Glycylcycline Antibiotics: Difference between revisions
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==Introduction== | ==Introduction== | ||
<br>Kristina Buschur<br><br>The ability of bacteria to quickly develop resistance to commonly used antibiotics is a huge hurdle in the path of disease treatment. The glycylcycline class of antibiotics is one recently-developed tool to combat this problem. | <br>Kristina Buschur<br><br>The ability of bacteria to quickly develop resistance to commonly used antibiotics is a huge hurdle in the path of disease treatment. Because of this, there is an ever-present need to develop new antibiotics that are use novel mechanisms to overcome multidrug-resistance and prevent microbial growth. The glycylcycline class of antibiotics is such one recently-developed tool to combat this problem. Derived from tetracycline, glycylcyclines have added substituents that interfere with the mechanisms bacteria employ to resist tetracycline, such as efflux pumps and ribosomal protection. Since tetracycline has been in wide use since the mid-1900s, many bacteria have since developed these mechanisms to prevent the harmful effects of tetracycline. <br><br> | ||
Currently tigecycline is the only antibiotic of the glycylcycline class in clinical use. The antibiotic | Currently tigecycline is the only antibiotic of the glycylcycline class in clinical use. Tigecycline was approved by the Food and Drug Administration in 2005, and is particularly useful in the treatment of infections of gram-positive bacteria, which are typically especially hard to treat. Penicillin-resistant Streptococcus pneumoniae, methicillin-resistant Staphylococcus aureus and Staphylococcus epidermidis, and vancomycin-resistant Enterococcus species are several examples of species that have developed an antibiotic resistance but are still affected by tigecycline. The antibiotic is structurally very similar to minocycline and similarly binds to the bacterial 30S ribosome unit. The manner in which the molecule binds prevents amino-acyl tRNAs from binding to the A site of the ribosome and subsequently prevents peptide formation and bacterial growth. Furthermore, the main difference between tigecycline and minocycline is the addition of an N,N-dimethylglycylamido group which actually causes the molecule to bind to the ribosome up to five times more tightly and decreases the probability that resistance will develop. <br><br> | ||
Tigecycline is administered to a patient intravenously with a dose of 50 mg every 12 hours after an initial 100 mg loading dose. As with nearly all drugs, the antibiotic has several known side-effects, including nausea, vomiting, and diarrhea. | |||
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Revision as of 20:10, 15 April 2009
Introduction
Kristina Buschur
The ability of bacteria to quickly develop resistance to commonly used antibiotics is a huge hurdle in the path of disease treatment. Because of this, there is an ever-present need to develop new antibiotics that are use novel mechanisms to overcome multidrug-resistance and prevent microbial growth. The glycylcycline class of antibiotics is such one recently-developed tool to combat this problem. Derived from tetracycline, glycylcyclines have added substituents that interfere with the mechanisms bacteria employ to resist tetracycline, such as efflux pumps and ribosomal protection. Since tetracycline has been in wide use since the mid-1900s, many bacteria have since developed these mechanisms to prevent the harmful effects of tetracycline.
Currently tigecycline is the only antibiotic of the glycylcycline class in clinical use. Tigecycline was approved by the Food and Drug Administration in 2005, and is particularly useful in the treatment of infections of gram-positive bacteria, which are typically especially hard to treat. Penicillin-resistant Streptococcus pneumoniae, methicillin-resistant Staphylococcus aureus and Staphylococcus epidermidis, and vancomycin-resistant Enterococcus species are several examples of species that have developed an antibiotic resistance but are still affected by tigecycline. The antibiotic is structurally very similar to minocycline and similarly binds to the bacterial 30S ribosome unit. The manner in which the molecule binds prevents amino-acyl tRNAs from binding to the A site of the ribosome and subsequently prevents peptide formation and bacterial growth. Furthermore, the main difference between tigecycline and minocycline is the addition of an N,N-dimethylglycylamido group which actually causes the molecule to bind to the ribosome up to five times more tightly and decreases the probability that resistance will develop.
Tigecycline is administered to a patient intravenously with a dose of 50 mg every 12 hours after an initial 100 mg loading dose. As with nearly all drugs, the antibiotic has several known side-effects, including nausea, vomiting, and diarrhea.
Section 1
Include some current research in each topic, with at least one figure showing data.
Section 2
Include some current research in each topic, with at least one figure showing data.
Section 3
Include some current research in each topic, with at least one figure showing data.
Conclusion
Overall paper length should be 3,000 words, with at least 3 figures.
References
Edited by student of Joan Slonczewski for BIOL 238 Microbiology, 2009, Kenyon College.
