Acinetobacter baumannii complex: Difference between revisions
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Acinetobacter baumannii complex
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*Contains ''Acinetobacter baumannii'', ''[[Acinetobacter nosocomialis]]'', and ''[[Acinetobacter pittii]]'' |
*Contains ''Acinetobacter baumannii'', ''[[Acinetobacter nosocomialis]]'', and ''[[Acinetobacter pittii]]'' |
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*Non-motile, non-fermenting [[Stain::Gram-negative]] [[Shape::bacillus]] |
*Non-motile, non-fermenting [[Stain::Gram-negative]] [[Shape::bacillus]] |
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=== Antimicrobial Resistance === |
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* A number of mechanisms |
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* Carbapenem resistance is usually mediated by acquisition of OXA-type class D [[Carbapenemases|carbapenemase]] |
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** Less common mechanisms include acquisition of class B (VIM, IMP, and NDM) [[carbapenemases]], loss of outer membrane CarO protein, and modification of AdeABC efflux pump |
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== Management == |
== Management == |
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* Infection must be distinguished from colonization of the airway or wound |
* Infection must be distinguished from colonization of the airway or wound |
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* Resistance may be mediated by a number of [[β-lactamases]], including OXA-24/40-like carbapenemases, |
* Resistance may be mediated by a number of [[β-lactamases]], including OXA-24/40-like carbapenemases, OXA-23-like carbapenemases, and metallo-β-lactamases, and often has [[sulbactam]] resistance |
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* Often have concurrent aminoglycoside-modifying enzymes or 16S rRNA methyltransferases, which confer resistance to [[aminoglycosides]] including [[plazomicin]] |
* Often have concurrent aminoglycoside-modifying enzymes or 16S rRNA methyltransferases, which confer resistance to [[aminoglycosides]] including [[plazomicin]] |
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* Refer to ESCMID guidelines[[CiteRef::paul2022eu]] |
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* Single-agent treatment may be sufficient for mild infections |
* Single-agent treatment may be sufficient for mild infections |
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** High-dose [[ampicillin-sulbactam]] is preferred, at a dose of either 9 g IV q8h infused over 4 hours, or 27 g IV q24h continuous infusion |
** High-dose [[ampicillin-sulbactam]] is preferred, at a dose of either 9 g IV q8h infused over 4 hours, or 27 g IV q24h continuous infusion |
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** If susceptible, [[polymixin B]] or high-dose [[tigecycline]] |
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* Combination treatment with at least two agents that have ''in vitro'' activity for most other infections |
* Combination treatment with at least two agents that have ''in vitro'' activity for most other infections |
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** Options include [[ |
** Options include [[minocycline]], [[tigecycline]], [[aminoglycosides]], or [[polymyxin B]] |
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** [[Ampicillin-sulbactam]] may remain effective in non-susceptible isolates when used at high doses |
** [[Ampicillin-sulbactam]] may remain effective in non-susceptible isolates when used at high doses |
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** [[Fosfomycin]] and [[rifampin]] are not recommended |
** [[Fosfomycin]] and [[rifampin]] are not recommended |
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** After clinical improvement, step down to single-agent therapy |
** After clinical improvement, step down to single-agent therapy |
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* [[Cefiderocol]] should generally be avoided |
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{{DISPLAYTITLE:''Acinetobacter baumannii'' complex}} |
{{DISPLAYTITLE:''Acinetobacter baumannii'' complex}} |
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[[Category:Gram-negative bacilli]] |
[[Category:Gram-negative bacilli]] |
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Latest revision as of 02:33, 14 November 2024
Background
Microbiology
- Contains Acinetobacter baumannii, Acinetobacter nosocomialis, and Acinetobacter pittii
- Non-motile, non-fermenting Gram-negative bacillus
Antimicrobial Resistance
- A number of mechanisms
- Carbapenem resistance is usually mediated by acquisition of OXA-type class D carbapenemase
- Less common mechanisms include acquisition of class B (VIM, IMP, and NDM) carbapenemases, loss of outer membrane CarO protein, and modification of AdeABC efflux pump
Management
- Choice of antibiotic depends on susceptibility testing
- Possible options include:
- Cefepime, ceftriaxone, and cefotaxime
- Cefiderocol
- Carbapenems
- Tigecycline
- Colistin and polymyxin B (though Acinetobacter junii has inherent resistance)
- Aminoglycosides may not penetrate well into lungs and brain, so are usually avoided
- Bacteriophages are promising
Carbapenem-Resistant Acinetobacter baumannii
- Infection must be distinguished from colonization of the airway or wound
- Resistance may be mediated by a number of β-lactamases, including OXA-24/40-like carbapenemases, OXA-23-like carbapenemases, and metallo-β-lactamases, and often has sulbactam resistance
- Often have concurrent aminoglycoside-modifying enzymes or 16S rRNA methyltransferases, which confer resistance to aminoglycosides including plazomicin
- Refer to ESCMID guidelines1
- Single-agent treatment may be sufficient for mild infections
- High-dose ampicillin-sulbactam is preferred, at a dose of either 9 g IV q8h infused over 4 hours, or 27 g IV q24h continuous infusion
- If susceptible, polymixin B or high-dose tigecycline
- Combination treatment with at least two agents that have in vitro activity for most other infections
- Options include minocycline, tigecycline, aminoglycosides, or polymyxin B
- Ampicillin-sulbactam may remain effective in non-susceptible isolates when used at high doses
- Fosfomycin and rifampin are not recommended
- After clinical improvement, step down to single-agent therapy
- Cefiderocol should generally be avoided
References
- ^ Mical Paul, Elena Carrara, Pilar Retamar, Thomas Tängdén, Roni Bitterman, Robert A. Bonomo, Jan de Waele, George L. Daikos, Murat Akova, Stephan Harbarth, Celine Pulcini, José Garnacho-Montero, Katja Seme, Mario Tumbarello, Paul Christoffer Lindemann, Sumanth Gandra, Yunsong Yu, Matteo Bassetti, Johan W. Mouton, Evelina Tacconelli, Jesús Rodríguez-Baño. European Society of Clinical Microbiology and Infectious Diseases (ESCMID) guidelines for the treatment of infections caused by multidrug-resistant Gram-negative bacilli (endorsed by European society of intensive care medicine). Clinical Microbiology and Infection. 2022;28(4):521-547. doi:10.1016/j.cmi.2021.11.025.
