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1
Terico, Adrienne T., and Jason C. Gallagher. "Beta-Lactam Hypersensitivity and Cross-Reactivity." Journal of Pharmacy Practice 27, no. 6 (August 14, 2014): 530–44. http://dx.doi.org/10.1177/0897190014546109.
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Penicillin is the most frequently reported cause of drug allergy, and cross-reactivity of penicillins with other beta-lactam antibiotics is an area of debate. This review evaluates the available data on immunoglobulin E-mediated penicillin hypersensitivity and cross-reactivity with cephalosporin, carbapenem, and monobactam antibiotics. A MEDLINE search was conducted from 1950 to October 2013, and selected references from review articles were also evaluated. There is a wide variety in reported incidences of cross-reactivity between penicillins and cephalosporins or carbapenems, with early retrospective studies suggesting up to 41.7% and 47.4% cross-reactivity, respectively. Conversely, the use of monobactam antibiotics is frequently employed in the case of a penicillin allergy, as prescribers believe that there is no cross-reactivity between the 2 drug classes. More recent prospective studies suggest that the rates of cross-reactivity with cephalosporins and carbapenems are <5% and <1%, respectively. Similarities in penicillin and cephalosporin side chains may play a role in cross-reactivity between these classes. Cross-reactivity with monobactams is essentially negligible; however, there are some clinical data to support an interaction between ceftazidime and aztreonam, due to the similarity of their side chains. The data reviewed suggest that avoidance of other beta-lactams in patients with type 1 hypersensitivity to penicillins should be reconsidered.
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Bradley, Nicole, Yuman Lee, and Dana Weinstein. "Overview of Beta-Lactam Allergy and the Role of the Pharmacist in Management." Allergies 1, no. 2 (June 17, 2021): 128–36. http://dx.doi.org/10.3390/allergies1020011.
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Unverified beta-lactam allergies are a substantial public health problem, as the majority of patients labeled as beta-lactam allergic do not have clinically significant allergies that may hinder the use beta-lactam therapy when indicated. Outdated or inaccurate beta-lactam or penicillin allergies can result in serious consequences, including suboptimal antibiotic therapy, increased risk of adverse effects, and use of broader spectrum antibiotics than indicated, which may contribute to antimicrobial resistance. The purpose of this review is to provide an overview of beta-lactam allergy and highlight the role of pharmacists in managing beta-lactam allergies. Studies have shown that pharmacists can play a vital role in allergy assessment, penicillin skin testing, beta-lactam desensitization, evaluation of beta-lactam cross-reactivity and recommending appropriate antibiotic therapy in patients with beta-lactam allergies.
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Asada, K., Y. Inaba, E. Tateda-Suzuki, K. Kuwahara-Arai, T. Ito, and K. Hiramatsu. "Evolution and resistance expression of MRSA. Evaluation of beta-lactam antibiotics against a set of isogenic strains with different types of phenotypic expression." Acta Biochimica Polonica 42, no. 4 (December 31, 1995): 517–24. http://dx.doi.org/10.18388/abp.1995_4905.
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Methicillin-resistant Staphylococcus aureus (MRSA) has two mechanisms of resistance to beta-lactam antibiotics; one is mediated by mecA gene expression, and the other by penicillinase production. It has been generally accepted in the clinical field that beta-lactam antibiotics are not the drugs of choice for MRSA infection. In this report, however, ampicillin and penicillin G were shown to have relatively good activity against MRSA if combined with a beta-lactamase inhibitor, sulbactam. These beta-lactam antibiotics were found to have relatively high binding affinities to PBP2', the mecA-encoded MRSA-specific penicillin-binding protein. The possible therapeutic application of sulbactam/ampicillin against MRSA infection in combination with arbekacin, an aminoglycoside antibiotic newly developed and introduced into clinical use in Japan, is discussed.
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Wong, Tiffany, Adelle Atkinson, Geert t’Jong, Michael J. Rieder, Edmond S. Chan, and Elissa M. Abrams. "Beta-lactam allergy in the paediatric population." Paediatrics & Child Health 25, no. 1 (February 2020): 62. http://dx.doi.org/10.1093/pch/pxz179.
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Abstract Beta-lactam allergy is commonly diagnosed in paediatric patients, but over 90% of individuals reporting this allergy are able to tolerate the medications prescribed after evaluation by an allergist. Beta-lactam allergy labels are associated with negative clinical and administrative outcomes, including use of less desirable alternative antibiotics, longer hospitalizations, increasing antibiotic-resistant infections, and greater medical costs. Also, children with true IgE-mediated allergy to penicillin medications are often advised to avoid all beta-lactam antibiotics, including cephalosporins, which is likely unnecessary in greater than 97% of those reporting penicillin allergies. Most patients can be safely treated with penicillin or amoxicillin if they do not have a history compatible with IgE-mediated or systemic, delayed reactions such as Stevens-Johnson syndrome (SJS), serum sickness-like reactions, drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome, or acute generalized exanthematous pustulosis (AGEP). Guidance is provided on how to stratify risk of beta-lactam allergy, and on test dosing and monitoring in the outpatient setting for patients deemed low risk. Guidance for patients at higher risk of beta-lactam allergy includes criteria for appropriate referral to allergists and the use of alternative antimicrobials, such as cephalosporins, while awaiting specialist assessment.
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Burroughs, Susan F., and Gerhard J. Johnson. "Beta-Lactam Antibiotics Inhibit Agonist-Stimulated Platelet Calcium Influx." Thrombosis and Haemostasis 69, no. 05 (1993): 503–8. http://dx.doi.org/10.1055/s-0038-1651641.
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Summary(β-lactam antibiotics cause platelet dysfunction with reversible agonist-receptor inhibition, irreversible [14C]-penicillin binding, and inhibition of agonist-stimulated elevation in cytosolic Ca2+ ([Ca2+]i), occurring after 24 h exposure in vitro and after in vivo treatment. We investigated β-lactam antibiotic-induced inhibition of rises in [Ca2+]i stimulated by thrombin, sodium arachidonate or A23187 to determine whether Ca2+ influx or intracellular release was primarily affected. The mean rise in [Ca2+]i, measured with fura-2-AM, was inhibited 43.7-84.1% by penicillin when the extracellular Ca2+ concentration ([Ca2+]e) was 1 mM, but was significantly less inhibited when [Ca2+]e was <1 μM. NiCl2 (2 mM), that blocks Ca2+ influx, caused inhibition comparable to penicillin. MnCl2 (1 mM), that quenches the intracellular fura-2 signal, significantly decreased the rise in 1 mM [Ca2+]i when [Ca2+]e was 1 mM, but did not increase the inhibition caused by penicillin. Penicillin did not inhibit the rise in [Ca2+]i stimulated by inositol-1,4,5-trisphosphate or GTPγS. Therefore, β-lactam antibiotics inhibit agonist-induced elevations of [Ca2+]i primarily through inhibition of Ca2+ influx, which probably accounts for the irreversible inhibition of platelet function seen after prolonged in vitro or in vivo treatment.
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Lepage, S., M. Galleni, B. Lakaye, B. Joris, I. Thamm, and J. M. Frere. "Kinetic properties of the Bacillus licheniformis penicillin-binding proteins." Biochemical Journal 309, no. 1 (July 1, 1995): 49–53. http://dx.doi.org/10.1042/bj3090049.
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In the analysis of the interactions between beta-lactam antibiotics and their target enzymes, it is often difficult to estimate the kinetic properties of the molecules which react rapidly with their targets and in consequence behave as the most efficient antibiotics. The combined utilization of fluorescein-labelled penicillins and of a new competition method has allowed an accurate determination of the high second-order rate constants characterizing the acylation of Bacillus licheniformis penicillin-binding protein 1 (PBP1) by penicillins and cephalosporins. Strategies were devised for measuring high acylation rates while avoiding titration effects. The method was also suitable for measuring the PBP kinetic parameters in intact cells. These results also confirmed that PBP1 is probably the main target of most beta-lactam antibiotics. Cephalexin, however, reacted faster with PBP3.
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Zaman, Rashed, Pranab Karmaker, SM Naimul Hasan, M. Hamidur Rahman, and Ariful Haque. "Drifted catalytic properties of β-lactamases due to unconstrained use of antibiotics." Journal of Bio-Science 19 (December 19, 2012): 37–42. http://dx.doi.org/10.3329/jbs.v19i0.12999.
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Context: Antibiotic resistance is an old problem with new face as the rate of infections due to multidrug resistant bacteria is increasing everyday and the number of new antibiotics to overwhelm the problem is becoming smaller. Major mechanism beneath this growing resistance is concomitant with the changes in ?-lactamases catalytic activity and its functional enhancement. Objectives: In ?-lactamases secreting clinical isolates at least 10% are extended-spectrum ?-lactamases (ESBL) that are not even treatable with ?-lactamases inhibitor like clavulanic acids. This implies that the catalytic domains of ?-lactamases have been mutated towards higher pathogenicity. The aim of the present study is to define the changes in ?-lactamases catalytic efficiency against ?-lactam antibiotics and its inhibitors. Materials and Methods: In this research work we have used multiple drug resistant (MDR) strains from surgical site of infections. A rapid method was used for specific detection of bacterial ?-lactamases that uses ?-lactam antibiotics as substrates. In this, the end products (open beta-lactam ring forms) generated after separately incubating substrates with ?-lactamases producing strains. Those end products of antibiotics were highly fluorescent after specific treatment and could be analyzed visually under long-wave UV lamp for efficiency. Results: ?-lactamases secreting strains are variably capable of defending ?-lactam antibiotics. Interestingly, one of the E. coli strain secretes ESBL, this means that the strain is resistant against clavulanic acid. However, the most fascinating fact of the finding is that ideally the ?-lactamases supposed to hydrolyze Penicillin by default but in our isolates, ?-lactamases are not able to hydrolyze penicillin instead they hydrolyze amoxicillin, a derivative which replaced clinical use of penicillin. In addition to that we have identified the presence of New Delhi Metalo- beta- lactamase in one of the clinical isolates. Conclusion: Rate of evolution in microbes is very high. Thus we presume that some of the amino acids in the functional domain of ?-lactamases have been changed respective to extinct use of penicillin whereas it is effective against clinically used other beta lactam antibiotics. DOI: http://dx.doi.org/10.3329/jbs.v19i0.12999 J. bio-sci. 19 37-42, 2011
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Derakhshandeh, Maryam, and Majid Monajjemi. "Nano drug deliverer for ampicillin, clavulanic acid, imipenem, penicillin g and ticarcillin." Nexo Revista Científica 33, no. 01 (July 20, 2020): 121–36. http://dx.doi.org/10.5377/nexo.v33i01.10052.
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Ampicillin belonging to the penicillin group of beta lactam antibiotics. Ampicillin is able to penetrate Gram positive and some Gram-negative bacteria. Imipenem (Primaxin) is an intravenous β-lactam antibiotic discovered by Merck scientists Burton Christensen, William Leanza, and Kenneth Wildonger in 1980 Ampicillin, Clavulanic acid, Imipenem, Penicillin G and Ticarcillin properties for the drug delivery with binding to SWCNNTs and SWBNNTs have been studied. Penicillin and its alteration Penicillin G or phenoxyacetic acid for Penicillin V is used for large scale production. Penicillin and other cell wall inhibitors are primarily specific against Gram positive bacteria because of higher percentage of peptidoglycan in the cell walls of these organisms. It was the first member of the carbapenem class of antibiotics. Based on our previous works we have modeled and simulated a drug delivery system of those antibiotics. The investigation of those antibiotics in binding with single-walled carbon nanotube (SWCNT) and SWBNNTs have been studied by theoretical methods. It has been established the best structural and functional of those antibiotics.
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Higazi, Abd Al-Roof, and Michael Mayer. "In Vitro Inhibition of Urokinase by Penicillins." Thrombosis and Haemostasis 60, no. 02 (1988): 305–7. http://dx.doi.org/10.1055/s-0038-1647049.
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SummaryUrokinase activity was assayed by a two-stage globinolytic method and by a direct chromogenic assay. With both methods, the enzyme activity was found to be inhibited by penicillins. The inhibition by penicillin G, carbenicillin, cloxacillin and penicilloic acid was dose-dependent. The Kj of penicillin G and urokinase with the S-2444 as substrate is 4 mM. This compound exhibited a competitive pattern of inhibition. Ampicillin and 6-amino penicillanic acid failed to inhibit urokinase. These results imply that hydrophobic side chains of penicillins interact with the active site of urokinase. The present observation could be relevant in clinical situation in which high doses of beta-lactam antibiotics could modulate the endogenous fibrinolytic activity of circulating urokinase.
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Connelly, Sheila, Todd Parsley, Hui Ge, and Michael Kaleko. "Identification, Characterization, and Formulation of a Novel Carbapenemase Intended to Prevent Antibiotic-Mediated Gut Dysbiosis." Microorganisms 7, no. 1 (January 16, 2019): 22. http://dx.doi.org/10.3390/microorganisms7010022.
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Antibiotics can damage the gut microbiome leading to opportunistic infections and the emergence of antibiotic resistance. Microbiome protection via antibiotic inactivation in the gastrointestinal (GI) tract represents a strategy to limit antibiotic exposure of the colonic microbiota. Proof of concept for this approach was achieved with an orally-administered beta-lactamase enzyme, SYN-004 (ribaxamase), that was demonstrated to degrade ceftriaxone excreted into the GI tract and protect the gut microbiome from antibiotic-mediated dysbiosis. Ribaxamase efficiently degrades penicillin and cephalosporin beta-lactam antibiotics, but is not active against carbapenems. To expand this microbiome protection strategy to include all classes of beta-lactams, three distinct carbapenemases were evaluated for manufacturability, antibiotic degradation spectrum, and stability in human intestinal fluid. E. coli production strains were generated for P2A, a novel metallo-enzyme isolated from B. cereus, New Delhi metallo-beta-lactamase (NDM), and Klebsiella pneumoniae carbapenemase (KPC). While all three enzymes effectively inactivated a broad range of antibiotics, including penicillins, most cephalosporins, and carbapenems in vitro, only P2A retained biological activity when incubated with human chyme. As functional stability in the intestinal tract is a key requirement for an orally-delivered enzyme, P2A was chosen as a potential clinical candidate. An enteric formulation of P2A was developed, called SYN-006, that was inert under high acid conditions, with enzyme dissolution occurring at pH > 5.5. SYN-006 has the potential to expand microbiome protection via antibiotic inactivation to include all classes of beta-lactam antibiotics.
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Salamone, Francine R. "Sulbactam/Ampicillin." Infection Control & Hospital Epidemiology 9, no. 7 (July 1988): 323–27. http://dx.doi.org/10.1086/645863.
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Sulbactam/ampicillin was recently marketed for use in several infections caused by beta-lactamase-producing organisms. Sulbactam is the second beta-lactamase inhibitor to become available in the United States. Interest in inhibition of beta-lactamases arose in the late 1960s when a combination consisting of an antibacterial agent and an enzyme inhibitor was found effective in the treatment of certain resistant gram-negative infections. It is now well accepted that the addition of a beta-lactamase inhibitor to a beta-lactam antibiotic may expand its usefulness in a variety of infections.The penicillin derivatives, known as beta-lactam antibiotics, possess a four-membered ring (beta-lactam ring) fused to a second ring (Figure). It is the beta-lactam ring that is essential for the inhibition of bacterial cell wall synthesis and subsequent bactericidal activity of these agents. The development of resistance to beta-lactam antibiotics may occur by a number of mechanisms, although the most important is bacterial production of enzymes (beta-lactamases) that are capable of beta-lactam ring hydrolysis and inactivation.Sulbactam resembles the penicillin derivatives in structure (Figure) and is able to preserve their activity by its ability to inhibit the action of beta-lactamases, particularly those of the Richmond classes II-V (gram-negative) and the group A beta-lactamases (gram-positive). Sulbactam is referred to as a “suicide inhibitor” because while forming an irreversible complex with the enzyme, it is destroyed in the process. By virtue of its ability to render the beta-lactamases inactive, sulbactam has been combined with ampicillin in an effort to restore its activity against a number of pathogens that have developed resistance by this mechanism.
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Ahsan, Sunjukta, Anindita Bhowmik, Sharmistha Goswami, and Nasir Uddin. "Detection of New Delhi Metallo b Lactamase gene in Uropathogenic E. coli." Bangladesh Journal of Microbiology 36, no. 1 (December 8, 2019): 29–33. http://dx.doi.org/10.3329/bjm.v36i1.44280.
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The rapid dissemination of antibiotic resistant E. coli is now a worldwide problem. In this study, a total of twenty E. coli obtained from stool were selected to determine resistance to beta lactam antibiotics. Beta–Lactamase are enzymes produced by bacteria that provide multi resistance to beta lactam antibiotics such as penicillin, cephalosporin, cephamycin and carbapenems. Of these isolates (n = 20), 35% were found resistant to Amoxicillin Clavulanate, 5% to Imipenem, 50% to Ceftriaxone and 75% to Ampicillin. PCR amplification confirmed the presence of the New Delhi beta-lactamase gene (blaNDM) in one isolate (5%, n=20). Plasmids of variable sizes were found in all the isolates. Beta lactam antibiotics are now commonly used for the treatment of disease. Resistance of 50% of the isolates to Ceftriaxone is alarming as this indicates that an alternative drug may soon need to replace this antibiotic for successful treatment. The finding of this study is also of public health concern as plasmids were found in most isolates and these mobile genetic elements can be transferred among clinical bacteria, thereby disseminating antibiotic resistance further limiting treatment options.
Bangladesh J Microbiol, Volume 36 Number 1 June 2019, pp 29-33
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Bouchard, Sylvie, Geneviève Robitaille, Fatiha Karam, Jean-Marc Daigle, and Mélanie Tardif. "PP43 Decision-Making Tool In Case Of Beta-Lactam Allergy: How To Help Clinicians?" International Journal of Technology Assessment in Health Care 35, S1 (2019): 45. http://dx.doi.org/10.1017/s0266462319002034.
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IntroductionBeta-lactams (BLs), especially penicillins, are the most commonly used antibiotics, particularly in primary care, and one of the most reported drug allergies. Fearing cross-reactivity, clinicians refrain from prescribing another BL (e.g., cephalosporin or carbapenem) to penicillin-allergic patients. This can have significant consequences for the patients and the health-care system (e.g., exposure to broad-spectrum antibiotics, increased risk adverse effects, and increased healthcare costs).MethodsTo assess the absolute cross-reactivity risk, two systematic reviews with meta-analysis were conducted. Then, an approach based on a knowledge mobilization framework considering scientific, contextual and experiential evidences was used. Focus groups with stakeholders, including primary care clinicians, pediatricians, infectious disease specialists and allergists/immunologists, were also held to meet the needs of all actors concerned.ResultsFollowing this work, it appears that true allergies to penicillin are very rare. Indeed, in patients with a history of penicillin allergy, very few are truly allergic and thus the risk of cross-reaction with another BL is even lower, varying according to structural and physicochemical similarities with alleged-penicillin. Moreover, the risk of having an anaphylactic reaction after penicillin exposure is very low, especially among children. As well, in patients with confirmed penicillin allergy, the observed reactions are usually delayed non-severe skin reactions. However, with a confirmed penicillin allergy, it is important to remain cautious when administering a new BL, especially if the initial reaction was serious or severe. Based on these key messages, a decision aid including an algorithm was developed. Likewise, individualized algorithms for common infections met in primary care were produced.ConclusionsFrom this work, health professionals non-specialized in allergology should be able to better manage the risks attributed to penicillin allergies. Therefore, patients should receive the most effective and safe antibiotics to treat their clinical conditions in primary care.
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Jamin, M., C. Damblon, S. Millier, R. Hakenbeck, and J. M. Frère. "Penicillin-binding protein 2x of Streptococcus pneumoniae: enzymic activities and interactions with β-lactams." Biochemical Journal 292, no. 3 (June 15, 1993): 735–41. http://dx.doi.org/10.1042/bj2920735.
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The high-molecular-mass penicillin-binding protein (PBP) 2x, one of the primary targets of beta-lactam antibiotics in Streptococcus pneumoniae, has been produced as a soluble form and purified in large amounts. It has been shown to catalyse hydrolysis and transfer reactions with different ester and thiolester substrates and its catalytic behaviour was often similar to that of the soluble DD-peptidase from Streptomyces R61. This provided an easy method to monitor the activity of the PBP. For the first time, a reliable kinetic study of the interaction between a lethal target and beta-lactam antibiotics has been performed. Characteristic kinetic parameters were obtained with different beta-lactam compounds. These results not only validated the mechanism established with non-essential extracellular enzymes, but will also constitute the basis for comparative studies of the low-affinity variants from penicillin-resistant strains.
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Slaught, Matthew John, Daniel W. Bougie, and Richard H. Aster. "Cross-Reactivity of Drug-Dependent Antibodies in Patients with Immune Thrombocytopenia Induced By Beta-Lactam Antibiotics." Blood 134, Supplement_1 (November 13, 2019): 2350. http://dx.doi.org/10.1182/blood-2019-131375.
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More than 50 beta lactam (BL) antibiotics are now in active use for treatment of a wide range of bacterial infections. BL antibiotics are among the most common drugs capable of inducing antibodies (DDAbs) that cause drug-induced immune thrombocytopenia (DITP). Most DDAbs are highly specific for the sensitizing drug but beta lactams all have a common core structure and many similarities among side groups that are added to augment potency and modify specificity, raising the possibility that a DDAb specific for one BL may cross-react with another. We studied DDAbs from 33 patients with DITP induced by 9 commonly used BL drugs to determine whether patterns of cross-reactivity exist that might influence the choice of an alternative antibiotic in a patient with BL-induced DITP. DDAbs were demonstrated in a flow cytometric assay considered to be "positive" when immunoglobulins in patient serum but not normal serum react with normal platelets in the presence, but not in the absence of drug (Blood 2018;131:1486). DDAbs detected in the 33 patients were specific for 9 different BL drugs that were divided into two groups, "penicillins" (Group 1) and cephalosporins (Group 2) on the basis of structural similarities (Figure 1). In Group 1 were 19 DDAbs specific for amoxicillin (2), nafcillin (4) and piperacillin (13). Structurally similar ampicillin and penicillin were also tested with these abs. In Group 2 were 14 DDAbs specific for cefadroxil (1), cefepime (2), ceftazidime (2), ceftizoxime (1), ceftriaxone (7) and cephalexin 1). Cross-reactions identified within these groups of DDAbs are shown in Tables 1 and 2. Cross-reactions, many quite strong (S) were observed among DDAbs specific for drugs in both structural groups (Tables 1 and 2). Particularly noteworthy were cross-reactions of the 19 Group 1 DDAbs with ampicillin (6) and penicillin (6) (Table 1) and of the 14 Group 2 DDAbs with cefepime (6), ceftizoxazole (6) and ceftriaxone (3) (Table 2). The findings show that platelet-specific DDAbs induced by beta lactam antibiotics, in contrast with those induced by medications like quinine, sulfamethoxazole and vancomycin, commonly cross-react with other antibiotics of this class. In patients with immune thrombocytopenia induced by a beta lactam antibiotic, it may be prudent to avoid switching to another beta lactam or, if this is necessary, to monitor platelet counts carefully. Disclosures No relevant conflicts of interest to declare.
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Sameed, Muhammad, Christine Nwaiser, Prashant Bhandari, and Sarah A. Schmalzle. "Meropenem-induced Stevens-Johnson syndrome/toxic epidermal necrolysis in a patient with known type IV penicillin hypersensitivity." BMJ Case Reports 12, no. 8 (August 2019): e230144. http://dx.doi.org/10.1136/bcr-2019-230144.
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Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are considered variants of a disease continuum that results in a life-threatening exfoliative mucocutaneous disease. These are categorised as type IV cell-mediated delayed hypersensitivity reactions, and antibiotics are often implicated as a cause. Penicillins and other beta-lactam antibiotics are known to cause both immediate and delayed hypersensitivity reactions. While immediate IgE-mediated cross-reactivity between penicillins and carbapenems is well studied, less information on the risk of type IV delayed cell-mediated cross-reactivity between the two is available. We present a case of meropenem-induced SJS in a patient with documented history of SJS from amoxicillin. There are few cases of cross-reactivity with carbapenems reported in the literature, but based on the potential for life-threatening reaction, it is likely prudent to avoid the use of any beta-lactams in a patient with a history of SJS, TEN or any other severe cutaneous adverse reactions to another beta-lactam antibiotic.
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Derakhshandeh, Maryam, and Majid Monajjemi. "Nano Drug Deliverer for Ampicillin, Clavulanic Acid, Imipenem, Penicillin G and Ticarcillin." Journal of Computational and Theoretical Nanoscience 13, no. 10 (October 1, 2016): 7144–55. http://dx.doi.org/10.1166/jctn.2016.5964.
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Ampicillin, Clavulanic acid, Imipenem, Penicillin G and Ticarcillin properties for the drug delivery with binding to SWCNNTs and SWBNNTs have been studied. Penicillin and its alteration Penicillin G or phenoxyacetic acid for Penicillin V is used for large scale production. Penicillin and other cell wall inhibitors are primarily specific against Gram positive bacteria because of higher percentage of peptidoglycan in the cell walls of these organisms. Ampicillin belonging to the penicillin group of beta lactam antibiotics, ampicillin is able to penetrate Gram positive and some Gram-negative bacteria. Imipenem (Primaxin) is an intravenous β-lactam antibiotic discovered by Merck scientists Burton Christensen, William Leanza, and Kenneth Wildonger in 1980. It was the first member of the carbapenem class of antibiotics. Based on our previous works we have modeled and simulated a drug delivery system of those antibiotics. The investigation of those antibiotics in binding with single-walled carbon nanotube (SWCNT) and SWBNNTs have been studied by theoretical methods. It has been established the best structural and functional of those antibiotics. A number of computational chemistry studies carried out to understand the conformational preferences that may be attributed to stereo electronic effects. These results show the minimized structure of mentioned antibiotics with SWCNTs and SWBNNTs, calculated potential energy for important dihedral angles, and the effect of temperature on geometry of optimized structure. NMR by GIAO approximation, have been applied for determination of the situation in antibiotics-SWCNT and shifting. This model provides an atomistic analysis of the antibiotics-SWCNT strategy and its implications for further investigations of drugs.
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Shweta, Fnu, Pooja Gurram, Natalia E. Castillo Almeida, Douglas Challener, Edison J. Cano, Miguel Park, Prasanna Narayanan, Lee Skrupky, Gerald Volcheck, and Abinash Virk. "153. Development of a Pathway for Removal of Inappropriate Penicillin Allergy Labels in Hospitalized Patients." Open Forum Infectious Diseases 7, Supplement_1 (October 1, 2020): S86—S87. http://dx.doi.org/10.1093/ofid/ofaa439.198.
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Abstract Background More than 90% of reported penicillin allergies are found inaccurate when formally assessed. These allergy labels lead to decreased utilization of first-line beta-lactam antibiotics, and adverse clinical outcomes. The objective of this study was to develop a multi-disciplinary approach to decrease inaccurate labeling among hospitalized patients with documented penicillin allergy. Methods A team of clinicians, pharmacists, and nurses utilized the DMAIC quality strategy to improve accuracy of penicillin allergy labeling. Allergic reactions were stratified to develop a penicillin allergy de-labeling algorithm (Figure 1). Admission to the intensive care unit (ICU) for anaphylaxis was defined as a balancing measure. We reviewed baseline data from patients with a documented penicillin allergy admitted to a single inpatient floor at Mayo Clinic, Rochester between June and October 2019. A cause and effect diagram was used to conduct a root cause analysis. The intervention was then applied to patients who reported penicillin allergy admitted to the same floor from November 2019 to January 2020. Study data were collected and basic descriptive statistics generated. Figure 1: Penicillin allergy delabeling algorithm Results 96 patients were included in the control group with mean age of 71 years (range 65–84 years) and 55% females. Breakdown of documented allergic reactions are represented in Figure 2. 58 (60%) received an antibiotic for a median duration of 1.5 days (IQR: 0 – 6). Of these, 7(12%) received penicillin-class antibiotics, and 41 (70.6%) received non-beta-lactam antibiotics. 2 (2%) of these patients were de-labeled without any penicillin skin tests. Detailed metrics of each PDSA cycle are shown in Table 1. During PDSA cycle 2, inaccurate penicillin documentation was removed in 9/19 (47.4%) of hospitalized patients. There were no ICU admissions for anaphylaxis. Figure 2: Graphic representation of proportion of type of documented allergic reactions to penicillin Table 1: Metrics and outcomes at baseline and during successive PDSA cycles Conclusion Various factors contribute to penicillin allergy mislabeling. Our comprehensive algorithm addresses nuances of penicillin allergic reactions and increased accurate penicillin allergy labeling in 47.4% of the cases. Beta-lactam use also increased to 37% through our pilot project while maintaining patient safety. A multi-disciplinary and patient-centered approach aligned with institutional workflows is necessary to improve patient outcomes. Disclosures All Authors: No reported disclosures
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Alves, Janine F., Guilherme H. Paula, Rânio C. F. Silva, Paulo V. T. Leão, Karen M. Leão, Edmar S. Nicolau, and Marco A. P. Silva. "Residues of antibiotics in milk: persistence and quality interference." Canadian Journal of Animal Science 100, no. 1 (March 1, 2020): 93–101. http://dx.doi.org/10.1139/cjas-2018-0224.
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The objective of this study was (i) to analyze antibiotic residues, two which were beta-lactam antibiotics, one tetracycline, and one quinolone in the milk of lactating animals; (ii) to evaluate the interference of the drug ceftiofur which is considered as discard-zero. The SNAPduo™ ST Plus kit was used to evaluate the presence of beta-lactam antibiotics and tetracyclines in natural milk. Medications based on penicillin, ceftiofur, enrofloxacin, and oxytetracycline were used. As expected, the milk from control animals and animals administered with enrofloxacin did not present antibiotic residue because it is not one of the classes detected by the SNAPduo™ ST Plus kit, and thus it was used to prove the efficiency of the test. Ceftiofur, known as a “discard-zero” antibiotic, tested positive for the SNAPduo™ ST Plus kit and the BetaStar Combo® “S” test. Chemical residues were detected in cow’s milk treated with different groups of antibiotics after the withdrawal time indicated in the package inserts of the medicines used.
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Meetschen, Ute, and Michael Petz. "Capillary Gas Chromatographic Method for Determination of Benzylpenicillin and Other Beta-Lactam Antibiotics in Milk." Journal of AOAC INTERNATIONAL 73, no. 3 (May 1, 1990): 373–79. http://dx.doi.org/10.1093/jaoac/73.3.373.
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Abstract A capillary gas chromatographic method Is described for determining residues of beta-lactam antibiotic residues In milk, with specificity for benzylpenlclllln (penicillin G), phenoxymethylpenlcillin, methlclllln, oxacillin, cloxaclllln, dlcloxaclllln, and nafclllln. Residues are extracted from milk with acetonitrlle. Samples are cleaned up by partitioning between aqueous and organic phases at different pH values. The penicillin residues are methylated with dlazomethane to render them amenable to determination by gas chromatography on a methyl silicone fused silica column. Samples are introduced by spllt/splltless injection using a programmed temperature vaporization injector and are detected by nitrogenselective thermionic detection, internal standardization Is used for quantitation. The limits of detection for all penicillins are well below 1 /μg/kg. Recoveries of spiked samples at 3 and 10 μg/kg are in the range of 42-85% (coefficients of variation 2-5%) and 41-92% (coefficients of variation 3- 7%), respectively.
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Kanu, Joseph Sam, Mohammed Khogali, Katrina Hann, Wenjing Tao, Shuwary Barlatt, James Komeh, Joy Johnson, et al. "National Antibiotic Consumption for Human Use in Sierra Leone (2017–2019): A Cross-Sectional Study." Tropical Medicine and Infectious Disease 6, no. 2 (May 13, 2021): 77. http://dx.doi.org/10.3390/tropicalmed6020077.
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Monitoring antibiotic consumption is crucial to tackling antimicrobial resistance. However, currently there is no system in Sierra Leone for recording and reporting on antibiotic consumption. We therefore conducted a cross-sectional study to assess national antibiotic consumption expressed as defined daily dose (DDD) per 1000 inhabitants per day using all registered and imported antibiotics (categorized under the subgroup J01 under the anatomical and therapeutic classification (ATC) system) as a proxy. Between 2017–2019, total cumulative consumption of antibiotics was 19 DDD per 1000 inhabitants per day. The vast majority consisted of oral antibiotics (98.4%), while parenteral antibiotics made up 1.6%. According to therapeutic/pharmacological subgroups (ATC level 3), beta-lactam/penicillins, quinolones, and other antibacterials (mainly oral metronidazole) comprised 65% of total consumption. According to WHO Access, Watch, and Reserve (AWaRe), 65% of antibiotics consumed were Access, 31% were Watch, and no Reserve antibiotics were reported. The top ten oral antibiotics represented 97% of total oral antibiotics consumed, with metronidazole (35%) and ciprofloxacin (15%) together constituting half of the total. Of parenteral antibiotics consumed, procaine penicillin (32%) and ceftriaxone (19%) together comprised half of the total. Policy recommendations at global and national levels have been made to improve monitoring of antibiotic consumption and antibiotic stewardship.
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Okerman, Lieve, Katia De Wasch, Jan Van Hoof, and Walter Smedts. "Simultaneous Determination of Different Antibiotic Residues in Bovine and in Porcine Kidneys by Solid-Phase Fluorescence Immunoassay." Journal of AOAC INTERNATIONAL 86, no. 2 (March 1, 2003): 236–40. http://dx.doi.org/10.1093/jaoac/86.2.236.
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Abstract Parallux®, a solid-phase fluorescence immunoassay (SPFIA) developed for antibiotic residue detection in milk, was used for analysis of bovine and porcine kidney tissue. Four tetracyclines, 2 broad-spectrum cephalosporins, 3 beta-lactam antibiotics, and cephapirin were detected in one run after minimal sample preparation. This commercially available test system is designed as cartridges, each with a combination of 1–4 tests. One cartridge can be used to detect 4 analytes in the same sample, or 1 or 2 analytes in different samples. The cartridge with the combination tetracyclines–ceftiofur–penicillin–cephapirin was selected because tetracyclines, beta-lactam antibiotics as well as cephalosporins, are registered for oral or parenteral use in bovines and pigs in Europe. The test is qualitative and is recommended only for screening. Tetracycline, oxytetracycline, chlortetracycline, and doxycycline were easily detected at 300 ppb with the tetracyclines channel; ceftiofur at 1000 ppb and cefquinome at 200 ppb with the ceftiofur channel; penicillin G, ampicillin, and amoxicillin at 50 ppb with the penicillin channel; and cephapirin at 100 ppb with the cephapirin channel. These levels are equal to or lower than the corresponding maximal residue limits in kidney tissue. Cephalexin was not detected. The SPFIA test can be used as an alternative to classical inhibition tests and for post-screening inhibitor- positive kidneys, because it detects 3 specific groups of antibiotics, which enables selection of specific confirmatory methods for identification and quantification.
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Verdier, Marie-Clémence, Olivier Tribut, Pierre Tattevin, Yves Le Tulzo, Christian Michelet, and Danièle Bentué-Ferrer. "Simultaneous Determination of 12 β-Lactam Antibiotics in Human Plasma by High-Performance Liquid Chromatography with UV Detection: Application to Therapeutic Drug Monitoring." Antimicrobial Agents and Chemotherapy 55, no. 10 (July 25, 2011): 4873–79. http://dx.doi.org/10.1128/aac.00533-11.
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ABSTRACTA rapid and specific high-performance liquid chromatography method with UV detection (HPLC-UV) for the simultaneous determination of 12 beta-lactam antibiotics (amoxicillin, cefepime, cefotaxime, ceftazidime, ceftriaxone, cloxacillin, imipenem, meropenem, oxacillin, penicillin G, piperacillin, and ticarcillin) in small samples of human plasma is described. Extraction consisted of protein precipitation by acetonitrile. An Atlantis T3 analytical column with a linear gradient of acetonitrile and a pH 2 phosphoric acid solution was used for separation. Wavelength photodiode array detection was set either at 210 nm, 230 nm, or 298 nm according to the compound. This method is accurate and reproducible (coefficient of variation [CV] < 8%), allowing quantification of beta-lactam plasma levels from 5 to 250 μg/ml without interference with other common drugs. This technique is easy to use in routine therapeutic drug monitoring of beta-lactam antibiotics.
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Ferreira, R. C., J. T. Park, D. Camelo, D. F. De Almeida, and L. C. Ferreira. "Interactions of Yersinia pestis penicillin-binding proteins with beta- lactam antibiotics." Antimicrobial Agents and Chemotherapy 39, no. 8 (August 1, 1995): 1853–55. http://dx.doi.org/10.1128/aac.39.8.1853.
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Jensen, Anders, Oskar Valdórsson, Niels Frimodt-Møller, Susan Hollingshead, and Mogens Kilian. "Commensal Streptococci Serve as a Reservoir for β-Lactam Resistance Genes in Streptococcus pneumoniae." Antimicrobial Agents and Chemotherapy 59, no. 6 (April 6, 2015): 3529–40. http://dx.doi.org/10.1128/aac.00429-15.
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ABSTRACTStreptococcus pneumoniaeis a leading cause of pneumonia, meningitis, septicemia, and middle ear infections. The incidence ofS. pneumoniaeisolates that are not susceptible to penicillin has risen worldwide and may be above 20% in some countries. Beta-lactam antibiotic resistance in pneumococci is associated with significant sequence polymorphism in penicillin-binding proteins (PBPs). Commensal streptococci, especiallyS. mitisandS. oralis, have been identified as putative donors of mutated gene fragments. However, no studies have compared sequences of the involvedpbpgenes in large collections of commensal streptococci with those ofS. pneumoniae. We therefore investigated the sequence diversity of the transpeptidase region of the threepbpgenes,pbp2x,pbp2b, andpbp1ain 107, 96, and 88 susceptible and nonsusceptible strains of commensal streptococci, respectively, at the nucleotide and amino acid levels to determine to what extent homologous recombination between commensal streptococci andS. pneumoniaeplays a role in the development of beta-lactam resistance inS. pneumoniae. In contrast to pneumococci, extensive sequence variation in the transpeptidase region ofpbp2x,pbp2b, andpbp1awas observed in both susceptible and nonsusceptible strains of commensal streptococci, conceivably reflecting the genetic diversity of the many evolutionary lineages of commensal streptococci combined with the recombination events occurring with intra- and interspecies homologues. Our data support the notion that resistance to beta-lactam antibiotics in pneumococci is due to sequences acquired from commensal Mitis group streptococci, especiallyS. mitis. However, several amino acid alterations previously linked to beta-lactam resistance in pneumococci appear to represent species signatures of the donor strain rather than being causal of resistance.
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AGÓCS, ATTILA, PÁL HERCZEGH, FERENC SZTARICSKAI, ZSUZSA GÁL, and FERENC HERNÁDI. "A Trimer of Phenoxymethyl Penicillin Sulphone: Synthesis of a New .BETA.-Lactam Podand." Journal of Antibiotics 55, no. 5 (2002): 524–27. http://dx.doi.org/10.7164/antibiotics.55.524.
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Burroughs, SF, and GJ Johnson. "Beta-lactam antibiotic-induced platelet dysfunction: evidence for irreversible inhibition of platelet activation in vitro and in vivo after prolonged exposure to penicillin." Blood 75, no. 7 (April 1, 1990): 1473–80. http://dx.doi.org/10.1182/blood.v75.7.1473.1473.
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Abstract beta-Lactam antibiotics cause platelet dysfunction with bleeding complications. Previous in vitro studies documented reversible inhibition of agonist-receptor interaction. This mechanism is inadequate to explain the effect of beta-lactam antibiotics in vivo. Platelet function does not return to normal immediately after drug treatment, implying irreversible inhibition of platelet function. We report here evidence of irreversible platelet functional and biochemical abnormalities after in vitro and in vivo exposure to beta-lactam antibiotics. Irreversible binding of [14C]-penicillin (Pen) occurred in vitro. After 24 hours' in vitro incubation with 10 to 20 mmol/L Pen, or ex vivo after antibiotic treatment, irreversible functional impairment occurred; but no irreversible inhibition of alpha 2 adrenergic receptors, measured with [3H]-yohimbine, or high-affinity thromboxane A2/prostaglandin H2 (TXA2/PGH2) receptors, measured with agonist [3H]-U46619 and antagonist [3H]-SQ29548, occurred. However, low- affinity platelet TXA2/PGH2 receptors were decreased 40% after Pen exposure in vitro or in vivo, indicating irreversible membrane alteration. Two postreceptor biochemical events were irreversibly inhibited in platelets incubated with Pen for 24 hours in vitro or ex vivo after antibiotic treatment. Thromboxane synthesis was inhibited 28.3% to 81.7%. Agonist-induced rises in cytosolic calcium ([Ca2+]i) were inhibited 40.1% to 67.5% in vitro and 26.6% to 52.2% ex vivo. Therefore, Pen binds to platelets after prolonged exposure, resulting in irreversible dysfunction attributable to inhibition of TXA2 synthesis and impairment of the rise in [Ca2+]i. The loss of low- affinity TXA2/PGH2 receptors suggests that the primary site of action of these drugs is on the platelet membrane.
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Burroughs, SF, and GJ Johnson. "Beta-lactam antibiotic-induced platelet dysfunction: evidence for irreversible inhibition of platelet activation in vitro and in vivo after prolonged exposure to penicillin." Blood 75, no. 7 (April 1, 1990): 1473–80. http://dx.doi.org/10.1182/blood.v75.7.1473.bloodjournal7571473.
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beta-Lactam antibiotics cause platelet dysfunction with bleeding complications. Previous in vitro studies documented reversible inhibition of agonist-receptor interaction. This mechanism is inadequate to explain the effect of beta-lactam antibiotics in vivo. Platelet function does not return to normal immediately after drug treatment, implying irreversible inhibition of platelet function. We report here evidence of irreversible platelet functional and biochemical abnormalities after in vitro and in vivo exposure to beta-lactam antibiotics. Irreversible binding of [14C]-penicillin (Pen) occurred in vitro. After 24 hours' in vitro incubation with 10 to 20 mmol/L Pen, or ex vivo after antibiotic treatment, irreversible functional impairment occurred; but no irreversible inhibition of alpha 2 adrenergic receptors, measured with [3H]-yohimbine, or high-affinity thromboxane A2/prostaglandin H2 (TXA2/PGH2) receptors, measured with agonist [3H]-U46619 and antagonist [3H]-SQ29548, occurred. However, low- affinity platelet TXA2/PGH2 receptors were decreased 40% after Pen exposure in vitro or in vivo, indicating irreversible membrane alteration. Two postreceptor biochemical events were irreversibly inhibited in platelets incubated with Pen for 24 hours in vitro or ex vivo after antibiotic treatment. Thromboxane synthesis was inhibited 28.3% to 81.7%. Agonist-induced rises in cytosolic calcium ([Ca2+]i) were inhibited 40.1% to 67.5% in vitro and 26.6% to 52.2% ex vivo. Therefore, Pen binds to platelets after prolonged exposure, resulting in irreversible dysfunction attributable to inhibition of TXA2 synthesis and impairment of the rise in [Ca2+]i. The loss of low- affinity TXA2/PGH2 receptors suggests that the primary site of action of these drugs is on the platelet membrane.
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Linggarjati, Shiwi, Dita Diana Parti, and Elly Nurus Sakinah. "Antibiotic sensitivity on pathogenic bacteria causing bacterial vaginosis." Majalah Obstetri & Ginekologi 29, no. 1 (April 28, 2021): 18. http://dx.doi.org/10.20473/mog.v29i12021.18-22.
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Objectives: To identify the sensitivity of antibiotics to pathogenic bacteria that cause Bacterial Vaginosis (BV).Materials and Methods: This type of research was an observational study with a sample of six specimens. The data were taken using primary data from patients who were swabbed in the vagina and then diagnosed BV with amsel criteria on vaginal secretion specimens carried out at Tanggul health center on January 23-February 23, 2020. The specimens were sent to Parahita Clinical Laboratory for bacterial identification and adjusted for sensitivity with CLSI using vitek 2 compact tool.Results: The results of this study identified the bacteria that caused bacterial vaginosis, the E. coli and K. pneumoniae with one sample of suspected ESBL. ESBL is a beta lactamase enzyme produced by bacteria and can induce bacterial resistance to penicillin, cephalosporin generation 1, 2, and 3. The types of bacteria found were E. coli and K. pneumoniae with high sensitivity antibiotics tested including piperacillin/tazobactam, ceftazidime, cefepime, ertapenem, meropenem, amikacin, gentamicin, tigecycline, and nitrofurantoin. Antibiotics with high levels of resistance tested against these bacteria included: ampicillin, amoxicillin, and ampicillin/sulbactam due to the mechanism of beta-lactam antibiotic resistance in the production of beta lactamase from bacteria.Conclusion: The type of bacteria found was E. coli and K. pneumoniae with high resistance levels in beta lactam antibiotics.
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Brito, Roseane Brandão de, and Roberto Gonçalves Junqueira. "Determination of Beta-Lactam residues in milk by high performance liquid chromatography." Brazilian Archives of Biology and Technology 49, spe (January 2006): 41–46. http://dx.doi.org/10.1590/s1516-89132006000200007.
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A high performance liquid chromatographic method to assay beta-lactam residues in milk was developed and validated. Milk samples were spiked with standard solutions and deproteinated. The extract was cleaned-up on C18 SPE cartridge, the antibiotics eluted with acetonitrile:water (50:50 v/v) and derivatized with acetic anhydride and 1-methyl-imidazole solution containing HgCl2. The chromatographic analysis was performed on C18 column using mobile phase consisting of acetonitrile and phosphate buffer (pH 6.5) in the presence of Na2S2O3 gradient and detection at 325 nm. The method was selective for ampicillin, penicillin G and penicillin V, the latter used as internal standard. Average recoveries for ampicillin and penicillin G ranged, respectively, from 60.0% to 104.9% and from 82.7% to 109.2%, with coefficients of variation from 11.1% to 24.6%, and from 2.1% to 25.2%, indicating accuracy and precision. Detection limit of 4.0 µg/L for ampicillin and 3.0 µg/L for penicillin G, and quantification limits of 4.0 µg/L for both were estimated.
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Gross, M. E., K. P. Giron, J. D. Septimus, E. O. Mason, and D. M. Musher. "Antimicrobial activities of beta-lactam antibiotics and gentamicin against penicillin-susceptible and penicillin-resistant pneumococci." Antimicrobial Agents and Chemotherapy 39, no. 5 (May 1, 1995): 1166–68. http://dx.doi.org/10.1128/aac.39.5.1166.
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Stankevich, A. A., I. B. Bykova, N. R. Efimochkina, and I. M. Netyaga. "SENSITIVITY TO ANTIBIOTICS OF BACTERIA OF THE GENUS KLEBSIELLA ISOLATED FROM FOODS." Problems of Veterinary Sanitation, Hygiene and Ecology 1, no. 2 (2018): 64–68. http://dx.doi.org/10.36871/vet.san.hyg.ecol.201802011.
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Antibiotic resistance of enterobacteria contaminating food products of animal origin has become one of the serious health problems in recent years. Increased resistance of bacteria of Klebsiella genus to antimicrobials leads to their adaptation and spread of high - and multi-resistant strains. The study of 44 samples of poultry meat, dairy products and food established that the frequency of detection of Klebsiella is 22%. Most of the isolated food isolates were sensitive to beta-lactam antibiotics, cephalosporins, fluoroquinolones and chloramphenicol. In 30% of cases resistance of Кlebsiell food isolates to penicillin and ampicillin, tetracycline antibiotics, gentamicin, streptomycin and nitrofurantoin was found. The presence of dissociation processes of Klebsiella food isolates and antibiotic resistance formation is shown.
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Song, Youchan, Zachary Nelson, and Krista Gens. "171. Effectiveness and Feasibility of Pharmacist-Driven Penicillin Allergy De-Labeling Pilot Program." Open Forum Infectious Diseases 7, Supplement_1 (October 1, 2020): S93. http://dx.doi.org/10.1093/ofid/ofaa439.215.
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Abstract Background Prevalence of true hypersensitivity to penicillins is low (0.5–2%). Documented penicillin allergies have been associated with an increased risk of adverse outcomes, including methicillin resistant Staphylococcus aureus infections, Clostridioides difficile infections, and surgical site infections. “De-labeling” of inappropriately documented allergies can decrease the use of unnecessary broad-spectrum antibiotics and prevent negative outcomes, but labor-intensive skin testing and oral challenges can be a barrier to program implementation. The goal of this project is to assess the effectiveness and feasibility of a pharmacist-led penicillin allergy de-labeling process that does not involve skin testing or oral challenges. Methods Adult patients with penicillin allergies were identified using a report within the electronic health record during a 3-month pilot period. Patients identified were interviewed by an infectious diseases pharmacy resident, and an allergy history was assessed utilizing a standardized checklist. The patients’ answers determined the ability to de-label via pharmacist utilization of an evidence-based and standardized checklist developed for this project. All documentation included a detailed patient allergy history along with a beta-lactam cross-reactivity chart to help guide future antibiotic choices. Results 66 patients were interviewed during the pilot. 12 patients (18%) met criteria for de-labeling and consented to the removal of the allergy. 4 patients (6%) met criteria for de-labeling but declined the removal of the allergy. Average time spent during patient interview was 5.2 minutes per patient. 58.3% of patients (7/12) who were de-labeled were subsequently prescribed a beta-lactam, and 100% (7/7) were able to tolerate the agents. 1 out of 4 patients (25%) who declined de-labeling but had their allergy updated to reflect intolerance was prescribed beta-lactams and was able to tolerate the agents (1/1, 100%). Conclusion A pharmacist-led penicillin allergy de-labeling process utilizing a standardized checklist is an effective method for removing penicillin allergies in patients who do not have a true allergy to penicillins. This pharmacist-led process is a feasible method for sites unable to perform oral challenges or skin testing. Disclosures All Authors: No reported disclosures
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Watkins, Andrew, Lee Amaya, Macey Wolfe, John Schoen, Erica Stohs, Sara May, Mark Rupp, Trevor Craig Van Schooneveld, Bryan Alexander, and Scott Bergman. "Use of a Beta-Lactam Graded Challenge Process at an Academic Medical Center." Infection Control & Hospital Epidemiology 41, S1 (October 2020): s502. http://dx.doi.org/10.1017/ice.2020.1183.
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Background: A penicillin allergy guidance document containing an algorithm for challenging penicillin allergic patients with β-lactams was developed by the antimicrobial stewardship program (ASP). As part of this algorithm, a “graded challenge” order set was created containing antimicrobial orders and safety medications along with monitoring instructions. The process is designed to challenge patients at low risk of reaction with infusions of 1% of the target dose, then 10%, and finally the full dose, each 30 minutes apart. We evaluated outcomes from the order set. Methods: Orders of the graded challenge over 17 months (March 2018 through July 2019) were reviewed retrospectively. Data were collected on ordering and outcomes of the challenges and allergy documentation. Use was evaluated based on ASP-recommended indications: history of IgE-mediated or unknown reaction plus (1) no previous β-lactam tolerance and the reaction occurred >10 years ago, or (2) previous β-lactam tolerance, now requiring a different β-lactam for treatment. Only administered challenges were included and descriptive statistics were utilized. Results: Of 67 orders, 57 graded challenges were administered to 56 patients. The most common allergies were penicillins (87.7%) and cephalosporins (38.6%), with the most common reactions being unknown (41.7%) or hives (22%). The most common antibiotics challenged were ceftriaxone (43.9%), cefepime (21.1%), and cefazolin (5.3%). Antibiotics given prior to challenge included vancomycin (48.2%), fluoroquinolones (35.7%), carbapenems (21.4%), aztreonam (19.6%), and clindamycin (12.5%). The median duration of challenged antibiotic was 6 days. The infectious diseases service was consulted on 59.6% of challenges and 75.4% of challenges were administered in non-ICU settings. There was 1 reaction (1.8%) involving a rash with the second infusion, which was treated with oral diphenhydramine and had no lasting effects. Based on indications, 80.7% of challenges were aligned with ASP guidance criteria. The most common use outside of these criteria was in patients without IgE-mediated reactions (10.5%). Most of these had minor rashes and could have received a full dose of a cephalosporin. Allergy information was updated in the electronic health record after 91.2% of challenges. Conclusions: We demonstrated the utility of a graded challenge process at our academic medical center. It was well tolerated, ordered frequently by noninfectious diseases clinicians, administered primarily in non-ICU settings, and regularly resulted in updated allergy information in the medical record. With many patients initially receiving broad-spectrum antibiotics with high costs or increased rates of adverse effects, graded challenges can potentially prevent the use of suboptimal therapies with minimal time and resource investment.Funding: NoneDisclosures: Scott Bergman reports a research grant from Merck.
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Verhaegen, J., and L. Verbist. "In-vitro activity of 21 beta-lactam antibiotics against penicillin- susceptible and penicillin-resistant Streptococcus pneumoniae." Journal of Antimicrobial Chemotherapy 41, no. 3 (March 1, 1998): 381–85. http://dx.doi.org/10.1093/jac/41.3.381.
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Shaw, Bryan G., Inela Masic, Nancy Gorgi, Niree Kalfayan, Elise M. Gilbert, Viktorija O. Barr, Michael G. Ison, and Milena M. McLaughlin. "Appropriateness of Beta-Lactam Allergy Record Updates After an Allergy Service Consult." Journal of Pharmacy Practice 33, no. 3 (September 4, 2018): 243–46. http://dx.doi.org/10.1177/0897190018797767.
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Background: Many patients with a self-reported penicillin allergy go on to tolerate beta-lactam antibiotics. Allergy specialists may be consulted to determine the nature and extent of the allergy. However, electronic allergy records must be appropriately updated such that recommendations are carried forward. Objective: To determine the percentage of patients who have their electronic allergy record updated after an allergy service consult (ASC). Methods: This was a retrospective study of patients with at least 1 documented beta-lactam allergy and had an ASC during (inpatient) or prior to (outpatient) hospital admission at Northwestern Memorial Hospital and Prentice Women’s Hospital in Chicago, Illinois. Results: Within the study period, a total of 26 526 patients were identified as having a documented antibiotic allergy, with 21 657 patients (81.6% of patients with allergies) having a listed beta-lactam allergy. Of these patients, 1689 (7.8%) patients were identified as having an ASC during or prior to admission, with 598 patients meeting inclusion criteria. Changes in the allergy record were recommended by the ASC for 62% (n = 371) of patients; however, the allergy record was updated after the ASC in 74.9% (n = 278) of patients. Conclusion: ASC recommendations to delabel a patient as beta-lactam allergic must result in updating the allergy record in order to optimize future treatment. Given the low proportion of allergy-labeled patients tested, programs outside formal ASCs should be considered.
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Salmanov, A. G., V. I. Mamchich, V. V. Potochilova, E. L. Rudneva, and M. A. Chaika. "IS AN ACUTE CHOLECYSTITIS A LOCAL INFECTION? ANTIBIOTIC THERAPY PROBLEMS." Kharkiv Surgical School, no. 3 (March 20, 2020): 19–26. http://dx.doi.org/10.37699/2308-7005.3.2020.04.
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Summary. Objective: to improve the results of surgical treatment of destructive forms of acute cholecystitis, taking into account the sensitivity of the isolated microflora to antibiotics.
Materials and methods. 347 patients with acute cholecystitis (AC) have been operated in the surgical department of Kiev Regional Clinical Hospital in 2016 – 2019. The control group included 275 AC patients operated on in 2013–2015, similar in sex, age, comorbidities, treatment and surgical tactics to each other, but with an empirical choice of antibiotic therapy. Bacteriological studies were performed to 237 patients with destructive forms of acute cholecystitis, where 531 microflora isolates were seeded.
Results and discussion. The AC treatment group patients (n=347) were arranged according to Tokyo guidelines (2013) into 3 grades. Mild course (grade I, n=38, 11 %), microbiological studies were not conducted. Antibiotic prophylaxis with beta-lactam antibiotics was used. At moderately severe AC (grade II, n = 260, 75 %) escalation antibiotic therapy was carried out. At severe disease (grade III, n = 49, 14 %) de-escalation antibiotic therapy was performed.
Most often intestinal group microflora was sown. The highest sensitivity of microflora was marked for linezolid - 100 %. Also high sensitivity of microflora was revealed to beta-lactam antibiotics - 83.3 % (penicillins, cephalosporins, monobactams, and carbapenems).
The highest resistance was marked for unprotected penicillins: penicillin — 67.7 %, ampicillin — 83.3 %, amoxicillin — 100 %, oxacillin — 100 %; among cephalosporins: cefixime — 75.0 %, cefuroxime — 66.7 %; among fluoroquinolones: lomefloxacin and pefloxa-cin — 100 % resistance to seeded aerobic microflora.
In the control group (n=275) purulent complications were noted in 9.8 % (27 patients), fatal cases — 6, the total mortality rate was 2.18 %, postoperative — 1.45 % (4 patients). In the study group (n = 347), the number of purulent complications was reduced to 4 % (p˂0.01), the total mortality rate was reduced to 0.58 % (p˂0.05).
Conclusions: 1. Acute obstructive cholecystitis, acute emphysematous (gas) cholecystitis and AC complicated by choledocholithiasis or cholangitis are referred to the local abdominal infectious process. 2. Infection is not a leading factor on first stage for emphysematous, vascular and post-traumatic forms of AC, but it develops in a destructive gall bladder on second stage. 3. For the patients of the first grade by Tokio guideline 2013 we recommend the use of antibiotic prophylaxis. Under moderate grade — escalation antibiotic therapy and under severe grade of the AC — de-escalation antibiotic therapy, followed by the use of selective antibacterial agents should be administered. 4. The highest selective sensitivity of seeded microflora in patients with destructive forms of AC was marked for oxazolidinones (linezolid) — (100 %), as well as for beta-lactam antibiotics (83.3 %). 5. The control group patients had decreased number of suppurations (from 9.8 to 4 %; p<0.01), and decreased mortality rate (from 2.18 to 0.58 %; p<0.05).
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Tucker, Kendall J., YoungYoon Ham, Haley K. Holmer, Caitlin M. McCracken, Ellie Sukerman, James Lewis, and Jessina C. McGregor. "162. Assessment of Beta-lactam Allergies as Rationale for Receipt of Vancomycin for Surgical Prophylaxis." Open Forum Infectious Diseases 7, Supplement_1 (October 1, 2020): S90. http://dx.doi.org/10.1093/ofid/ofaa439.207.
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Abstract Background Beta-lactam (BL) antibiotics are first-line agents for most patients receiving antimicrobial prophylaxis in surgical procedures. Despite evidence showing low cross-reactivity between classes of BLs, patients with allergies commonly receive vancomycin as an alternative to avoid allergic reaction. The objective of this study was to identify potentially inappropriate use of vancomycin surgical prophylaxis among patients with reported BL allergies. Methods Adult patients (≥18 years) receiving vancomycin for surgical prophylaxis with a reported penicillin and/or cephalosporin allergy at our institution between August 2017 to July 2018 were retrospectively evaluated for potential eligibility for penicillin allergy testing and/or receipt of standard prophylaxis. Surgery type and allergy history were extracted from the electronic medical record. Per our institution’s penicillin-testing protocol, patients with IgE-mediated reactions < 10 years ago were eligible for penicillin skin testing (PST), mild reactions or IgE-mediated reaction > 10 years ago were eligible for direct oral amoxicillin challenge, and severe non-IgE mediated allergies were ineligible for penicillin allergy evaluation or BL prophylaxis. Results Among 830 patients who received vancomycin for surgical prophylaxis, 196 reported BL allergy and were included in the analysis (155 with penicillin allergy alone; 21 with cephalosporin allergy; 20 with both cephalosporin and penicillin allergy). Approximately 40% of surgeries were orthopedic. Six patients were ineligible for BL prophylaxis. Per institutional protocol, 73 of 155 patients (48%) may have qualified for PST; 81 of 155 (52%) patients may have received a direct oral amoxicillin challenge. Only 3 of 22 patients with history of methicillin-resistant Staphylococcus aureus appropriately received additional prophylaxis with vancomycin and a BL. Conclusion Patients with BL allergies often qualify for receipt of a first-line BL antibiotic. An opportunity exists for improved BL allergy assessment as an antimicrobial stewardship intervention. Future studies should evaluate outcomes associated with BL allergy evaluation and delabeling in patients receiving surgical prophylaxis. Disclosures All Authors: No reported disclosures
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Kufel, Wesley D., Julie Ann Justo, P. Brandon Bookstaver, and Lisa M. Avery. "Penicillin Allergy Assessment and Skin Testing in the Outpatient Setting." Pharmacy 7, no. 3 (September 19, 2019): 136. http://dx.doi.org/10.3390/pharmacy7030136.
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Penicillin allergies are among of the most commonly reported allergies, yet only 10% of these patients are truly allergic. This leads to potential inadvertent negative consequences for patients and makes treatment decisions challenging for clinicians. Thus, allergy assessment and penicillin skin testing (PST) are important management strategies to reconcile and clarify labeled penicillin allergies. While PST is more common in the inpatient setting where the results will immediately impact antibiotic management, this process is becoming of increasing importance in the outpatient setting. PST in the outpatient setting allows clinicians to proactively de-label and educate patients accordingly so beta-lactam antibiotics may be appropriately prescribed when necessary for future infections. While allergists have primarily been responsible for PST in the outpatient setting, there is an increasing role for pharmacist involvement in the process. This review highlights the importance of penicillin allergy assessments, considerations for PST in the outpatient setting, education and advocacy for patients and clinicians, and the pharmacist’s role in outpatient PST.
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Liao, X., and R. E. Hancock. "Susceptibility to beta-lactam antibiotics of Pseudomonas aeruginosa overproducing penicillin-binding protein 3." Antimicrobial Agents and Chemotherapy 41, no. 5 (May 1997): 1158–61. http://dx.doi.org/10.1128/aac.41.5.1158.
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By using a broad-host-range vector, pUCP27, the Pseudomonas aeruginosa and Escherichia coli pbpB genes, which encode penicillin-binding protein 3 (PBP3), were separately overexpressed in a P. aeruginosa strain, PAO4089, that is deficient in producing chromosomal beta-lactamase. Susceptibility studies indicated that overproduction of the P. aeruginosa PBP3 in PAO4089 resulted in twofold-increased resistance to aztreonam, fourfold-increased resistance to cefepime and cefsulodin, and eightfold-increased resistance to ceftazidime, whereas overproduction of the P. aeruginosa PBP3 in PAO4089 did not affect susceptibility to PBP1-targeted cephaloridine or PBP2-targeted imipenem. Similar results were obtained with PAO4089 overproducing E. coli PBP3, with the exception that there was no influence on the MICs or minimal bactericidal concentrations of cefsulodin and cefepime, which have very low affinities for E. coli PBP3. These data are consistent with the conclusion that PBP3 has to achieve a certain level of saturation, with beta-lactams targeted to this protein, to result in cell inhibition or death.
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RAJKOWSKI, KATHLEEN T., JAMES T. PEELER, and JAMES W. MESSER. "Detectability Levels of Four Beta-Lactam Antibiotics in Eight Milk Products Using the AOAC Bacillus stearothermophilus Disc Assay." Journal of Food Protection 49, no. 9 (September 1, 1986): 687–90. http://dx.doi.org/10.4315/0362-028x-49.9.687.
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The 50% dectability level (ED50) of the Bacillus stearothermophilus disc assay in raw, pasteurized whole, protein-fortified lowfat, lowfat, and skim milks, half-and-half, heavy cream and goat's milk was determined for penicillin G, ampicillin, cloxacillin and cephapirin. Results demonstrate a lower level of detectability with PM agar than with A4 agar for ampicillin, cloxacillin and penicillin. Ranges of detection using PM agar at 64°C were 0.0025 to 0.0042 IU/ml (0.0016 to 0.0026 μg/ml) for penicillin G, 0.0021 to 0.0042 μg/ml for ampicillin, 0.0030 to 0.0059 μg/ml for cephapirin and 0.0167 to 0.0334 μg/ml for cloxacillin. Liquid penicillinase is recommended when performing the confirmation test for beta-lactam identification.
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Bhatt, Shivangi, and Neepa Pandhi. "Wide Spread Prevalence of β-Lactam Resistance among Bacterial Species Obtained from Non-Clinical Samples." International Journal of Applied Sciences and Biotechnology 3, no. 2 (June 25, 2015): 248–55. http://dx.doi.org/10.3126/ijasbt.v3i2.12480.
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The potential threats of bacterial resistance, especially widespread multi-drug resistance, are of major concern. The scenario of a patient dying from an infection caused by a multi-drug resistant organism is now a reality. Infections caused by resistant strains of bacteria are related to higher morbidity and mortality. β-Lactam antibiotics are a broad class of antibiotics, consisting of penicillin, cephalosporin, Monobactam, and carbapenems. β-lactam antibiotics are used to treat various infections. β-lactamases are enzymes responsible to provide resistance to β-lactam antibiotics. Among Gram-negative bacteria, the emergence of resistance to expanded-spectrum cephalosporin has been a major concern. Initially a limited number of bacterial species that could mutate to hyper produce their chromosomal class C β-lactamase were found but now, resistance appeared in large number of bacterial species due to the production of TEM- or SHV-type ESBLs. In our study non clinical samples were selected to study the prevalence of drug resistance. After placing the various generations of β-lactam drugs we found that they were also resistant up to 4th generation of β-lactam drugs. This study confirms the growing incidences of β-lactam resistant strains in bacterial species of community origin.Int J Appl Sci Biotechnol, Vol 3(2): 248-255 DOI: http://dx.doi.org/10.3126/ijasbt.v3i2.12480
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Ikeda, Fumiaki, Yoshiko Yokota, Akiko Ikemoto, Noriko Teratani, Kyoichi Shimomura, and Harushige Kanno. "Interaction of Beta-Lactam Antibiotics with the Penicillin-Binding Proteins of Penicillin-Resistant Streptococcus pneumoniae." Chemotherapy 41, no. 3 (1995): 159–64. http://dx.doi.org/10.1159/000239338.
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Hornak, Joseph Patrik, and David Reynoso. "44. Antibiotic Class-Based Distribution and Analysis of Reported Beta-Lactam Allergies amongst Hospitalized Patients." Open Forum Infectious Diseases 7, Supplement_1 (October 1, 2020): S45. http://dx.doi.org/10.1093/ofid/ofaa439.089.
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Abstract Background Reported β-lactam allergy (BLA) is very common, yet less than 10% of these patients exhibit true hypersensitivity. When faced with reported BLAs, physicians often choose alternative antibiotics which can be associated with C. difficile infection, drug-resistance development, poorer outcomes, & increased costs. Effective identification of these patients is necessary for subsequent, appropriate BLA “de-labeling.” Here, we conducted a single-center analysis of alternative antibiotic utilization amongst patients reporting BLA and compare the frequency of drug-resistant infections and C. difficile infection in allergic & non-allergic patients. Methods This is a retrospective review of adult patients hospitalized at The University of Texas Medical Branch from 1/1/2015 to 12/31/2019. Pooled electronic medical records were filtered by antibiotic orders and reported allergies to penicillins or cephalosporins. Patients with drug-resistant and/or C. difficile infection (CDI) were identified by ICD-10 codes. Microsoft Excel & MedCalc were used for statistical calculations. Results Data were available for 118,326 patients and 9.3% (11,982) reported a BLA, with the highest rates seen in those receiving aztreonam (85.9%, 530/617) & clindamycin (33.7%, 3949/11718). Amongst patients reporting BLA, high ratios-of-consumption (relative to all patients receiving antibiotics) were seen with aztreonam (7.0), clindamycin (2.7), cephalosporin/β-lactamase inhibitors (2.4), & daptomycin (2.1). Compared to the non-BLA population, BLA patients more frequently experienced MRSA infection (3.0% vs 1.5%, OR 1.99, 95% CI 1.79–2.23, p< 0.0001), β-lactam resistance (1.2% vs 0.6%, OR 2.07, 95% CI 1.72–2.49, p< 0.0001), and CDI (1.2% vs 0.7%, OR 1.85, 95% CI 1.54–2.23, p< 0.0001). Conclusion Our measured BLA rate matches approximate expectations near 10%. Moreover, these patients experienced significantly higher frequencies of drug-resistant bacterial infections and CDI. Targeted inpatient penicillin allergy testing stands to be particularly effective in those patients receiving disproportionately utilized alternative agents (e.g. aztreonam, clindamycin, daptomycin). β-lactam allergy “de-labeling” in these patients is likely a valuable antimicrobial stewardship target. Disclosures All Authors: No reported disclosures
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Rodionov, D. G., and E. E. Ishiguro. "Effects of inhibitors of protein synthesis on lysis of Escherichia coli induced by beta-lactam antibiotics." Antimicrobial Agents and Chemotherapy 40, no. 4 (April 1996): 899–903. http://dx.doi.org/10.1128/aac.40.4.899.
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The role of protein synthesis in ampicillin-induced lysis of Escherichia coli was investigated. The inhibition of protein synthesis through amino acid deprivation resulted in the rapid development of ampicillin tolerance as a consequence of the stringent response, as previously reported. In contrast, inhibition of protein synthesis by use of ribosome inhibitors such as chloramphenicol did not readily confer ampicillin tolerance and, in fact, promoted the development of both stages of the ampicillin-induced lysis process, i.e., (i) an ampicillin-dependent stage which apparently involves the interaction of penicillin-binding proteins with ampicillin and (ii) an ampicillin-independent stage which may represent the events leading to the deregulation of peptidoglycan hydrolase activity. We propose that lysis was facilitated when protein synthesis was inhibited because the production of new penicillin-binding proteins to replace those which were ampicillin inhibited was prevented under these conditions.
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Mukhopadhyay, S., and P. Chakrabarti. "Altered permeability and beta-lactam resistance in a mutant of Mycobacterium smegmatis." Antimicrobial Agents and Chemotherapy 41, no. 8 (August 1997): 1721–24. http://dx.doi.org/10.1128/aac.41.8.1721.
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Beta-lactam resistance in mycobacteria results from an interplay between the following: (i) beta-lactamase production, (ii) affinity of the penicillin-binding proteins (PBPs) for the drugs, and (iii) permeation of the drugs. A laboratory mutant of Mycobacterium smegmatis was studied in order to evaluate the roles of these factors in beta-lactam resistance. Mutant M13 was between 7- and 78-fold more resistant than the wild type to cephaloridine, cefoxitin, cefazolin, cefamandole, and cephalothin. Increased beta-lactamase activity toward these antibiotics was not observed in the mutant. The PBP profiles of the wild type and M13 were comparable. However, the affinities of PBP 1 for the beta-lactams tested were lower for the mutant than for the wild type. The permeation of the drugs measured in intact cells was lower for M13 than for the parent strain. The liposome swelling technique, which could be used for cephaloridine, also supported this view. Reduced permeation was not restricted to the beta-lactams alone. Glycine uptake was also lower in M13. Taken together, the results suggest that decreased affinities of PBP 1 for beta-lactams, combined with the decreased permeability of the cell wall of the mutant, lead to the development of high-level acquired beta-lactam resistance.
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Chambers, H. F. "Methicillin-resistant staphylococci." Clinical Microbiology Reviews 1, no. 2 (April 1988): 173–86. http://dx.doi.org/10.1128/cmr.1.2.173.
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Strains of staphylococci resistant to methicillin were identified immediately after introduction of this drug. Methicillin-resistant strains have unusual properties, the most notable of which is extreme variability in expression of the resistance trait. The conditions associated with this heterogeneous expression of resistance are described. Methicillin resistance is associated with production of a unique penicillin-binding protein (PBP), 2a, which is bound and inactivated only at high concentrations of beta-lactam antibiotics. PBP2a appears to be encoded by the mec determinant, which also is unique to methicillin-resistant strains. The relationships between PBP2a and expression of resistance and implications for the mechanism of resistance are discussed. The heterogeneous expression of methicillin resistance by staphylococci poses problems in the detection of resistant strains. Experience with several susceptibility test methods is reviewed and guidelines for performance of these tests are given. Treatment of infections caused by methicillin-resistant staphylococci is discussed. Vancomycin is the treatment of choice. Alternatives have been few because methicillin-resistant strains often are resistant to multiple antibiotics in addition to beta-lactam antibiotics. New agents which are active against methicillin-resistant staphylococci are becoming available, and their potential role in treatment is discussed.
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Al-Charrakh, Alaa Hani. "Frequency and antimicrobial resistance of bacteria isolated from oral and topical medicaments from Hilla, Iraq." Journal of Infection in Developing Countries 6, no. 06 (March 26, 2012): 489–94. http://dx.doi.org/10.3855/jidc.1817.
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Introduction: The presence of microorganisms in pharmaceuticals is undesirable because they may cause spoilage of the product and may present an infection hazard to the consumers or patients. Methodology: A total of 102 samples of oral and topical non-sterile pharmaceutical products were collected at random from different drug houses and pharmacies in Iraq, to investigate the microbial contamination of these products. Bacterial isolates recovered from these medicaments were subjected to susceptibility testing against various antibiotics by disk diffusion method according to Clinical and Laboratory Standards (CLSI) guidelines. Results: The results revealed that the occurrence of Gram-positive bacteria was in oral and topical medicaments while Gram-negative bacteria were only detected in topical medicaments. More than 58% of Bacillus isolates were resistant to lincomycin and Bacillus mycoides isolates were resistant to beta-lactam antibiotics and trimethoprim-sulfamethoxazole. Staphylococcus spp. showed a relatively high resistance to ampicillin, amoxicillin, penicillin, tetracycline, and trimethoprim-sulfamethoxazole. S. epidermidis had the highest number of multi-resistant isolates. Furthermore, 87.5% of isolated Gram-negative rods showed high resistance to beta-lactam antibiotics and 75% of them were highly resistant to erythromycin. One isolate of Pseudomonas aeruginosa was the most resistant among all Gram-negative rod isolates. Conclusion: The high rate of resistance to antimicrobial agents of bacterial isolates recovered from oral and topical medicaments in this study may indicate a widespread antibiotic resistance among bacteria isolated from different sources, including those of anthropological and environmental origin.
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Tracy, Michael, Anna Wanahita, Yevgeny Shuhatovich, Elizabeth A. Goldsmith, Jill E. Clarridge, and Daniel M. Musher. "Antibiotic Susceptibilities of Genetically Characterized Streptococcus milleri Group Strains." Antimicrobial Agents and Chemotherapy 45, no. 5 (May 1, 2001): 1511–14. http://dx.doi.org/10.1128/aac.45.5.1511-1514.2001.
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ABSTRACT Previous studies of the antibiotic susceptibility ofStreptococcus milleri group organisms have distinguished among species by using phenotypic techniques. Using 44 isolates that were speciated by 16S rRNA gene sequencing, we studied the MICs and minimum bactericidal concentrations of penicillin, ampicillin, ceftriaxone, and clindamycin for Streptococcus intermedius, Streptococcus constellatus, and Streptococcus anginosus. None of the organisms was resistant to beta-lactam antibiotics, although a few isolates were intermediately resistant; one strain of S. anginosus was tolerant to ampicillin, and another was tolerant to ceftriaxone. Six isolates were resistant to clindamycin, with representation from each of the three species. Relatively small differences in antibiotic susceptibilities among species of the S. milleri group show that speciation is unlikely to be important in selecting an antibiotic to treat infection caused by one of these isolates.
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Aiswarya P. Nath, Arul Balasubramanian, and Kothai Ramalingam. "Cephalosporins : An imperative antibiotic over the generations." International Journal of Research in Pharmaceutical Sciences 11, no. 1 (January 20, 2020): 623–29. http://dx.doi.org/10.26452/ijrps.v11i1.1866.
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Cephalosporins are the most commonly prescribed class of antibiotics, and its structure and pharmacology are similar to that of penicillin. It's a bactericidal, and its structure contains beta-lactam ring, as like of penicillin, which intervenes in bacterial cell wall synthesis. Cephalosporins are derived from the mold Acremonium (previously called as Cephalosporium). It was first discovered in 1945; scientists have been improving the structure of cephalosporins to make it more effective against a wider range of bacteria. Whenever the structure of cephalosporins modified, a new "generation" of cephalosporins are made. So far, there are five generations of cephalosporins available. They are prescribed against various organisms and infections. The cephalosporin antibiotics interfere with cell-wall synthesis of bacteria, leading to the breakdown of the infectious organism. To achieve this effect, the antibiotic must cross the bacterial cell wall and bind to the penicillin-binding proteins. Various generations of cephalosporins, mechanisms of resistance, pharmacokinetics, adverse reactions, and their clinical use were reviewed in this article. Most of the cephalosporins are available as parenteral, but the oral formulations are also available for certain drugs. Rather than learn all cephalosporins, it is reasonable for the clinician to be familiar with selected cephalosporins among the parenteral and oral formulations.