[Sensitivity of Streptococcus A and B towards penicillin G, penicillin V, ampicillin and amoxicillin].
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Amoxicillin↗
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Results for “Penicillin G”
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Infective endocarditis caused by Streptococcus bovis resistant to the lethal effect of penicillin G.
Penicillin G alone is generally recommended for the treatment of infective endocarditis caused by Streptococcus bovis because clinical isolates of S bovis are represented as being uniformly and markedly susceptible to penicillin G. However, two strains of S bovis recovered from two patients with bacterial endocarditis were resistant to the lethal effect of penicillin G. Combination therapy, cefazolin sodium and gentamicin sulfate in patient 1 and penicillin G and gentamicin in patient 2, was necessary; synergy, as manifested by lethal activity against the infecting strains, was demonstrated in the laboratory. We stress the need to determine the minimal lethal concentration of penicillin G for clinical isolates of S bovis. Until such information is available, particularly in life-threatening infections, combination drug therapy, consisting of an aminocyclitol added to a beta-lactam antimicrobic, should be used.
Cefazolin↗
Conformations of penicillin G: crystal structure of procaine penicillin G monohydrate and a refinement of the structure of potassium penicillin G.
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Crystallography↗
Stabilizing effect of penicillin G sulfoxide, a competitive inhibitor of penicillin G acylase: its practical applications.
We have found that penicillin G sulfoxide (pen G SO) behaves as a general stabilizing agent of two bacterial penicillin G acylases (PGAs) from E. coli and from K. citrophila), and this role is related to a strong inhibitory effect on the enzymes. The stabilizing effect has been observed during two different inactivation processes: (i) thermal inactivation of soluble enzymes at alkaline pH, and (ii) inactivation of immobilized enzymes as a consequence of covalent multiinteraction with highly activated agarose aldehyde gels. At the same time, pen G SO behaves as a strong competitive inhibitor of these two enzymes. The inhibition constant is more than 10-fold lower than the one corresponding to another smaller competitive inhibitor, phenylacetic acid (PAA), the structure of which is exactly the acyl donor moiety corresponding to pen G SO. In turn, PAA hardly exerts any stabilizing effect on PGAs. The stabilizing effect of pen G SO allowed the preparation of derivatives of these PGAs preserving full catalytic activity in spite of being 1,400- and 650-fold more stable than the corresponding soluble or one-point attached immobilized enzymes.
Enzyme Stability↗
[Treatment of syphilis using a depot penicillin G preparation based on serum penicillin level determination].
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Delayed-Action Preparations↗
Evaluation of three newer methods for investigating protein interactions of penicillin G.
THE INTERACTION OF PENICILLIN G WITH HUMAN SERUM PROTEINS WAS EVALUATED BY THREE DIFFERENT TECHNIQUES: rate of dialysis, cross-linked dextran exclusion, and ultracentrifugation. The rate-of-dialysis technique demonstrated that penicillin G binding to serum was immediate but incompletely reversible. Cross-linked dextran adsorbed or trapped significant amounts of penicillin G, necessitating correction factors of more than 10%. Ultracentrifugation was found to be the most reliable method for quantitative protein-binding determinations of penicillins.
Blood Proteins↗
"Comparably massive" penicillin G therapy in renal failure.
Impairment of penicillin G excretion in renal failure may result in life-threatening, dose-related toxicity. We report a method for achieving a desired mean serum penicillin G concentration in patients with renal failure, with minimal risk of both undertreatment and drug toxicity. The method is based on the linear relation between the total plasma clearance of penicillin G (Cpen) and the endogenous creatinine clearance. The daily maintenance dose of penicillin G (units) is defined by the product, Cpen (ml/min) times desired mean serum penicillin G concentration (mug/ml) times 2300. Application of this method to patients with various degrees of renal impairment by either constant-rate infusion or intermittent infusion gave serum penicillin G concentrations within the desired range in all but 1 of 15 instances. On the basis of these observations, practical guidelines for "comparably massive" penicillin G therapy are suggested.
Adult↗
[Evaluation of the biliary excretion of penicillin G. (author's transl)].
Biliary excretion of penicillin G was studied experimentally by perfusion of isolated rabbit liver. Under these conditions, bile recovery accounted for 5% of the amount of penicillin G added to the perfusing blood (10 mg); peak biliary level averaged 135.3 micrograms/ml. In man after intravenous administration of a 599 mg dose of penicillin G (1 MU) to patients provided with T-tube drainage (n = 10), the maximum biliary concentration averaged 18.0 +/- 8.0 micrograms/ml at 2 hours; biliary recovery of penicillin G accounts for 0.12% of the administered dose. The excretion of penicillin G in the juice collected through duodenal tubing in normal subjects averaged 0.07% of the administered dose (599 mg IV). Per-operative assays showed that the concentration determined at 1 hour after intravenous administration of the drug (599 mg) in the gallbladder bile (45.7 +/- 16.7 micrograms/ml) and common duct bile (93.5 +/- 16.3 micrograms/ml) were definitely higher (4.5--9 times) than the serum levels measured simultaneously. The biliary excretion of penicillin G is compared with the biliary elimination of a certain number of beta-lactam derivatives studied under the same conditions (ampicillin, metampicillin, carbenicillin, cefalothin, cefaloridine, cefacetrile, cefalexin, cefazolin).
Animals↗
Effects of site-directed mutations on processing and activities of penicillin G acylase from Escherichia coli ATCC 11105.
Penicillin G acylase from Escherichia coli ATCC 11105 is synthesized from its precursor polypeptide into a catalytically active heterodimer via a complex posttranslational processing pathway. Substitutions in the pair of aminoacyl residues at the cleavage site for processing the small and large subunits were made. Their processing phenotypes and penicillin G acylase activities were analyzed. By the introduction of a prolyl residue at either position, the processing of the small subunit was blocked without a change in enzymatic activity. Four other substitutions had no effect. At the site for processing the large subunit, four substitutions out of the seven examined blocked processing. In general, penicillin G acylase activity seemed to be proportional to the efficiency of the large-subunit-processing step. Ser-290 is an amino acid critical for processing and also for the enzymatic activity of penicillin G acylase. In the mutant pAATC, in which Ser-290 is mutated to Cys, the precursor is processed, but there is no detectable enzymatic activity. This suggests that there is a difference in the structural requirements for the processing pathway and for enzymatic activity. Recombination analysis of several mutants demonstrated that the small subunit can be processed only when the large subunit is processed first. Some site-directed mutants from which signal peptides were removed showed partial processing phenotypes and reduced enzymatic activities. Their expression showed that the prerequisite for penicillin G acylase activity is the efficient processing of the large subunit and that the maturation of the small subunit does not affect the enzymatic activity.
DNA Mutational Analysis↗
Streptococcal pharyngitis in children. A comparison of four treatment schedules with intramuscular penicillin G benzathine.
Four hundred children with streptococcal pharyngitis were treated randomly with single injections in groups of 100 each (1) with 600,000 units of penicillin G benzathine, (2) 1.2 million units of penicillin G benzathine, (3) 600,000 units of penicillin G benzathine and 600,000 units of penicillin G procaine, or (4) 900,000 units of penicillin G benzathine and 300,000 units of penicillin G procaine. Clinical response and severity of local reaction were judged in a double-blind manner at 24, 48, and 72 hours; throat cultures were taken then, and at 10, 21, and 42 days. Although the clinical response to 900,000 units of penicillin G benzathine and 300,000 units of penicillin G procaine was equal to 1.2 million units of penicillin G benzathine, the former cleared the streptococci more quickly, greatly reduced the incidence and severity of local reactions, and offered optimal therapy for streptococcal pharyngitis in the pediatric age group.
Age Factors↗
Pharmacokinetics of penicillin G in the turkey.
Parmacokinetics of penicillin G was determined for the turkey. The study was prompted by the isolation of a sulfonamide-resistant strain of Pasteurella multocida from tissues of turkeys involved in an outbreak of fowl cholera and the subsequent discovery that little pharmacologic information was available concerning other antimicrobial agents in that species. Penicillin G was chosen for study because P multocida is susceptible to this antibiotic. The elimination of the antibiotic followed first-order kinetics, and the half-life was found to be 0.5 hours. Parenteral administration of benzathine-procaine penicillin G resulted in higher concentrations, which persisted for longer periods than did procaine or potassium salts of the antibiotic.
Animals↗
Production of rat homocytotropic antibodies using low dose, long term oral exposure to penicillin G.
Sera from 15 patients with immediate hypersensitivity reactions to penicillin G gave positive responses in the rat mast cell test (RMCT) indicating the presence of IgE-type antibodies in the sera. Five sera were from patients who had had reactions to penicillin 15 to 22 years previously without known re-exposure to this antigen. To explore the possibility that non-therapeutic exposure to penicillin may have produced continued sensitization in these patients, an animal model system was developed to explore the efficacy of low dose, long term oral exposure to penicillin G in rats for producing homocytotropic antibodies in these animals. It was found that when rats were given penicillin G in their drinking water at concentrations of 0.1 to 1 U/ml over a period of 1 to 3 months they produced serum IgE and IgGa antibodies. In addition, IgE antibodies were actively bound to the peritoneal mast cells of these animals. The presence of circulating or cell bound antibodies was detected using the rat mast cell test. It was also shown that rats given penicillin G orally for 1 month were more prone to antibody production after a single intramuscular injection of penicillin G compared to a control group receiving only the intramuscular injection of this antigen. The results of this study are discussed in terms of possible non-therapeutic sensitization towards penicillin G in the human population.
Administration, Oral↗
Effect of 60Co-irradiation on penicillin G procaine in veterinary mastitis products.
The effect of 60Co-irradiation on penicillin G procaine in a peanut oil-based veterinary mastitis product was examined by reversed-phase high-performance liquid chromatography (HPLC). The HPLC method is capable of separating and quantifying procaine, penicillin G, and various degradation compounds. Penicillin G recovery from a placebo formulation was 100.4% with a relative standard deviation of less than 1%. When irradiated at 4.0 Mrads, the penicillin G in two product lots decreased slightly (approximately 1-2%) with a corresponding increase in two compounds inherently present in bulk penicillin G powder. These compounds may be formed in abundance by treating penicillin G in an acidic solution. From the mass spectrometric analysis and the relative retention data with authentic compounds, these compounds were identified as benzylpenilloaldehyde and benzylpenaldic acid. Values obtained by the HPLC method on the product irradiated and stored at various temperatures correlated well with those of the microbiological assay. No significant decrease in the procaine was detected even after 4.0-Mrad irradiation. The HPLC method is applicable for analysis of other beta-lactam antibiotics.
Animals↗
[In vitro antibacterial effects of spectinomycin and penicillin G on Neisseria gonorrhoeae singly and in combination (author's transl)].
The antibacterial effects of spectinomycin and penicillin G on clinical isolates of Neisseria gonorrhoeae were studied. The concentrations of penicillin G at which the isolates showed drug sensitivity ranged widely from 0.011 to 6.25 mug/ml. Some of the isolates were resistant to penicillin G. Sensitivity to spectinomycin was observed at the drug concentrations ranging from 3.13 to 12.5 mug/ml. About 60% of the isolates were sensitive to 6.25 mug/ml of spectinomycin, and those isolates which were resistant to penicillin G showed good sensitivity to spectinomycin. No correlation in sensitivity was noted between the two drugs. Tests for their bactericidal activities on bouillon media revealed that the addition of spectinomycin at the concentration of 12.5 mug/ml or over produced a marked bactericidal effect in a short time while penicillin G exhibited a bactericidal or bacteriostatic effect depending upon the concentration used. A synergistic effect of a penicillin and an aminoglycoside antibiotic was observed in these isolates of N. gonorrhoea as was in the isolates of Pseudomonas aeruginosa. Where penicillin G and spectinomycin were used in combination, a simultaneous addition of both the drugs produced the most marked synergistic effect. Morphology of N. gonorrhoeae cells exposed to either of these drugs was examined under a scanning electron microscope. Exposure to spectinomycin at the level of 6.25 mug/ml resulted in almost no morphological change. At 6.25 mug/ml of the drug, however, a roughened cell surface, a bleb-like structure or a state suggesting the loosening of such a bleb-like structure was noted. The addition of penicillin G at 0.19 mug/ml led to an impairment of cell division at one hour of exposure and to cell swelling and lysis with further exposure. At 1.19 mug/ml of the drug, these processes of cell swelling and lysis took place early.
Drug Combinations↗
Antimicrobial susceptibility testing of pneumococci: determination of Kirby-Bauer breakpoints for penicillin G, erythromycin, clindamycin, tetracycline, chloramphenicol, and rifampin.
Antimicrobial susceptibility testing of pneumococci is now essential to monitor for the presence of resistance to agents such as the penicillins, macrolides, lincomycins, chloramphenicol, and tetracycline. In this study, clinical isolates of a selection of resistant South African strains were tested for antimicrobial susceptibility by minimal inhibitory concentration (MIC) determination and by a modified Kirby-Bauer disk diffusion technique, using Mueller-Hinton medium supplemented with 5% horse blood. Disk diffusion breakpoints were determined for penicillin G, erythromycin, clindamycin, tetracycline, chloramphenicol, and rifampin. Reliable results were obtained on disk diffusion for all these agents except for penicillin G. With 6-mug penicillin G disks, zones of strains with intermediate penicillin susceptibility overlapped those of sensitive and resistant strains. With 5-mug methicillin disks, clearer separation of strains based on susceptibility to penicillin G occurred. Strains with zones of <35 mm around penicillin G disks and <25 mm around methicillin disks should have penicillin G MICs determined to confirm their resistance to penicillin G. In view of the potential for pneumococci to be resistant to the agents used in this study, antimicrobial susceptibility of all clinically significant isolates should be determined.
Chloramphenicol↗
Renal tubular transport of penicillin G and carbenicillin in the rat.
The pattern of transport of penicillin G and carbenicillin was examined directly in the rat kidney by means of micropuncture studies. Samples of plasma, tubular fluid, and urine were assayed for antibiotic content by an agar diffusion technique. Secretion accounted for 67% of the penicillin G but for only 37% of the carbenicillin present in the proximal tubule. No further net secretion of either agent could be detected in the distal nephron. Net secretion of penicillin G decreased from 67% in the distal tubule to 60% in the urine (P less than 0.05%); this reduction correlated with reabsorption of water from the collecting ducts. Both penicillin G and carbenicillin were secreted by the proximal tubule of the rat nephron, but the latter was secreted at a lower rate than the former. A significant fraction of penicillin G was reabsorbed from the collecting ducts under conditions of maximal antidiuresis.
Animals↗
Biosynthesis of peptidoglycan in Gaffkya homari. The mode of action of penicillin G and mecillinam.
The effect of the beta-lactam antibiotics penicillin G and mecillinam on the incorporation of peptidoglycan into pre-formed cell wall peptidoglycan was studied with wall membrane enzyme preparations from Gaffkya homari. Using UDP-N-acetylglucosamine (UDP-GlcNAc) and UDP-N-acetylmuramyl-pentapeptide (UDP-MurNAc-pentapeptide) as precursors the incorporation of peptidoglycan into the pre-existing cell wall of G. homari was inhibited to an extent of 50% (ID50 value) at a concentration of 0.25 mug of penicillin G/ml. With UDP-GlcNAc and UDP-MurNAc-tetrapeptide as precursors the ID50 value was about 2500-fold greater (630 mug/ml). The inhibition by penicillin G of the incorporation of peptidoglycan from UDP-MurNAc-[14C]Lys-pentapeptide could be overcome by addition of non-radioactive UDP-MurNAc-tetrapeptide to the incubation mixture. In the presence of 5 mug of penicillin G/ml the incorporation of peptidoglycan formed from the mixture of UDP-MurNAc-Ala-DGlu-Lys-D-[14C]Ala-D[14C]Ala and non-radioactive UDP-MurNAc-tetrapeptide proceeded virtually without release of D-[14C]alanine by transpeptidase activity. The enzyme preparation also exhibited DD-carboxypeptidase activity which was only slightly more sensitive to penicillin G and mecillinam than was the incorporation of peptidoglycan into the cell wall. Since the ID50 values for the beta-lactam antibiotics are similar to the concentrations required to inhibit the growth of G. homari to an extent of 50%, the DD-carboxypeptidase must be the killing site of both penicillin G and mecillinam.
Azepines↗
Effects of cephalothin and penicillin G on platelet function in vitro.
High concentrations of cephalothin or penicillin G inhibit a number of the functions of human or rabbit platelets in citrated platelet-rich plasma (PRP) and in suspensions of washed platelets. The reactions shown to be inhibited are: ADP-induced shape change and the primary and secondary phases of aggregation and release induced by ADP or adrenaline in human cirtated PRP; release and aggregation of washed human platelets exposed to collagen, thrombin, vasopressin, or the ionophore A 23,187; aggregation of washed human platelets exposed to phytohaemagglutinin from Phaseolus vulgaris (PHA) or polylysine; release induced by concanavalin A or PHA in suspensions of washed platelets from rabbits; platelet adherence to a collagen-coated surface or to the damaged intimal surface of the rabbit aorta; platelet factor 3 availability; lysis of rabbit platelets by an antiserum directed against them; and clot retraction. Neither antibiotic affected serotonin-induced aggregation; a high concentration of cephalothin slightly inhibited the initial rate of serotonin uptake. Penicilloic acid showed about half the inhibitory effect of penicillin G on ADP-induced aggregation. In citrated human platelet-rich plasma, ampicillin and oxacillin inhibited ADP-induced aggregation to the same extent as similar concentrations of penicillin G; in suspensions of washed platelets, however, ampicillin was less inhibitory than penicillin G or oxacillin. Platelet ultrastructure, assessed by transmission electron microscopy, was not visibly altered. Evidence that the antibiotics become bound to platelets is the finding that platelets incubated with the antibiotics ans resuspended in fresh media showed less response to aggregating agents compared with control platelets. Penicillin G and related antibiotics may be inhibitory because they coat the platelet surface. Their effects on platelet functions are probably responsible for excessive bleeding and increased bleeding times observed in patients and volunteers receiving high doses of these antibiotics.
Antibodies↗