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Biomedical subjects

Y Aujard

Publications and source records attributed to Y Aujard.

At least 91 records · Page 5Linked to original sources
PubMed1989

[Staphylococcal toxic shock in children].

Toxic shock syndrome (TSS) is reported in 2 children. TSS occurred 10 days after an accidental injury of the fore foot in one case and 5 days following surgery for severe uretero-vesical reflux in the other. The clinical illness was defined by the case definition formulated for epidemiologic studies (CDC, 1982). The diagnosis was confirmed by isolation of a Staphylococcus aureus strain producing TSST, at the infected site. Toxin-induced mediators such as interleukin I and Tumor Necrosis Factor have been incriminated in septic shock with multivisceral involvement. As in our 2 cases, the syndrome may be delayed or even absent.

Adolescent↗
PubMed1988

Treatment of type III von Willebrand's disease with solvent/detergent-treated factor VIII concentrates.

An intermediate purity concentrate of factor VIII, treated with solvent and detergent (SD), was successfully used for treatment of intracerebral hematoma in a newborn with type III von Willebrand's disease. At the present time, the SD process used for the preparation of this factor VIII concentrate seems to be one of the most effective methods for viral inactivation. In this product, the biological properties of factor VIII and von Willebrand factor are preserved. Thus, the intermediate purity factor VIII SD concentrate could be used instead of frozen cryoprecipitate, as a safer therapy in the treatment of von Willebrand's disease.

Bleeding Time↗
PubMed1987

[Evaluation of the bactericidal curves of beta-lactam and aminoglycoside combinations at the concentrations obtained in the cerebrospinal fluid in Haemophilus influenzae meningitis].

The prognosis and sequelae of patients with Haemophilus influenzae meningitis were related to concentrations of bacteria in the cerebrospinal fluid (CSF). Rapid bacterial killing and rapid reduction of organisms in vivo in CSF are critical to the outcome. In our patients colony counts of Haemophilus influenzae in CSF were 10(2)/ml - 10(9)/ml (mean 10(5)/ml). Killing kinetics were determined for amoxicillin and cefotaxime, alone and in combination with amikacin, against 35 clinical strains of Haemophilus influenzae (43% beta-lactamase-positive) at concentrations of these antibiotics comparable to those attained in the CSF following systemic administration. Antibiotics concentrations were: amoxicillin: 5 mg/ml, cefotaxime: 3.8 mg/l, amikacin: 1.8 mg/l. Mean killing curves with beta-lactamase-negative strains showed that a bactericidal effect was observed at 18 h for amoxicillin, at 5 h for cefotaxime, at 5 h for amoxicillin plus amikacin and at 2 h 30 for cefotaxime plus amikacin. Against beta-lactamase-positive strains a bactericidal effect was observed at 5 h for cefotaxime, at 2 h 30 for cefotaxime plus amikacin and at 18 h for amoxicillin plus amikacin. The finding of significantly increased killing rates of Haemophilus influenzae by amikacin at low concentration in the presence of either ampicillin or cefotaxime suggests that combined therapy may be beneficial in the treatment of meningitis caused by Haemophilus influenzae.

Amikacin↗
PubMed1987

[Treatment of neonatal infections: the place of cephalosporins].

The most commonly used antibiotic combination as a first-line treatment in neonates is ampicillin and an aminoglycoside. The increasing resistance of E. coli to ampicillin requires another choice. Good activity against group B Streptococci and E. coli, good CSF penetration and fewer side-effects are in favour of third generation cephalosporins as part of the antibiotic therapy. If a Listeria infection has not been excluded at the beginning of treatment, a triple combination may be given: ampicillin + third generation cephalosporin + aminoglycoside during the first 48 hours. The prognosis of enterobacterial meningitis has improved with third generation cephalosporins. As the other beta-lactam antibiotics, they modify the intestinal microbial ecosystem.

Bacterial Infections↗
PubMed1987

Urinary excretion of N-acetyl-glucosaminidase and beta-2-microglobulin as early markers of gentamicin nephrotoxicity in neonates.

A prospective study in 16 healthy and 16 gentamicin-treated neonates was undertaken to compare the urinary excretion of proximal tubular markers such as beta 2-microglobulin (beta 2-m) and total N-acetyl-beta-D-glucosaminidase (NAG) and its isoenzymatic form NAGB. beta 2-m excretion was not related to postnatal age in control full-term neonates; it was significantly increased in gentamicin-treated full-term neonates. The urinary excretion of the lysosomal markers, total NAG and NAGB, rose significantly with postnatal age in control group. fMean values for total NAG and NAGB were significantly higher in the treated group but the isoenzymatic profile (NAGB/total NAG X 100) was not modified by gentamicin treatment.

Acetylglucosaminidase↗
PubMed1987

[Importance of the study of the minimal bactericidal time of serum in the choice of optimal treatment of neonatal septicemias].

Rapid eradication of bacteria in bloodstream is critical for the outcome in neonatal bacterial sepsis. Two groups of neonates with E. coli K1 sepsis without purulent meningitis were studied. Group I (n = 14) received cefotaxime IV (100 mg.kg-1 D-1) plus netilmicin (4 mg.kg-1 D-1); group II (n = 8) received amoxicillin/clavulanic acid IV (100/10 mg.kg-1 D-1) plus netilmicin (4 mg.kg-1 D-1). Both groups were identical. For all strains MICs of cefotaxime, amoxicillin/clavulanic acid, netilmicin were less than 0.2, 4 and 1 mg/l respectively. Serum bactericidal activity (SBA) was determined for each patient (peak sample). The SBA was defined as the greatest dilution in which 99,99% of the inoculum was killed. Time-kill curves were performed with 1:16 dilutions of peak serum samples to measure the kinetic of bacterial killing. The minimal bactericidal time of serum (MBTS) was defined as the minimal time required to observe a decrease of more than 4 log CFU/ml of the bacterial inoculum. Samples (10 microliters) were taken at 1 h intervals over a 6 h period and at 24 h for quantitative culture. All patients cured. Median SBA were respectively 1/128 and 1/64 for group I and II. However, mean MBTS for groups I and II were respectively 1.2 h +/- 0.8 and 3.9 h +/- 1.4. Killing was more rapid in group I (p less than 0.01). The MBTS may be a clinically useful adjunctive test when optimal therapy would be expected.

Amoxicillin↗
PubMed1987

[Prevention of nephrotoxicity of amphotericin B during the treatment of deep candidiasis].

Previous observations suggest that tubulo-glomerular feedback could be involved in amphotericin B nephrotoxicity. We then investigated the influence of sodium status on the occurrence of renal damage during amphotericin B therapy. A retrospective survey demonstrated that impaired renal function occurred during therapy in 67 per cent of the patients who received amphotericin B alone and in 12 per cent of the patients who received amphotericin B and ticarcillin (parenteral sodium supplement of 100-150 meq per day). Prospective studies were then undertaken both in adults and children. Intravenous sodium supplement was given intravenously as routine prophylaxis with amphotericin B therapy. In all courses amphotericin B was successfully administered without deterioration in renal function. These results support the hypothesis that parenteral sodium supplementation reduces the frequency of developing impaired renal function during amphotericin B therapy.

Adult↗
PubMed1986

[A Parisian case of congenital malaria].

A case of symptomatic congenital malaria (Plasmodium vivax) was diagnosed and treated in a 3 week-old girl in Paris. This led to discuss the characteristics of transplacental contamination and symptomatology of congenital malaria and the methods for diagnosis and treatment of this very rare disease.

Chloroquine↗
PubMed1986

[Optimum choice of antibiotic treatment in neonatal infections due to group B streptococci].

Morbidity and mortality among neonates with group B streptococcal infections remain high. As delays in bacterial killing may be responsible for these poor results, there is a need for studies into killing kinetics. We investigated antimicrobial sensitivity and killing effect time lags for penicillin, ampicillin and mezlocillin, alone and in combination with gentamicin or amikacin, against 20 strains of group B streptococci isolated in cultures of blood and cerebrospinal fluid from neonates. A culture of each strain (10(5) germs/ml) was exposed to the antibiotics individually or in combination. Antibiotics were used in the concentrations achieved clinically. Surviving bacteria were counted after 2 h 30, 4 h 30 and 24 h. incubation. Mean killing curves showed that the time interval until onset of a killing effect was 24 hours with either penicillin or ampicillin alone, against 4 h 30 with penicillin-amikacin or ampicillin-gentamicin. The most rapid killing effect (2 h 30) was observed with mezlocillin alone and ampicillin-amikacin. No antagonism was found between mezlocillin and aminoglycosides. Choice of the best antibiotic treatment for group B streptococcal infections should be based on both the rapidity of the in vitro killing effect and the antibiotic's diffusion into the site of the infection.

Amikacin↗
PubMed1986

[Amniotic fluid and neonatal infection].

Bacterial contamination of amniotic fluid (AF) leads to a fetal contamination and, in less than 10% of cases, to an infection. A rupture of the membranes longer than 24 hours increases the frequency of bacterial contamination/infection of the fetus. However an AF contamination, due to a pathogen bacteria found in the vaginal flora, is possible trough intact membranes. Quantitative bacteriological studies of AF allows to predict an high risk of fetal infection. Antibacterial substances are found in AF, specially a zinc protein complex which has bacteriostatic activity against E. Coli and Streptococcus B in, respective, 68% and 36% of caucasian women. Heavy contamination, virulence of the pathogen and neonatal immunity are, with AF antibacterial factors, the parameters explaining why an AF contamination can lead to fetal/neonatal infection.

Amniotic Fluid↗