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Chapter 16 : Antimicrobial Resistance in Campylobacter

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Abstract:

This chapter provides a review of prevalence and trends of resistance in and isolated from humans in different parts of the world and a more thorough description of the mechanisms of resistance, origin, spread, and clinical consequences of resistance. Aminoglycosides exhibit rapid and significant bactericidal effects in vitro and should initially be included for the treatment of bacteremia in patients who appear very ill. The only mechanism of chloramphenicol resistance identified in occurs through modification of chloramphenicol by chloramphenicol acetyltransferase, which prevents its binding to the ribosome. The majority of contacts between Tet(O) and the ribosome are mediated by the rRNA, and one interaction with ribosomal protein S12. Most of the antimicrobials used in veterinary medicine are tetracyclines and macrolides, which result in high and continuous selective pressure for the animal-colonizing bacteria, ultimately resulting in the acquisition of antimicrobial resistance genes. Investigation into the mechanisms of action of antimicrobials, as well as the transfer of resistance determinants, is necessary to gain effective control of antimicrobial resistance. Epidemiological and microbiological studies show that poultry is the most important source for quinolone-susceptible and quinolone-resistant infections in humans. Trends over time for macrolide resistance show stable low rates in most countries, and macrolides should remain the drug class of choice for and enteritis.

Citation: Engberg J, Gerner-Smidt P, Keelan M, Taylor D. 2006. Antimicrobial Resistance in Campylobacter, p 269-292. In Aarestrup F (ed), Antimicrobial Resistance in Bacteria of Animal Origin. ASM Press, Washington, DC. doi: 10.1128/9781555817534.ch16

Key Concept Ranking

Outer Membrane Proteins
0.4742716
Campylobacter coli
0.45169926
Campylobacter jejuni
0.45169926
Campylobacter coli
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Figures

Image of Figure 1.
Figure 1.

Trends for quinolone resistance rates (in percentages) among and combined from human sources around the world. The bars represent both nalidixic acid and fluoroquinolone resistance and are based on mean values of resistance from numerous reports. Updated and modified from reference . Additional data are from references , and , and V. Prouzet-Mauléon (personal communication).

Citation: Engberg J, Gerner-Smidt P, Keelan M, Taylor D. 2006. Antimicrobial Resistance in Campylobacter, p 269-292. In Aarestrup F (ed), Antimicrobial Resistance in Bacteria of Animal Origin. ASM Press, Washington, DC. doi: 10.1128/9781555817534.ch16
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Image of Figure 2.
Figure 2.

Quinolone resistance rates (in percentages) among (Denmark, The Netherlands, and Norway) and and combined (Finland, Sweden, the United Kingdom, and the United States) by history of travel. Data are from references , and .

Citation: Engberg J, Gerner-Smidt P, Keelan M, Taylor D. 2006. Antimicrobial Resistance in Campylobacter, p 269-292. In Aarestrup F (ed), Antimicrobial Resistance in Bacteria of Animal Origin. ASM Press, Washington, DC. doi: 10.1128/9781555817534.ch16
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Image of Figure 3.
Figure 3.

(A) Elongation cycle of protein synthesis; (B) inhibition by tetracycline (Tc); (C) model for Tet(O) action. (A) In the absence of antibiotics, the aa-tRNA–EF-Tu–GTP ternary complex catalyzes the binding of aa-tRNA to the open A site on the pretranslocation-state (Pre) ribosome. (B) Tc initially binds to the posttranslation-state (Post) ribosome and induces a conformational change (or steric clash) that blocks the aa-tRNA–EF-Tu–GTP ternary complex from occupying the A site, effectively inhibiting further protein synthesis. (C) If Tet(O) is present, it recognizes the Tc-blocked ribosome by virtue of its open A site, prolonged pausing, and possibly by a drug-induced conformational change. The interaction of Tet(O) with the ribosome induces rearrangements in the A site and triggers the release of Tc from the primary binding site prior to GTP hydrolysis. Tet(O) then hydrolyzes the bound GTP and likely leaves the ribosome with the GTPase-associated region in a configuration compatible with EF-Tu binding, thereby allowing protein synthesis to continue. Adapted from references and .

Citation: Engberg J, Gerner-Smidt P, Keelan M, Taylor D. 2006. Antimicrobial Resistance in Campylobacter, p 269-292. In Aarestrup F (ed), Antimicrobial Resistance in Bacteria of Animal Origin. ASM Press, Washington, DC. doi: 10.1128/9781555817534.ch16
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Download as Powerpoint

References

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Tables

Generic image for table
Table 1.

Erythromycin or azithromycin resistance rates among , , and and combined isolated from humans worldwide since 1997

Citation: Engberg J, Gerner-Smidt P, Keelan M, Taylor D. 2006. Antimicrobial Resistance in Campylobacter, p 269-292. In Aarestrup F (ed), Antimicrobial Resistance in Bacteria of Animal Origin. ASM Press, Washington, DC. doi: 10.1128/9781555817534.ch16
Generic image for table
Table 2.

Antibiotics and their resistance mechanisms in Campylobacterspp.

Citation: Engberg J, Gerner-Smidt P, Keelan M, Taylor D. 2006. Antimicrobial Resistance in Campylobacter, p 269-292. In Aarestrup F (ed), Antimicrobial Resistance in Bacteria of Animal Origin. ASM Press, Washington, DC. doi: 10.1128/9781555817534.ch16
Generic image for table
Table 3.

Antimicrobial agents transported by CmeABC in C. jejuni

Citation: Engberg J, Gerner-Smidt P, Keelan M, Taylor D. 2006. Antimicrobial Resistance in Campylobacter, p 269-292. In Aarestrup F (ed), Antimicrobial Resistance in Bacteria of Animal Origin. ASM Press, Washington, DC. doi: 10.1128/9781555817534.ch16
Generic image for table
Table 4.

Studies evaluating the duration of illness in patients infected with quinolone-resistant strains versus quinolone-susceptible strains

Citation: Engberg J, Gerner-Smidt P, Keelan M, Taylor D. 2006. Antimicrobial Resistance in Campylobacter, p 269-292. In Aarestrup F (ed), Antimicrobial Resistance in Bacteria of Animal Origin. ASM Press, Washington, DC. doi: 10.1128/9781555817534.ch16
Generic image for table
Table 5.

Campylobacter

Citation: Engberg J, Gerner-Smidt P, Keelan M, Taylor D. 2006. Antimicrobial Resistance in Campylobacter, p 269-292. In Aarestrup F (ed), Antimicrobial Resistance in Bacteria of Animal Origin. ASM Press, Washington, DC. doi: 10.1128/9781555817534.ch16

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