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Biomedical subjects

R H Alford

Publications and source records attributed to R H Alford.

At least 19 recordsLinked to original sources
PubMed1987

Nosocomial infectious balanoposthitis in neutropenic patients.

We have reported balanoposthitis as a source of fever and bacteremia in two neutropenic uncircumcised patients. The etiologic organisms were Pseudomonas aeruginosa in one case and Providencia stuartii in the other. In one patient, the diagnosis was delayed by the presence of a condom catheter. This emphasizes the importance of personal hygiene in uncircumcised men about to undergo immunosuppressive therapy, and the need for judicious use of condom catheters in such patients.

Agranulocytosis↗
PubMed1986

Ketoconazole's inhibition of fungal antigen-induced thymidine uptake by lymphocytes from patients with psoriasis.

Ketoconazole, an oral antifungal imidazole, has been effective in some refractory cases of psoriasis, particularly those with scalp involvement, perhaps because of suppression of Pityrosporum ovale. To assess an ancillary immunologically mediated role for ketoconazole, its effects were evaluated on psoriatic patients' lymphocyte function. Ketoconazole in vitro markedly inhibited Pityrosporum antigen-induced lymphocyte blastogenesis as indicated by impairment of cellular tritiated thymidine uptake. Ketoconazole likewise inhibited lymphocyte uptake of other pyrimidine nucleosides by both normal and psoriatic lymphocytes. Neither imidazole or an investigational triazole antifungal (Bay n7133) inhibited the uptake. Thus, ketoconazole potentially could affect psoriasis in seborrheic areas of skin by a direct antifungal action or indirectly by suppressing fungal antigen-induced lymphocyte-mediated immune responses affecting the skin.

Antigens, Fungal↗
PubMed1986

Discrepancies between disk diffusion and broth susceptibility studies of the activity of ticarcillin plus clavulanic acid against ticarcillin-resistant Pseudomonas aeruginosa.

Ticarcillin and clavulanic acid in combination were tested against 40 Pseudomonas aeruginosa isolates resistant to ticarcillin by disk diffusion. A total of 21 isolates (53%) were susceptible to ticarcillin-clavulanate by disk diffusion, under currently recommended criteria for ticarcillin susceptibility. Macro-broth dilution tests (ticarcillin plus clavulanic acid, 2 micrograms/ml) confirmed susceptibility (MIC less than or equal to 64 micrograms/ml) of only 8 (38%) of 21 isolates. Time-kill studies of disk diffusion susceptible isolates indicated 2 log10 or greater killing of most isolates at 6 h in broth containing ticarcillin (64 micrograms/ml) combined with clavulanic acid (1, 2, 5, or 10 micrograms/ml). After 6 h, regrowth was common in all concentrations of clavulanic acid except 10 micrograms/ml. Regrowth populations were resistant to ticarcillin-clavulanate by MIC determination. Poor bactericidal activity of ticarcillin-clavulanate against ticarcillin-resistant P. aeruginosa was confirmed, as most isolates did not undergo 99.9% or greater killing at 24 h in all concentrations of clavulanic acid. Serotype O-11 was our most common serotype and was associated with disk diffusion "pseudosusceptibility." Concomitant disk diffusion testing of ticarcillin-clavulanate and ticarcillin is recommended for testing the susceptibility of P. aeruginosa to ticarcillin-clavulanate by disk diffusion. P. aeruginosa isolates resistant to ticarcillin should as a rule be considered also resistant to ticarcillin-clavulanate, despite apparent susceptibility by disk diffusion.

Clavulanic Acid↗
PubMed1985

Failure of chloramphenicol and cefotaxime therapy in Klebsiella meningitis: possible role of antibiotic antagonism.

We have described a patient with Klebsiella pneumoniae meningitis who was treated with cefotaxime and chloramphenicol concomitantly, and whose slow initial resolution and subsequent relapse plus in vitro evidence of antagonism of cefotaxime appear to indicate that chloramphenicol interfered with the activity of the cephalosporin. Thus, concomitant use of chloramphenicol should probably be avoided or used advisedly in adults with gram-negative bacillary meningitis susceptible to a third generation cephalosporin.

Brain Diseases↗
PubMed1984

Antagonism by chloramphenicol of broad-spectrum beta-lactam antibiotics against Klebsiella pneumoniae.

Chloramphenicol combined with cefotaxime, moxalactam, cefoperazone, aztreonam, or imipenem was tested in vitro against clinical isolates of Klebsiella pneumoniae. By time-kill cultures (killing curves), chloramphenicol interfered with activity of all five beta-lactams. When chloramphenicol was added before the beta-lactams, the action of cefotaxime, moxalactam, or cefoperazone against all isolates was antagonized at all times tested. The action of aztreonam was antagonized against four of six isolates. With imipenem, antagonism occurred against half of the isolates at some time during 24 h when chloramphenicol was added simultaneously, provided that a sufficient inoculum of K. pneumoniae was employed. Generally, less antagonism resulted when chloramphenicol was added after the cephalosporins. Interference of bactericidal activity of three new cephalosporins by chloramphenicol has potential clinical relevance to the therapy of gram-negative bacillary meningitis. The lesser antagonism of aztreonam and imipenem by chloramphenicol is of uncertain clinical relevance but indicates that this in vitro phenomenon may apply to a wide range of beta-lactam antibiotics.

Anti-Bacterial Agents↗
PubMed1983

Comparison of ketoconazole and amphotericin B in interference with thymidine uptake by and blastogenesis of lymphocytes stimulated with Histoplasma capsulatum antigens.

Human peripheral blood lymphocytes stimulated with Histoplasma capsulatum yeasts were exposed in culture to graded concentrations of ketoconazole or amphotericin B and subsequently assessed for membrane integrity, thymidine uptake, and blastogenesis. Lymphocyte reactivity varied with concentration and duration of exposure to ketoconazole. Overt membrane toxicity resulted from exposure to 40 micrograms of ketoconazole per ml for 5 days, diminished thymidine uptake occurred with concentrations as low as 5 micrograms/ml, and 15 to 20 micrograms/ml caused a marked decrease in thymidine uptake and eventually diminished blastogenesis. The antilymphocyte action of ketoconazole was neutralized by increasing the concentration of human serum in cultures to 40% regardless of its cholesterol content. Amphotericin B activity was qualitatively similar but less pronounced.

Amphotericin B↗
PubMed1983

Histoplasma infection of abdominal aortic aneurysms.

Fungal endarteritis resulting from progressive disseminated histoplasmosis may cause arterial aneurysms, or lead to infection of pre-existing aneurysms. Three patients with Histoplasma capsulatum infections of abdominal aortic aneurysms are reported. All had previous disseminated histoplasmosis and atherosclerotic peripheral vascular disease. All were considered cured of systemic infection when their aneurysms were discovered. Atherosclerotic vascular lesions may become infected during the course of systemic fungal disease and may serve as a haven for viable organisms in patients whose dissemination recurs despite seemingly adequate antifungal therapy. In treating these patients, resection of all infected arterial tissue, revascularization through uninfected tissues, and long-term antimicrobial therapy are recommended.

Adult↗
PubMed1982

Conditions associated with relapse of amphotericin B-treated disseminated histoplasmosis.

Progressive disseminated histoplasmosis (PDH) is a rare consequence of infection with Histoplasmia capsulatum. Usually fatal if untreated, PDH generally is cured by appropriate amphotericin B treatment. Of 31 persons with uncomplicated PDH treated with amphotericin B, we found that relapse occurred in five (16%) after an interval of up to nine years after initial therapy. Review of these five cases and 31 additional relapsing cases from the literature indicates that fungal endocarditis or endarteritis without surgical treatment, underlying lymphoreticular neoplasm, and amphotericin B dosage of less than 2 g appear to be associated with relapse of PDH.

Aged↗
PubMed1981

Evolution of antimicrobial resistance and nosocomial infection. Lessons from the Vanderbilt experience.

The development of antimicrobial resistance by bacteria has had profound effects of the clinical use of antibiotics, especially in hospital-acquired infections. In 1973, a large outbreak of nosocomial infections due to Serratia marcescens began at the Vanderbilt University medical complex, a major characteristic of which was high-level resistance to gentamicin and carbenicillin. Investigation of the outbreak and subsequent in vitro studies have shown that the evolution and epidemiology of this high-level resistance operated at three levels of organizations: (1) dissemination of individual strains, (2) dissemination of a plasmid among different strains and (3) movement of a discrete genetic element, or transposon, between plasmids. The investigations of this outbreak and other studies reviewed support the concept that resistant strains can evoke as a result of R-plasmid exchange within the hospital environment, providing an opportunity for control of this exchange can be interrupted.

Carbenicillin↗
PubMed1981

Bacteremia and bacteriuria after transrectal prostatic biopsy.

To determine the efficacy of parenteral gentamicin versus povidone-iodine enema (P.I.E.) in preventing infectious complications, a randomized study was undertaken in 40 patients undergoing transrectal needle prostatic biopsy. In 69 per cent of patients not receiving P.I.E. bacteremia developed, and 32 per cent acquired bacteriuria; whereas only 19 per cent of patients given P.I.E. alone or in combination with gentamicin because bacteremic, and 9.5 per cent had postbiopsy bacteriuria. Thus, P.I.E. provided a safe and effective means for preventing most bacteremia and bacteriuria associated with transrectal biopsy of the prostate.

Adult↗
PubMed1981

Ceforanide kinetics in renal insufficiency.

Ceforanide (500 mg) was infused intravenously over 30 min into six normal subjects, 10 nondialysis patients with renal insufficiency, and six hemodialysis patients. Dialysis patients received two ceforanide infusions, one immediately before dialysis and another during an interdialysis period. Sequential plasma samples over 24 to 72 hr were assayed for ceforanide. Peak ceforanide levels (mean = 69 +/- 12 micrograms/ml) and volumes of distribution did not vary with creatinine clearance (Clcr, ml/min/1.73 m2) and both plasma clearance and renal clearance decreased linearly as Clcr decreased. Mean nonrenal clearance (4.6 +/- 1.8 ml/min/1.73 m2) did not vary with Clcr. Mean half-life was 3 hr in the normal subjects, increasing to approximately 25 hr in patients with severe renal insufficiency. Hemodialysis resulted in a removal of approximately 21% of the dose of ceforanide. Dosing recommendations for patients with renal insufficiency are provided.

Adult↗
PubMed1981

Superior activity of N-formimidoyl thienamycin against gentamicin-resistant Pseudomonas aeruginosa.

N-Formimidoyl thienamycin (N-F-thienamycin), cefotaxime, moxalactam, and cefsulodin were tested by agar dilution against 125 isolates of Pseudomonas aeruginosa, Serratia marcescens, Klebsiella pneumoniae, and Providencia stuartii. Against gentamicin-susceptible P. aeruginosa, N-F-thienamycin and cefsulodin were most active. Only N-F-thienamycin inhibited gentamicin-resistant P. aeruginosa at less than or equal to 4 microgram/ml. N-F-thienamycin's activity equaled or surpassed that of the other antibiotics tested against both the gentamicin-susceptible and -resistant Enterobacteriaceae.

Anti-Bacterial Agents↗