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Biomedical subjects

S A Chartrand

Publications and source records attributed to S A Chartrand.

53 records · Page 3Linked to original sources
PubMed1987

Selective and differential medium for recovery of Pseudomonas cepacia from the respiratory tracts of patients with cystic fibrosis.

A selective and differential medium, OFPBL (oxidation-fermentation base supplemented with agar, lactose, and two antimicrobial agents), for the isolation of Pseudomonas cepacia from respiratory specimens of patients with cystic fibrosis was developed and tested. Among 725 specimens submitted from seven centers over a 4- to 6-month period, 58 (8%) yielded P. cepacia on OFPBL; only 19 of these were recovered on MacConkey or sheep blood agar (P less than 0.001). No isolate was recovered on MacConkey or sheep blood agar alone. Ranges of recovery rates among centers were 0 to 15% on OFPBL and 0 to 10% on MacConkey or sheep blood agar. Ninety percent of P. cepacia isolates were detected on OFPBL in less than or equal to 3 days. Other nonfermenters and yeasts isolated on OFPBL were distinguished from P. cepacia by failure to acidify the medium. The new medium was clearly superior to MacConkey and sheep blood agars for the isolation of P. cepacia from the respiratory secretions of patients with cystic fibrosis.

Culture Media↗
PubMed1986

Buccal cellulitis reevaluated.

We studied 72 children (17 prospectively) with acute buccal cellulitis. The median age was 11 months. Fifty-five percent of patients were bacteremic, and three children without meningeal signs or symptoms had concomitant meningitis. Cellulitis aspirate cultures (eight of 35 positive) and urine bacterial antigen tests (13 of 27 positive) were useful in making an etiologic diagnosis. Infections due to other bacteria were clinically indistinguishable from those due to Haemophilus influenzae type b. The right cheek was affected more often than the left, and only 23 (32%) of 72 patients had otitis media ipsilateral to the involved cheek. The pathogenesis of buccal cellulitis likely involves direct mucous membrane invasion rather than spread from the ipsilateral middle ear.

Acute Disease↗
PubMed1986

Aztreonam therapy for serious gram-negative infections in children.

Fifty-nine children were enrolled in an open trial of aztreonam, a monocyclic beta-lactam, therapy for serious gram-negative infections. Thirty-six infections were microbiologically evaluable and received five or more days of therapy. Patients' ages ranged from 3 days to 12 years, and diagnoses included pyelonephritis or cystitis (20), deep soft tissue or joint infection (seven), septicemia (four), pneumonia (three), peritonitis, and epiglottitis. Causative bacteria included Escherichia coli and other Enterobacteriaceae, Pseudomonas aeruginosa, and Haemophilus influenzae. The standard regimen was 30 mg/kg every six or eight hours intravenously. All isolates were aztreonam-susceptible and were eradicated during therapy. Two patients had microbiologic relapses: a patient with Salmonella choleraesuis meningitis who was initially treated for only ten days and a patient with E coli pyelonephritis. Clinical cure was achieved in 31 of 36 children. Pharmacokinetic studies performed in six children demonstrated no difference in serum concentrations or pharmacokinetic variables between day 1 and day 7 of therapy. Although several patients had transient eosinophilia (eight), elevated levels of aminotransferase (seven), or thrombocytosis (ten), no clinically significant adverse effects were noted. In this initial, uncontrolled study, aztreonam was effective and safe in the treatment of a variety of serious gram-negative infections in children.

Aztreonam↗
PubMed1986

Cefuroxime versus ampicillin plus chloramphenicol in childhood bacterial meningitis: a multicenter randomized controlled trial.

In a multicenter randomized trial, 107 children with bacterial meningitis were initially given either cefuroxime or ampicillin plus chloramphenicol. Patients were alternately assigned to 7- or 10-day courses of the designated antimicrobial regimen. CSF isolates included Haemophilus influenzae type b (89, of which 25% were beta-lactamase positive), Streptococcus pneumoniae, and Neisseria meningitidis. Although mean CSF bactericidal titers against Haemophilus isolates were 1:6 in each treatment group, H. influenzae was cultured from CSF in four of 39 patients receiving cefuroxime, 24 to 48 hours after initiation of therapy, compared with none of 40 patients given ampicillin plus chloramphenicol (P = 0.11). Clinical cure rates were similar (95%); one death occurred in each group. One child given cefuroxime had persistent meningitis after 5 days of therapy, and mastoiditis with secondary bacteremia developed in one on day 10. Three patients had relapse or reinfection. One patient who received cefuroxime for 10 days had a relapse of epiglottitis 17 days later, and of the patients given ampicillin plus chloramphenicol, one had a relapse of meningitis 1 week after 7 days of therapy, and bacteremia developed in one 42 days after completion of 10 days of therapy. No increase in either in-hospital complications or relapses occurred with a 7-day treatment course. Proof of the equivalence of the antibiotic regimens and the efficacy of 7-day courses of treatment, as well as the consequences of delayed CSF sterilization, will require additional investigation.

Adolescent↗
PubMed1986

Prostaglandin synthetase inhibition in group B streptococcal shock: hematologic and hemodynamic effects.

A rabbit model of group B Streptococcal (GBS) shock was used to study the effects of prostaglandin synthetase inhibition on the hemodynamic and hematologic response to GBS shock. The infusion of heat-killed GBS in groups I and II produced significant decreases in mean arterial pressure, neutrophil counts, and platelet counts (p less than 0.05), and significant rises in concentrations of thromboxane B2 and 6-Keto-PGF1 alpha, the stable metabolites of thromboxane A2 and prostacyclin (p less than 0.05). Administration of indomethacin (4 mg/kg) after GBS infusion (group II) was associated with a significant rise in mean arterial pressure and a significant decline in thromboxane B2 and 6-Keto-PGF1 alpha concentrations (p less than 0.05) but had no effect on GBS-induced hematologic alterations. Indomethacin administration before GBS infusion (group III) prevented alterations in mean arterial pressure and was associated with a decrease in thromboxane B2 and 6-Keto-PGF1 alpha concentrations. Indomethacin in group III did not prevent neutropenia and thrombocytopenia and may have exacerbated neutropenia. Alteration of experimental GBS shock with prostaglandin synthetase inhibition produces disparate hemodynamic and hematologic response.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

The comparison of myocardial dysfunction in three forms of experimental septic shock.

A rabbit model of septic shock was used to determine if myocardial dysfunction is a common component of shock due to diverse neonatal pathogens, and prostaglandins modulate septic myocardial dysfunction. The infusion of heat-killed Escherichia coli (group I), Haemophilus influenzae (group II), or Staphylococcus epidermidis (group III) produced significant decreases in the first derivative of left ventricular pressure with respect to time (p less than 0.05). Each organism also produced significant changes in mean arterial pressure, cardiac output, and heart rate, while pulmonary artery pressure was altered in groups I and III. Saline-infused control animals (group IV) exhibited no significant changes in any hemodynamic variable. Blood gas variables were not significantly changed in any group. These cardiovascular changes appeared dependent on arachidonic acid metabolism since indomethacin pretreatment prevented the cardiovascular changes induced by bacterial infusion. These results suggest that septic myocardial dysfunction is a common component of gram-negative and gram-positive septic shock, and that myocardial dysfunction is modulated by prostaglandin products.

Animals↗
PubMed1985

Myocardial dysfunction in group B streptococcal shock.

A rabbit model of group B Streptococcal (GBS) shock was used to determine if myocardial dysfunction contributes to GBS shock and, if so, to ascertain if prostaglandins modulate this dysfunction. The infusion of heat-killed GBS (group I) produced a dramatic decrease in the first derivative of left ventricular pressure with respect to time (LVdP/dt) from baseline values (p less than 0.05). LVdP/dt remained stable in rabbits pretreated with indomethacin (group II) and in saline-infused control rabbits (group III), and was significantly different at 30 min from LVdP/dt in group I (p less than 0.05). Values for group I mean arterial pressure, cardiac output, pulmonary vascular resistance, and heart rate and for pH and pO2 after GBS infusion were all significantly different from baseline values and from postinfusion values for groups II and III (p less than 0.05). Systemic vascular resistance and left ventricular end diastolic pressure did not change significantly in any group at any time interval. These results indicate a primary role for myocardial dysfunction in the pathogenesis of GBS shock, and suggest strongly that prostaglandins modulate GBS-induced myocardial dysfunction.

Animals↗
PubMed1984

Moxalactam therapy of Haemophilus influenzae type b meningitis in children.

Thirty-four children with Haemophilus influenzae type b meningitis were given prospectively either moxalactam (200 mg/kg/day) or ampicillin (400 mg/kg/day) plus chloramphenicol (75 mg/kg/day). One patient in each group died. The mean duration of fever, clinical response, sequential cerebrospinal fluid findings, and incidence of neurologic sequelae were similar between groups. Moxalactam cerebrospinal fluid bioactivity was significantly greater than that of ampicillin or chloramphenicol throughout therapy. Neutropenia, liver enzyme abnormalities, and diarrhea were not significantly different. In eight of 11 patients given moxalactam (versus one of 14 controls) there was complete elimination of gram-negative aerobic flora in the stools by day 10 (P = 0.002); however, none acquired Clostridium difficile. Moxalactam in effective therapy for H. influenzae type b meningitis.

Ampicillin↗
PubMed1983

Cefoperazone pharmacokinetics in acute childhood meningitis.

We studied the serum pharmacokinetics and cerebrospinal fluid concentrations of cefoperazone in 15 children with acute meningitis. Mean cefoperazone concentrations of 117 micrograms/ml in the serum and 3.8 micrograms/ml in the cerebrospinal fluid were noted 2 hours after a single 100 mg/kg dose. Following multiple 50 or 100 mg/kg doses, the mean peak serum cefoperazone concentrations were 232 and 498 micrograms/ml, respectively, with an overall mean elimination phase half-life of 2.12 hours. The data best fit a linear, two-compartment model. Cerebrospinal fluid concentrations 1.5 to 2.5 hours after the end of cefoperazone infusions ranged from 1.4 to 19.2 micrograms/ml for all doses and states of illness. This represented 1.2% to 6.4% of simultaneous serum values. The cerebrospinal fluid inhibitory titer was greater than or equal to 1:16 in 17 of 18 specimens tested against a strain of Haemophilus influenzae type b resistant to both chloramphenicol and ampicillin. In the doses given, cefoperazone produces adequate cerebrospinal fluid concentrations and bioactivity to treat the common bacterial forms of acute meningitis in infants and children.

Acute Disease↗
PubMed1983

In vitro activity of CI-919 (AT-2266), an oral antipseudomonal compound.

We tested CI-919 (AT-2266), a nalidixic acid analog, against 555 gram-positive and gram-negative bacteria, using microbroth or agar dilution methods. The activity of CI-919 was compared with those of cephalosporins, tobramycin, ticarcillin, dicloxacillin, rifampin, chloramphenicol, ampicillin, and trimethoprimsulfamethoxazole. The minimal inhibitory concentrations of CI-919 for 90% of isolates were (in micrograms per milliliter): Pseudomonas spp. (including Pseudomonas aeruginosa), 4.0; Enterobacteriaceae, 0.5; Staphylococcus spp., 2.0; Haemophilus influenzae, 0.12; Campylobacter jejuni, 0.12; and enterococci, 16. The minimal inhibitory concentrations of CI-919 for 90% of 82 tobramycin-resistant, gram-negative strains was 4.0 micrograms/ml. CI-919 was bactericidal for most isolates, showing no cross-resistance with unrelated antimicrobial agents, and was stable for 11 weeks at temperatures ranging from 22 to -70 degrees C. Inoculum size and media pH had little effect on the antibacterial activity of CI-919 for nine strains tested. CI-919 may be useful as an oral antibiotic for the treatment of infections due to diverse bacteria, including P. aeruginosa.

Anti-Bacterial Agents↗
PubMed1976

Persistent pleocytosis in bacterial meningitis.

Persistent pleocytosis of greater than 60 white blood cells/mm3 was commonly seen in children adequately treated for bacterial meningitis. It occurred in 13 of 21 (62%) children with Hemophilus influenzae meningitis and in 2 of 9 (22%) with pneumococcal meningitis. Pleocytosis alone cannot be used as an indication of prolonging therapy; significance of persistent pleocytosis is not known.

Adolescent↗
PubMedDate not supplied

Staphylococcal pneumonia in infants and children.

Records were reviewed of 79 infants and children with acute Staphylococcus aureus pneumonia admitted to our hospitals during a 13 1/2-year period from 1965 to 1978. Primary staphylococcal pneumonia was diagnosed in 61 infants (median age, 6 months) and secondary pneumonia (disseminated disease) was present in 18 children (median age, 5.5 years). Fever and signs of pleural effusion and respiratory distress were common in primary disease while fever and a toxic appearance were frequent with disseminated illness. Lobar consolidation was the most common initial roentgenographic abnormality and effusions were detected in 80% of infants with primary pneumonia and 61% of those with secondary disease. In the first 12 to 36 hours after admission 22 (28%) infants showed rapid progression of the roentgenographic abnormalities associated with worsening of the clinical condition. S. aureus was grown in blood cultures from 29% of patients with primary disease and from 89% of those with disseminated disease. The case fatality rate was 25%; factors having a significant adverse influence on the rate were admission before 1972, treatment with ineffective antibiotics, bilateral and/or multilobe pulmonary involvement and a white blood cell count of less than or equal to 10,000 cells/cu mm.

Adolescent↗