Tigecycline: Difference between revisions

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*Complicated Bacterial Peritonitis
*Complicated Bacterial Peritonitis
*Complicated Skin and Skin Structure Infection
*Complicated Skin and Skin Structure Infection
*Complicated Skin and Skin Structure [[E. Coli]] Infection
*Complicated Skin and Skin Structure ''[[E. coli]]'' Infection
*Complicated Skin and Skin Structure ''[[Enterococcus faecalis]]'' Infection,  
*Complicated Skin and Skin Structure ''[[Enterococcus faecalis]]'' Infection,  
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==Mechanism of action==
==Mechanism of action==
The drug evades the Tet(A-E) efflux pumps<ref name=Petersen>  Petersen PJ, Jacobus NV, Weiss WJ et al. In vitro and in vivo antibacterial activities of a novel glycylcycline, the 9-t-butylglycylamido derivative of minocycline (GAR-936). Antimicrob Agents Chemother  1999; 43: 738–44</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 Neisseria spp.<ref>Milatovic D, Schmitz FJ, Verhoef J et al. Activities of the glycylcycline tigecycline  (GAR-936) against 1,924 recent European clinical bacterial isolates. Antimicrob Agents Chemother 2003; 47: 400–4</ref>
The drug evades the Tet(A-E) efflux pumps<ref name=Petersen>{{citation
 
| author = Petersen PJ, Jacobus NV, Weiss WJ et al
| title = In vitro and in vivo antibacterial activities of a novel glycylcycline, the 9-t-butylglycylamido derivative of minocycline (GAR-936)
| journal = Antimicrob Agents Chemother  
  | 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|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.''
| title = Activities of the glycylcycline tigecycline  (GAR-936) against 1,924 recent European clinical bacterial isolates.  
| journal = Antimicrob Agents Chemother | year = 2003 | volume = 47 | pages = 400–4
| url = http://jac.oxfordjournals.org/cgi/ijlink?linkType=ABST&journalCode=aac&resid=47/1/400}}</ref>
==Administration==
It is given intravenously, but should not be administered simultaneously, through common tubing, with [[amphotericin B]], [[chlorpromazine]], [[methylprednisolone]], or [[voriconazole]].
   
   
==References==
==References==
{{reflist|2}}
{{reflist|2}}

Revision as of 12:56, 23 May 2010

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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]

  • Complicated Appendicitis
  • Complicated Bacterial Peritonitis
  • Complicated Skin and Skin Structure Infection
  • Complicated Skin and Skin Structure E. coli Infection
  • Complicated Skin and Skin Structure Enterococcus faecalis Infection,

  • Infectious Disease of Abdomen
  • Intra-Abdominal Abscess*
  • Legionella pneumophila Pneumonia
  • Streptococcal Pneumonia

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

  1. ↑ 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. ↑ 2.0 2.1 Chopra I (1986), "Genetic and biochemical basis of tetracycline resistance", J Antimicrob Chemother 18 (Suppl C): 51–6
  3. ↑ Tigecycline IV, American Society of Health-System Pharmacists
  4. ↑ 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
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