Recent publications
Classical Zn²⁺-dependent deac(et)ylases play fundamental regulatory roles in life and are well characterized in eukaryotes regarding their structures, substrates and physiological roles. In bacteria, however, classical deacylases are less well understood. We construct a Generalized Profile (GP) and identify thousands of uncharacterized classical deacylases in bacteria, which are grouped into five clusters. Systematic structural and functional characterization of representative enzymes from each cluster reveal high functional diversity, including polyamine deacylases and protein deacylases with various acyl-chain type preferences. These data are supported by multiple crystal structures of enzymes from different clusters. Through this extensive analysis, we define the structural requirements of substrate selectivity, and discovered bacterial de-d-/l-lactylases and long-chain deacylases. Importantly, bacterial deacylases are inhibited by archetypal HDAC inhibitors, as supported by co-crystal structures with the inhibitors SAHA and TSA, and setting the ground for drug repurposing strategies to fight bacterial infections. Thus, we provide a systematic structure-function analysis of classical deacylases in bacteria and reveal the basis of substrate specificity, acyl-chain preference and inhibition.
An over‐the‐counter product berberine (a major alkaloid in goldenseal) is a substrate of the uptake transporter OCT1 and the metabolizing enzyme CYP2D6. The two genes exhibit common functional polymorphisms. Approximately 9% of Europeans and white Americans are either poor CYP2D6 metabolizers or poor OCT1 transporters. In this study, we investigated the effects of OCT1 and CYP2D6 polymorphisms on berberine pharmacokinetics in humans. We confirmed in vitro that berberine is an OCT1 substrate ( K M of 7.0 μM, CL int of 306 ± 29 μL/min/mg). Common OCT1 alleles *3 to *6 showed uptake reduced by at least 65% and Oct1/2 knockout mice showed 3.2‐fold higher AUCs in liver perfusion experiments. However, in humans, poor OCT1 transporters did not show any differences in berberine pharmacokinetics compared with reference participants. In contrast, CYP2D6 polymorphisms significantly affected berberine metabolism, but exclusively in females. Females who were poor CYP2D6 metabolizers had an 80% lower M1‐to‐berberine ratio. General linear model analyses suggest strong synergistic, rather than additive, effects between female sex and CYP2D6 genotype. Overall, berberine displayed low oral bioavailability, yet females had a 2.8‐fold higher AUC and a 3.6‐fold higher C max than males ( P < 0.001). These effects were only partially attributable to the sex‐ CYP2D6 genotype interaction. In conclusion, despite berberine being an OCT1 substrate, OCT1 deficiency did not affect berberine pharmacokinetics in humans. In contrast, CYP2D6 emerges as a critical enzyme for berberine metabolism in females, but not in males, highlighting sex‐specific differences. We suggest that factors beyond CYP2D6 metabolism are determining berberine's systemic exposure, especially in males (NCT05463003).
Objectives: Previous research has shown that living alone and being quarantined during the COVID-19 pandemic were associated with poorer mental health and well-being. The aim of this study was to examine whether self-compassion buffered these adverse effects. Methods: 435 German adults were surveyed in three waves over six weeks. In all three waves, participants were asked whether they lived alone and whether they were quarantined. Self-compassion, mental health, and well-being were also assessed in all three waves. Results: In linear structural equation models adjusted for age, gender, and the respective outcome measure at T1, higher self-compassion at T2 was associated with better mental health and well-being at T3. However, there was no evidence that living alone and quarantine at T1 were associated with mental health and well-being at T3, or that self-compassion moderated these effects. Conclusions: Our study spanned six weeks, and one possible explanation for our nonsignificant findings is that the mental health effects of living alone, quarantine, and self-compassion are rather short-lived. In addition, individuals living alone and individuals in quarantine may not necessarily have been socially isolated or felt lonely, which may explain why no associations with mental health were found.
Key Clinical Message
Not only germline but also postzygotic mutations in the RASA1 or EPHB4 genes can lead to capillary malformation‐arteriovenous malformation (CM‐AVM) syndrome. As it is not always possible to clinically distinguish between constitutional variants and postzygotic mosaicism, a sufficiently high sequencing depth must be used in genetic diagnostics to detect both.
Abstract
Capillary malformation‐arteriovenous malformation (CM‐AVM) syndrome, with or without Parkes Weber syndrome, is a rare autosomal dominant disease caused by pathogenic RASA1 or EPHB4 variants. Up to 80% of CM‐AVM cases have an affected parent. Gene panel sequencing was performed for a 4‐year‐old girl with multiple CMs, two capillary stains on the left leg, and associated overgrowth of the second toe. We also reviewed published cases with mosaic RASA1 and EPHB4 mutations. A mosaic RASA1 loss‐of‐function mutation was detected with a variant allele frequency (VAF) of 20% in the blood and oral epithelial cells of the index patient. The literature review illustrates that the severity of the clinical phenotype does not correlate with the VAF. We also identified a germline nonsense variant in the patient's TEK gene. However, inactivating TEK variants do not cause a vascular phenotype but can confer an increased risk for primary congenital glaucoma with variable expressivity. The case presented here illustrates that the choice of the sequencing depth of a diagnostic next‐generation sequencing test for CM‐AVM patients should always take mosaicism into account and that a good knowledge of the sequenced genes and associated disease mechanisms is necessary for adequate genetic counseling.
Aromatic monomers obtained by selective depolymerization of the lignin β‐O‐4 motif are typically phenolic and contain (oxygenated) alkyl substitutions. This work reveals the potential of a one‐pot catalytic lignin β‐O‐4 depolymerization cascade strategy that yields a uniform set of methoxylated aromatics without alkyl side‐chains. This cascade consists of the selective acceptorless dehydrogenation of the γ‐hydroxy group, a subsequent retro‐aldol reaction that cleaves the Cα−Cβ bond, followed by in situ acceptorless decarbonylation of the formed aldehydes. This three‐step cascade reaction, catalyzed by an iridium(I)‐BINAP complex, resulted in 75 % selectivity for 1,2‐dimethoxybenzene from G‐type lignin dimers, alongside syngas (CO : H2≈1.4 : 1). Applying this method to a synthetic G‐type polymer, 11 wt % 1,2‐dimethoxybenzene was obtained. This versatile compound can be easily transformed into 3,4‐dimethoxyphenol, a valuable precursor for pharmaceutical synthesis, through an enzymatic catalytic approach. Moreover, the hydrodeoxygenation potential of 1,2‐dimethoxybenzene offers a pathway to produce valuable cyclohexane or benzene derivatives, presenting enticing opportunities for sustainable chemical transformations without the necessity for phenolic mixture upgrading via dealkylation.
Polyethylene (PE) is the most commonly used plastic type in the world, contributing significantly to the plastic waste crisis. Microbial degradation of PE in natural environments is unlikely due to its inert saturated carbon‐carbon backbones, which are difficult to break down by enzymes, challenging the development of a biocatalytic recycling method for PE waste. Here, we demonstrated the depolymerization of low‐molecular‐weight (LMW) PE using an enzyme cascade that included a catalase‐peroxidase, an alcohol dehydrogenase, a Baeyer Villiger monooxygenase, and a lipase after the polymer was chemically pretreated with m‐chloroperoxybenzoic acid (mCPBA) and ultrasonication. In a preparative experiment with gram‐scale pretreated polymers, GC‐MS and weight loss determinations confirmed ~27 % polymer conversion including the formation of medium‐size functionalized molecules such as ω‐hydroxycarboxylic acids and α,ω‐carboxylic acids. Additional analyses of LMWPE‐nanoparticles using AFM showed that enzymatic depolymerization reduced the sizes of these mCPBA‐ and enzyme‐treated LMWPE‐nanoparticles. This multi‐enzyme catalytic concept with distinct chemical steps represents a unique starting point for future development of bio‐based recycling methods for polyolefin waste.
Two-percent glutaraldehyde has sufficient bactericidal and yeasticidal activity in 3 min, mycobactericidal activity in 10 min and fungicidal activity in 30 min. The antimicrobial activity of glutaraldehyde is explained by protein coagulation and inhibition of macromolecular synthesis. Cell wall and membrane modifications are cellular defence mechanisms. Glutaraldehyde can significantly reduce biofilm formation in P. aeruginosa and has low to moderate biofilm removal rates (2%–82%). Biofilm fixation by glutaraldehyde is usually strong (62%–97%). Susceptibility to glutaraldehyde is not significantly altered by exposure of E. coli, Salmonella spp. and P. aeruginosa to subinhibitory concentrations. Cross-tolerance to other aldehydes may occur in E. coli, Halomonas spp. and B. cepacia. Hydrogen peroxide has the ability to induce a function that reduces the killing effect of aldehydes in E. coli. Few isolates of M. chelonae from endoscope washer-disinfectors were resistant to glutaraldehyde in suspension and carrier tests and also caused endoscope-associated pseudo-outbreaks. Very few M. gordonae isolates were insufficiently reduced by 2.5% glutaraldehyde in 10 min in suspension tests. Very few P. aeruginosa isolates were resistant to glutaraldehyde in suspension tests and caused an endoscope-associated pseudo-outbreak. The overall probability of resistance to glutaraldehyde of practical relevance is very low for most species in the absence of biofilm, with mainly M. chelonae having a higher probability of resistance.
Peracetic acid has bactericidal activity (1.6%, 3–5 min), yeasticidal activity (0.25%, 1 min) and tuberculocidal activity (0.25% in 1 min). However, some food-associated fungi and Mycobacterium spp. are not sufficiently killed under these conditions. The antimicrobial activity of peracetic acid is explained by non-specific oxidation and disruption of cell wall permeability. No specific cellular defence mechanisms against peracetic acid have been described. Peracetic acid partially inhibits or even prevents biofilm formation. Biofilm removal is poor to moderate (0%–63%). Biofilm fixation by peracetic acid ranges from 0% to 54%. High MIC values have been reported for some meat-borne L. monocytogenes isolates, their relevance is uncertain. Low-level exposure does not alter the susceptibility of C. sakazakii, L. monocytogenes, S. enterica and Y. enterocolitica. Virulence genes may be induced (S. aureus) or reduced (L. monocytogenes). S. Typhimurium survivors of low-level exposure may be viable but not culturable. Peracetic acid can convert various beta-lactam antibiotics in wastewater, thereby reducing selection pressure. No peracetic acid-resistant isolates have been described with insufficient efficacy in suspension tests or tests under practical conditions at use concentrations, or with a contamination of disinfectants. The overall probability of resistance to peracetic acid of practical relevance is very low in the absence of biofilm.
Hydrogen peroxide has bactericidal (0.3%, 30 min) and yeasticidal (3%, 10 min) activity against most species, but an inconsistent fungicidal and mycobactericidal activity. Its antimicrobial activity is explained by oxidation of cellular components and damage to the cytoplasmatic membrane. Peroxidases and catalases, encoded by various genes, are important cellular defence mechanisms. Hydrogen peroxide can increase or decrease biofilm formation, depending on the species and the concentration of hydrogen peroxide. Biofilm removal is moderate in most studies (10%–89%). Its biofilm-fixing potential is unknown. High MIC values have been reported for meat-borne L. monocytogenes and clinical A. baumannii isolates, but their relevance is uncertain. Low-level exposure does not significantly alter the susceptibility of most species, but may increase catalase activity and cause cross-tolerance to aldehydes and hypochlorous acid. Only one Acinetobacter spp. spacecraft isolate with hydrogen peroxide resistance has been described (insufficient efficacy in suspension tests), but no resistant isolates have been found that failed the requirements of tests under practical conditions, or with a contamination of disinfectants. The overall probability of resistance to hydrogen peroxide of practical relevance is very low in the absence of biofilm.
Instrument disinfectants can be based on different types of biocidal active substances such as benzalkonium chloride, DDAC, glutaraldehyde, hydrogen peroxide, peracetic acid and sodium hypochlorite. Validated reprocessing of non-critical and semi-critical medical devices is expected to provide a health benefit to patients. A low adaptive response combined with a frequently observed inhibition of biofilm formation and removal of existing biofilm cannot be attributed to any of the biocidal active substances. Overall, the use of peracetic acid on surfaces of instruments where biofilm formation is to be inhibited (e.g. flexible endoscopes) seems to be the most appropriate option due to the low selection pressure, mainly inhibition of biofilm formation and mainly moderate removal of biofilm. Hydrogen peroxide and sodium hypochlorite also have a low selection pressure and can moderately remove biofilm, but they could also increase biofilm formation in a relevant number of species. They appear to be suitable for use on instrument surfaces where the enhancement of biofilm formation is of minor importance. Benzalkonium chloride seems to be the least suitable biocidal active substance, taking into account the often observed strong and stable adaptive response, the cross-tolerance with some other biocidal active substances and the inconclusive effect on biofilm formation and removal.
Wound and mucosal antiseptics can be based on chlorhexidine digluconate, polyhexanide, hydrogen peroxide, sodium hypochlorite, povidone iodine or octenidine dihydrochloride. Silver can also be used as an antimicrobial agent in wound treatment, for example, in wound dressings. A health benefit can be expected at least in patients with infected or critically colonised wounds. Povidone iodine has been shown to have a low adaptive response, an inconsistent effect on biofilm formation and a moderate or strong removal of existing biofilm. Sodium hypochlorite and hydrogen peroxide also showed a low adaptive response, but may enhance biofilm formation and have mostly a moderate ability to remove biofilm. Limited data with octenidine dihydrochloride shows an inconsistent picture. Polyhexanide can show a strong adaptive response, mainly in Gram-positive species. Its ability to remove biofilm is mostly moderate. Chlorhexidine digluconate and silver can both often show a strong adaptive response, mainly in Gram-negative species. Silver can moderately inhibit biofilm formation, whereas the effect of chlorhexidine digluconate is lower. For biofilm removal, silver usually has a moderate effect, whereas the effect of chlorhexidine digluconate is usually poor or moderate. Overall, povidone iodine seems to have the lowest selection pressure and chlorhexidine digluconate the highest.
Polihexanide (PHMB) is mostly bactericidal at 0.016–0.02% (1 h) and yeasticidal at 0.1% (5 min). Fungicidal and mycobactericidal activity is species dependent. Its antimicrobial activity is explained by membrane damage. Cellular defence mechanisms include biodegradation of PHMB in A. westerdijkiae, Sphingomonas spp. and Azospirillum spp., tolerance genes in S. cerevisiae and E. coli and point mutation in P. lilacinum. PHMB reduces biofilm mass in developing and existing biofilms in several species. The effect of PHMB on biofilm fixation is unknown. High MIC values indicating tolerance to PHMB have been reported for isolates of P. lilacinum (50,000 mg/l). Low-level exposure results in no MIC change in 32 species, a weak MIC change in 18 species and a strong MIC change in 6 species, which are only stable in E. faecalis and S. aureus, resulting in MIC values as high as 31.3 mg/l (E. faecalis) and 23.5 mg/l (S. aureus). Cross-tolerance to other biocidal agents has not been reported. Cross-resistance to gentamicin has been reported in E. coli. PHMB-resistant isolates have been described in an outbreak of keratitis (Fusarium spp.) and with contaminated disinfectants (P. lilacinum). The overall probability of resistance to PHMB of practical relevance is low in the absence of biofilm.
Antimicrobial soaps are usually based on chlorhexidine digluconate, povidone iodine, triclosan, benzalkonium chloride, DDAC, octenidine dihydrochloride, polyhexanide or sodium hypochlorite. Evidence of a health benefit is inconsistent. Routine antiseptic body washing of ICU patients appears to prevent catheter-associated bloodstream infections, and bundles including antiseptic body washes on MRSA carriers may reduce transmission or infection. Benzalkonium chloride, triclosan, chlorhexidine digluconate and DDAC can cause a large and stable MIC increase, mainly in Gram-negative bacteria. Cross-tolerance between benzalkonium chloride, triclosan and chlorhexidine digluconate is common. Horizontal gene transfer can be induced by chlorhexidine digluconate, polihexanide and triclosan in E. coli. Efflux pump genes may be upregulated in some species by benzalkonium chloride, chlorhexidine digluconate, triclosan and octenidine dihydrochloride. Some risks may be potentially serious for the development of antibiotic resistance. The least adaptive reaction is seen with povidone iodine, sodium hypochlorite and octenidine dihydrochloride. The use of antimicrobial soaps should be restricted to applications where there is an expected health benefit and should not be used for routine hand washing at home, for surgical scrubbing (preference for alcohol-based hand rubs without selection pressure) and for hygienic hand washing (preference for plain soap).
Sodium hypochlorite has bactericidal (5000 mg/l, 30 min) and yeasticidal (1000 mg/l, 5 min) activity. Tuberculocidal activity was reported at 1000 mg/l available chlorine in 10 min. The antimicrobial effect of sodium hypochlorite is explained by damage to cellular components and disruption of cell membranes. Cell defence occurs through energy conservation, biofilm formation and the VBNC state. Sodium hypochlorite at 1–5 mg/l mostly increases biofilm mass, whereas 100–5050 mg/l sodium hypochlorite decreases biofilm formation in most species. Moderate removal of biofilm occurs in young biofilms (mostly 21%–87%), less removal is found in mature biofilms. Elevated MIC values indicating tolerance to sodium hypochlorite have been reported in some clinical isolates, but their relevance is uncertain. In bacterial species, there is little or no increase in MIC (≤4-fold) after low-level exposure. Sodium hypochlorite-resistant isolates have been reported for Methylobacterium spp. and R. erythropolis, with insufficient bactericidal activity in suspension tests compared to culture collection strains. No cross-resistance to antibiotics has been reported for S. aureus, but in selected strains of Salmonella spp. Cross-tolerance may be seen to benzalkonium chloride, another quaternary ammonium compound, and alkylamine (L. monocytogenes) or sodium nitrite and hydrogen peroxide (E. coli). The overall probability of resistance to sodium hypochlorite of practical relevance is very low in the absence of biofilm.
Octenidine dihydrochloride (OCT), usually in combination with 2% phenoxyethanol, is bactericidal (1 min) and yeasticidal (30 s–2 min) at 0.1%. Its mycobactericidal activity is unknown. Its antimicrobial activity is explained by membrane disruption and alteration of cellular structural integrity. Cellular defence mechanisms include efflux pumps in A. baumannii and P. aeruginosa. OCT reduces biofilm mass in developing and existing biofilms in several species. The effect of OCT on biofilm fixation is unknown. High MIC values indicating tolerance to OCT have been reported for isolates of S. salivarius (800 mg/l) and S. mutans (120 mg/l). Low-level exposure results in no MIC change in three species, a weak MIC change in six species and a strong and stable MIC change in P. aeruginosa, resulting in an MIC value as high as 128 mg/l. Cross-tolerance to chlorhexidine may occur in P. aeruginosa. Cross-resistance to selected antibiotics may also occur. OCT-resistant isolates have been described in an outbreak of B. cepacia complex infections or colonisations in intensive care patients caused by a contaminated commercial mouthwash (0.1% OCT). A recall of a commercial mouthwash contaminated with B. cepacia complex has also been reported. The overall probability of resistance to OCT of practical relevance is low in the absence of biofilm.
Propan-2-ol has sufficient bactericidal activity at 70% in 15 s, yeasticidal activity at 50% in 5 min, incomplete fungicidal activity at 70% in 10 min and tuberculocidal activity at 60% in 5 min. The antimicrobial effect of propan-2-ol is explained by the non-specific denaturation of proteins and deformation of membranes. No specific cellular defence mechanisms against propan-2-ol have been described. Propan-2-ol between 40% and 95% can significantly increase biofilm formation in S. aureus and S. epidermidis. The effect of propan-2-ol on biofilm fixation is unknown. Biofilm removal by 70% propan-2-ol is very low at 0% for P. aeruginosa and S. aureus. E. faecium isolates with a relative tolerance to 23% propan-2-ol have been described. Exposure to 1–6% propan-2-ol can increase biofilm formation in S. aureus, and 2.5% propan-2-ol can increase surface attachment in L. monocytogenes. Biofilm development of C. albicans can be inhibited by 2% propan-2-ol. Susceptibility to propan-2-ol can be significantly reduced by exposing E. coli to sublethal concentrations. No propan-2-ol-resistant isolates have been described with an insufficient efficacy in suspension tests or tests under practical conditions compared to culture collection strains or with a contamination of disinfectants. The overall probability of resistance to propan-2-ol of practical relevance is very low in the absence of biofilm.
For biocides and disinfectants, terms such as “resistance”, “tolerance”, “decreased susceptibility”, “reduced susceptibility”, “insusceptibility” and “acquired reduced susceptibility” are used. On the basis of a recent proposal, isolates with increased MIC values compared to reference strains of the same species and isolates that are insufficiently killed by concentrations of a disinfectant solution below those for use (suspension tests or tests under practical conditions) are considered to be tolerant. Isolates are considered to be resistant if they are able to survive or multiply in a disinfectant solution, with or without direct evidence of infection as a result of the contamination, and if they are insufficiently killed by use concentrations of a disinfectant solution in suspension tests or in a test under practical conditions compared to culture collection strains of the same species or strains from efficacy standards (e.g. European norms). European standards exist among others for the determination of bactericidal, fungicidal and mycobactericidal activity. They also define minimum efficacy requirements using culture collection strains.
Triclosan at 1% is mostly bactericidal (3 min) and yeasticidal (1 min). Mycobactericidal activity is unknown. The antimicrobial effect of triclosan is explained by blocking the enoyl acyl carrier protein reductase and by affecting several cellular processes. Efflux pumps, membrane and gene expression changes, and the use of triclosan as the sole carbon source are cellular defence mechanisms. Biofilm formation was reduced in S. aureus, S. enteritidis, S. mutans, and A. fumigatus, but not in P. aeruginosa and mixed biofilms. No relevant biofilm reduction was reported with 1–30 mg/l triclosan in A. naeslundii, S. oralis, and S. gordonii (1 h exposure), but a significant reduction with 1000–3000 mg/l triclosan in L. innocua, L. monocytogenes, L. welshimeri, and P. acnes (18–24 h exposure). Elevated MICs have been reported in many species, but their relevance is uncertain. Low-level exposure results in no MIC change in 33 species, a weak MIC change in 27 species, and a strong MIC change in 33 species (13 of which are stable), resulting in MIC values as high as 8000 mg/l (E. coli) or 3000 mg/l (Salmonella spp.). Cross-tolerance to chlorhexidine, benzalkonium chloride, hexachlorophene, and selected antibiotics may occur in many species. Horizontal gene transfer can be induced in E. coli. P. aeruginosa and S. marcescens isolates have been isolated in liquid soaps causing infections. K. oxytoca, S. liquefaciens, S. sonnei, E. gergoviae, S. odorifera, and E. cloacae have been detected in liquid soaps (0.15%–0.65% triclosan). The overall probability of resistance to triclosan of practical relevance is low to moderate in the absence of biofilm.
Surface disinfectants can be based on different types of biocidal active substances such as benzalkonium chloride, DDAC, glutaraldehyde, alcohols, hydrogen peroxide, silver (mostly in combination with hydrogen peroxide), peracetic acid and sodium hypochlorite. A health benefit was reported only in outbreak situations or in special care units for products based on different types of biocidal agents, but not for routine use on hospital floors, surfaces in patient rooms or wards. A low adaptive response combined with mostly an inhibition of biofilm formation and removal of existing biofilm cannot be attributed to any of the biocidal active substances. Overall, on surfaces where biofilm formation should be inhibited, the use of peracetic acid seems to be the most appropriate option (low selection pressure, mainly inhibition of biofilm formation, mainly moderate removal of biofilm). Hydrogen peroxide and sodium hypochlorite also have a low selection pressure and can moderately remove biofilm, but they increased biofilm formation in a relevant number of species. They seem to be suitable for surfaces where the enhancement of biofilm formation is of minor importance. Benzalkonium chloride seems to be the least suitable biocidal active substance, taking into account the often observed strong and stable adaptive response, the cross-tolerance with other biocidal active substances and the inconclusive effect on biofilm formation and removal.
Chlorhexidine digluconate (CHG) is bactericidal at 2–4% (5 min) except Enterococcus spp., S. epidermidis, MRSA and P. stuartii and yeasticidal at 2% (5 min). General mycobactericidal activity is not expected. Its antimicrobial activity is explained by cell adsorption resulting in precipitation of bacterial cytoplasm. Cellular defence mechanisms include resistance genes, cell membrane alterations, efflux pumps and plasmids. CHG reduces biofilm mass in developing and existing biofilms mostly poorly or moderately in several species. The effect of CHG on biofilm fixation is unknown. High MIC values indicating tolerance to CHG have been reported for isolates of B. subtilis, E. faecalis, K. pneumoniae and Proteus spp. (10,000 mg/l). Low-level exposure results in no MIC change in 53 species, a weak MIC change in 56 species and a strong MIC change in 43 species, which are stable in nine species, resulting in MIC values as high as 2048 mg/l (S. marcescens) and 1024 mg/l (P. aeruginosa). Low-level exposure can upregulate efflux pump genes, mostly increase biofilm formation and induce horizontal gene transfer (E. coli). Cross-tolerance to triclosan, benzalkonium chloride, hydrogen peroxide and selected antibiotics may occur. CHG-resistant isolates have been described in outbreaks and pseudo-outbreaks (A. xylosoxidans, B. cepacia, P. mirabilis, P. pickettii, MRSA, S. epidermidis, S. haemolyticus, S. marscescens) and with contaminated disinfectants (11 Gram-negative species). The overall probability of resistance to CHG of practical relevance is low to moderate in the absence of biofilm.
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Greifswald, Germany
Head of institution
Prof. Hannelore Weber