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D J Krogstad

Publications and source records attributed to D J Krogstad.

At least 91 records · Page 5Linked to original sources
PubMed1980

Defective killing of enterococci: a common property of antimicrobial agents acting on the cell wall.

We tested the ability of antimicrobial agents that act on the cell wall to kill enterococci and found defective killing (a minimal bactericidal concentration/minimal inhibitory concentration ratio of greater than or equal to 32) with both beta-lactams (penicillin G and cephalothin) and non-beta-lactams (vancomycin, cycloserine, and bacitracin). Our results indicate that the resistance of enterococci to antimicrobial killing spans the spectrum of agents known to inhibit cell wall synthesis and suggest that the mechanism responsible for enterococcal resistance to killing by these drugs may be a defective autolytic enzyme system.

Anti-Bacterial Agents↗
PubMed1980

Medicine in Malawi.

Explore the source record for details and available documents.

Delivery of Health Care↗
PubMed1978

Plasmid-mediated resistance to antibiotic synergism in enterococci.

Mating experiments have shown that high-level resistance (minimal inhibitory concentration greater than 2,000 microgram/ml) to streptomycin and kanamycin, and resistance to penicillin-streptomycin and penicillin-kanamycin synergism are transferable by conjugation from resistant clinical isolates of enterococci to a sensitive recipient strain. Cesium chloride-ethidium bromide ultracentrifugation revealed a satellite (plasmid) band in resistant clinical isolates and the transconjugant strains but not in the sensitive recipient. Examination of these satellite bands by agarose gel electrophoresis and electron microscopy demonstrated a common plasmid with a weight of 45 megadaltons. Novobiocin treatment of a resistant clinical isolate produced simultaneous loss of high-level resistance to streptomycin and kanamycin, and of resistance to penicillin-aminoglycoside synergism. These results suggest that (a) high-level resistance to streptomycin and kanamycin among some clinical isolates of enterococci is associated with a 45 megadalton plasmid, and (b) the same plasmid is also responsible for the resistance to penicillin-aminoglycoside synergism observed in these strains.

Aminoglycosides↗
PubMed1978

Aminoglycoside-inactivating enzymes in clinical isolates of Streptococcus faecalis. An explanation for resistance to antibiotic synergism.

Clinical isolates of enterococci (Streptococcus faecalis) with high-level resistance to both streptomycin and kanamycin (minimal inhibitory concentration >2,000 mug/ml), and resistant to synergism with penicillin and streptomycin or kanamycin were examined for aminoglycoside-inactivating enzymes. All of the 10 strains studied had streptomycin adenylyltransferase and neomycin phosphotransferase activities; the latter enzyme phosphorylated amikacin as well as its normal substrates, such as kanamycin. Substrate profiles of the neomycin phosphotransferase activity suggested that phosphorylation occurred at the 3'-hydroxyl position, i.e., aminoglycoside 3'-phosphotransferase. A transconjugant strain, which acquired high-level aminoglycoside resistance and resistance to antibiotic synergism after mating with a resistant clinical isolate, also acquired both enzyme activities. Quantitative phosphorylation of amikacin in vitro by a sonicate of the transconjugant strain inactivated the antibiotic, as measured by bioassay, and the phosphorylated drug failed to produce synergism when combined with penicillin against a strain sensitive to penicillin-amikacin synergism.No differences were found in the sensitivity of ribosomes from a sensitive and resistant strain when examined in vitro using polyuridylic acid directed [(14)C]-phenylalanine incorporation in the presence of streptomycin, kanamycin, or amikacin. Therefore, we conclude that aminoglycoside-inactivating enzymes are responsible for the aminoglycoside resistance, and resistance to antibiotic synergism observed in these strains.

Aminoglycosides↗
PubMed1978

Amebiasis: epidemiologic studies in the United States, 1971-1974.

Seven investigations of suspected foci of amebiasis between October 1971 and June 1974 lead to three conclusions. (1) A number of laboratories have vastly overdiagnosed amebiasis and have reported leukocytes in stools as Entamoeba histolytica. Two laboratories found to be in error were in community hospitals, and one was at a teaching hospital associated with a medical school and a school of public health. These three laboratories had been diagnosing more than 1200 cases of amebiasis a year for 20 years. (2) When amebiasis does occur, it is likely to be misdiagnosed. In one outbreak with four cases and three deaths, amebiasis was not diagnosed until two patients had died and another was critically ill. Sporadic cases may be mistakenly diagnosed as ulcerative colitis and inappropriately treated with steroids. (3) Foci of endemic amebiasis continue to exist in the United States, both in institutions and in noninstitutional settings.

Amebiasis↗
PubMed1977

Resistance to six aminoglycosidic aminocyclitol antibiotics among enterococci: prevalence, evolution, and relationship to synergism with penicillin.

Two hundred and three recent clinical isolates of enterococci were tested for susceptibility to streptomycin, kanamycin, amikacin, gentamicin, sisomicin, and tobramycin. Depending upon the source of the isolate, 36 to 54% of the enterococci demonstrated high-level resistance (minimal inhibitory concentration, >2,000 mug/ml) to streptomycin, 16 to 49% to kanamycin, and 0 to 14% to amikacin. None of the strains was highly resistant to gentamicin, sisomicin, or tobramycin. A comparison with isolates of enterococci obtained in 1968 revealed that there has been a decrease in prevalence of high-level resistance among organisms isolated from wound cultures in 1976. However, no decrease in resistance to streptomycin or kanamycin was demonstrated among blood or urine isolates. Penicillin, combined with gentamicin, sisomicin, or tobramycin, was synergistic against all 10 strains of Streptococcus faecalis subjected to formal testing. For streptomycin and kanamycin, the presence or absence of synergism with penicillin correlated with the absence or presence of high-level aminoglycoside resistance. High-level resistance to amikacin was seen in only 1 of the 10 strains. Nonetheless, combinations of penicillin plus amikacin failed to produce synergistic killing against 6 of the 10 strains. Indeed, the combination was synergistic only against those four strains that were susceptible to high levels of kanamycin.

Aminoglycosides↗
PubMed1976

Pneumocystis carinii pneumonia in the United States: epidemiologic, diagnostic, and clinical features.

Analysis of 194 patients with confirmed Pneumocystis carinii pneumonia in the United States over a 3-year period revealed that P. carinii pneumonia occurred almost exclusively in the immunosuppressed host who had a serious underlying disease. The epidemiologic features of pneumocystis pneumonia primarily reflected those of the underlying disease. P. carinii was identified antermortem in 81% of the cases usually by biopsy or needle aspiration of the lung, procedures associated with considerable morbidity and morbidity and mortality. Laboratory identification of P. carinii was usually accurate, but errors resulting from fault staining tecnique occurred. Most patients had been ill less than 2 weeks with bilateral diffuse interstitial pneumonia. Leukopenia (white blood cell count less than or equal to 3,00/mm3) and probably severe hypoxia were negative prognostic factors. Although treatment with pentamidine was effective, the drug frequently cased adverse reactions, particularly impaired renal function, when given with other nephrotoxic agents.

Adolescent↗
PubMed1975

A prospective study of the effects of ultralow volume (ULV) aerial application of malathion on epidemic Plasmodium falciparum malaria. IV. Epidemiologic aspects.

In the Miragoane Valley of Haiti a consistent pattern in the incidence of Plasmodium falciparum malaria over a 10-year period made it possible to predict an annual outbreak and perform a prospective study to test the effects of aerial ultralow volume (ULV) malathion on epidemic levels of this disease. At the end of October 1972, after epidemic levels (100 cases/month/10,000 population) had been reached, spray operations were begun. The first spray cycle produced a sharp and immediate drop in populations of the vector Anopheles albimanus, followed 4 weeks later by a decrease in the incidence of malaria throughout the valley. Although the incidence of malaria was similar in sprayed and unsprayed areas prior to the effect of ULV malathion (176.1 and 198.7 cases/month/10,000 population, respectively), it was significantly different during the subsequent 3 months (16.8 cases/month/10,000 population in sprayed areas and 65.4 in unsprayed; p less than 0.001). Travel histories indicated that only 4% of all cases had spent a night away from home during the 4 weeks prior to onset of symptoms; therefore, we concluded that these incidence data represent malaria transmission in the valley. Results of the study indicate that aerial spraying of ULV malathion can interrupt epidemic transmission of P. falciparum malaria by a susceptible vector.

Adolescent↗
PubMedDate not supplied

Accumulation of chloroquine by membrane preparations from Plasmodium falciparum.

Chloroquine susceptibility and resistance have been associated respectively with the uptake and efflux of chloroquine by Plasmodium falciparum. We made membrane preparations from parasitized and unparasitized red cells in order to study chloroquine accumulation in a cell-free system. The accumulation of [3H]chloroquine by these preparations is inhibited by unlabeled chloroquine and thus is specific. Only membranes from parasitized red cells demonstrate time-dependent chloroquine accumulation; membranes from unparasitized red cells do not. Chloroquine accumulation is eliminated by detergent (0.05% Triton X-100) and reduced by a hypertonic medium, consistent with accumulation inside membrane vesicles rather than binding to membranes. Accumulation is energy dependent; it has a specific requirement for ATP, which cannot be replaced with GTP, CTP, UTP, TTP or ADP, an apparent Km of 21 microM and an apparent Vmax of 4.6 pmol (mg protein)-1 h-1. Vesicle acidification is MgATP dependent, and is reversed by NH4Cl. Chloroquine accumulation is inhibited by reduced medium pH, N-ethylmaleimide or oligomycin, but not by vanadate or ouabain. These studies demonstrate that membrane vesicles prepared from parasitized red cells provide a model system for the study of chloroquine accumulation by P. falciparum.

Acetylcholine↗
PubMedDate not supplied

Reliability of disc diffusion susceptibility testing.

We retested 2,181 bacteria-antibiotic combinations with the Kirby-Bauer disc-diffusion technique and found interpretive changes with 120 (5.5%). Most changes (101 of 120) were single steps (i.e. from R to I, I to R or S, or S to I). Of the 19 remaining, 10 of them were from R to S and nine from S to R. These changes were significantly more frequent for combinations with zone diameters clustered near interpretive breakpoints (within 2mm) than for other combinations, and there was a linear relationship between decreased reproducibility and increased clustering near interpretive breakpoints. Based on an analysis of all susceptibility testing results performed in 1978, combinations most commonly clustered near interpretive breakpoints included: Ampicillin with Klebsiella pneumoniae; erythromycin with enterococci; chloramphenicol with Serratia marcescens; gentamicin with Pseudomonas aeruginosa and enterocci; and tetracycline with Enterobacter spp., Escherichia coli, and K. pneumoniae.

Anti-Bacterial Agents↗