Propionibacterium acnes is developing gradual increase in resistance to oral tetracyclines

Nakase, Keisuke; Nakaminami, Hidemasa; Takenaka, Yuko; Hayashi, Nobuyuki; Kawashima, Makoto; Noguchi, Norihisa

doi:10.1099/jmm.0.000392

Cited by 23 publications

(18 citation statements)

References 19 publications

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“…Therefore, we need to analyze the complete sequence of pTZC1 in the other C. acnes isolates because pTZC1 has a possibility to differ in C. acnes strains. Until now, the decreased susceptibility of C. acnes to tetracyclines was caused by the acquisition of mutations in 16S rRNA and the S10 ribosomal protein, whereas an extrachromosomal resistance determinant has not been reported in C. acnes (17,18). Our findings strongly suggest that dissemination of the strains carrying pTZC1 will cause increased prevalence of C. acnes strains with decreased susceptibility to tetracyclines in the future.…”

Section: Discussionmentioning

confidence: 65%

Transferable Multidrug-Resistance Plasmid Carrying a Novel Macrolide-Clindamycin Resistance Gene, erm (50), in Cutibacterium acnes

Aoki

Nakase

Nakaminami

et al. 2020

Antimicrob Agents Chemother

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Antimicrobial-resistant Cutibacterium acnes strains have emerged and disseminated throughout the world. The 23S rRNA mutation and erm(X) gene are known as the major resistance determinants of macrolides and clindamycin in C. acnes. We isolated eight high-level macrolide-clindamycin-resistant C. acnes strains with no known resistance determinants, such as 23S rRNA mutation and erm(X), from different acne patients in 2008 between 2013 and 2015. The aim of this study was to identify the novel mechanisms of resistance in C. acnes. Whole-genome sequencing revealed the existence of a plasmid DNA, denoted pTZC1 (length, 31,440 bp), carrying the novel macrolide-clindamycin resistance gene erm(50) and tetracycline resistance gene tet(W). pTZC1 was detected in all C. acnes isolates (eight strains) exhibiting high-level macrolide-clindamycin resistance, with no known resistance determinants (MIC of clarithromycin, ≥256 μg/ml; clindamycin, ≥256 μg/ml). Transconjugation experiments demonstrated that the pTZC1 was horizontally transferred among C. acnes strains and conferred resistance to macrolides, clindamycin, and tetracyclines. Our data showed, for the first time, the existence of a transferable multidrug-resistant plasmid in C. acnes. Increased prevalence of this plasmid will be a great threat to antimicrobial therapy for acne vulgaris.

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Section: Discussionmentioning

confidence: 65%

Transferable Multidrug-Resistance Plasmid Carrying a Novel Macrolide-Clindamycin Resistance Gene, erm (50), in Cutibacterium acnes

Aoki

Nakase

Nakaminami

et al. 2020

Antimicrob Agents Chemother

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“…Tetracycline resistance is associated with chromosomal point mutation in the 16s rRNA gene of C. acnes [69]. C. acnes becomes less susceptible to doxycycline when amino acid is substituted in the ribosomal S10 protein [131].…”

Section: Acne Treatment and Skin Microbesmentioning

confidence: 99%

Potential Role of the Microbiome in Acne: A Comprehensive Review

Lee

Byun

Kim

2019

JCM

199

195

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Acne is a highly prevalent inflammatory skin condition involving sebaceous sties. Although it clearly develops from an interplay of multiple factors, the exact cause of acne remains elusive. It is increasingly believed that the interaction between skin microbes and host immunity plays an important role in this disease, with perturbed microbial composition and activity found in acne patients. Cutibacterium acnes (C. acnes; formerly called Propionibacterium acnes) is commonly found in sebum-rich areas and its over-proliferation has long been thought to contribute to the disease. However, information provided by advanced metagenomic sequencing has indicated that the cutaneous microbiota in acne patients and acne-free individuals differ at the virulent-specific lineage level. Acne also has close connections with the gastrointestinal tract, and many argue that the gut microbiota could be involved in the pathogenic process of acne. The emotions of stress (e.g., depression and anxiety), for instance, have been hypothesized to aggravate acne by altering the gut microbiota and increasing intestinal permeability, potentially contributing to skin inflammation. Over the years, an expanding body of research has highlighted the presence of a gut–brain–skin axis that connects gut microbes, oral probiotics, and diet, currently an area of intense scrutiny, to acne severity. This review concentrates on the skin and gut microbes in acne, the role that the gut–brain–skin axis plays in the immunobiology of acne, and newly emerging microbiome-based therapies that can be applied to treat acne.

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“…Unfortunately, resistance to these antibiotics is beginning to emerge. 56 However, recent work has demonstrated that natural products from Staphylococcus epidermidis , such as succinic acid, can effectively inhibit the growth of P. acnes . 56 Gaining a better understanding of the molecular mechanism by which products like succinic acid inhibit P. acnes growth may provide the basis of naturally based small molecules that more effectively target this organism and prevent infection from occurring.…”

Section: Precision Treatment For Skin Infectionsmentioning

confidence: 99%

Precision antimicrobial therapeutics: the path of least resistance?

Spaulding

Klein

Schreiber

et al. 2018

npj Biofilms Microbiomes

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The emergence of drug-resistant pathogens has led to a decline in the efficacy of traditional antimicrobial therapy. The rise in resistance has been driven by widespread use, and in some cases misuse, of antibacterial agents in treating a variety of infections. A growing body of research has begun to elucidate the harmful effects of broad-spectrum antibiotic therapy on the beneficial host microbiota. To combat these threats, increasing effort is being directed toward the development of precision antimicrobial therapeutics that target key virulence determinants of specific pathogens while leaving the remainder of the host microbiota undisturbed. This includes the recent development of small molecules termed “mannosides” that specifically target uropathogenic E. coli (UPEC). Mannosides are glycomimetics of the natural mannosylated host receptor for type 1 pili, extracellular appendages that promotes UPEC colonization in the intestine. Type 1 pili are also critical for colonization and infection in the bladder. In both cases, mannosides act as molecular decoys which potently prevent bacteria from binding to host tissues. In mice, oral treatment with mannosides simultaneously clears active bladder infection and removes intestinal UPEC while leaving the gut microbiota structure relatively unchanged. Similar treatment strategies successfully target other pathogens, like adherent-invasive E. coli (AIEC), an organism associated with Crohn’s disease (CD), in mouse models. While not without its challenges, antibiotic-sparing therapeutic approaches hold great promise in a variety of disease systems, including UTI, CD, otitis media (OM), and others. In this perspective we highlight the benefits, progress, and roadblocks to the development of precision antimicrobial therapeutics.

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Propionibacterium acnes is developing gradual increase in resistance to oral tetracyclines

Cited by 23 publications

References 19 publications

Transferable Multidrug-Resistance Plasmid Carrying a Novel Macrolide-Clindamycin Resistance Gene, erm (50), in Cutibacterium acnes

Transferable Multidrug-Resistance Plasmid Carrying a Novel Macrolide-Clindamycin Resistance Gene, erm (50), in Cutibacterium acnes

Potential Role of the Microbiome in Acne: A Comprehensive Review

Precision antimicrobial therapeutics: the path of least resistance?

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