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B Fantin

Publications and source records attributed to B Fantin.

At least 19 recordsLinked to original sources
PubMed2001

[Experimental models: interaction of Synercid with other anti-Gram positive agents].

EXPERIMENTAL DATA: In case of resistance to quinupristin, the bacteriostatic synergism is preserved but the in vivo bactericidal effect of Synercid declines. On the other hand, no selection of resistant mutants has been observed. In case of isolated resistance to dafopristin, there is no reduction in the bactericidal effect of Synercid; there is however a possible risk of selecting resistant mutants. To become resistant to Synercid, S. aureus strains have to become resistant to both quinupristin and dafopristin, a highly unlikely situation. POTENTIAL COMBINATIONS: Among the combinations of Synercid with other antibiotics, the combination with vancomycin would have particular interest for clinical applications, increasing bactericidal activity. This would be the case for severe S. aureus infections with a large inoculum and even more so for meti-R resistant strains with a C-MLSB phenotype. Combination with rifampicin would be another possibility, but only for strains not resistant to quinupristin.

Animals↗
PubMed2001

[Purulent meningitis].

Purulent meningitis is a bacterial infection of the subarachnoid space. It constitutes a diagnostic and therapeutic emergency. The vital and functional prognosis is always engaged and depends on the rapidity and the adequacy of management. Treatment is based on a bactericidal antibiotic treatment which is at first empirically prescribed, on the basis of the underlying condition, the clinical examination and the epidemiological context, and then adjusted according to the micro-organism isolated from the cerebrospinal fluid. The recent emergence and increase of penicillin-resistant Streptococcus pneumoniae has led to a modification of antibiotic guidelines.

Anti-Bacterial Agents↗
PubMed2001

Consequences of VanE-type resistance on efficacy of glycopeptides in vitro and in experimental endocarditis due to Enterococcus faecalis.

The consequences on glycopeptide activity of low-level resistance to vancomycin due to VanE-type resistance were evaluated in vitro and in experimental endocarditis caused by Enterococcus faecalis BM4405 (MICs of vancomycin and teicoplanin: 16 and 0.5 microg/ml, respectively), its susceptible derivative BM4405-1, and susceptible E. faecalis JH2-2. After 24 h of incubation, vancomycin at 8 microg/ml was not active against E. faecalis BM4405 whereas it was bacteriostatic against strains BM4405-1 and JH2-2. Against all three strains, vancomycin at 30 microg/ml and teicoplanin at 8 or 30 microg/ml were bacteriostatic but bactericidal when combined with gentamicin. In rabbits with aortic endocarditis due to VanE-type resistant strain BM4405, treatment with a standard dose of vancomycin generated subinhibitory plasma concentrations (i.e., peak of 36.3 +/- 2.1 microg/ml and trough of 6.0 +/- 2.2 microg/ml) and led to no significant reduction in mean aortic valve vegetation counts compared to no treatment of control animals. In contrast, a higher dosing regimen of vancomycin (i.e., resulting in a peak of 38.3 +/- 5.2 microg/ml and a trough of 15.0 +/- 8.3 microg/ml), providing plasma concentrations above the MIC for the entire dosing interval, led to significant and similar activities against all three strains, which were enhanced by combination with gentamicin. Treatment with teicoplanin led to results similar to those obtained with vancomycin at a high dose. No subpopulations with increased resistance to glycopeptides were selected in vitro or in vivo. In conclusion, the use of a high dose of vancomycin was necessary for the treatment of experimental enterococcal endocarditis due to VanE-type strains.

Animals↗
PubMed2001

Activities of the combination of quinupristin-dalfopristin with rifampin in vitro and in experimental endocarditis due to Staphylococcus aureus strains with various phenotypes of resistance to macrolide-lincosamide-streptogramin antibiotics.

We evaluated the activities of quinupristin-dalfopristin (Q-D), alone or in combination with rifampin, against three strains of Staphylococcus aureus susceptible to rifampin (MIC, 0.06 microg/ml) and to Q-D (MICs, 0.5 to 1 microg/ml) but displaying various phenotypes of resistance to macrolide-lincosamide-streptogramin antibiotics: S. aureus HM1054 was susceptible to quinupristin and dalfopristin (MICs of 8 and 4 microg/ml, respectively); for S. aureus RP13, the MIC of dalfopristin was high (MICs of quinupristin and dalfopristin for strain RP13, 8 and 32 microg/ml, respectively); and S. aureus HM1054R was obtained after conjugative transfer of macrolide-lincosamide-streptogramin B constitutive resistance to HM1054, and the MIC of quinupristin for this strain was high (MICs of quinupristin and dalfopristin, 64 and 4 microg/ml, respectively). In vitro time-kill curve studies showed an additive effect [corrected] between Q-D and rifampin, at a concentration of four times the MIC, against the three strains. Rabbits with aortic endocarditis were treated 4 days with Q-D, rifampin, or their combination. In vivo, the combination was highly bactericidal and synergistic against strains susceptible to quinupristin (HM1054 and RP13) and sterilized 94% of the animals. In contrast, the combination was neither synergistic nor bactericidal against the quinupristin-resistant strain (HM1054R) and did not prevent the emergence of mutants resistant to rifampin. We conclude that the in vivo synergistic and bactericidal activity of the combination of Q-D and rifampin against S. aureus is predicted by the absence of resistance to quinupristin but not by in vitro combination studies.

Animals↗
PubMed2001

Clinical evaluation of the management of community-acquired pneumonia by general practitioners in France.

STUDY OBJECTIVES: To evaluate the management of community-acquired pneumonia (CAP) by general practitioners (GPs) in terms of clinical efficiency and adherence to official recommendations. DESIGN: Prospective cohort study. SETTING: Community-based study from 11 French counties. PATIENTS: Adult patients clinically suspected of having CAP who were seen by GPs were included after confirmation of the presence of an infiltrate on chest radiographs. INTERVENTION: The management of the patients was left to the discretion of the GP. MEASUREMENTS AND RESULTS: One hundred thirty patients were included in the study, and 13 patients (10%) were immediately hospitalized because of the severity of the pneumonia. The remaining 117 patients were treated as outpatients: 108 of 117 patients (92%) were cured, and 9 patients were subsequently hospitalized because of the failure of ambulatory treatment. Diagnostic error (n = 6) rather than antibiotic failure (n = 3) was the most frequent cause of the failure of ambulatory treatment. Only 40% of the patients received an initial antibiotic treatment that was in agreement with French recommendations. However, the rate of antibiotic failure leading to hospitalization was low (3 of 117 patients; 2.6%) and similar for patients treated or not according to recommendations (p > 0.5). Overall, five patients (4%) died; all deaths occurred during hospitalization and were related to the severity of the underlying disease but not to the choice of antibiotic treatment. CONCLUSIONS: The management of CAP by GPs was clinically effective despite a poor adherence to official recommendations. Our results suggest that adequate assessment of severity rather than adherence to recommendations for antibiotic treatment had an impact on clinical outcome of CAP managed by GPs.

AIDS-Related Opportunistic Infections↗
PubMed2000

Association between nasal carriage of Staphylococcus aureus and infection in liver transplant recipients.

We reviewed the records of 87 patients who underwent liver transplantation and who were screened by use of nasal swabs on the day before surgery. Twenty-four patients harbored methicillin-susceptible Staphylococcus aureus (MSSA), and 8 harbored methicillin-resistant S. aureus (MRSA). MSSA infection occurred in 3 (12.5%) of 24 MSSA carriers and in 2 (3.2%) of 63 noncarriers (nonsignificant). In contrast, MRSA infection occurred more frequently in MRSA carriers (7 [87.5%] of 8) than in MRSA noncarriers (8 [10.1%] of 79; P<.001). Nasal carriage of MRSA is associated with a very high risk of MRSA infection in liver transplant recipients.

Adolescent↗
PubMed2000

Activity of LY333328 combined with gentamicin in vitro and in rabbit experimental endocarditis due to vancomycin-susceptible or -resistant Enterococcus faecalis.

We investigated the activity of LY333328 alone and combined with gentamicin, both in vitro and in a rabbit model of experimental endocarditis, against the susceptible strain Enterococcus faecalis JH2-2 and its two glycopeptide-resistant transconjugants, BM4316 (VanA) and BM4275 (VanB). MICs of LY333328 and gentamicin were 2 and 16 microgram/ml, respectively, for the three strains. In vitro, LY333328 alone was bactericidal at 24 h against JH2-2 at a concentration of 2 microgram/ml and against BM4316 and BM4275 at a concentration of 30 microgram/ml. The combination of LY333328 and gentamicin (4 microgram/ml) was synergistic and bactericidal after 24 h of incubation against the three strains at LY333328 concentrations of 2 microgram/ml for JH2-2 and 8 microgram/ml for BM4275 and BM4316. The combination of LY333328 and gentamicin was the only regimen demonstrating in vitro bactericidal activity against BM4316. In vivo, intravenous treatment with LY333328 alone, providing peak and trough serum levels of 83.3 +/- 1.3 and 3.8 +/- 0.2 microgram/ml, respectively, was inactive against BM4316 and BM4275 and selected mutants resistant to LY333328 in half of the rabbits infected with the VanA-type strain (MICs, 8 to 20 microgram/ml). However, the LY333328-gentamicin combination was active against the three strains and prevented the emergence of mutants resistant to both components of the combination. We conclude that the LY333328-gentamicin combination might be of interest for the treatment of enterococcal infections, particularly against VanA-type strains.

Animals↗
PubMed2000

Influence of resistance to streptogramin A type antibiotics on the activity of quinupristin-dalfopristin in vitro and in experimental endocarditis due to Staphylococcus aureus.

We evaluated the activity of quinupristin-dalfopristin (Q-D) against three clinical strains of Staphylococcus aureus susceptible to Q (MIC, 8 microg/ml) and Q-D (MICs, 0.5 to 1 microg/ml) but displaying various levels of susceptibility to D. D was active against S. aureus HM 1054 (MIC, 4 microg/ml) and had reduced activity against S. aureus RP 13 and S. aureus N 95 (MICs, 32 and 64 microg/ml, respectively). In vitro, Q-D at a concentration two times the MIC (2xMIC) produced reductions of 4.3, 3.9, and 5.8 log(10) CFU/ml after 24 h of incubation for HM 1054, RP 13, and N 95, respectively. Comparable killing was obtained at 8xMIC. Q-D-resistant mutants were selected in vitro at a frequency of 2 x 10(-8) to 2 x 10(-7) for the three strains on agar containing 2xMIC of Q-D; no resistant bacteria were detected at 4xMIC. Rabbits with aortic endocarditis were treated for 4 days with Q-D at 30 mg/kg of body weight intramuscularly (i.m.) three times a day (t.i.d.) or vancomycin at 50 mg/kg i.m. t.i.d. In vivo, Q-D and vancomycin were similarly active and bactericidal against the three tested strains compared to the results for control animals (P < 0.01). Among animals infected with RP 13 and treated with Q-D, one rabbit retained Q-D-resistant mutants that were resistant to Q and to high levels of D (MICs, 64, >256, and 8 microg/ml for Q, D, and Q-D, respectively). We conclude that the bactericidal activity of Q-D against strains with reduced susceptibility to D and susceptible to Q-D is retained and is comparable to that of vancomycin. Acquisition of resistance to both Q and D is necessary to select resistance to Q-D.

Animals↗
PubMed2000

Bactericidal activity of gentamicin against Enterococcus faecalis in vitro and in vivo.

The activity of gentamicin at various concentrations against two strains of Enterococcus faecalis was investigated in vitro and in a rabbit model of aortic endocarditis. In vitro, gentamicin at 0.5 to 4 times the MIC failed to reduce the number of bacteria at 24 h. Rabbit or human serum dramatically increased gentamicin activity, leading to a >/=3-log(10) CFU/ml decrease in bacterial counts when the drug concentration exceeded the MIC. Susceptibility testing in the presence of serum was predictive of in vivo activity, since gentamicin alone significantly reduced the number of surviving bacteria in the vegetations if the peak-to-MIC ratio was greater than 1. However, gentamicin selected resistant mutants in rabbits. The intrinsic activity of gentamicin should be taken into account in evaluation of combinations of gentamicin and cell wall-active agents against enterococci.

Animals↗
PubMed1999

Influence of socioeconomic status on features and outcome of community-acquired pneumonia.

The influence of socioeconomic status on the features and evolution of community-acquired pneumonia in 107 consecutive hospitalized patients was investigated. Thirty-four (31.8%) patients were considered to have a low socioeconomic status. These patients were more likely immigrants, middle-aged, with fewer comorbid illnesses, and were more often tobacco, alcohol, or drug consumers (P<0.01). The distribution of etiologies was significantly different according to socioeconomic status, with tuberculosis occurring more frequently in the low socioeconomic group (P < 0.05). Low socioeconomic status was not associated with a more severe presentation or outcome of pneumonia but was an independent factor that predicted a significantly longer length of hospitalization (5.9 days longer; 95% confidence interval, 2.2-9.5 days; P<0.003), entailing a substantial excess cost per hospital stay.

Adult↗
PubMed1999

Activity and diffusion of LY333328 in experimental endocarditis due to vancomycin-resistant Enterococcus faecalis.

The activity of LY333328 against Enterococcus faecalis JH2-2, which is susceptible to glycopeptides, and against its transconjugants E. faecalis BM4281 and BM4316, with VanB and VanA phenotypes, respectively, was investigated. LY333328 was active in vitro against the three strains, for which MICs were 2 microg/ml on agar and 0.25 microg/ml in broth. LY333328 was bactericidal in broth against E. faecalis JH2-2 and BM4281 at a concentration of 8 microg/ml and against BM4316 at a concentration of 30 microg/ml. The protein binding of LY333328 to rabbit serum was >99%, and the bactericidal activity of LY333328 in broth was reduced when it was tested in the presence of 90% rabbit serum. Autoradiographic studies performed in rabbits with enterococcal endocarditis showed that 14[C]LY333328 was distributed heterogeneously throughout cardiac vegetations. In rabbits with aortic endocarditis, a regimen of 20 mg of LY333328 per kg of body weight administered intramuscularly twice a day for 5 days after a loading dose of 40 mg/kg was active against the three strains in vivo (P < 0.01), whereas vancomycin was not active against the VanB-type strain and teicoplanin was not active against the VanA-type strain. We conclude that the activity of LY333328 is not significantly modified by acquired resistance to glycopeptides in E. faecalis either in vitro or in experimental endocarditis.

Animals↗
PubMed1999

Two-step acquisition of resistance to the teicoplanin-gentamicin combination by VanB-type Enterococcus faecalis in vitro and in experimental endocarditis.

The activity of vancomycin and teicoplanin combined with gentamicin was investigated in vitro against strains of Enterococcus faecalis resistant to vancomycin and susceptible to teicoplanin (VanB type) and against mutants that had acquired resistance to teicoplanin by three different mechanisms. In vitro, gentamicin selected mutants with two- to sixfold increases in the level of resistance to this antibiotic at frequencies of 10(-6) to 10(-7). Teicoplanin selected teicoplanin-resistant mutants at similar frequencies. Both mutations were required to abolish the activity of the gentamicin-teicoplanin combination. As expected, simultaneous acquisition of the two types of mutations was not observed. In therapy with gentamicin or teicoplanin alone, each selected mutants in three of seven rabbits with aortic endocarditis due to VanB-type E. faecalis BM4275. The vancomycin-gentamicin combination selected mutants that were resistant to gentamicin and to the combination. In contrast, the teicoplanin-gentamicin regimen prevented the emergence of mutants resistant to one or both components of the combination. These results suggest that two mutations are also required to suppress the in vivo activity of the teicoplanin-gentamicin combination.

Animals↗
PubMed1998

[The contribution of experimental models to the physiopathology and treatment of infectious endocarditis].

The model of experimental endocarditis can be used for the investigation of the different steps in the physiopathologic process leading to the formation of the infected cardiac vegetation. It has also greatly contributed to the knowledge of the characteristics of the infected vegetation. These data allow a better understanding of the therapeutic consequences (both preventive and curative) of the physiopathologic process.

Animals↗
PubMed1998

Regression of rectal stenosis secondary to neoplasm in an HIV1-positive patient with gancyclovir antiviral therapy: report of a case.

PURPOSE: The case of a human immunodeficiency virus-positive patient with rectal stenosis caused by a tumor that completely regressed in response to gancyclovir is presented. METHODS: Several biopsies from the tumoral mass failed to show any stigmata of non-Hodgkin's lymphoma, adenocarcinoma, or Kaposi sarcoma. No parasites could be detected in rectal biopsies. Viral inclusions showing both Epstein-Barr virus and cytomegalovirus on immunostained sections suggested an unusual form of viral infection. RESULTS: Antiviral therapy (gancyclovir 10 mg/kg/day) had a dramatic effect on pain and discharge of blood, and suppressed rectal difficulties within three days of therapy. The antiviral treatment was stopped at Day 10 because of leukopenia. Endoscopic and histologic examinations revealed normal rectal mucosa after 3, 6, 9, 12, and 18 months of follow-up. CONCLUSION: This is the first case of complete and long-term regression of a rectal stenosis secondary to a tumoral mass in response to antiviral therapy in patients with human immunodeficiency virus.

Antiviral Agents↗
PubMed1998

Critical importance of in vivo amoxicillin and cefotaxime concentrations for synergy in treatment of experimental Enterococcus faecalis endocarditis.

The synergy between amoxicillin and cefotaxime against two strains of Enterococcus faecalis (JH2-2 and 6370) in vitro and in rabbit endocarditis was investigated. In vitro synergy was obtained only when amoxicillin concentrations were below the MBC and when cefotaxime concentrations were above 1 microg/ml. No synergy was observed in vivo, because of the short period of time during which these pharmacologic requirements were achieved.

Amoxicillin↗