Editing Antibiotic (section)

==Pharmacodynamics==
{{Main|Antimicrobial pharmacodynamics}}
The successful outcome of antimicrobial therapy with antibacterial compounds depends on several factors. These include [[immune system|host defense mechanisms]], the location of infection, and the pharmacokinetic and pharmacodynamic properties of the antibacterial.<ref name="Pankey2004"/> The bactericidal activity of antibacterials may depend on the bacterial growth phase, and it often requires ongoing metabolic activity and division of bacterial cells.<ref name="Bactericidal action of daptomycin against stationary-phase and nondividing Staphylococcus aureus cells"/> These findings are based on laboratory studies, and in clinical settings have also been shown to eliminate bacterial infection.<ref name="Pankey2004"/><ref>{{cite book |vauthors=Pelczar MJ, Chan EC, Krieg NR |year=2010 |contribution=Host-Parasite Interaction; Nonspecific Host Resistance |title=Microbiology Concepts and Applications |edition=6th |publisher=McGraw-Hill |location=New York |pages=478–479}}</ref> Since the activity of antibacterials depends frequently on its concentration,<ref name="Rhee2004"/> ''in vitro'' characterization of antibacterial activity commonly includes the determination of the [[minimum inhibitory concentration]] and minimum bactericidal concentration of an antibacterial.<ref name="Pankey2004"/><ref name="Agar and broth dilution methods to determine the minimal inhibitory concentration (MIC)of antimicrobial substances"/>
To predict clinical outcome, the antimicrobial activity of an antibacterial is usually combined with its [[pharmacokinetics|pharmacokinetic]] profile, and several pharmacological parameters are used as markers of drug efficacy.<ref>{{cite journal | vauthors = Dalhoff A, Ambrose PG, Mouton JW | title = A long journey from minimum inhibitory concentration testing to clinically predictive breakpoints: deterministic and probabilistic approaches in deriving breakpoints | journal = Infection | volume = 37 | issue = 4 | pages = 296–305 | date = August 2009 | pmid = 19629383 | doi = 10.1007/s15010-009-7108-9 | s2cid = 20538901 }}</ref>

===Combination therapy===

In important infectious diseases, including tuberculosis, [[combination therapy]] (i.e., the concurrent application of two or more antibiotics) has been used to delay or prevent the emergence of resistance. In acute bacterial infections, antibiotics as part of combination therapy are prescribed for their [[drug synergy|synergistic]] effects to improve treatment outcome as the combined effect of both antibiotics is better than their individual effect.<ref name="Antagonism between bacteriostatic">{{cite journal | vauthors = Ocampo PS, Lázár V, Papp B, Arnoldini M, Abel zur Wiesch P, Busa-Fekete R, Fekete G, Pál C, Ackermann M, Bonhoeffer S | title = Antagonism between bacteriostatic and bactericidal antibiotics is prevalent | journal = Antimicrobial Agents and Chemotherapy | volume = 58 | issue = 8 | pages = 4573–82 | date = August 2014 | pmid = 24867991 | pmc = 4135978 | doi = 10.1128/AAC.02463-14 }}</ref><ref name="Bollenbach - interactions">{{cite journal | vauthors = Bollenbach T | title = Antimicrobial interactions: mechanisms and implications for drug discovery and resistance evolution | journal = Current Opinion in Microbiology | volume = 27 | pages = 1–9 | date = October 2015 | pmid = 26042389 | doi = 10.1016/j.mib.2015.05.008 | doi-access = free | title-link = doi }}</ref> [[Fosfomycin]] has the highest number of synergistic combinations among antibiotics and is almost always used as a partner drug.<ref>{{cite journal | vauthors = Antonello RM, Principe L, Maraolo AE, Viaggi V, Pol R, Fabbiani M, Montagnani F, Lovecchio A, Luzzati R, Di Bella S | title = Fosfomycin as Partner Drug for Systemic Infection Management. A Systematic Review of Its Synergistic Properties from In Vitro and In Vivo Studies | journal = Antibiotics | volume = 9 | issue = 8 | pages = 500 | date = August 2020 | pmid = 32785114 | pmc = 7460049 | doi = 10.3390/antibiotics9080500 | doi-access = free | title-link = doi }}</ref> [[Methicillin-resistant Staphylococcus aureus|Methicillin-resistant ''Staphylococcus aureus'']] infections may be treated with a combination therapy of [[fusidic acid]] and rifampicin.<ref name="Antagonism between bacteriostatic"/> Antibiotics used in combination may also be antagonistic and the combined effects of the two antibiotics may be less than if one of the antibiotics was given as a [[monotherapy]].<ref name="Antagonism between bacteriostatic"/> For example, [[chloramphenicol]] and [[tetracyclines]] are antagonists to [[penicillin]]s. However, this can vary depending on the species of bacteria.<ref>{{cite web |url=http://medical-dictionary.thefreedictionary.com/antibiotic+antagonism |title=antagonism |access-date=25 August 2014 |archive-date=26 August 2014 |archive-url=https://web.archive.org/web/20140826115751/http://medical-dictionary.thefreedictionary.com/antibiotic+antagonism |url-status=live }}</ref> In general, combinations of a bacteriostatic antibiotic and bactericidal antibiotic are antagonistic.<ref name="Antagonism between bacteriostatic"/><ref name="Bollenbach - interactions"/>

In addition to combining one antibiotic with another, antibiotics are sometimes co-administered with resistance-modifying agents. For example, [[β-lactam antibiotics]] may be used in combination with [[beta-lactamase inhibitor|β-lactamase inhibitor]]s, such as [[clavulanic acid]] or [[sulbactam]], when a patient is infected with a [[Beta-lactamase|β-lactamase]]-producing strain of bacteria.<ref>{{cite journal | vauthors = Drawz SM, Bonomo RA | title = Three decades of beta-lactamase inhibitors | journal = Clinical Microbiology Reviews | volume = 23 | issue = 1 | pages = 160–201 | date = January 2010 | pmid = 20065329 | pmc = 2806661 | doi = 10.1128/CMR.00037-09 }}</ref>