MECHANIZMY OPORNOŚCI
PAŁECZEK ACINETOBACTER SPP.
NA ANTYBIOTYKI NIE b-LAKTAMOWE
Marcin Zmudziński, Eugenia Gospodarek,
Krzysztof Gierlotka
Katedra i Zakład Mikrobiologii, Collegium Medicum im. L. Rydygiera
w Bydgoszczy, Uniwersytet Mikołaja Kopernika w Toruniu,
ul. M. Skłodowskiej-Curie 9, 85-094 Bydgoszcz, tel. (52) 5854480,
e-mail: kizmikrob@cm.umk.pl
Wpłynęło w sierpniu 2005 r.
1. Wprowadzenie.
2. Oporność pałeczek Acinetobacter spp. na
aminoglikozydy. 3. Oporność pałeczek Acinetobacter
spp. na
tetracykliny. 4. Oporność pałeczek Acinetobacter
spp. na
fluorochinolony. 5. Oporność Acinetobacter
spp. na sulfonamidy i
trimetoprim. 6. Oporność Acinetobacter
spp. na chloramfenikol. 7. Zastosowanie kolistyny w
zakażeniach pałeczkami Acinetobacter spp.
8. Antybiotykoterapia złożona w leczeniu zakażeń Acinetobacter
spp. 9. Podsumowanie
Mechanisms of the resistance of
Acinetobacter spp. to non-b-lactamas
Abstract:
In recent years Acinetobacter spp. have emerged as
important nosocomial
pathogens which are known to express a variety of resistance
mechanisms. They do not posses any important virulence factors. The
danger of these agents resides in their capability to acquire
and
develop resistance to multiple classes of useful antibiotics
to the
extent that it could be considered as a significant virulence factor.
In this way, they can adapt to new environmental conditions. It is
important to know the mechanisms of resistance to non-b-lactam
antibiotics because some of Acinetobacter spp.
exhibit resistance to
all b-lactams, including
carbapenems, and reduced susceptibility to
polymyxins.
Apart from b-lactams,
aminoglycosides fluoroquinolones and tetracyclines are widely
used for
treating Acinetobacter spp. infections. Acinetobacter
spp. resistance
to aminoglycosides results from the production of
aminoglycoside -modifying enzymes such as acetyltransferases (AAC),
nucleotidyltransferases (ANT, AAD) and phosphotransferases (APH).
Resistance to fluoroquinolones has been linked to mutations in
the
quinolone-resistance-determining-region (QRDR) of gyrA, parC genes and
a decrease in quinolone accumulation due to the decreased
uptake or
increased efflux. The main mechanisms responsible for tetracycline
resistance have been identified as the expression of efflux pumps
tet(A), tet(B) and ribosomal protection (tetM).
Combination therapy is used to widen the
antymicrobial spectrum, minimize toxicity and prevent the emergence of
resistant mutants.
1. Introduction.
2. Resistance of Acinetobacter
spp. to
aminoglycosides.
3. Resistance of Acinetobacter spp
to
tetracyclines. 4. Resistance of Acinetobacter
spp. to
fluoroquinolones. 5. Resistance of Acinetobacter
spp. to sulfamethoxazole-trimethoprim. 6. Resistance
of Acinetobacter
spp to chloramphenikol. 7. Use of colistin in
infections
caused by
Acinetobacter spp.
8. Combination therapy in infections caused by
Acinetobacter spp. 9. Summary
Słowa kluczowe: antybiotyki nie
b-laktamome,
Acinetobacter, oporność
Key words: Acinetobacter,
non-b-lactam antibiotics,
resistance
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