Τόμος 12 (1994) – Τεύχος 4 – Άρθρο 2 – Επιθεώρηση Κλινικής Φαρμακολογίας και Φαρμακοκινητικής-Ελληνική Έκδοση – Volume 12 (1994) – Issue 4 – Article 2 – Epitheorese Klinikes Farmakologias και Farmakokinetikes-Greek Edition

Από | | Άρθρο - Article, Αστέριος Σ. Τσιφτσόγλου - Asterios S. Tsiftsoglou, Δήμητρα Γεννηματά,D. Gennimata, Πλήρες Κείμενο στα Ελληνικά - Full Text in Greek

 

Τίτλος – Title

Μη­χα­νι­σμοί Ανάπτυξης Αντίστασης (Ανθεκτικότητας) των Μικροοργανισμών στα Αντιβιοτικά

Mechanisms of Microorganisms Resistance to Antibiotics
Συγγραφέας – Author

Δήμητρα Γεννηματά και Αστέριος Σ. Τσιφτσόγλου

Εργαστήριο Φαρμακολογίας, Τμήμα Φαρμακευτικής, Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης, Θεσσαλονίκη 540 06, Μακεδονία, Ελλάδα

D. Gennimata and A. Tsiftsoglou

Laboratory of Pharmacology, Department of Pharmacy, Aristotelian University of Thessaliniki, Thessaloniki, Macedonia, Greece
Παραπομπή – Citation

Γεννηματά,Δ.,  Τσιφτσόγλου,Α.Σ. : Μη­χα­νι­σμοί Ανάπτυξης Αντίστασης (Ανθεκτικότητας) των Μικροοργανισμών στα Αντιβιοτικά , Επιθεώρηση Κλιν. Φαρμακολ. Φαρμακοκινητ. 12 : 167-180 (1994)

Gennimata,D., Tsiftsoglou,M. : Mechanisms of Microorganisms Resistance to Antibiotics , Epitheorese Klin. Farmakol. Farmakokinet. 12 : 167-180 (1994)
Ημερομηνία Δημοσιευσης – Publication Date
22-12-1994
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Λέξεις κλειδιά – Keywords

Αντίσταση μικροοργανισμών στα αντιβιοτικά, βιοχημικοί και γενετικοί μηχανισμοί, γενετικοί δείκτες αντίστασης, θεραπευτική λοιμώξεων

Microorganisms resistance to antibiotics, biochemical and genetic mechanisms, resistance genetic determinants, infectious diseases therapeutics
Λοιποί Όροι – Other Terms

Άρθρο

Article
Περίληψη – Summary

Τα α­ντι­βιο­τι­κά, τα οποία α­πο­τε­λούν δευ­τε­ρο­γε­νείς με­τα­βο­λί­τες μι­κρο­ορ­γα­νι­σμών, εί­ναι μια α­πό τις συ­χνό­τε­ρα χο­ρη­γού­με­νες ο­μά­δες φαρ­μά­κων για τη θε­ρα­πεί­α των λοι­μώ­ξε­ων. Ω­στό­σο, οι μι­κρο­ορ­γα­νι­σμοί, ε­να­ντί­ον των ο­ποί­ων χρη­σι­μο­ποι­ο­ύ­νται, α­να­πτύσ­σουν συ­χνά α­ντί­στα­ση στα α­ντι­βιο­τι­κά. ‘Å­ôóé, α­παι­τεί­ται συ­νε­χώς η α­νά­πτυ­ξη νέ­ων α­ντι­μι­κρο­βια­κών πα­ρα­γό­ντων ή/και η τρο­πο­ποί­η­ση των ή­δη υ­παρ­χό­ντων, χω­ρίς ταυ­το­χρό­νως να ε­ξα­σφα­λί­ζε­ται η α­πο­τε­λε­σμα­τι­κό­τη­τά τους, α­φού εί­ναι πολύ πι­θα­νό οι μι­κρο­ορ­γα­νι­σμοί να εμ­φα­νί­σουν α­ντί­στα­ση και σε αυ­τούς. Η α­ντί­στα­ση των μι­κρο­ορ­γα­νι­σμών στα α­ντι­βιο­τι­κά μπο­ρεί να εκ­δη­λω­θεί εί­τε με α­δυ­να­μί­α ει­σό­δου του α­ντι­βιο­τι­κού στο κύτ­τα­ρο ή/και με με­τα­τρο­πή του στό­χου του α­ντι­μι­κρο­βια­κού ή/και με α­πε­νερ­γο­ποί­ηση του α­ντι­βιο­τι­κού α­πό τρο­πο­ποι­η­τι­κά έν­ζυ­μα και πα­ρου­σιά­ζει τις πε­ρισ­σό­τε­ρες φο­ρές γε­νε­τι­κή αι­τιο­λο­γί­α. Με­τα­τρο­πές στη δο­μή ή/και στην έκ­φρα­ση του γε­νε­τι­κού υ­λι­κού (με­ταλ­λά­ξεις), κα­θώς ε­πί­σης και στην πρό­σλη­ψη γε­νε­τι­κών χαρακτήρων (μεταφορά, ανασυνδυασμός), μπο­ρούν να οδηγήσουν στην εμφάνιση ανθεκτικών κλώνων που επικρατούν κάτω από την επιλεκτική πίεση την οποία ασκεί η διαρκής και α­νε­ξέ­λε­γκτη χρή­ση των α­ντι­μι­κρο­βια­κών. Οι γε­νε­τι­κοί δεί­κτες α­ντί­στα­σης ε­ντο­πίζο­νται στο χρω­μα­τό­σω­μα ή/και σε ε­ξω­χρω­μα­το­σω­μα­τι­κά στοι­χεί­α. Ο ρό­λος που παί­ζουν τα πλα­σμί­δια στη δια­τή­ρη­ση και με­τά­δο­ση των γε­νε­τι­κών χα­ρα­κτή­ρων α­ντί­στα­σης εί­ναι κα­θο­ρι­στι­κός. Ο έ­λεγ­χος στη χρή­ση των α­ντι­μι­κρο­βια­κών σε συν­δυα­σμό με τη χά­ρα­ξη κα­τευ­θυ­ντη­ρί­ων γραμ­μών για την α­ντι­μι­κρο­βια­κή θε­ρα­πεί­α των λοι­μώ­ξε­ων θε­ω­ρού­νται α­πα­ραί­τη­τες προ­ϋ­πο­θέ­σεις στον πε­ριο­ρι­σμό της ε­ξά­πλω­σης της α­ντί­στα­σης στα α­ντι­βιο­τι­κά. TÝ­ëïò, υπο­γραμ­μί­ζε­ται ό­τι η πα­ρου­σί­α γε­νε­τι­κών δει­κτών α­ντί­στα­σης σε α­ντι­μι­κρο­βια­κά στο πλα­σμι­δια­κό υ­λι­κό των μι­κρο­ορ­γα­νι­σμών συ­νε­τέ­λε­σε ου­σια­στι­κά στην α­νά­πτυ­ξη της τε­χνο­λο­γί­ας α­να­συν­δυα­σμέ­νου DNA (rDNA), της γε­νετι­κής μη­χα­νι­κής και της με­τα­φο­ράς γο­νι­δί­ων και της εκ­φρα­σής τους σε άλ­λους μι­κρο­ορ­γα­νι­σμούς και ι­δια­ί­τε­ρα σε κύτ­τα­ρα θη­λα­στι­κών, για πα­ρα­γω­γή νέ­ων προ­ϊ­ό­ντων δια­γνω­στι­κής και θε­ρα­πευ­τι­κής ση­μα­σί­ας.

Antibiotics are among the widely used drugs for treatment of bacterial infections. However, microorganisms quite often become re­sistant to antibiotics. There­fore, a growing chain of new or/and modified antimicrobial agents is ne­ces­si­tated, but warrants of effectivity can not be of­fered since it is quite pos­sible that microorgan­isms will develop resistance to them, sooner or later. Several biochemical and genetic mecha­nisms have been proposed to explain the devel­opment of resistance in bacteria. Drug resistance can be natural or acquired and in most cases is due to genetic events (mutations) occurring either on the bacterial chromosome or in extrachromo­somal elements (plasmids, transposons). The in­volvement of extrachromosomal elements in main­tenance and transfer of resistance genes is crucial. Drug resistance can be expressed pheno­typically as inadequate transport of drug, meta­bolic inacti­vation of the antibiotic or altered target sites, where the drug actually acts (cell wall, ribo­somes, DNA). Drug resistance genetic determi­nants can be transmitted among bacteria either by transfor­mation, conjugation or/and phage transduction. Furthermore, drug resistance ge­netic determi­nants may be transferred among bacteria and other species in the microcosmos (horizontal transfer). These mechanisms of ex­change of ge­netic material contribute to extensive spread of infection and increasing demand for new drugs to counteract resistant infections in the clinic. There­fore antimicrobial agents must be used only when it is absolutely necessary and not recklessly in an attempt to restrict development of resistant bacteria and decrease spreading of in­fectious dis­eases. Finally, one must mention the fact that the presence of drug resistance genetic determinants on plasmids contributed to the de­velopment of re­combinant DNA (rDNA) technol­ogy and transfer of genetic material into both bac­teria and mammals. All these eventually led to the expression of genes in other microorganisms and development of several products of biotechnology of rDNA.
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