Tigecycline: Difference between revisions
imported>Howard C. Berkowitz mNo edit summary |
imported>Howard C. Berkowitz No edit summary |
||
| Line 42: | Line 42: | ||
| journal = Antimicrob Agents Chemother | | journal = Antimicrob Agents Chemother | ||
| year = 1999 | volume = 43 | pages= 738–44 | | year = 1999 | volume = 43 | pages= 738–44 | ||
| url = http://jac.oxfordjournals.org/cgi/ijlink?linkType=ABST&journalCode=aac&resid=43/4/738}}</ref> which account for most acquired resistance to [[tetracycline]] and [[minocycline]] in [[Enterobacteriaceae]] and [[Acinetobacter spp.]]; also the Tet(K) pumps, which occur widely in [[staphylococci]] conferring resistance to tetracycline though not [[minocycline]] or [[doxycycline]].<ref name=Chopra/> It binds to bacterial ribosomes that have been modified by the Tet(M) protein,<ref name=Petersen> a mechanism that compromises all available tetracyclines, and which is frequent in Gram-positive cocci and | | url = http://jac.oxfordjournals.org/cgi/ijlink?linkType=ABST&journalCode=aac&resid=43/4/738}}</ref> which account for most acquired resistance to [[tetracycline]] and [[minocycline]] in ''[[Enterobacteriaceae]]'' and ''[[Acinetobacter|Acinetobacter spp.]]''; also the Tet(K) pumps, which occur widely in [[staphylococci]] conferring resistance to tetracycline though not [[minocycline]] or [[doxycycline]].<ref name=Chopra/> It binds to bacterial ribosomes that have been modified by the Tet(M) protein,<ref name=Petersen> a mechanism that compromises all available tetracyclines, and which is frequent in Gram-positive cocci and ''[[Neisseriae]]'' spp.<ref>{{citation | ||
| author = Milatovic D, Schmitz FJ, Verhoef J ''et al.'' | | author = Milatovic D, Schmitz FJ, Verhoef J ''et al.'' | ||
| title = Activities of the glycylcycline tigecycline (GAR-936) against 1,924 recent European clinical bacterial isolates. | | title = Activities of the glycylcycline tigecycline (GAR-936) against 1,924 recent European clinical bacterial isolates. | ||
Revision as of 11:56, 23 May 2010
Tigecycline is the first commercially available antibiotic of the glycylcycline class, which are a new family based on tetracyclines, but with molecular modifications to evade some, but not all, tetracycline resistance mechanisms. [1] Tetracycline resistance... [2]
Its labeled indications are:[3]
|
|
|
Mechanism of action
The drug evades the Tet(A-E) efflux pumps[4] which account for most acquired resistance to tetracycline and minocycline in Enterobacteriaceae and Acinetobacter spp.; also the Tet(K) pumps, which occur widely in staphylococci conferring resistance to tetracycline though not minocycline or doxycycline.[2] It binds to bacterial ribosomes that have been modified by the Tet(M) protein,Cite error: Closing </ref> missing for <ref> tag
Administration
It is given intravenously, but should not be administered simultaneously, through common tubing, with amphotericin B, chlorpromazine, methylprednisolone, or voriconazole.
References
- ↑ David M. Livermore (2005), "Tigecycline: what is it, and where should it be used?", Journal of Antimicrobial Chemotherapy 56 (4): 611-614, DOI:10.1093/jac/dki291
- ↑ 2.0 2.1 Chopra I (1986), "Genetic and biochemical basis of tetracycline resistance", J Antimicrob Chemother 18 (Suppl C): 51–6
- ↑ Tigecycline IV, American Society of Health-System Pharmacists
- ↑ Petersen PJ, Jacobus NV, Weiss WJ et al (1999), "In vitro and in vivo antibacterial activities of a novel glycylcycline, the 9-t-butylglycylamido derivative of minocycline (GAR-936)", Antimicrob Agents Chemother 43: 738–44