Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ERYTHROMYCIN”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources

NTP Toxicology and Carcinogenesis Studies of Erythromycin Stearate (CAS No. 643-22-1) in F344/N Rats and B6C3F1 Mice (Feed Studies).

Toxicology and carcinogenesis studies of erythromycin stearate (USP grade, greater than 96% pure) were conducted by administering the antibiotic in feed to groups of F344/N rats and B6C3F1 mice of each sex for 14 days, 13 weeks, or 2 years. Erythromycin stearate was studied because of its widespread use in humans as a broad-spectrum macrolide antibiotic and because of the lack of adequate long-term studies for carcinogenicity. Fourteen-Day and Thirteen-Week Studies: In the 14-day studies, none of the rats (at dietary concentrations up to 50,000 ppm) and 2/5 female mice that received 50,000 ppm died before the end of the studies. Final mean body weights of male rats that received 12,500, 25,000, or 50,000 ppm were 10%, 30%, or 36% lower, respectively, than that of controls; final mean body weights of female rats were 10%, 12%, or 32% lower. None of the dosed mouse groups gained weight. The final mean body weight of male mice that received 50,000 ppm was 10% lower than that of controls. In the 13-week studies, none of the rats or mice (at dietary concentrations up to 20,000 ppm) died before the end of the studies. Final mean body weights of the 20,000-ppm groups of rats were more than 12% lower than that of the controls for males and 7% lower for females. Final mean body weights of mice that received 10,000 or 20,000 ppm were 15% or 19% lower than that of controls for males and 5% or 14% lower for females. Multinucleated syncytial hepatocytes were observed in 10/10 male rats that received 20,000 ppm but in 0/10 male rats that received 10,000 ppm. No compound-related gross or microscopic pathologic effects were observed in mice. Based on these results, 2-year studies of erythromycin stearate were conducted by feeding diets containing 0, 5,000, or 10,000 ppm erythromycin stearate to groups of 50 rats of each sex for 103 weeks. Diets containing 0, 2,500, or 5,000 ppm were fed to groups of 50 mice of each sex for 103 weeks. Body Weight and Survival in the Two-Year Studies: Mean body weights of high dose male rats were comparable to those of controls throughout the studies. Mean body weights of high dose female rats were 5%-10% lower than those of controls. Mean body weights of dosed and control mice were comparable. The average daily feed consumption was similar for dosed and control male and female rats. For mice, estimated daily feed consumption by low and high dose males was similar to that of the controls and by low and high dose females was 92% that of the controls. The average amount of erythromycin stearate consumed per day was approximately 180 or 370 mg/kg for male rats and 210 or 435 mg/kg for female rats; for mice, the average amounts were 270 or 545 mg/kg for males and 250 or 500 mg/kg for females. No significant differences in survival were observed between any groups of rats or mice of either sex (final survival-- male rats: control, 28/50; low dose, 23/50; high dose, 27/50; female rats: 29/50; 30/50; 38/50; male mice: 34/50; 33/50; 40/50; female mice: 38/50; 34/50; 40/50). Nonneoplastic and Neoplastic Effects in the Two-Year Studies: Granulomas of the liver were observed at increased incidences in high dose rats (male: 1/50; 2/50; 10/50; female: 18/50; 27/50; 43/50). Granulomatous inflammation or granulomas of the spleen were observed in dosed female rats (0/48; 1/49; 3/50). Reticulum cell hyperplasia in the bone marrow occurred at increased incidences in high dose female rats (10/50; 14/50; 25/50). Squamous cell papillomas of the oral mucosa were observed in 1/50 control, 2/50 low dose, and 3/50 high dose female rats. These tumors were considered to be marginal and not related to exposure. Hyperplasia of the oral mucosa was not observed. Pheochromocytomas of the adrenal gland in female rats occurred with a positive trend (1/50; 4/49; 5/50). The incidences in the dosed groups are similar to the average historical incidence (9%) of this tumor in untreated control female F344/N rats at the study laboratory. This marginal tumor increase is not considered to be biologically important. No increases in incidences of study laboratory. This marginal tumor increase is not considered to be biologically important. No increases in incidences of neoplasms were observed at any site in dosed male rats. Inflammation in the glandular stomach was observed at increased incidences in dosed male mice (1/49; 4/50; 6/50). Lymphoid hyperplasia in the urinary bladder was observed at increased incidences in dosed female mice (1/50; 9/47; 7/48). No increases in incidences of neoplasms were observed at any site in dosed male or female mice. Genetic Toxicology: Erythromycin stearate was not mutagenic in Salmonella typhimurium strains TA98, TA100, TA1535, or TA1537 when tested both with or without exogenous metabolic activation. Erythromycin stearate demonstrated equivocal mutagenicity in the mouse L5178Y lymphoma cell assay in the absence of exogenous metabolic activation (S9); erythromycin stearate was not mutagenic in the presence of S9. Treatment of cultured Chinese hamster ovary cells with erythromycin stearate did not produce an increase in the frequency of sister chromatid exchanges or chromosomal aberrations in either the presence or absence of metabolic activation. Audit: The data, documents, and pathology materials from the 2-year studies of erythromycin stearate have been audited. The audit findings show that the conduct of the studies is documented adequately and support the data and results given in this Technical Report. Conclusions: Under the conditions of these 2-year studies, there was no evidence of carcinogenic activity of erythromycin stearate for male or female F344/N rats administered erythromycin stearate in the diet at 5,000 or 10,000 ppm. There was no evidence of carcinogenic activity of erythromycin stearate for male or female B6C3F1 mice administered erythromycin stearate in the diet at 2,500 or 5,000 ppm. Dose-related increases in the incidences of granulomas of the liver were observed in male and female rats. The absence of any biologically important chemical-associated effects in mice suggests that higher doses could have been given to male and female mice. Synonyms: erythrocin stearate; erythromycin octadecanoate Trade Names: Abbotcine; Bristamycin; Dowmycin E; Eratrex; Erypar; Ethril; Gallimycin; HSDB 4178; OE 7; Pantomicina; Pfizer-E; SK-Erythromycin; Wyamycin S

Journal Article↗

Influence of erythromycin A on the microbial populations in aquaculture sediment microcosms.

Degradation of erythromycin A was studied using two sediment samples obtained from the salmon and trout hatchery sites at Hupp Springs (HS) and Goldendale (GD), Washington, United States. The former site had been treated for 3 years with erythromycin-medicated feed prior to the experiments, and the latter site had not been treated with any antibiotic for at least 6 years. The two sediment microcosms treated with either N-[methyl-14C]erythromycin A or [1,3,5,7,9,11,13-14C]erythromycin A showed S-curves for erythromycin A mineralization with a prolonged lag time of 120 days, except for GD microcosms treated with [1,3,5,7,9,11,13-14C]erythromycin A. We proposed a simplified logistic model to interpret the mineralization curves under the assumption of the low densities of initial populations metabolizing erythromycin A. The model was helpful for knowing the biological potential for erythromycin A degradation in sediments. Although erythromycin A added to the two sediment microcosms did not significantly alter the numbers of total viable aerobic bacteria or erythromycin-resistant bacteria, it affected the bacterial composition. The influence on the bacterial composition appeared to be greater in GD microcosms without pre-exposure to antibiotics. PCR-RFLP and DNA sequence analyses of the 16S ribosomal RNA gene and the erythromycin esterase (ere) gene revealed that ereA type 2 (ereA2) was present in potentially erythromycin-degrading Pseudomonas spp. strains GD100, GD200, HS100, HS200 and HS300, isolated from erythromycin-treated and non-treated GD and HS microcosms. Erythromycin A appeared to influence the development and proliferation of strain GD200, possibly via the lateral gene transfer of ereA2.

Anti-Bacterial Agents↗

Open-Label, parallel-group, multicenter, randomized study of cefprozil versus erythromycin in children with group A streptococcal pharyngitis/tonsillitis.

BACKGROUND: Cefprozil and erythromycin are acceptable alternatives to penicillin in the treatment of pharyngitis/tonsillitis due to group A beta-hemolytic streptococcus (GABHS). OBJECTIVE: The purpose of this trial was to determine the relative efficacy and tolerability of cefprozil and erythromycin in the treatment of pediatric pharyngitis/tonsillitis due to GABHS. METHODS: This trial compared the bacteriologic and clinical efficacy of erythromycin and cefprozil in children 2 to 12 years of age with culture-documented GABHS pharyngitis/ tonsillitis. Children who were allergic to penicillin, cefprozil, or erythromycin were excluded. Patients were prospectively randomly assigned to receive 10 days of oral therapy with either cefprozil suspension 15 mg/kg per day in 2 divided doses or erythromycin ethylsuccinate suspension 30 mg/kg per day in 3 divided doses. Primary efficacy end points were bacteriologic and clinical response 2 to 8 days after treatment ended. The frequency and severity of adverse events and their relationship to treatment were also assessed. RESULTS: A total of 199 patients were enrolled and treated (cefprozil, 99; erythromycin, 100); 12 patients in the cefprozil group and 15 in the erythromycin group were not evaluable. The GABHS eradication rate was significantly higher with cefprozil (95%) than with erythromycin (74%) (P = 0.001). The posttreatment carrier rate was lower in the cefprozil group (5%) than in the erythromycin group (18%) (95% CI, -22.3 to -3.8). Clinical cure rate was 90% (78/87) with cefprozil and 91% (77/85) with erythromycin (P = 0.95) (treatment group difference, -0.93; 95% CI, -9.9% to 8.0%). The overall incidence of drug-related adverse events was not significantly different in the 2 groups (11% with cef- prozil, 18% with erythromycin). The most common adverse events were diarrhea and vomiting. Two patients in the erythromycin group discontinued therapy because of adverse events. CONCLUSIONS: The bacteriologic eradication rate was significantly greater with cefprozil compared with erythromycin in children with pharyngitis/tonsillitis. Both cefprozil and erythromycin produced a clinical cure in >90% of patients.

Anti-Bacterial Agents↗

Tonsillar penetration of erythromycin and its 2'-acetyl ester in patients with chronic tonsillitis.

Concentrations of erythromycin and 2'-acetyl erythromycin were analysed in serum or plasma and tonsil tissue after repeated dosage of erythromycin acistrate (EA), a new erythromycin prodrug, in two separate studies in 61 young patients. The reference preparations were: (1) enterocoated tablets of erythromycin base (EB enterotablets, (2) erythromycin base as enterocoated pellets (EB enterocapsules) and (3) erythromycin stearate (ES). All drugs were given 500 mg tid for three days before scheduled tonsillectomy. Tonsils were removed about 3 h after intake of the last dose. Blood samples were collected at 0, 2 and 6 h and at the time of tonsillectomy. At all time points EA produced several-fold higher total drug (erythromycin + 2'-acetyl erythromycin) concentrations in serum or plasma than any of the reference preparations. Similarly, after EA the mean total antibiotic levels in tonsil tissue exceeded the erythromycin levels after the reference preparations by at least a factor of 3. Tonsil/serum or plasma ratios of the total antibiotic were quite similar with all preparations (means 38-50%). Peak erythromycin levels in circulation did not differ significantly from each other in spite of two nonabsorbers after EB enterotablets. The same was true of tonsil tissue. There were, however, 15 tonsils with undetectable erythromycin: 4/25 (16%) with EA, 5/12 (42%) with EB enterotablets, 2/12 (17%) with EB enterocapsules and 4/12 (33%) with ES. The degree of hydrolysis of 2'-acetyl erythromycin to erythromycin was 23-43% higher in tonsil tissue than in circulation.

Adolescent↗

Characterization of erythromycin resistance in Campylobacter jejuni and Campylobacter coli.

The mechanism of resistance to erythromycin, the drug of choice in the treatment of campylobacter gastroenteritis, was investigated. Erythromycin resistance (MICs, greater than 1,024 micrograms/ml) in three clinical isolates of Campylobacter jejuni and one C. coli isolate was determined to be constitutive and chromosomally mediated. In vivo protein synthesis in erythromycin-susceptible C. jejuni and C. coli strains was completely inhibited by low levels of erythromycin (5 micrograms/ml), whereas a high concentration of the antibiotic (100 micrograms/ml) had no effect on protein synthesis in erythromycin-resistant strains. Biological assays showed that extracellular degradation of erythromycin was not responsible for erythromycin resistance in strains of Campylobacter species. The rates and amounts of uptake of [14C]erythromycin by resistant and susceptible campylobacter cells were determined to be similar. Binding assays with purified campylobacter 70S ribosomes as well as 50S ribosomal subunits showed that those from erythromycin-resistant strans bound much less [14C]erythromycin than did those from susceptible strains. Genomic DNA from C. coli UA585 was used to transform erythromycin resistance to C. coli UA417. The erythromycin resistance marker was associated with a 240-kb SmaI fragment of the C. coli UA585 genome. Our results rule out erythromycin inactivation or efflux and are not consistent with the production of an RNA methylase, although they are consistent with a mutational mechanism of resistance due to a change in a ribosomal protein gene. This study constitutes a detailed biochemical and genetic characterization of erythromycin resistance in Campylobacter species.

Bacterial Proteins↗

Erythromycin enhances gastric emptying in patients with gastroparesis after vagotomy and antrectomy.

We studied the effect of erythromycin on gastric emptying in nine patients with gastroparesis following truncal vagotomy and antrectomy, and assessed their clinical response to chronic oral erythromycin. Gastric emptying was evaluated using a solid-phase radio-labeled meal. Patients were studied after erythromycin 200 mg intravenously (N = 9) and after an oral suspension of erythromycin 200 mg (N = 7) each given 15 min after ingestion of the meal. Three parameters of gastric emptying were analyzed: half-emptying time (T1/2), area under the curve, and percent gastric residual at 2 hr. Nine patients were subsequently placed on oral suspension erythromycin 150 mg three times a day before meals (range 125-250 mg three times a day) and symptoms of nausea, vomiting, postprandial fullness, and abdominal pain were assessed before and after erythromycin. Intravenous erythromycin markedly accelerated the gastric emptying (all three parameters studied) of solids (P < 0.01) in seven of nine patients with postsurgical gastroparesis [baseline T1/2 154 +/- 15 min; after intravenous erythromycin, T1/2 56 +/- 17 min (mean +/- SEM)]. Oral erythromycin enhanced (P < 0.05) the gastric emptying rate (T1/2, area under the curve) in five of seven patients (baseline T1/2 146 +/- 16 min; after oral erythromycin, T1/2 87 +/- 20 min). Of the nine patients who were placed on oral maintenance erythromycin, three showed clinical improvement after two weeks. In summary, erythromycin significantly enhances gastric emptying in many patients with vagotomy and antrectomy-induced gastroparesis; however, only a small subset of patients respond clinically to chronic oral erythromycin.

Administration, Oral↗

Erythromycin enhances solid-phase gastric emptying in induced-hyperglycemia in patients with truncal vagotomy and pyloroplasty.

Erythromycin has been found to be a gastrointestinal prokinetic agent while acute hyperglycemia has been associated with delayed gastric emptying in healthy controls and diabetics. The aim of this study was to investigate whether hyperglycemia, per se, alters gastric motility, during erythromycin-induced acceleration of gastric emptying of solids in patients with truncal vagotomy and pyloroplasty (TVP) and the role of vagus nerves. Eight TVP patients and six controls underwent scintigraphic measurement of gastric emptying of a solid meal, during placebo in normoglycemia (5-8.9 mmol/liter glucose) or 200 mg intravenous erythromycin lactobionate in normo- or hyperglycemia (16-19 mmol/liter glucose) induced by intravenous glucose infusion, on separate days in random order. In the TVP patients during normoglycemia, the erythromycin compared to placebo accelerated the meal gastric half-emptying time (T1/2), (37.12 +/- 6.87 vs 91.88 +/- 11.53, P < 0.001) and decreased the lag-phase duration (P < 0.001) and the percentage of meal retained in the stomach at 120 min (P < 0.001). Erythromycin in hyperglycemia compared to normoglycemia increased T1/2 (61.25 +/- 10.67 vs 37.12 +/- 6.87, P < 0.001), prolonged lag-phase duration (P < 0.001), and the percentage of isotope retained in the stomach at 120 min (P < 0.001). The T1/2, the lag phase duration, and the meal retained in the stomach at 120 min, after giving placebo was significantly increased, compared to erythromycin administration in hyperglycemia (P < 0.001). Significant differences among patients and controls were found during gastric emptying after giving placebo and after erythromycin in hyperglycemia (P = 0.04 and P = 0.007, respectively), while nonsignificant differences were found after giving erythromycin in normoglycemia. We conclude that the effect of erythromycin-induced acceleration on gastric emptying is related to the plasma glucose level. Hyperglycemia reduces the erythromycin-induced acceleration of gastric emptying of solids in both controls and TVP patients. A significant increase in the delay of gastric emptying was achieved in TVP patients compared to controls after giving erythromycin in hyperglycemia and after placebo. Despite the inhibitory effect of induced hyperglycemia on gastric emptying, erythromycin is still able to accelerate the emptying rate and could prove to be a useful prokinetic agent under hyperglycemic conditions. Hyperglycemia may indicate a cholinergic-antagonist pathway that delays the erythromycin-induced acceleration of gastric emptying of solids and is more evident in vagotomized patients than controls, who retain the functional integrity of the vagus nerves.

Adult↗

The differential antibacterial and gastrointestinal effects of erythromycin and its chiral isolates.

The use of erythromycin has been limited by the gastrointestinal side effect properties, which include abdominal distress and diarrhea. To evaluate the possibility of reducing the toxicity of erythromycin, studies were undertaken to separate erythromycin into chiral isolates and then to test the activity of these chiral isolates on gastrointestinal contractility and bacteriostatic actions. Gastrointestinal contractility was obtained by the use of isolated strips of a rat colon. Antibacterial activity was used by obtaining the MICs of erythromycin and isolated agents against Enterococcus faecalis ATCC 29212. ANOVA was performed using the SPSS v.10 to determine statistical differences in the MICs and the amplitude and frequency of spike bursts. Results were expressed as mean+/-SE (N=5). The MICs (microg/mL) of erythromycin (racemate), chiral isolate X, and chiral isolate Y were 0.45+/-0.29, 0.53+/-0.24 (n.s.), and 0.2+/-0.07 (P<or=0.001), respectively. Erythromycin (racemate) at 10 mol/L, 10 mol/L, 5x10 mol/L, 10 mol/L, and 10 mol/L concentrations caused the amplitude of spike bursts to increase by 18+/-7% (P=n.s.), 43+/-10% (P<or=0.05), 55+/-12% (P<or=0.001), 121+/-23% (P<or=0.001), and 163+/-16% (P<or=0.001), respectively. The chiral isolate Y increased the amplitude of spike bursts at the same concentrations as tested above: 32+/-11% (P<or=0.05), 48+/-14% (P<or=0.001), 84+/-13% (P<or=0.001), 112+/-18% (P<or=0.001), and 121+/-13% (P<or=0.001), respectively. Chiral isolate X caused much reduced effect on the amplitude of spike bursts: 9+/-6% (P=n.s.), 27+/-12% (P=n.s.), 27+/-12% (P=n.s.), 30+/-11% (P=n.s.), and 30+/-11.2% (P=n.s.), respectively. EC50 for erythromycin (mixture) was 0.4x10 mol/L, and for erythromycin Y, it was 0.8x10 mol/L. The addition of erythromycin at 10 mol/L caused the frequency of spike bursts to increase 11+/-7% at 10 mol/L, 5x10 mol/L, 10 mol/L, and 10 mol/L; the changes were 13+/-10% (P=n.s.), 13+/-10% (P=n.s.), 22+/-13% (P=ns), and 39+/-30% (P<or=0.05), respectively. Chiral isolate Y of erythromycin, changed the frequency of spike bursts by 26+/-21% (P=n.s.); 35+/-20% (P=n.s.), 39+/-30% (P=n.s.), 41+/-37% (P=n.s.), and 44+/-36% (P=n.s.) at the respective concentrations as discussed above. Chiral isolate X altered the frequency of spike bursts at the same concentrations as 40+/-30% (P=n.s.), 45+/-30% (P=n.s.), 62+/-41% (P=n.s.), 62+/-41% (P=n.s.), and 52+/-35% (P=n.s.), respectively. Data indicate that erythromycin (racemate) and chiral isolates X and Y possess similar antibacterial activity. It was also shown that erythromycin and chiral isolate Y increase significantly the amplitude of spike bursts compared with baseline. Isolate X does not increase the amplitude of spike bursts in a dose-dependent manner. The frequency of spike bursts is not significantly changed in the presence of erythromycin or the 2 chiral isolates.

Action Potentials↗

Erythromycin-inducible resistance in Staphylococcus aureus: requirements for induction.

At least two functionally different types of ribosomes are found in strains of Staphylococcus aureus which display "dissociated" resistance to erythromycin. One type of ribosome is found under conditions of growth in ordinary nutrient broth, and the second is formed during growth in the presence of erythromycin. In these strains, erythromycin acts as an inducer of resistance to three different classes of inhibitors of the 50S ribosomal subunit-the macrolides, lincosamides, and streptogramin B-type antibiotics. The optimal inducing concentration of erythromycin is between 10(-8) and 10(-7)m. Concentrations as low as 10(-9)m can produce a 10-fold increase in resistant cells over the uninduced, background level, whereas concentrations greater than 10(-7)m block induction owing to inhibition of protein synthesis. Resistant cells begin to appear within 5 to 10 min after addition of erythromycin (to 10(-7)m), and within 40 min (i.e., about one generation) more than 90% of the entire culture is resistant to erythromycin as well as to lincomycin and vernamycin B(alpha). A resistant culture becomes sensitive if grown for 90 min in the absence of erythromycin. The process of induction is inhibited by chloramphenicol and streptovaricin, which inhibit protein and ribonucleic acid synthesis, respectively, but not by novobiocin, which inhibits deoxyribonucleic acid synthesis. Resistant cells produced in this manner fail to concentrate (14)C-erythromycin and (14)C-lincomycin, but not (14)C-chloramphenicol. Constitutively erythromycin-resistant strains which do not require the presence of erythromycin for expression of resistance can be selected on media containing antibiotics which belong to any one of the three classes. Two patterns of constitutive resistance have been found. These are (i) generalized constitutive resistance-which involves resistance in the absence of erythromycin to all members of each of the three cited classes of 50S subunit inhibitors which were tested, and (ii) partial constitutive resistance-which involves different degrees of resistance, in the absence of erythromycin, to various members of the three classes. Several different patterns of variable constitutivity are possible. 50S ribosomal subunits isolated from induced or constitutively resistant cells show decreased ability to bind erythromycin and lincomycin, and possible enzymatic inactivation of these antibiotics has been rigorously excluded. The induced change, therefore involves modification of ribosome structure rather than modification of the antibiotic.

Anti-Bacterial Agents↗

Mutation and cloning of eryG, the structural gene for erythromycin O-methyltransferase from Saccharopolyspora erythraea, and expression of eryG in Escherichia coli.

A mutant strain derived by chemical mutagenesis of Saccharopolyspora erythraea (formerly known as Streptomyces erythreus) was isolated that accumulated erythromycin C and, to a lesser extent, its precursor, erythromycin D, with little or no production of erythromycin A or erythromycin B (the 3"-O-methylation products of erythromycin C and D, respectively). This mutant lacked detectable erythromycin O-methyltransferase activity with erythromycin C, erythromycin D, or the analogs 2-norerythromycin C and 2-norerythromycin D as substrates. A 4.5-kilobase DNA fragment from S. erythraea originating approximately 5 kilobases from the erythromycin resistance gene ermE was identified that regenerated the parental phenotype and restored erythromycin O-methyltransferase activity when transformed into the erythromycin O-methyltransferase-negative mutant. Erythromycin O-methyltransferase activity was detected when the 4.5-kilobase fragment was fused to the lacZ promoter and introduced into Escherichia coli. The activity was dependent on the orientation of the DNA relative to lacZ. We have designated this genotype eryG in agreement with Weber et al. (J.M. Weber, B. Schoner, and R. Losick, Gene 75:235-241, 1989). It thus appears that a single enzyme catalyzes all of the 3"-O-methylation reactions of the erythromycin biosynthetic pathway in S. erythraea and that eryG codes for the structural gene of this enzyme.

Chromatography, High Pressure Liquid↗

Azithromycin is as effective as and better tolerated than erythromycin estolate for the treatment of pertussis.

OBJECTIVE: Although universal immunization against Bordetella pertussis (whooping cough) infection has resulted in dramatic reductions in the incidence of pertussis, outbreaks continue to occur in countries with excellent vaccine coverage. Treatment of infection may ameliorate symptom severity during the catarrhal phase of pertussis but has no effect on established paroxysms, emesis, or apnea if given during the paroxysmal or convalescent phases. Erythromycin, recommended for treatment of pertussis to prevent transmission of infection, is poorly tolerated because of gastrointestinal side effects. We compared the safety and efficacy of erythromycin with azithromycin for treatment of pertussis in a large, randomized, controlled trial that enrolled children from primary care practices in 1 American and 11 Canadian urban centers. METHODS: Children who were 6 months to 16 years of age and had cough illness that was suspected to be or was culture confirmed as pertussis were randomized to azithromycin (10 mg/kg on day 1 and 5 mg/kg on days 2-5 as a single dose) or erythromycin estolate (40 mg/kg/day in 3 divided doses for 10 days) with stratification by center. The primary outcome measure was bacteriologic cure of infection as determined by cultures of nasopharyngeal aspirates. Culture-positive participants had a second aspirate collected at the end of therapy (days 5-7 for azithromycin, days 10-12 for erythromycin) and 1 week after therapy. Bacteriologic cure was defined as negative cultures at the end of therapy. Bacteriologic relapse was defined as a positive culture 1 week after completion of therapy and after a negative end-of-therapy culture. Secondary outcomes were pertussis diagnosed by serology and polymerase chain reaction (PCR), treatment-associated adverse events, compliance, and presence of clinical symptoms at the end of the treatment course. Serology was performed using standard enzyme-linked immunosorbent assay methods. A participant was considered to have pertussis when the PCR was positive or a 4-fold increase in pertussis toxin antibody between baseline and follow-up visits was observed. PCR was performed using a 1046-bp ClaI DNA fragment from B pertussis. Adverse events (nausea, vomiting, diarrhea, any gastrointestinal complaint, or other) were determined by a parent-completed diary that was reviewed with study personnel during study visits. Compliance was measured by review of the parent medication diary during study visits and observation of medication containers by the pharmacist at study completion. Symptoms were determined by history collected by study personnel at enrollment and subsequently from the diary. The design of the study was an equivalence trial, aimed at demonstrating that the bacteriologic failure rates with the 2 therapies did not differ by >8%. For the safety analysis, all participants who received at least 1 dose of study drug were included. In the per-protocol efficacy analysis, all culture-positive participants with end-of-treatment cultures were considered. RESULTS: A total of 477 children were enrolled and randomly assigned to either azithromycin (n = 239) or erythromycin (n = 238). Of these children, 114 (24%) grew B pertussis from nasopharyngeal specimens (azithromycin group: 58 of 239 [24%]; erythromycin group: 56 of 238 [23%]); these children composed the efficacy cohort for the per-protocol and intention-to-treat analyses. Serology and PCR added 52 children to the number considered to have pertussis for a total of 35% (166 of 477) of all children who presented with cough illness. In the safety analysis (antibiotic side effects, compliance) and comparison of cough symptoms after treatment, all randomized children are reported in their assigned treatment group. At end of therapy, bacterial eradication was demonstrated in all 53 patients in the azithromycin group and all 53 patients in the erythromycin group with follow-up cultures available (eradication 100%; 95% confidence interval [CI]: 93.3-100). No bacterial recurrence was demonstrated in children with 1 week posttreatment nasopharyngeal cultures available (51 and 53 participants in the azithromycin and erythromycin arms, respectively [0%, 95% CI: 0-7.0; and 0%, 95% CI: 0-6.7]). No serious adverse events attributable to study drug were observed. Gastrointestinal adverse events were reported less frequently in azithromycin (18.8%; 45 of 239) than in erythromycin estolate (41.2%; 98 of 238) recipients (90% CI on difference: -29.0% to -15.7%) as a result of less nausea (2.9% vs 8.4%; 95% CI: -8.9% to -2.0%), less vomiting (5.0% vs 13.0%; 95% CI: -4.9% to -1.4%), and less diarrhea (7.1% vs 11.8%; 95% CI: -9.0% to -0.3%). Children who were randomized to azithromycin were much more likely to have complied with antimicrobial therapy over the treatment period. In the azithromycin group, 90% of children took 100% of prescribed doses, whereas only 55% of children in the erythromycin group took 100% of prescribed doses. CONCLUSIONS: In this large, multicenter, randomized trial, we found that azithromycin is as effective as erythromycin estolate for the treatment of pertussis in children. Gastrointestinal adverse events were much more common with erythromycin treatment than azithromycin. Compliance with therapy was markedly better with azithromycin than with erythromycin in this study.

Adolescent↗

[The phenotype and genotype patterns of erythromycin-resistant Streptococcus pneumoniae].

OBJECTIVE: To investigate the resistance phenotypes and genotypes in erythromycin-resistant Streptococcus (S.) pneumoniae. METHODS: The minimum inhibitory concentration (MIC) of erythromycin, clindamycin, penicillin and fluoroquinolones against 192 strains of S. pneumoniae was tested with broth microdilution method according to the guidelines of the National Committee for Clinical Laboratory Standards. Of 148 clinical isolates of erythromycin resistant S. pneumoniae, the macrolide resistance phenotypes were observed by the erythromycin-clindamycin-spiramycin triple-disc test and erythromycin resistance genes were detected by polymerase chain reaction. RESULTS: 42.7% S. pneumoniae isolates was resistant (intermediate and resistant) to penicillin while the resistance rates to erythromycin and clindamycin were 77.6% and 66.7% respectively. The ermB gene, being the most prevalent, was detected in 79.1% of the 148 erythromycin-resistant strains. The main phenotype (85.1%) of erythromycin-resistant strains was constitutive macrolide, lincosamide, and streptogramin B resistance phenotype (cMLS). Erythromycin MICs for S. pneumoniae ermB-positive isolates were higher than those for mefA-positive isolates. 74.4% of the ermB-positive isolates demonstrated erythromycin MICs of > 16.0 micro g/ml, and the erythromycin MICs for mefA-positive isolates ranged from 0.5 approximately 4.0 micro g/ml. CONCLUSIONS: The resistance rate of S. pneumoniae to erythromycin is high in China. The main phenotype is cMLS. Ribosomal modification (ermB gene coded) is the main resistance mechanism against erythromycin in S. pneumoniae

Anti-Bacterial Agents↗

Gastrointestinal behavior of orally administered radiolabeled erythromycin pellets in man as determined by gamma scintigraphy.

The behavior of single 250-mg doses of a multiparticulate form of erythromycin base (ERYC(R)), each including five pellets radiolabeled with neutron-activated samarium-153, was observed by gamma scintigraphy in seven male subjects under fasting and nonfasting conditions. The residence time and locus of radiolabeled pellets within regions of the gastrointestinal tract were determined and were correlated with plasma concentrations of erythromycin at coincident time points. Administration of food 30 minutes postdosing reduced fasting plasma erythromycin Cmax and area under the plasma erythromycin versus time curve (AUC) values by 43% and 54%, respectively. Mean peak plasma concentration of erythromycin (Cmax) in the fasting state was 1.64 micrograms/mL versus 0.94 micrograms/mL in the nonfasting state. Total oral bioavailability, as determined by mean AUC (0-infinity) of the plasma erythromycin concentration versus time curve, was 7.6 hr/micrograms/mL in the fasted state, versus 3.5 hr/micrograms/mL in the nonfasting state. Mean time to peak plasma erythromycin concentration (tmax) in the fasting state was 3.3 hours, versus 2.3 hours in the nonfasting state. Plasma concentrations of erythromycin in both fasting and nonfasting states were within acceptable therapeutic ranges. Evidence provided by this study: 1) indicates that pellet erosion and absorption of active erythromycin base begins when the enteric-coated pellets reach the highly vascular mucosa of the jejunum and proximal ileum, and is essentially completed within the ileum, with a significant portion absorbed in the medial-to-distal ileum; 2) confirms that acceptable therapeutic plasma levels of erythromycin are attained in nonfasting subjects (Cmax = 0.94 microgram/mL) and that superior plasma erythromycin concentrations (Cmax = 1.64 micrograms/mL) are achieved by administration of the dose on an empty stomach 1 to 2 hours before or after meals; 3) corroborates other comparative studies reporting greater fasting bioavailability with this multiparticulate dosage form of erythromycin base than with reference single tablet or particle-in-tablet formulations; and 4) indicates that neutron activation of stable isotopes incorporated as a normal excipient in industrially-produced formulations provides an effective means for in vivo evaluation of dosage forms through gamma scintigraphy.

Administration, Oral↗

Erythromycin acts through a cholinergic pathway to improve canine-delayed gastric emptying following vagotomy and Roux-Y antrectomy.

We have demonstrated that erythromycin improves gastric emptying in dogs following truncal vagotomy and Roux-en-Y antrectomy (VRYA). To explore its mechanism of action we studied gastric emptying and myoelectric activity in a canine Roux model and administered atropine simultaneously with erythromycin. Tachyphylaxis was evaluated following short-term administration. Four dogs with delayed gastric emptying following VRYA were studied. Radionuclide solid gastric emptying was measured, with simultaneous myoelectric recordings obtained from the duodenum and Roux limb. Study groups were: (1) saline control (VRYA dogs); (2) erythromycin 1 mg/kg iv over 1 hr; (3) erythromycin 3 mg/kg po tid for 1 week, with repeat studies using erythromycin 1 mg/kg iv over 1 hr; and (4) atropine 0.5 mg/kg iv bolus, followed by a 1-hr infusion of atropine 0.05 mg/kg and erythromycin 1 mg/kg. Control Roux animals had severe gastric retention (73 +/- 5% at 2 hr, compared to 27 +/- 6% following iv erythromycin (P less than 0.01). Clustered spike bursts were observed in the Roux limb following erythromycin. Atropine abolished the gastrokinetic response and suppressed the myoelectric response to erythromycin (81 +/- 3% retention at 2 hr, P less than 0.01 compared to erythromycin alone). The response to erythromycin was unchanged after 1 week of tid administration (40 +/- 14% retention at 2 hr postprandial, P = NS). Erythromycin improves gastric emptying in VRYA dogs via a cholinergic pathway and does not exhibit tachyphylaxis following short-term administration.

Anastomosis, Roux-en-Y↗

Effect of antrectomy and truncal vagotomy on erythromycin induced pancreatic polypeptide secretion.

Erythromycin, a motilin agonist, enhances gastrointestinal motility but also stimulates endogenous pancreatic polypeptide (PP) secretion. We investigated whether the effect of erythromycin on PP release is dependent on (1) prokinetic activity of erythromycin generated from the antrum and (2) the long vagus nerve since erythromycin acts via cholinergic neurons. Erythromycin induced PP secretion was determined in 14 patients with antrectomy (6 patients with Billroth I type anastomosis, 8 patients with Billroth II type anastomosis), in 6 patients with truncal vagotomy and pyloroplasty but without gastric resection and in 8 healthy controls. Plasma PP levels in response to erythromycin (3 mg/kg i.v.) were determined at regular intervals for 180 min. Erythromycin induced a significant increase in plasma PP in the control subjects from 22 +/- 4 pmol/l (basal) to 49 +/- 4 pmol/l at 10 min. In the patients with truncal vagotomy plasma PP secretion after erythromycin was significantly (P < 0.05) increased (peak increment vs. basal: 98 +/- 10 pmol/l vs. 27 +/- 2 pmol/l) and prolonged compared to controls. In the patients with antrectomy no significant increases in plasma PP over basal were observed after erythromycin infusion. It is concluded that erythromycin stimulates PP secretion in healthy controls. The PP response to erythromycin is exaggerated after truncal vagotomy but absent after antrectomy indicating that the antrum is essential for erythromycin induced PP secretion.

Adult↗

Electrophysiological mechanisms in a canine model of erythromycin-associated long QT syndrome.

BACKGROUND: Erythromycin is known to prolong ventricular repolarization and has been associated with the occurrence of torsades de pointes. In this study, we have investigated potential mechanisms in vivo and in vitro for induction of an acquired long QT syndrome by erythromycin. METHODS AND RESULTS: Ventricular electrograms and endocardial monophasic action potentials were recorded in anesthetized open-chest dogs before and after administration of 40 to 120 mg/kg of erythromycin lactobionate. Conventional microelectrode techniques were used to record transmembrane action potentials in isolated dog Purkinje fibers and papillary muscles. Erythromycin at concentrations > 20 mg/L prolonged action potential duration. At higher concentrations (100 to 200 mg/L), erythromycin induced phase 2 and phase 3 early afterdepolarizations (EADs) both in vivo and in vitro. The effects of erythromycin on repolarization were more marked in Purkinje fibers than in papillary muscle. Pretreatment of Purkinje fibers with erythromycin antagonized the effects of dofetilide, a selective delayed-rectifier potassium channel (IK) blocker. Pretreatment with prazosin or tetrodotoxin had no effect on erythromycin-induced changes in action potential duration. CONCLUSIONS: These pharmacological studies suggest that erythromycin prolongs repolarization to a large extent by block of IK. In turn, prolongation of action potential duration resulting from erythromycin's actions on IK may promote the development of EADs. The induction of ventricular arrhythmias observed clinically after exposure to erythromycin may be related to the development of EADs. The rarity of occurrence of ventricular arrhythmias suggests that other predisposing factors contribute to the acquired long QT syndrome associated with erythromycin.

Action Potentials↗

In-vivo kinetics of the interaction between midazolam and erythromycin in rats, taking account of metabolic intermediate complex formation.

To predict, quantitatively, the extent of drug interaction during repeated administration of a metabolic inhibitor, we analysed the effects of erythromycin treatment under several regimens on the area under the concentration curve (AUC) of midazolam in rats. Midazolam was administered into the portal vein 12 h after erythromycin treatment for 1, 2 or 3 days, or 12, 24, 36, 48, 72 and 96 h after erythromycin treatment for 4 days, and the plasma-concentration profiles of midazolam were analysed to assess the AUC. Moreover, the contents of total cytochrome P450 and inactive metabolic intermediate (MI) complex were simultaneously quantitated. While the AUC value of midazolam was not affected by the administration of erythromycin for 1 day, repeated administration of erythromycin evoked an increase in AUC ratio (AUC in erythromycin-treated rats/AUC in vehicle-treated rats), which reached a maximum value of 1.99 at 12 h after 4 days' treatment with erythromycin. The total content of cytochrome P450 in liver microsomes was unaffected by erythromycin treatment. Although the MI complex was undetectable after 1 day's treatment with erythromycin, its content increased with duration of erythromycin treatment, and the complex disappeared after the end of erythromycin treatment with a half-life of 12.3 h. In conclusion, the interaction between erythromycin and midazolam could be well predicted when the formation of MI complex in the liver was taken into account.

Animals↗

Clinically significant hearing loss in renal allograft recipients treated with intravenous erythromycin.

BACKGROUND: Hearing loss is generally regarded as a rare side effect of erythromycin therapy. However, our own clinical experiences in erythromycin-treated patients led us to suspect that this complication may be more common among renal allograft recipients. The purpose of this study was to evaluate the incidence, predisposing factors, clinical characteristics, and outcomes of erythromycin-induced hearing loss among renal allograft recipients. METHODS: We reviewed medical records of renal transplant patients treated for pneumonia with intravenous erythromycin lactobionate. Patients were evaluated for the occurrence of clinically significant hearing loss (including onset, duration, and reversibility), other signs and symptoms of ototoxicity (vertigo and tinnitus), daily erythromycin dose and duration of treatment, concurrent ototoxic drug therapy, renal and hepatic function, and history of previous otic disease. RESULTS: Eleven (32%) of 34 courses of intravenous erythromycin therapy resulted in hearing loss. The incidence of hearing loss was 53% (eight of 15 courses) in patients treated with 4 g of erythromycin daily compared with 16% (three of 19 courses) among those receiving 2 g/d (P = .05). In addition, courses of erythromycin were longer in those suffering auditory toxicity (9.6 +/- 4.7 days) than in nontoxic patients (5.7 +/- 3.6 days) (P < .05). Hepatic and renal function did not differ between toxic and nontoxic patients. All episodes of erythromycin-induced hearing loss were reversible. CONCLUSIONS: We conclude that clinically significant hearing loss occurs in more than 30% of renal allograft recipients treated for pneumonia with intravenous erythromycin lactobionate. Patients who require prolonged courses of erythromycin and those treated with 4 g/d are at particular risk for the development of auditory toxicity. With prompt recognition and modification of therapy, erythromycin-induced hearing loss appears to be completely reversible.

Adult↗