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MECHANIZMY OPORNOŚCI
PAŁECZEK ACINETOBACTER SPP.
NA ANTYBIOTYKI b-LAKTAMOWE
Marcin Zmudziński, Eugenia Gospodarek
Katedra i Zakład Mikrobiologii, Collegium Medicum w Bydgoszczy,
Uniwersytet Mikołaja Kopernika w Toruniu, ul. M. Skłodowskiej-Curie
9, 85-094 Bydgoszcz, tel. (052) 585 34 81, 585 44 80, e-mail:
kiemikrob@cm.umk.pl
Wpłynęło w czerwcu 2005 r.
1. Wprowadzenie. 2. Antybiotyki
aktywne wobec pałeczek Acinetobacter spp.
3. Antybiotykoterapia złożona w leczeniu
zakażeń wywołanych przez pałeczki Acinetobacter spp.
4. b-laktamazy
pałeczek Acinetobacter spp. 4.1. Klasa
A b-laktamaz. 4.2. Klasa
B b-laktamaz. 4.3. Klasa
C b-laktamaz. 4.4. Klasa
D b-laktamaz. 5. Zmiana
białek wiążących penicyliny. 6. Zmiana
przepuszczalności osłon komórkowych. 7. Wypływ
(„efflux") antybiotyków z wnętrza komórki. 8. Podsumowanie
Mechanisms of resistance to b-lactams in Acinetobacter
spp.
Abstract: Acinetobacter spp.
has emerged as a serious nosocomial pathogen in many
countries mainly due to its resistance to b-lactams,
which are the most frequently used antibiotics. These bacteria
appears to have a propensity for developing
antibiotic resistance extremely fast. Many mechanisms of resistance
to b-lactams have been identified in this
species. Acinetobacter spp. is
responsible for the production of all classes of
b-lactamases. The most important b-lactamases
are cefalosporinases, which are C class b-lactamases,
A class b-lactamases, OXA enzymes, which
are D class b-lactamases and B class
b-lactamases also known as metallo-b-lactamases.
ESBL, related to the narrow spectrum TEM and SHV type
b-laktamases, have not yet been detected
m Acinetobacter spp. The only type of ESBL identified in this
agent were non-TEM and non-SHV type ESBL: PER, VEB and CTX-M.
Acinetobacter spp. all produce OXA-type
b-lactamases that hydrolyze carbapenems
OXA-23, OXA-24, OXA-25, OXA-26, OXA-27, OXA-40, OXA-51 and OXA-58,
which have already been identified and described. Other mechanisms
include alteration of PBPs and the reduction of penetration rate
across the outer membrane. Combination of these two mechanisms with
the production of OXA-type b-lactamases
or with class C cephalosporinases can lead to resistance to
carbapenems. The reduced expression of PBPs or loss of some outer
membrane proteins are related to the increased MIC of carbapenems.
Efflux pump system does not appear to influence the resistance to
b-lactams. The most active agents against Acinetobacter spp.
in this group are imipenem, meropenem, ampicillin or cefaperazon
with sulbactam and colistin. Combination therapy can be effective in
patients with severe infections caused by multidrug resistant
strains of Acinetobacter spp.
1. Introduction. 2. The
most active agents against Acinetobacter spp.
3. Combination therapy in treating infections
caused by Acinetobacter spp. 4. b-lactamases
in Acinetobacter spp. 4.1. Class
A b-lactamases. 4.2. Class
B b-lactamases. 4.3. Class
C b-lactamases. 4.4. Class
D b-lactamases. 5. Alterations
of penicillin-binding proteins. 6. Efflux
pump system. 7. Loss of outer
membrane proteins. 8. Summary
Słowa kluczowe: Acinetobacter, b-laktamowe
antybiotyki, b-laktamazy, PBP
Key words: Acinetobacter, b-lactam
antibiotics, b-lactamases, PBP
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