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[Effects of cefdinir in pediatric infectious diseases].
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[Reevaluation of current antimicrobials. cefdinir (discussion)].
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Cefdinir--a new oral cephalosporin.
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The effects of quinolones on the adherence of type-1 fimbriated Escherichia coli to mannosylated agarose beads.
Bacterial adherence is reported to be antagonized by several classes of antibiotics including quinolones, beta-lactams and tetracyclines, based primarily on in-vitro studies in which bacterial cells are exposed to antimicrobials, incubated in the presence of uroepithelial cells (UECs) and assessed for adherence by light microscopy. Some problems associated with the use of this approach, include low sensitivity, high variability and, in the case of adherence of mannose-sensitive Escherichia coli interference by mannose-containing uromucoid. To avoid these problems, mannosylated agarose beads (MABs) were used as a model for UECs. Adherence of E. coli strain AAEC356, which is constitutive for type-1 fimbrial expression, was maximal with 3 x 10(4) beads/mL and 1 x 10(8) bacterial cells/mL co-incubated for 35 min at 37 degrees C. Those bacterial cultures showed 40-60% adherence to MABs but only 4-10% adherence to UECs. This study reports a novel method to detect mannose-sensitive bacterial adherence, using MABs, in order to determine the effects of quinolones, cefdinir and tetracycline on E. coli adherence. Cefdinir and the quinolones ciprofloxacin, enoxacin and PD131628 caused significant reductions in the adherence of AAEC356 to UECs at concentrations equivalent to 1/2 x MIC, while up to 1 x MIC of these antibiotics had no significant effect on adherence to MABs. A direct comparison of UEC to MAB-based techniques showed that PD131628, at concentrations equivalent to 1/16x, 1/4x, 1/2x and 1 x MIC, had no effect on bacterial adherence to MABs, while reductions of 34%, 38%, 87% and 85% respectively were seen in adherence to UECs. The anti-adherent effect mediated by quinolones may not therefore be related to the specific interaction between type-1 fimbriae and mannosylated receptors. While quinolones and cefdinir had no effect on overall bacterial adherence to MABs, there was a decrease in the ability of alpha-methyl-D-mannoside (alpha-MM) to inhibit competitively this adherence. Concurrent exposure of PD131628 or cefdinir with tetracycline prevented this, suggesting that protein synthesis is required for this effect.
[Antibacterial activity and beta-lactamase stability of eleven oral cephalosporins].
Oral cephalosporins (cefixime, cefdinir, cefetamet, ceftibuten, cefpodoxime, loracarbef, cefprozil, cefuroxime, cefaclor, cefadroxil and BAY 3522) were compared by their antibacterial profile including stability against new beta-lactamases. Both activity and antibacterial spectrum of compounds structurally related to third generation parenteral cephalosporins (of the oximino class) were superior to established compounds. Activity against staphylococci was found to be highest for cefdinir, cefprozil and BAY 3522. Cefetamet, ceftibuten and cefixime demonstrate no clinically meaningful antistaphylococcal activity while the other compounds investigated demonstrate intermediate activity. The antibacterial spectrum was broadest for cefdinir and cefpodoxime. New oral cephalosporins are equally inactive as established compounds against Enterobacter spp., Morganella, Listeria, Pseudomonas and Acinetobacter spp., methicillin-resistant staphylococci, Enterococcus spp., penicillin-resistant pneumococci and anaerobes. New extended broad-spectrum betalactamases (TEM-3, TEM-5, TEM-6, TEM-7, SHV-2, SHV-3, SHV-4, SHV-5, CMY-1, CMY-2, and CTX-M) are active against the majority of oral cephalosporins. Ceftibuten, cefetamet, cefixime and cefdinir were stable against some of these enzymes even to a higher extent than parenteral cephalosporins. New oral cephalosporins should improve the therapeutic perspectives of oral cephalosporins due to their higher activity against pathogens marginally susceptible to established compounds (higher multiplicity of maximum plasma concentrations over MICs of the pathogens) and furthermore by including in their spectrum organisms resistant to established absorbable cephalosporins (e.g. Proteus spp., Providencia spp., Citrobacter spp., and Serratia spp.).
In vitro selection of resistance in haemophilus influenzae by 4 quinolones and 5 beta-lactams.
We tested abilities of ciprofloxacin, levofloxacin, gatifloxacin, moxifloxacin, amoxicillin, amoxicillin/clavulanate, cefixime, cefpodoxime, and cefdinir to select resistant mutants in 5 beta-lactamase positive and 5 beta-lactamase negative Haemophilus influenzae strains by single and multistep methodology. In multistep tests, amoxicillin, amoxicillin/clavulanate and cefpodoxime exposure did not cause >4-fold minimum inhibitory concentration (MIC) increase after 50 days. One mutant selected by cefdinir had one amino acid substitution (Gly490Glu) in PBP3 and became resistant to cefdinir. Cefixime exposure caused 8-fold MIC-increase in 1 strain with TEM but the mutant remained cefixime susceptible and had no alteration in PBP3 or TEM. Among 10 strains tested, ciprofloxacin, moxifloxacin, gatifloxacin, levofloxacin caused >4-fold MIC increase in 6, 6, 5, and 2 strain, respectively. Despite the increases in quinolone MICs, none of the mutants became resistant to quinolones by established criteria. Quinolone selected mutants had quindone resistance-determining region (QRDR) alterations in GyrA, GyrB, ParC, ParE. Four quinolone mutants had no QRDR alterations. Among beta-lactams cefdinir and cefixime selected one mutant each with higher MICs however amoxicillin, amoxicillin/clavulanate, and cefpodoxime exposure did not select resistant mutants.
Effects of zinc oxide on the attachment of Staphylococcus aureus strains.
We examined the attachment of Staphylococcus aureus to plastic tissue-culture coverslips after incubation for 24 h. The attachment to coverslips was weaker in rabbit plasma with 5% zinc oxide (ZnO) than in the control rabbit plasma without ZnO (P < 0.01). Plasma coagulation by S. aureus strains was not detected in plasma with 5% ZnO after incubation for 24 h. The membranous structure (an immature biofilm) was formed on the coverslips by S. aureus cells in plasma after incubation for 24 h. The colony counts of S. aureus cells on the membranous structures were lower in plasma with 5% ZnO, plasma with 0.2% hinokitiol, plasma with 5% ZnO + 0.2% hinokitiol, plasma with cefdinir at 4 minimum inhibitory concentration (MIC) and plasma with levofloxacin at 4 MIC, than in the control plasma after incubation for 24 h (P < 0.01). The colonies on the membranous structures completely disappeared in the case of plasma with 5% ZnO and 0.2% hinokitiol. The colony counts on membranous structures were lower in plasma with cefdinir at 4 MIC or levofloxacin at 4 MIC containing 5% ZnO than in plasma with cefdinir at 4 MIC or levofloxacin at 4 MIC only, (P < 0.05). The MICs of hinokitiol against S. aureus strains peaked at an MIC distribution of 16-32 micrograms/ml. The peak shifted to below 1 microgram/ml by adding 5% ZnO in agar plate method. The results suggest that the attachment of S. aureus cells to the coverslips is suppressed in the presence of 5% ZnO and that antistaphylococcal activities of cefdinir, levofloxacin and hinokitiol increase in the presence of 5% ZnO.
Activity of nine oral agents against gram-positive and gram-negative bacteria encountered in community-acquired infections: use of pharmacokinetic/pharmacodynamic breakpoints in the comparative assessment of beta-lactam and macrolide antimicrobial agents.
BACKGROUND: The application of pharmacokinetic (PK) and pharmacodynamic (PD) data in conjunction with minimum inhibitory concentrations (MICs) of antibacterial agents has been shown to allow for improved selection and appropriate dosing of antimicrobial agents for specific infections, increasing the likelihood of bacteriologic cure and, through this, reducing the risk for the development of resistant organisms. OBJECTIVES: This study was undertaken to provide data on current levels of resistance among common community-acquired bacterial species to 7 betalactam antimicrobial agents (including the combination product amoxicillin/clavulanate), azithromycin, and clarithromycin, determined through application of the PK/PD breakpoints based on time-above-MIC for the beta-lactams and the nonazalide macrolide clarithromycin, and on 24-hour serum area under the curve divided by MIC for the azalide macrolide azithromycin. METHODS: The antimicrobial products tested were amoxicillin/clavylanate, cefpodoxime, cefdinir, cefditoren, cefprozil, cefuroxime, cefixime, azithromycin, and clarithromycin. The bacterial species comprised 70 penicillin-susceptible, 68 penicillin-intermediate, and 69 penicillin-resistant strains of Streptococcus pneumoniae; 46 beta-lactamase-positive and 54 beta-lactamase-negative strains of Haemophilus influenzae; 49 strains of Moraxella catarrhalis; and 100 methicillin-sensitive strains of Staphylococcus aureus (MSSA). Strains were isolated from clinical specimens obtained from outpatient-acquired infections in 1 clinical center in the Northeast and 1 in the north-central area of the United States within the past 2 years. National Committee for Clinical Laboratory Standards microdilution MIC methodology was used. PK/PD breakpoints were obtained from previously published studies and were based on blood values. RESULTS: Amoxicillin/clavulanate was the product to which the greatest percentage of susceptible, intermediate, and resistant strains of pneumococci were sensitive at the PK/PD breakpoint, followed by cefditoren, cefpodoxime, cefuroxime, cefdinir, and cefprozil. None of the cephalosporins were active against penicillin-resistant pneumococci. Cefditoren and cefpodozime were the agents to which the greatest percentage of beta-lactamase-positive and beta-lactamase-negative strains of H influenzae were sensitive, followed by amoxicillin/clavulanate, cefdinir, and cefuroxime. Cefprozil was inactive against H influenzae. All of the beta-lactam products were active against M catarrhalis. All but cefpodoxime, cefditoren, and cefixime were active against MSSA. CONCLUSIONS: In this study, based on PK/PD breakpoints, amoxicillin/clavulanate had the best overall activity of the 9 antimicrobial products tested. Cefpodoxime and cefditoren were active against >or=90% of strains of penicillin-susceptible and penicillin-intermediate pneumococci, H influenzae, and M catarrhalis. The macrolides azithromycin and clarithromycin were active against penicillin-susceptible and penicillin-intermediate pneumococci and M catarrhalis; they were inactive against H influenzae and penicillin-resistant pneumococci.
Evaluating the need, timing and best choice of antibiotic therapy for acute otitis media and tonsillopharyngitis infections in children.
Deciding whether an antibiotic is necessary, when to begin therapy and selecting an optimal drug is an everyday challenge in clinical practice. In vitro susceptibility testing which determines the minimum concentration necessary for a particular antibiotic to inhibit or kill most strains of a bacterial species and pharmacodynamic modeling are useful but have limitations. The need for antibiotic therapy for acute otitis media (AOM) has been recently questioned. However, explanations for uniformly positive results with many antibiotic and placebo comparative trials include overdiagnosis of AOM at study entry, inclusion of patients with mild or uncomplicated AOM and broad criteria for the definition of clinical success. Recurrent and persistent AOM does not have as favorable a natural history as uncomplicated AOM; children below 2 years of age benefit most from antibiotic therapy. Selecting the best choice among the many antibiotics that can be used to treat AOM has become more complex over the last decade due to escalating antibiotic resistance among the pathogens that cause this infection. Broader spectrum antibiotics such as cefdinir, the newly introduced third generation cephalosporin, have their most prominent use in the treatment of persistent and recurrent AOM. In the early 1950s and 1960s penicillin clearly was the best available agent for the treatment of group A streptococcal (GAS) infections. In the 1970s the situation began to change as cephalosporin antibiotics became available. Superior eradication rates with cephalosporins such as cefdinir have now been well-documented. The leading hypothesis to explain the widening gap in efficacy between penicillin and cephalosporins relates to two major concepts: the presence of copathogens and differential alteration of the normal microbial ecology in the throat as a consequence of the selected therapy. There are positive and negative consequences to early initiation of antibiotic therapy for GAS tonsillopharyngitis. Penicillin has persisting good efficacy in patients older than the age of 12 years and in those who have been ill for >2 days. Shortening therapy for GAS tonsillopharyngitis offers a therapeutic advantage. Cefpodoxime proxetil and cefdinir have a 5-day indication for the treatment of GAS tonsillopharyngitis. Antibiotics with lower side effect profile, infrequent dosing, good palatability in suspension formulation and efficacy with short duration of treatment may lead to better outcomes because noncompliance often results in failed therapy, persistence of infection and morbidity.
Efficacy of trimethoprim in murine experimental infection with a thymidine kinase-deficient mutant of Escherichia coli.
The antimicrobial activity of trimethoprim is antagonized by thymidine in in vitro susceptibility tests. The purpose of this investigation was to determine whether this antagonism also occurred during experimental infection in mice, which have high serum thymidine concentrations. We derived a mutant strain of Escherichia coli, TT-48, incapable of utilizing exogenous thymidine from parent strain E. coli KC-14 and then investigated the in vitro and in vivo antimicrobial activities of trimethoprim, sulfamethoxazole, cefdinir, and ofloxacin against these strains. E. coli TT-48 lacked the activity of thymidine kinase, which catalyzes the conversion of thymidine to thymidylate, but its growth curve remained close to that of the parent strain. The MICs of all of the antimicrobial agents tested, except cefdinir, for the mutant strain were slightly inferior to those for the parent strain. The bactericidal effect of trimethoprim against the parent strain was antagonized by thymidine at concentrations of more than 1 microg/ml, while that against the mutant strain was not affected by thymidine even at the highest concentration (10 microg/ml). The therapeutic efficacy of trimethoprim in experimental murine infections was significantly higher when the mutant rather than the parent strain was used, whereas the therapeutic efficacy of cefdinir or ofloxacin, whose antimicrobial action is independent of folic acid synthesis, was the same with both strains. Unexpectedly, sulfamethoxazole also had similar efficacy against both strains. Thus, high thymidine concentrations antagonized the antimicrobial activity of trimethoprim in vitro and in vivo.
Comparative in vitro activities of seven new beta-lactams, alone and in combination with beta-lactamase inhibitors, against clinical isolates resistant to third generation cephalosporins.
We examined the drug susceptibility pattern of Gram-negative bacilli to seven new beta-lactams. A total of 277 non-duplicate gramnegative bacilli strains belonging to the Enterobacteriaceae family, Pseudomonas and Acinetobacter species, isolated from various clinical samples were tested for susceptibility to imipenem, piperacillin/tazobactam, cefoperazone/sulbactam, ticarcillin/clavulanate, cefdinir, cefepime and cefpirome with the disk diffusion technique. The percentage resistance was low for imipenem (7.2%), piperacillin/tazobactam (2.8%), cefoperazone/sulbactam (5.4%). However, a high frequency of resistance was observed to ticarcillin/clavulanate (83.9%), cefdinir (70.6%), cefepime (45.5%) and cefpirome (84.4%). We conclude that imipenem, piperacillin/tazobactam and cefoperazone/sulbactam are effective antibiotics in our environment, whereas ticarcillin/clavulanate, cefdinir, cefepime and cefpirome are relatively uneffective.
RU 29 246, the active compound of the cephalosporin-prodrug-ester HR 916. I. Antibacterial activity in vitro.
The aminothiazolyl-cephalosporin RU 29 246 is the active metabolite of the prodrug-pivaloyl-oxyethyl-ester HR 916. RU 29 246 in vitro activity includes a wide range of clinically relevant bacterial pathogens. Against methicillin-sensitive Staphylococci RU 29 246 (MIC90 of 0.25 approximately 2 micrograms/ml) was clearly more active than cefaclor, cefuroxime, cefpodoxime, cefixime and ceftibuten, but slightly less active than cefdinir. RU 29 246 inhibited hemolytic Streptococci of the serogroups A, B, C and G as well as penicillin-sensitive Streptococcus pneumoniae at concentrations similar to cefdinir, cefpodoxime and cefuroxime (MIC90 less than or equal to 0.13 micrograms/ml), but less than the other oral cephalosporins investigated (cefixime, cefaclor and ceftibuten). MIC90s of RU 29 246 against Escherichia coli, Klebsiella pneumoniae, Klebsiella oxytoca, Salmonella spp., Shigella spp., Proteus mirabilis and Haemophilus influenzae were less than or equal to 0.5 micrograms/ml. Only RU 29 246 and cefdinir demonstrated moderate activity against Acinetobacter baumannii (MIC90 greater than or equal to 4 micrograms/ml). Most strains of Pseudomonas spp., Serratia marcescens, Enterobacter spp., Hafnia alvei and Bacteroides spp. were resistant to RU 29 246. RU 29 246 killed Escherichia coli and Staphylococcus aureus at a rate of 99% to 99.9% at concentrations of two times MIC. The pH value of the medium (range 5.5 to 8.5) and the inoculum size (range 10(5) to 10(7) cfu/ml) had no or only low influence on the antibacterial activity of RU 29 246. RU 29 246 is a broad spectrum cephalosporin including in its activity both Gram-positive and Gram-negative pathogens and therefore--depending on the bioavailability of its prodrug--looks promising as to its therapeutic perspective.
Acute streptococcal pharyngitis in pediatric medicine: current issues in diagnosis and management.
Group A beta-hemolytic streptococcus (GABHS) is the most common bacterial cause of acute pharyngitis. Although children infected with GABHS will recover clinically without antibiotics, treatment is recommended in order to prevent acute rheumatic fever and probably suppurative complications, hasten resolution of clinical signs and symptoms, and prevent transmission to close contacts. Streptococcal pharyngitis usually cannot be reliably distinguished from other etiologies on the basis of epidemiologic or physical findings, and therefore a throat culture or a rapid antigen detection test is generally necessary to confirm the diagnosis. All isolates of GABHS are sensitive to penicillins and cephalosporins, whereas resistance to macrolides has been identified in some geographic regions. The recommended first-line therapy for streptococcal pharyngitis is a 10-day course of penicillin V, usually given 2 or 3 times per day. A number of alternatives to penicillin V are available, including other penicillins, macrolides, and cephalosporins. As a class, the cephalosporins are noteworthy because they may provide somewhat higher bacteriologic eradication rates than penicillin V. Many cephalosporins can be administered twice daily, but they also must be given for 10 days. Two third-generation cephalosporins, cefdinir and cefpodoxime proxetil, are approved for use in a more convenient 5-day dosing schedule, thus possibly increasing the likelihood of adherence to the full course of therapy. Palatability is also an important consideration when prescribing antibiotics to children. In a series of studies, children preferred the pleasant strawberry-cream taste of cefdinir to that of amoxicillin/clavulanate, cefprozil, and azithromycin. Cefdinir may offer an alternative to penicillin V for children with streptococcal pharyngitis, particularly when compliance is a clinical concern.
Update on treating uncomplicated skin and skin structure infections.
Dermatologists treat a variety of uncomplicated skin and skin structure infections (uSSSIs) such as folliculitis, impetigo, erysipelas, cellulitis, furuncles, carbuncles, and non-perirectal abscesses. Most uSSSIs are caused by Staphylococcus aureus and Streptococcus pyogenes. The new extended-spectrum cephalosporins (cefdinir, cefpodoxime) offer efficacy against most Gram-positive and Gram-negative pathogens. Despite recently published guidelines, many physicians do not prescribe cephalosporins for uSSSIs out of concern that these agents will produce a hypersensitivity reaction in patients allergic to penicillin. Although the rate of cephalosporin reaction in penicillin-allergic patients is often quoted as up to 10%, this rate does not take into account the 1% to 3% risk for allergy to cephalosporin alone and the nonspecific increased risk of penicillin-allergic patients to develop hypersensitivity to other drugs. When these additional risks are considered, the likelihood of a reaction in known penicillin-allergic patients, especially to most third-generation and extended spectrum cephalosporins, becomes less than 1%. Cephalosporins with side chains unlike those of penicillin or ampicillin side chains are less likely to result in an allergic reaction in penicillin or ampicillin-allergic patients than cephalosporins with similar side chains. Although both cefdinir and cefpodoxime are considered to carry a very low risk of cross reactivity with penicillin or ampicillin, the former demonstrates better activity against S. aureus. Among the late-generation cephalosporins, cefdinir is the most potent oral agent when tested against oxacillin-susceptible staphylococci, 4- to 16-fold more active than cefprozil and cephalexin, respectively.
Emergence of cephem- and aztreonam-high-resistant Neisseria gonorrhoeae that does not produce beta-lactamase.
Regarding Neisseria gonorrhoeae, the National Committee for Clinical Laboratory Standards (NCCLS) has not defined the breakpoint minimum inhibitory concentration (MIC) for expanded spectrum cephems such as cefpodoxime and ceftizoxime, because of the absence of resistant strains to these antibiotics. To date, in gonococcal urethritis, after treatment with third generation cephems and aztreonam, clinical failures caused by resistant N. gonorrhoeae strains have not been reported. However, we experienced two clinical failures in patients with gonococcal urethritis treated with cefdinir and aztreonam. N. gonorrhoeae isolates from these two patients showed high-level MICs to these agents. The MIC of cefdinir was 1 microg/ml for both strains and that of aztreonam was 8 microg/ml for both strains, while the MICs of other beta-lactams were also higher than the NCCLS value, except for ceftriaxone, for which the MIC was 0.125 microg/ml for both strains. Moreover, the MICs of fluoroquinolones, tetracyclines, and erythromycin against these two isolates were higher than the NCCLS susceptibility value. These isolates were susceptible to spectinomycin. In N. gonorrhoeae, the emergence of these beta-lactam-resistant isolates is of serious concern. However, a more serious problem is that these isolates were already resistant to non-beta-lactam antimicrobials. In Japan, ceftriaxone has not been permitted for clinical use against gonococcal infections. Therefore, in Japan, patients with gonococcal urethritis caused by these resistant N. gonorrhoeae strains should be treated with cefodizime or spectinomycin.
Evaluation of oral antimicrobial agent levels in tooth extraction sites.
OBJECTIVE: The purpose of this study was to evaluate various oral antimicrobial agent levels in tooth extraction sites. STUDY DESIGN: The concentration of dental alveolar blood in extraction wounds after the oral administration of talampicillin (500 mg), cefaclor (500 mg), cefteram pivoxil (200 mg), cefuroxime axetil (250 mg), cefdinir (200 mg), and ofloxacin (100 mg) was determined in 338 patients and was assessed on the basis of its antimicrobial activity against Streptococcus isolated in odontogenic infections. RESULTS: The percentage of patients whose concentrations exceeded the minimum inhibitory concentration for 90% of Streptococcus was 62.5% to 100% for talampicillin at 30 to 360 minutes, 0% to 12.5% for cefaclor at 30 to 360 minutes, 18.2% to 100% for cefteram pivoxil at 30 to 480 minutes, 50% to 100% for cefuroxime axetil at 30 to 480 minutes, 0% to 50% for cefdinir at 16 to 290 minutes, and 0% to 40% for ofloxacin at 30 to 480 minutes. CONCLUSION: These results indicate that talampicillin, cefteram pivoxil, and cefuroxime axetil have minimum inhibitory concentration levels for 90% of Streptococcus in tooth sockets.