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PubMed2004

Penetration of fusidic acid and rifampicin into cerebrospinal fluid in low-grade inflammatory meningitis caused by Staphylococcus epidermidis.

Cerebrospinal fluid (CSF) concentration-time curves of rifampicin and fusidic acid were studied in a patient with post-operative meningitis caused by Staphylococcus epidermidis. The patient was treated with this combination of antimicrobial agents because of a severe hypersensitivity reaction to vancomycin. Peak CSF concentrations of rifampicin exceeded the MIC by > 60-fold, while those of fusidic acid just reached the MIC. CSF concentrations of fusidic acid were relatively stable within the range reported for patients with uninflamed meninges, but serum levels were surprisingly low. An increase in the metabolism of fusidic acid induced by rifampicin cannot be excluded.

Anti-Bacterial Agents↗
PubMed1990

Fusidic acid, an immunosuppressive drug with functions similar to cyclosporin A.

Fusidic acid, a tetracyclic triterpenoic acid, is used for local and systemic treatment of bacterial infections. Its in vitro effects on the human immune response were tested. Activated blood mononuclear cells released lower levels of interleukin (IL) 1 in the presence of nontoxic and clinically attainable levels of fuscidic acid (15 to 50 micrograms/mL). In contrast, the drug failed to affect the production of two other monocyte-derived cytokines, tumor necrosis factor (TNF)-alpha and IL 6. The production of the T-cell-derived cytokines, IL 2 and interferon-gamma (IFN-gamma), were also suppressed (IC50: 5 to 15 micrograms/mL). The early costimulatory effects of IL 1 and IL 6 on mouse thymocytes and human T cells were suppressed by similar levels of the drug, as was the hybridoma growth-promoting function of IL 6. T-cell proliferation induced by phytohemagglutinin or allogeneic cells was reversibly inhibited (IC50: 15 micrograms/mL). These functions of fusidic acid were strikingly similar to those of cyclosporin A. Because of the low toxicity of the former, it may have a role as a clinically useful suppressor of immunoinflammatory processes.

Adult↗
PubMed1997

A novel fusidic acid resistance gene from Streptomyces lividans 66 encodes a highly specific esterase.

Resistance to fusidic acid in Streptomyces lividans is due to secretion of an extracellular enzyme (FusH) that converts the steroid antibiotic into an inactive derivative. NH2-terminal and several internal amino acid sequences were prepared from the purified enzyme. Using one of the deduced oligonucleotides to probe a subgenomic DNA library, the fusH gene was cloned and sequenced. Sequence analysis located an ORF which, owing to the presence of two putative start codons, indicates a predicted protein with 520 or 509 amino acids. A signal peptide was identified by aligning the deduced amino acids with the N-terminal sequence determined for the mature enzyme. The C-terminal part of the deduced FusH contains a region of three tandemly repeated stretches of 50 amino acids, which is preceded and followed by amino acids showing high homology with the repeats. FusH was found to share a GDS motif with some deduced esterases. S. lividans transformants carrying fusH on a multicopy vector synthesized high levels of FusH. Purified FusH cleaved equally well an acetyl, a thioacetyl or a formyl group from the 16 beta-position of fusidic acid and its derivatives. However, a propionyl group at the 16 beta-position was attacked with difficulty and a 16 alpha-acetyl group was not hydrolysed at all. These data indicate that FusH is a highly specific esterase. The fusH gene is widely distributed among streptomycetes that modify fusidic acid to its inactive lactone derivative.

Amino Acid Sequence↗
PubMed2005

Gentamicin-loaded bone cement with clindamycin or fusidic acid added: biofilm formation and antibiotic release.

The formation of staphylococcal biofilms on experimental bone cements, loaded with 0.5 or 1.0 g of active gentamicin and an additional equivalent amount of gentamicin, clindamycin, or fusidic acid was investigated. The biofilms were formed in a modified Robbins device over a 3-day time span and the influence of the additional antibiotics was quantified by expressing the number of colony forming units relative to the corresponding bone cement containing only gentamicin. Combinations of gentamicin with either fusidic acid or clindamycin reduced growth of clinical isolates of both gentamicin-sensitive Staphylococcus aureus and gentamicin-resistant coagulase-negative staphylococci to approximately 28%. To determine whether adding a second antibiotic has influence on the gentamicin release, cement blocks were placed in phosphate buffer and aliquots were taken at designated sampling intervals. The influence of the additional antibiotics was quantified by expressing the percentage released of the total amount of antibiotic incorporated in the different bone cements. After 3 days, all bone cements had released similar percentages of gentamicin, whereas more clindamycin and fusidic acid were released after doubling their concentration in the bone cements. In conclusion, bone cements loaded with combinations of gentamicin and clindamycin or fusidic acid are more effective in preventing biofilm formation than bone cements with gentamicin as a single drug. In addition, the presence of clindamycin or fusidic acid in gentamicin-loaded bone cement has no influence on the total gentamicin release.

Biofilms↗
PubMed1996

Comparison of vancomycin, teicoplanin, metronidazole, and fusidic acid for the treatment of Clostridium difficile-associated diarrhea.

We conducted a prospective, randomized study to compare the efficacy of oral fusidic acid, oral metronidazole, oral vancomycin, and oral teicoplanin for the treatment of Clostridium difficile-associated diarrhea. Treatment resulted in clinical cure for 94% of the patients who were treated with vancomycin, 96% of those treated with teicoplanin, 93% of those treated with fusidic acid, and 94% of those treated with metronidazole. Clinical symptoms recurred in 16% of patients treated with vancomycin, 7% of those treated with teicoplanin, 28% of those treated with fusidic acid, and 16% of those treated with metronidazole. There was asymptomatic carriage of C. difficile toxin in 13% of patients treated with vancomycin, 4% of those treated with teicoplanin, 24% of those treated with fusidic acid, and 16% of those treated with metronidazole. No adverse effects related to therapy with vancomycin or teicoplanin were observed. Considering the costs of treatment, our findings suggest that metronidazole is the drug of choice for C. difficile-associated diarrhea and that glycopeptides should be reserved for patients who cannot tolerate metronidazole or who do not respond to treatment with this drug.

Administration, Oral↗
PubMed1989

Effects of fusidic acid on staphylococcal keratitis.

We treated 20 consecutive patients suffering from staphylococcal keratitis with topical fusidic acid 1% suspension in a carbomer gel. Fifteen (79%) of the isolated Staphylococcus epidermidis strains were resistant to methicillin, but all were sensitive to fusidic acid by in-vitro testing. The keratitis showed evidence of healing in 17 (85%) of the 20 patients. The healing times ranged between 5 and 21 days (mean 10.5 days). In this open clinical trial fusidic acid proved to be a safe and effective antibiotic for the treatment of staphylococcal keratitis.

Adolescent↗
PubMedDate not supplied

Fusidic acid for the treatment of antibiotic-associated colitis induced by Clostridium difficile.

Twenty courses of fusidic acid were given to 16 patients with antibiotic-associated colitis caused by Clostridium difficile. Fusidic acid was given in a dose of 0.5-1.5 g daily for seven to 21 days. Diarrhoea disappeared rapidly. Clinical relapse occurred after five courses and once when the patient was still on treatment. Clinical cure with persistence or reappearance of toxin occurred in four further patients. Nineteen courses of metronidazole were given to 19 patients who experienced six failures or relapses. Seven courses of vancomycin were given to five patients, three of whom had had relapse. Five patients healed without treatment. The relapses occurred only in old and prostrated patients. They often recurred several times in the same patient. 0.5 g of fusidic acid daily appears to be as effective as vancomycin and metronidazole for the treatment of C. difficile-induced colitis.

Adult↗
PubMed1993

[Mechanisms of adhesion of Staphylococci to biomaterials: effect of fusidic acid].

The production of slime, adherence to plastics and hydrophobicity are factors which regulate the colonisation of biomaterials by Staphylococci. The influence of fusidic acid on these 3 factors was studied by using 3 pairs of pathogenic strains of S. aureus and S. epidermidis. Each pair presented differences in the expression of one or several of these factors. The influence of fusidic acid was initially studied by determining the expression of these factors by these strains cultured in the presence of 0.03 mg/l and 0.5 mg/l of antibiotic. Hydrophobicity was measured by the Bath-test method, slime was detected by Trypan blue staining after fixation with Carnoy's fixative and adherence was determined on polystyrene. The variations observed were generally minor, except for S. epidermidis, high slime produces, which showed a reduced production. Using this collection of strains, we then selected mutants resistant to 2 micrograms/ml of fusidic acid. This resistance induced a reduction in the 3 colonisation factors and it can be proposed that strains resistant to fusidic acid have a lesser capacity to colonise than sensitive strains. The bacteria adhere to and colonise the majority of surfaces proposed to them [3, 7, 10]. This was the case for biomaterials used in medicine, whose number and diversity (catheters, prostheses) are continually increasing. Apart from thrombosis, the major complication is the development of infection. Coagulase positive or negative Staphylococci are very frequently responsible for this type of infection.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacterial Adhesion↗
PubMed1977

Morphological stages of Bacillus subtilis sporulation and resistance to fusidic acid.

During spore development of Bacillus subtilis both protein synthesis and sporulation become resistant to the antibiotic fusidic acid. This resistance develops at the time when asymmetric prespore septa are formed. Simultaneously ribosomes lose their ability to bind fusidic acid, as demonstrated by their affinity chromatography with the immobilized drug. Mutants resistant to fusidic acid during growth are oligosporogenous; their sporulation development is blocked before septum formation. These results indicate that normal ribosomes are needed for prespore septation sporulation; only after septation can protein synthesis be maintained, throughout the development period, by fusidate resistant ribosomes.

Bacillus subtilis↗
PubMed2002

Treatment of acute bacterial conjunctivitis: 1% fusidic acid viscous drops vs. 0.3% tobramycin drops.

BACKGROUND: A frequent cause of conjunctivitis is an acute bacterial infection, presenting with mucopurulent discharge and conjunctival hyperemia. The authors compared the clinical and microbiologic efficacy, safety and acceptability of 1% fusidic acid viscous drops (Fucithalmic) with 0.3% tobramycin ophthalmic solution (Tobrex) in the treatment of suspected bacterial conjunctivitis. METHODS: Patients were recruited at 20 sites in Ontario, Saskatchewan and Alberta from October 1995 to December 1998. Patients who presented to their primary care physician with suspected bacterial conjunctivitis, as identified by conjunctival hyperemia and purulent or mucopurulent discharge, were eligible for the study. Patients were randomly assigned to receive 7 days of treatment with either 1% fusidic acid (one drop applied twice daily) or 0.3% tobramycin (one to two drops applied four to six times daily). The investigators were blinded as to treatment status. Bacteriologic samples were taken from the inferior conjunctival cul-de-sac on day 0 and at the end of treatment. Signs and symptoms of conjunctivitis were assessed at baseline and after 3 and 7 days of treatment. The acceptability of treatment was assessed by having the patient or the parent or guardian complete a questionnaire on degree of compliance and ease of use after 3 and 7 days of treatment. RESULTS: Conjunctival swabs were obtained from 484 patients (410 over 9 years of age and 74 aged 2 to 9 years) to determine baseline bacteriology. Of the 484, 319 (65.9%) (63% of the older patients and 80% of those aged 2 to 9 years) had positive results of culture for bacteria. Ninety-four patients (19%) (63 [15%] of the older patients and 31 [42%] of those aged 2 to 9 years) had per-protocol pathogens as defined by quantitative bacteriology criteria. There was a direct correlation between the presence of mucopurulent discharge and the presence of per-protocol pathogens. There were no significant differences in clinical or bacteriologic efficacy between the treatment groups. Treatment compliance was similar between the treatment groups for the older patients; however, for those aged 2 to 9 years, compliance was significantly better in the fusidic acid group than in the tobramycin group (85% vs. 47%) (p < 0.001). Significantly more patients in the fusidic acid group than in the tobramycin group rated treatment as convenient or very convenient, particularly among younger patients (97% vs. 54%) (p < 0.001). INTERPRETATION: The clinical and bacteriologic efficacy of fusidic acid viscous drops combined with the convenience of a twice-daily dosage regimen establishes this antibiotic as first-line treatment for suspected acute bacterial conjunctivitis and a favourable alternative to other broad-spectrum antibiotics.

Adolescent↗
PubMed1980

Classification of polyene antibiotics according to their synergistic effect in combination with bleomycin A2 or fusidic acid.

Five polyene antibiotics were compared for their effects on colony formation of either Chinese hamster V79 or Saccharomyces cerevisiae cells. A 10 to 40 times higher concentration of amphotericin B (heptaene) or nystatin (degenerated heptaene) was necessary to inhibit colony formation of hamster cells than that needed to inhibit colony formation of yeast cells. In contrast, colony formation of both hamster and yeast cells was inhibited to the same extent by similar concentrations of filipin (pentaene), pentamycin (pentaene), or pimaricin (tetraene). The five polyene antibiotics were also compared for their effects on colony formation of either V79 or S. cerevisiae cells when combined with a nonpolyene antibiotic, fusidic acid or bleomycin A2. Amphotericin B or nystatin could augment the cytocidal effect of fusidic acid but not that of bleomycin A2, whereas pentamycin or pimaricin could augment the cytocidal effect of both fusidic acid and bleomycin A2 against hamster and yeast cells. Filipin was found to enhance the action of fusidic acid and bleomycin upon growth of mammalian cells, whereas the pentaene polyene significantly potentiated the action of fusidic acid, but not that of bleomycin A2, against S. cerevisiae. It was therefore suggested that these polyene antibiotics be classified into two groups: group 1 (pimaricin, pentamycin, and filipin) and group 2 (amphotericin B and nystatin).

Amphotericin B↗
PubMed1992

Anti-diabetogenic effect of fusidic acid in diabetes prone BB rats.

Fusidic acid and its sodium salt (fusidin) are anti-staphylococcal drugs. In vitro studies have shown that they prevent the lymphocyte co-stimulatory activities of the cytokines IL-1 and IL-6 in a manner similar to that of cyclosporin A, and prevent the inhibitory effect of IL-1 on glucose-induced insulin production. As IL-1 and IL-6 are thought to play a role in the pathogenesis of Type 1 diabetes, the aim of this study was to investigate whether fusidin could influence the disease incidence of the spontaneously diabetic BB rat model. Accordingly, a group of 50 BB rats receiving fusidin dissolved in their drinking water were compared to a control group of 55 rats over a period of 200 days. The incidence of diabetes was found to be 52% in the experimental group and 71% in the control group (P < 0.05). The degree of insulitis and the number of islets at histological examination were similar among the non-diabetic animals whereas the diabetic fusidin-treated animals showed a higher degree of islet preservation than the diabetic control rats. The results are highly indicative of an anti-diabetogenic effect of fusidin.

Administration, Oral↗
PubMed1997

Oral treatment of Staphylococcus spp. infected orthopaedic implants with fusidic acid or ofloxacin in combination with rifampicin.

Oral therapy of staphylococcal infection of orthopaedic implants with 900 mg/day rifampicin combined with either 1.5 g/day fusidic acid for 5 days followed by 1 g/day thereafter, or 600 mg/day ofloxacin was compared. Patients with an infected hip were treated for 6 months, with removal of any unstable prosthesis after 5 months' treatment and those with an infected knee prosthesis were treated for 9 months, with removal of the prosthesis after 6 months of treatment. Patients with infections of other type of bone implants were treated for 6 months with removal of the implant after 3 months of treatment, if necessary. Cure was defined as the absence of clinical, microbiological and radiological evidence of infection 12 months after completion of treatment. The treatment of 46 of the 52 included in the study was evaluated for safety and that of 42 was assessed for efficacy. Overall treatment was successful for 11 (55%) of 20 patients treated with rifampicin and fusidic acid group and for 11 (50%) of the 22 treated with rifampicin and ofloxacin. Treatment failed in four cases in each treatment group because of persistent infection. One patient given rifampicin and fusidic acid and three patients given rifampicin and ofloxacin failed treatment because of relapse. Superinfection led to failure in the remainder and was due to staphylococci in all but one case in which Acinetobacter calcoaceticus var. anitratus was isolated. There were no side effects related to study treatment. Oral treatment with rifampicin combined with fusidic acid may be a suitable alternative to the combination of rifampicin and ofloxacin for treating implant infections due to Staphylococcus spp. either when the patient is intolerant to quinolones or when the infecting organism is resistant to these drugs.

Administration, Oral↗
PubMed1976

Intravenous fusidic acid ('Fucidin') in the management of severe staphylococcal infections: a review of 46 cases.

Case reports are reviewed of 46 patients with severe, life-threatening infections, mainly staphylococcal, who were treated with intravenous fusidic acid. Overall, 22 (48%) patients survived and 24 died, 10 of these within 24 hours of commencing treatment with fusidic acid. Thirty-nine patients received unsuccessful antibiotic therapy prior to the administration of fusidic acid. It was not possible to relate prior antibiotic treatment to outcome, and, in such severe infections, complicating diseases had an adverse effect upon survival. It is concluded that intravenous fusidic acid ('Fucidin') has an important place in the treatment of severe staphylococcal infections.

Adolescent↗
PubMed1999

Fusidic acid in septicaemia and endocarditis.

The in vitro activity of fusidic acid against Staphylococcus aureus is confirmed in clinical studies which demonstrate that this antibiotic in combination with other agents, particularly beta-lactams, is efficacious in non-MRSA septicaemia. Some reports suggest that fusidic acid when used in combination, may significantly diminish the risk of relapse after cessation of therapy. However, in spite of over 30 years of use and its recommendation in a number of guidelines, published evidence is insufficient to allow reliable comment on the efficacy of the antibiotic in the treatment of endocarditis.

Anti-Bacterial Agents↗
PubMed1995

Purification and characterization of a novel extracellular Streptomyces lividans 66 enzyme inactivating fusidic acid.

The wild-type strain Streptomyces lividans 66 is resistant against the steroid-like antibiotic fusidic acid. Comparative studies of the wild-type strain and a fusidic acid-sensitive mutant allowed the identification of an extracellular enzyme which inactivates fusidic acid. With the help of a combination of ultrafiltration and chromatographies with Phenyl-Sepharose and an anion exchanger, the enzyme was highly purified. Its apparent molecular mass is 48 kDa, its optimal activity ranges between 45 and 55 degrees C, and its optimal pH is 6.0 to 9.0. It is stimulated by neither monovalent nor divalent ions. The enzyme acts as a specific esterase which removes the acetyl group at C-16 from fusidic acid. The resulting intermediate is unstable, and spontaneous lactonization between C-21 and C-16 occurs rapidly.

Acetates↗
PubMed1991

Inactivation of fusidic acid by resistant Streptomyces strains.

Streptomyces lividans and several other Streptomyces species are resistant to the steroid-like antibiotic fusidic acid. This resistance is mediated by structural modification of the antibiotic. Using TLC, CD, UV, IR, NMR and mass spectroscopy the structure of one of the resulting inactive compounds was determined. It is derived from fusidic acid by the loss of an acetyl group and the formation of a lactone ring between C-21 and C-16. In addition, helvolic acid, a compound closely related to fusidic acid, has been shown to be modified.

Chromatography, Thin Layer↗
PubMed1993

Penetration of fusidic acid into human brain tissue and cerebrospinal fluid.

Penetration of fusidic acid into brain tissue in six patients and cerebrospinal fluid in seven patients was determined. Tissue samples, taken during surgery revealed drug levels at about 7% of simultaneous serum concentrations. In contrast, cerebrospinal fluid concentrations were below 1% of serum levels. Since serum- and tissue levels of fusidic acid were far above the minimal inhibitory concentration (MICs) of staphylococci and streptococci, and since it has a long serum half-life of about 10 hours, it is a promising candidate for prophylaxis in neurosurgery.

Adult↗