to drug inactivation or resistance due to cell wall alterations.

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“…PM infection is often treated with antimicrobial agents that are efficacious in the respiratory tract, including cephalosporins, macrolides and lincosamides. Macrolides and lincosamides have the same mechanism of action and can also be used for the treatment of Mycoplasma species, Brachyspira hyodysenteriae and Lawsonia intracellularis 8–11 . The intensive administration of antimicrobials also facilitates the development of resistance through three main mechanisms: modification of target binding site, enzymatic inactivation of antimicrobials, and active efflux of antimicrobials 8 .…”

Section: Introductionmentioning

confidence: 99%

Antimicrobial susceptibility, serotypes and genotypes of Pasteurella multocida isolates associated with swine pneumonia in Taiwan

Yeh

Chang

et al. 2017

Veterinary Record

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(PM) can cause progressive atrophic rhinitis and suppurative bronchopneumonia in pigs. The present study performed antimicrobial susceptibility testing and serotype and genotype identification on the 62 PM strains isolated from the lungs of diseased pigs with respiratory symptoms. Antimicrobial susceptibility testing examined 13 antimicrobial agents (amoxicillin, cefazolin, doxycycline, flumequine, enrofloxacin, florfenicol, kanamycin, lincomycin, Linco-Spectin (lincomycin and spectinomycin), erythromycin, tylosin, tilmicosin and tiamulin). Antimicrobial resistance ratios were over 40% in all of the antimicrobial agents except for cefazolin. The highest levels of resistance (100%) were found for kanamycin, erythromycin and tylosin. The majority of isolated strains was serotype D:L6 (n=35) followed by A:L3 (n=17). Comparison of the antimicrobial resistance levels between the two serotypes showed that the antimicrobial resistance rates were higher in D:L6 than in A:L3 for all the tested antimicrobials except for tylosin and tilmicosin. For PM with (B),(T) or (42), the results showed no significant difference compared with non-resistance gene strains in phenotype. Pulsed-field gel electrophoresis genotyping usingI restriction digestion of the genomic DNA demonstrated that there were 17 distinct clusters with a similarity of 85% or more, and the genotyping result was similar to that of serotyping. The results of the present study demonstrated that the PM isolated from diseased pigs in Taiwan was resistant to multiple antimicrobials, and the distribution of antimicrobial resistance was associated with pulsotype and serotype.

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Macrolides and Lincosamides

Cited by 7 publications

References 53 publications

Same Exposure but Two Radically Different Responses to Antibiotics: Resilience of the Salivary Microbiome versus Long-Term Microbial Shifts in Feces

Same Exposure but Two Radically Different Responses to Antibiotics: Resilience of the Salivary Microbiome versus Long-Term Microbial Shifts in Feces

Acquired Inducible Antimicrobial Resistance in Gram-Positive Bacteria

Antimicrobial susceptibility, serotypes and genotypes of Pasteurella multocida isolates associated with swine pneumonia in Taiwan

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