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PubMedDate not supplied

Effect of fusidic acid on pancreatic islet allograft rejection.

We examined in fully mismatched rats, the survival of pancreatic islet allografts in recipients treated with either fusidic acid (FA), an antistaphyllococcal antibiotic that has been shown to possess an immunosuppressive effect in vitro and in vivo, or cyclosporin-A (CsA). Islets were isolated by collagenase digestion, separated from acinar tissue by handpicking under a dissecting microscope and transplanted into the liver by portal vein injection of streptozotocin(STZ)-induced diabetic rats. The results indicated that while a temporary immunosuppression with CsA achieved an indefinite islet allograft survival, FA administered to recipients daily was not able to prevent islet allograft rejection across a major histocompatibility barrier. We conclude that despite the fact that fusidic acid has been claimed to act as an-immunosuppressant drug in vitro with effects similar to those of CsA, unlike CsA, FA given either orally or by s.c. injection was not effective to prolong islet allograft survival in vivo.

Animals↗
PubMed1995

Depletion of small cytoplasmic RNA confers fusidic-acid resistance on Bacillus subtilis.

Bacillus subtilis small cytoplasmic RNA (scRNA) is a member of a signal recognition particle (SRP)-like RNA family. To analyze the function of scRNA in protein synthesis, a B. subtilis strain SC201NA was constructed in which the expression of intact scRNA is regulated by an IPTG-inducible promoter. In this strain, depletion of scRNA leads to deficient translation and sporulation as well as morphological changes. In addition, the growth of SC201NA in the absence of IPTG became fusidic-acid resistant. The acquisition of fusidic-acid resistant phenotype by depletion of scRNA suggested that scRNA is associated with elongation factor G (EF-G) in the translation process.

Bacillus subtilis↗
PubMed1999

[Pharmacokinetics of fusidic acid in patients with seriously infected burns].

The pharmacokinetics of fusidic acid (FA) were studied in 10 infected severe burns patients (35 +/- 5 yrs, 81 +/- 17 kg) i.e. 43 +/- 10% in 3rd degree. Treatment was given at the dose of 500 mg/8 hours (2-hour infusion). The kinetics of FA were evaluated on D1 (1st infusion) and at steady state on D4 (10th infusion), each sequence involving 9 whole blood samples. Samples were assayed by high-performance liquid chromatography. Data were analysed by a non-compartmental method. Mean duration of treatment, considered effective in all cases, was 5.9 +/- 2.1 days. The systemic safety of FA was felt to be good. Kinetic analysis revealed the existence of significant differences between D1 and D4 concerning the parameters Cmax, Cmin, AUC, Cl and Vss. These events are attributable to the non-linear nature of the human kinetics of FA. Accumulation ratios R1 and R2 did not differ i.e. 1.51 +/- 0.25 and R2 = 2.44 +/- 0.68. Kinetic modelling based upon the experimental tracing obtained on D1 revealed good coincidence of the predictive tracing in relation to data determined on D4. The dosage algorithm of 500 mg/8 hours was microbiologically satisfactory with Cmin measured on D1 and at steady state constantly greater than the MIC of the main organisms concerned (< to 2 micrograms/ml). Reduction in the parameters Cmax and AUC in comparison with a group of healthy subjects ultimately led to shortening of the mean T1/2 of FA. In the absence of impaired liver function, this is attributable to the known increase in hepatic clearances in burns patients and, to a certain extent, to the existence of translesional extra-hepatic clearance, which could contribute to the success of treatment.

Adult↗
PubMed1982

Determination of sodium fusidate and fusidic acid in dosage forms by high-performance liquid chromatography and a microbiological method.

A new High-performance liquid chromatographic (HPLC) method for the assay of sodium fusidate (I) or fusidic acid in dosage forms was developed and compared to a microbiological assay. A linear relationship was obtained between absolute peak area and amount of I(r = 0.99+) in the 50-1000-microgram/ml range. In the microbiological assay, Staphylococcus aureus (NCTC 6571) was the test organism, using an agar diffusion technique. With five test levels of the standard, potencies were interpolated from standard curve using a log transformation straight-line method with least-squares fitting (r = 0.99+). Both methods were applied to assay I (or fusidic acid) in tablets, a suspension, and an ointment. Excellent agreement was observed between results of the two methods.

Biological Assay↗
PubMed1990

Comparative in-vitro activities of ten fluoroquinolones and fusidic acid against Mycobacterium spp.

The in-vitro activities of eight new quinolones (A-56620, amifloxacin, difloxacin, CI-934, enoxacin, irloxacin, pefloxacin, temafloxacin), two reference fluoroquinolones (ciprofloxacin and ofloxacin) and fusidic acid against 147 mycobacterial strains, belonging to seven different species, were compared. Temafloxacin, ofloxacin and ciprofloxacin were the most active compounds. They only showed consistent activity against Mycobacterium tuberculosis, M. malmoense and M. fortuitum, but not against M. chelonei, M. avium, M. intracellulare and M. scrofulaceum. However, individual strains of these species were sometimes susceptible. The best overall in-vitro activity was obtained with temafloxacin, which often showed activity where other products were inactive. Fusidic acid merely displayed good activity against M. tuberculosis (MIC90 16 mg/l).

Anti-Infective Agents↗
PubMed1996

The dynamic structure of EF-G studied by fusidic acid resistance and internal revertants.

We have previously identified 20 different fusidic acid-resistant alleles of fusA, encoding mutant forms of the ribosomal translocase EF-G. One of these, P413L, is used here as the starting point in selections for internal revertants, identifying 20 different pseudo-wild-type forms of EF-G. We have also identified two alleles of fusA previously isolated as suppressors of 4.5 S RNA deficiency. All of these mutants are analysed in terms of their effects on the structural dynamics of EF-G. Most mutation conferring fusidic acid-resistance interfere with conformational changes of EF-G, but some may be located at a possible fusidic acid binding site. Revertants of the P413L mutations restore the function of EF-G with or without affecting the level of resistance to fusidic acid. The revertant mutations probably restore the balance between the GDP and GTP conformations of EF-G off the ribosome, and most of them are located close to the interface between the G domain and domain II. The procedure for the isolation of pseudo-wild-type forms of EF-G can be used to direct evolution progressively away from the wild-type while still maintaining the essential functions of EF-G.

Anti-Bacterial Agents↗
PubMedDate not supplied

Efficacy of penicillin G, flucloxacillin, cefazolin, fusidic acid, vancomycin, rifampicin and fosfomycin in muscular infections in mice due to Staphylococcus aureus.

Two strains each of sensitive, penicillinase-producing, methicillin-resistant and "tolerant" Staphylococcus aureus were used to infect mice intramuscularly. The mice were then treated with three doses each of fosfomycin, vancomycin, rifampicin, fusidic acid, penicillin G, flucloxacillin or cefazolin intravenously. Infections due to sensitive strains were effectively treated with all antibiotics investigated except fusidic acid. Fosfomycin, vancomycin, rifampicin and flucloxacillin showed the best activity against penicillinase-producing strains. Fosfomycin and vancomycin were equally effective against infections due to methicillin-resistant S. aureus. Infections caused by "tolerant" strains again responded best to fosfomycin, vancomycin and rifampicin.

Animals↗
PubMed1985

Fusidic acid in orthopaedic infections due to coagulase-negative staphylococci.

Twenty orthopaedic in-patients who developed an acute infection due to coagulase-negative staphylococci, and which was associated with a foreign body in 11 cases, were treated with fusidic acid. All patients were given oral medication, except for 1 child with acute osteomyelitis who was treated intravenously for the first 7 days. The mean daily dose was 21 mg/kg and the mean duration of treatment 20 days. Fusidic acid was given alone in 5 patients and concurrently with another antibiotic in the other 15 patients. All patients responded satisfactorily with resolution of the relevant signs and symptoms, although 1 patient relapsed subsequently. Mild side-effects were observed in 3 patients.

Administration, Oral↗
PubMedDate not supplied

Trimethoprim-polymyxin B sulfate cream versus fusidic acid cream in the treatment of pyodermas.

One hundred patients with a clinical diagnosis of a primary or secondary superficial pyoderma were entered into a double-blind study. They were allocated treatment with either trimethoprim-polymyxin B sulfate cream or fusidic acid cream according to a fully randomized treatment code. Data suitable for evaluation were obtained from 87 patients, and statistical analysis revealed trimethoprim-polymyxin B sulfate (TP) cream to be significantly better than fusidic acid cream in alleviation several of the individual signs and symptoms associated with pyogenic infection of the skin as well as in reducing the overall severity score at the end of the 2-week study period.

Administration, Topical↗
PubMed2001

In vitro activity of mezlocillin, meropenem, aztreonam, vancomycin, teicoplanin, ribostamycin and fusidic acid against Borrelia burgdorferi.

The in vitro susceptibility profile of Borrelia burgdorferi is not yet well defined for several antibiotics. Our study explored the in vitro susceptibility of B. burgdorferi to mezlocillin, meropenem, aztreonam, vancomycin, teicoplanin, ribostamycin and fusidic acid. Minimal inhibitory concentrations (MICs) and minimal borreliacidal concentrations (MBCs) were measured using a standardised colorimetric microdilution method and conventional subculture experiments. MIC values were lowest for mezlocillin (MIC(90), < or =0.06 mg/l) and meropenem (MIC(90), 0.33 mg/l). Vancomycin (MIC(90), 0.83 mg/l) was less effective in vitro. Borreliae proved to be resistant to aztreonam (MIC(90), >32 mg/l), teicoplanin (MIC(90), 6.6 mg/l), ribostamycin (MIC(90), 32 mg/l), and fusidic acid (MIC(90), >4 mg/l). The mean MBCs resulting in 100% killing of the final inoculum after 72 h of incubation were lowest for mezlocillin (MBC, 0.83 mg/l). This study gathered further data on the in vitro susceptibility patterns of the B. burgdorferi complex. The excellent in vitro effectiveness of acylamino-penicillin derivatives and their suitability for the therapy of Lyme disease is emphasised.

Anti-Bacterial Agents↗
PubMed1983

In-vitro effects of vancomycin, rifampicin, and fusidic acid, alone and in combination, against methicillin-resistant Staphylococcus aureus.

Minimal inhibitory and minimal bactericidal concentrations were determined for eighteen methicillin-resistant Staphylococcus aureus isolates, the majority also resistant to gentamicin, obtained from the blood of bacteraemic patients. Fifty per cent of organisms had a greater than four-fold difference in M.I.C. and M.B.C. for vancomycin, 83% for rifampicin, and 89% for fusidic acid. In-vitro effects of two-drug combinations of vancomycin, rifampicin, and fusidic acid demonstrated neither synergy nor antagonism when measured by a checkerboard dilution technique. The relevance of these findings to choice of therapy of serious infection due to methicillin-gentamicin resistant Staph. aureus is yet to be determined.

Culture Media↗
PubMed1985

Methicillin- and gentamicin-resistant Staphylococcus aureus: susceptibility to fosfomycin, cefamandole, N-formimidoyl-thienamycin, clindamycin, fusidic acid and vancomycin.

The in vitro activity of fosfomycin against 90 strains of methicillin- and gentamicin-resistant Staphylococcus aureus was studied in an in vitro microtitre system using Mueller-Hinton broth supplemented with glucose-6-phosphate. In parallel the antistaphylococcal activity of cefamandole, N-formimidoyl-thienamycin, clindamycin, fusidic acid and vancomycin was determined with the same organisms. The following MIC50 (MIC95) values were obtained: fosfomycin 8 (128) mg/l, cefamandole 8 (greater than 64) mg/l, clindamycin 0.25 (16) mg/l, fusidic acid less than 0.25 (less than 0.25) mg/l, vancomycin 1 (2) mg/l and N-formimidoyl-thienamycin 4 (16) mg/l. A high MIC/MBC ratio was noted for cefamandole, in contrast to fosfomycin.

Cefamandole↗
PubMedDate not supplied

Intranasal administration of fusidic acid cream in leprosy.

The effect of local treatment of nostrils with fusidic acid cream was investigated in 30 previously untreated lepromatous leprosy patients. The cream was applied in the nostrils after flushing the nostrils with normal saline, twice a day for a period of four weeks. It was found that 20 mg/gm of sodium fusidate was effective in reducing the morphological index of the nose-blow smear to zero in two weeks in majority of the patients. No untoward side effect was seen in any of the patients. Such nasal treatment along with multidrug therapy may help in reducing the patient's level of infectiousness to their contacts, since the nose is recognized to be an important portal of exit of M. leprae.

Administration, Intranasal↗
PubMedDate not supplied

Anti-HIV activity of dideoxynucleosides, foscarnet and fusidic acid is potentiated by human leukocyte interferon in blood-derived macrophages.

Blood-derived macrophages were acutely infected with HIV and treated with a combination of leucocyte interferon (IFN) and five anti-HIV drugs. HIV growth was assayed by quantitation of p24 antigen in the supernatant and in some experiments by determination of reverse transcriptase activity. Both IFN and all drugs, with the exception of fusidic acid, inhibited HIV growth in a dose-dependent manner. IFN in combination with zidovudine, dideoxycytidine or fusidic acid exerted a synergistic effect on HIV titers, while IFN combined with dideoxyinosine or foscarnet had an additive effect.

Cells, Cultured↗
PubMed1969

Fusidic acid: inhibition of factor T2 in reticulocyte protein synthesis.

The steroid antibiotic fusidic acid inhibits reticulocyte protein synthesis. This inhibition appears to be due to interference with the activity of the T(2) supernatant fraction, and strengthens the proposition that T(2) is functionally analogous to the G-factor of bacterial protein synthesis, which is also specifically inhibited by this antibiotic.

Adenosine Triphosphate↗
PubMedDate not supplied

Fusidic acid vs ofloxacin prophylaxis before cataract surgery.

PURPOSE: To evaluate the safety and efficacy of two self-administrated antibiotics in eliminating conjunctival microbial flora. METHODS: A total of 133 patients operated for cataract surgery were divided into three groups. The first group (A), 55 patients, received fusidic acid drops (1%) two times per day during the 3 days before the surgery; a second group (B), 55 patients, received ofloxacin (0.3%) four times per day during the 3 days before the surgery; and the third group (C), 23 patients, did not receive any topical antibiotic before the surgery. On the day of the surgery, cultures were taken from the lower fornix. RESULTS: In Group A, 28 cultures (50.9%) were sterile, and 27 (49.1%) were positive for the presence of microbial agents. In Group B, 25 cultures (45.4%) were sterile, and 30 (54.5%) were positive for the presence of microbial agents. In Group C, 5 cultures (21.7%) were sterile, and 18 (78.2%) were not. Staphylococcus epidermidis was the most common micro-organism isolated in all the groups. Statistical analysis does not reveal a significant difference between Groups A and B for the sterile cultures (p=0.7) (chi-square test), but a statistically significant difference is present between the treated and not treated patients (p= 0.05) (chi-square test). CONCLUSIONS: A preoperative prophylaxis is useful in eliminating conjunctival micro-organism, and both antibiotics (fusidic acid and ofloxacin) are efficient.

Anti-Bacterial Agents↗
PubMed1999

A Norwegian nosocomial outbreak of methicillin-resistant Staphylococcus aureus resistant to fusidic acid and susceptible to other antistaphylococcal agents.

In Norway, infections caused by methicillin resistant Staphylococcus aureus (MRSA) are still uncommon. From December 1993 to January 1997, MRSA was isolated from 22 people in Oslo county; 17 patients and five carriers (healthcare workers). A cluster of ten people (five patients and five healthcare workers) were associated with an outbreak at two hospitals in Oslo. The five patients were all admitted to the same intensive care unit (ICU) at Ullevål University Hospital between May-July 1995 (they were not transferred from abroad) and treated for acute neurological lesions. After surgery, four of them (one died) were transferred to another hospital for rehabilitation and training. The presence of MRSA was discovered in the patients and the five healthcare workers during the 10 months June 1995-March 1996. All cluster strains showed an unusual antibiotic resistance pattern in vitro, with a relatively low degree of methicillin resistance, resistance to fusidic acid, but sensitivity to all other anti-staphylococcal agents. A clonal spread of this fusidic acid resistant MRSA was supported by strain typing using pulsed-field gel electrophoresis (PFGE), which showed that all ten cluster strains belonged to one type or its subtype.

Adolescent↗
PubMed1998

The independent evolution of resistance to ciprofloxacin, rifampicin, and fusidic acid in methicillin-resistant Staphylococcus aureus in Australian teaching hospitals (1990-1995). Australian Group for Antimicrobial Resistance (AGAR).

Methicillin-resistant Staphylococcus aureus (MRSA) is endemic in teaching hospitals in eastern Australian states, with prevalence rates averaging 25-30% of all S. aureus. Between 1990 and 1995, 1467 non-duplicate MRSA isolates from clinically infected sites were tested in Sydney, Melbourne, and Brisbane as part of a national survey of staphylococcal susceptibility. We reviewed the differing evolution of resistance to ciprofloxacin, rifampicin, and fusidic acid. Despite similarities in community and hospital antibiotic use and MRSA prevalence rates, trends in resistance to the oral antibiotics in these cities have progressed independently of each other. In the 1995 survey in individual hospitals in Melbourne, 16-24% of strains were ciprofloxacin-resistant, compared with 80-100% in Sydney and 30-44% in Brisbane. There was great diversity of phage type patterns for ciprofloxacin-resistant strains, suggesting heterogeneous development of resistance. Rifampicin resistance was more closely associated with distinct dominant epidemic phage types, common to institutions in the same city, but without spread to the other cites. Between 1990 and 1995, these comprised 30-60% of all MRSA in Brisbane, compared with 5-10% in Melbourne and < 25% in Sydney. Fusidic acid resistance was uncommon and sporadic (< 5%), and was distributed equally between methicillin-resistant and methicillin-susceptible strains. Resistance to the oral agents in MRSA is due to a complex mix of antibiotic selection pressures and cross-infection with local and epidemic strains in closely related institutions. Each of these mechanisms can predominate, dependent on local factors and the antibiotics used.

Anti-Bacterial Agents↗