scholarly journals Profiles of Non-aureus staphylococci in retail pork and slaughterhouse carcasses: prevalence, antimicrobial resistance, and genetic determinant of fusidic acid resistance

2022 ◽  
Author(s):  
Yu Jin Yang ◽  
Gi Yong Lee ◽  
Sun Do Kim ◽  
Ji Heon Park ◽  
Soo In Lee ◽  
...  
Keyword(s):  
Antimicrobial Resistance ◽  
Fusidic Acid ◽  
Acid Resistance ◽  
Genetic Determinant

scholarly journals Frequent Emergence of Resistance in Clostridium difficile during Treatment of C. difficile-Associated Diarrhea with Fusidic Acid

2006 ◽  
Vol 50 (9) ◽  
pp. 3028-3032 ◽  
Author(s):  
T. Norén ◽  
M. Wullt ◽  
Thomas Åkerlund ◽  
E. Bäck ◽  
I. Odenholt ◽  
...  
Keyword(s):  
Clostridium Difficile ◽  
Treatment Failure ◽  
Fusidic Acid ◽  
Negative Impact ◽  
Acid Resistance ◽  
Clinical Recurrence ◽  
Acid Therapy ◽  
Emergence Of Resistance ◽  
Culture Positive

ABSTRACT Samples from patients with Clostridium difficile-associated diarrhea (CDAD) that were randomized to fusidic acid (n = 59) or metronidazole (n = 55) therapy for 7 days were cultured for Clostridium difficile in feces on days 1, 8 to 13, and 35 to 40. Of the patients who were culture positive only before treatment, 77% (36/47) were permanently cured (no treatment failure and no clinical recurrence), compared to 54% (22/41) of those with persistence of C. difficile at one or both follow-ups (P = 0.03). A similar association between bacterial persistence and a worse outcome of therapy was seen in both treatment groups. Resistance to fusidic acid was found in 1 of 88 pretherapy isolates available, plus in at least 1 subsequent isolate from 55% (11/20) of patients who remained culture-positive after fusidic acid therapy. In 10 of these 11 patients, the resistant follow-up isolate(s) belonged to the same PCR ribotype as the susceptible day 1 isolate, confirming frequent emergence of resistance to fusidic acid during treatment. Despite this, 5 of these 11 patients were permanently cured with fusidic acid, relative to 5 of 9 patients with susceptible C. difficile at follow-up (P = 1.0). None of the 36 PCR ribotypes of C. difficile identified was associated with any particular clinical outcome or emergence of fusidic acid resistance. In conclusion, culture positivity for C. difficile was common after both fusidic acid and metronidazole therapy and was associated with treatment failure or recurrence of CDAD. Development of resistance in C. difficile was frequent in patients given fusidic acid, but it was without apparent negative impact on therapeutic efficacy in the actual CDAD episode.

scholarly journals Fusidic acid resistance in Staphylococcus aureus nasal carriage strains in nine European countries

2014 ◽  
Vol 9 (6) ◽  
pp. 737-745 ◽  
Author(s):  
Casper DJ den Heijer ◽  
Evelien ME van Bijnen ◽  
W John Paget ◽  
Ellen E Stobberingh
Keyword(s):  
Staphylococcus Aureus ◽  
Fusidic Acid ◽  
Acid Resistance ◽  
Nasal Carriage ◽  
European Countries

scholarly journals Mutations in fusA Associated with Posttherapy Fusidic Acid Resistance in Clostridium difficile

2007 ◽  
Vol 51 (5) ◽  
pp. 1840-1843 ◽  
Author(s):  
T. Norén ◽  
T. Åkerlund ◽  
M. Wullt ◽  
L. G. Burman ◽  
M. Unemo
Keyword(s):  
Staphylococcus Aureus ◽  
Clostridium Difficile ◽  
Fusidic Acid ◽  
In Silico ◽  
Acid Resistance ◽  
Nonsynonymous Substitutions ◽  
Resistant Mutants

ABSTRACT In silico, we identified fusA (2,067 bp) in Clostridium difficile 630. Sequencing of fusA in posttherapy fusidic acid-resistant C. difficile isolates from 12 patients with C. difficile-associated diarrhea (CDAD) identified fusA mutations, one or two nonsynonymous substitutions, or in one case a deletion of one codon associated with resistance. Five of these mutations have previously been described in fusA of fusidic acid-resistant Staphylococcus aureus, but seven were novel fusA mutations. Fusidic acid monotherapy for CDAD seemed to rapidly select conserved resistant mutants.

Molecular analysis of fusidic acid resistance in Staphylococcus aureus

2003 ◽  
Vol 47 (2) ◽  
pp. 463-469 ◽  
Author(s):  
Silke Besier ◽  
Albrecht Ludwig ◽  
Volker Brade ◽  
Thomas A. Wichelhaus
Keyword(s):  
Staphylococcus Aureus ◽  
Molecular Analysis ◽  
Fusidic Acid ◽  
Acid Resistance

Fusidic Acid Resistance in Staphylococcus aureus Strains in an Interval of Ten Years (2001-2011)

2012 ◽  
Vol 32 (6) ◽  
pp. 1668-1672 ◽  
Author(s):  
Şebnem NERGİZ ◽  
Selahattin ATMACA ◽  
Tuncer ÖZEKİNCİ ◽  
Alicem TEKİN
Keyword(s):  
Staphylococcus Aureus ◽  
Fusidic Acid ◽  
Acid Resistance

scholarly journals A target-protection mechanism of antibiotic resistance at atomic resolution: insights into FusB-type fusidic acid resistance

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Jennifer H. Tomlinson ◽  
Gary S. Thompson ◽  
Arnout P. Kalverda ◽  
Anastasia Zhuravleva ◽  
Alex J. O’Neill
Keyword(s):  
Antibiotic Resistance ◽  
Fusidic Acid ◽  
Acid Resistance ◽  
Atomic Resolution ◽  
Protection Mechanism

scholarly journals Compensatory Adaptation to the Loss of Biological Fitness Associated with Acquisition of Fusidic Acid Resistance in Staphylococcus aureus

2005 ◽  
Vol 49 (4) ◽  
pp. 1426-1431 ◽  
Author(s):  
Silke Besier ◽  
Albrecht Ludwig ◽  
Volker Brade ◽  
Thomas A. Wichelhaus
Keyword(s):  
Staphylococcus Aureus ◽  
Amino Acid ◽  
Fusidic Acid ◽  
Wild Type Strain ◽  
Elongation Factor ◽  
Acid Resistance ◽  
Resistant Bacteria ◽  
Wild Type ◽  
Compensatory Adaptation

ABSTRACT Recent studies have shown that individual amino acid exchanges within elongation factor G (EF-G) cause fusidic acid resistance in Staphylococcus aureus. The data from the present study illustrate that the fusidic acid resistance-mediating amino acid substitutions P406L and H457Y are associated with a marked impairment of the biological fitness of S. aureus. In particular, strains producing EF-G derivatives with these mutations showed reduced growth, decreased plasma coagulase activity, and an impaired capability to compete with the isogenic wild-type strain. Second-site mutations within EF-G, such as A67T and S416F, that have been encountered in clinical fusidic acid-resistant isolates containing the amino acid exchanges P406L and H457Y, respectively, were shown not to contribute to resistance. Furthermore, the substitution A67T had no impact on the biological fitness in vitro. The exchange S416F, however, was found to function as a fitness-compensating mutation in S. aureus carrying the substitution H457Y in EF-G. In conclusion, the data presented in this report provide evidence at the molecular level that the deleterious effects of fusidic acid resistance-mediating exchanges within EF-G of S. aureus can be reduced considerably by specific compensating mutations in this target protein. This compensatory adaptation most likely plays a significant role in the stabilization of resistant bacteria within a given population.

scholarly journals Distribution of Fusidic Acid Resistance Determinants in Methicillin-ResistantStaphylococcus aureus

2010 ◽  
Vol 55 (3) ◽  
pp. 1173-1176 ◽  
Author(s):  
F. B. McLaws ◽  
A. R. Larsen ◽  
R. L. Skov ◽  
I. Chopra ◽  
A. J. O'Neill
Keyword(s):  
Fusidic Acid ◽  
Drug Target ◽  
Horizontal Transmission ◽  
Acid Resistance ◽  
Limited Data ◽  
Genetic Lineages ◽  
Resistance Determinants ◽  
Resistant Strains ◽  
Mrsa Strains ◽  
Insight Into

ABSTRACTThe prevalence of resistance to fusidic acid in clinical isolates ofStaphylococcus aureus, including methicillin-resistantS. aureus(MRSA), has increased in the past 2 decades. However, there are limited data regarding the relative importance in this process of the different staphylococcal determinants that mediate resistance to fusidic acid. Furthermore, the roles played by clonal dissemination of fusidic acid-resistant strains versus horizontal transmission of fusidic acid resistance determinants have not been investigated in detail. To gain insight into both issues, we examined fusidic acid resistance in 1,639 MRSA isolates collected in Denmark between 2003 and 2005. Resistance to fusidic acid (MIC, >1 μg/ml) was exhibited by 291 (17.6%) isolates. For the majority of these isolates (∼87%), resistance was attributed to carriage offusBorfusC, while the remainder harbored mutations in the gene (fusA) encoding the drug target (EF-G). The CC80-MRSA-IV clone carryingfusBaccounted for ∼61% of the resistant isolates in this collection, while a single CC5 clone harboringfusCrepresented ∼12% of the resistant strains. These findings emphasize the importance of clonal dissemination of fusidic acid resistance within European MRSA strains. Nonetheless, the distribution offusBandfusCacross several genetic lineages, and their presence on multiple genetic elements, indicates that horizontal transmission of fusidic acid resistance genes has also played an important role in the increasing prevalence of fusidic acid resistance in MRSA.

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