Mycobacterium Chelonae Medication

Updated: Nov 14, 2017
  • Author: Alfred Scott Lea, MD; Chief Editor: Michael Stuart Bronze, MD  more...
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Medication

Medication Summary

Antibiotic therapy for Mycobacterium chelonae infection is generally less intense compared with Mycobacterium abscessus infections since the organism does not possess the erm gene that is responsible for inducible macrolide resistance. [6] Like many of the nontuberculous mycobacteria (NTM), the in vitro susceptibilities of M chelonae do not always correspond to the clinical response and success seen in vivo. Therefore, it is recommended that susceptibility testing be obtained to guide treatment decisions, after careful consideration of the susceptibility test limitations. [25]

Susceptibility testing for M chelonae and related mycobacteria lacks standardization and is hampered by previous studies that considered the more resistant organism, M abscessus, to be the same as M chelonae. Microbiological studies published after 2000 are more likely to be reliable than those of the 1990s, especially if published before 1992.

Most M chelonae infections are uncomplicated, localized, and may resolve before treatment is rendered. Chronic, nonresolving infection requires antimicrobial therapy guided by appropriate identification and susceptibility testing. Empiric therapy should be avoided except in unusual circumstances. One should seek consultation from experts in the field if empiric therapy is required or when difficult, life-threatening clinical scenarios arise. The authors routinely seek outside opinions when encountering unusual and difficult cases.

Macrolide antibiotics are the cornerstone of treatment for M chelonae, and either clarithromycin or azithromycin is the agent of choice. [25] Macrolide monotherapy for localized disease may be sufficient, particularly when used with surgical debridement. The development of resistance during prolonged therapy has been described with macrolide monotherapy and is less common with aminoglycoside monotherapy. [25, 29, 40]

Disseminated infection is usually treated with at least 2 drugs that include a macrolide, and a parental agent, usually an aminoglycoside. [1, 29] Treatment duration for disseminated disease is recommended to be at least 6 months or until all symptoms and signs resolve. [29, 40]

Lung disease with M chelonae is treated with at least 2 drugs that are based on in vitro susceptibility testing. Tobramycin is the preferred aminoglycoside based on in vitro minimum inhibitory concentrations (MICs). [25, 29] Treatment duration should include 12 months of negative sputum cultures. [25]

Ocular disease is usually treated with a combination of topical antimicrobial agents that usually include aminoglycosides, macrolides, and quinolones for many weeks. [23] In vitro susceptibility testing for ocular infections uses the same MIC breakpoints as with systemic agents and may not be applicable to usage of topical agents. In a recent review of ocular NTM infections, M chelonae were greater than 90% susceptible in vitro to tobramycin, amikacin, clarithromycin, and azithromycin. With regards to the fluoroquinolones, gatifloxacin and ciprofloxacin were the most susceptible, at 93% and 73%, respectively, compared with levofloxacin and , at 39% and 64%, respectively. [41]

Bone and prosthetic joint infections require at least 6 months of appropriate therapy with a combination of antimicrobials agents based on in vitro susceptibilities. [27, 42]

Various antimicrobials, parenteral and oral, are summarized below that can be used in treatment of M chelonae infection if susceptible. In contrast to other NTM, tobramycin remains the aminoglycoside of choice compared with amikacin for M chelonae. [25, 29] Imipenem is the carbapenem of choice for treatment. M chelonae is universally resistant to cefoxitin in vitro. Approximately 20% of M chelonae isolates have a susceptible MIC to doxycycline. [29] Tigecycline has been shown to have good in vitro activity against M chelonae, but it does not have an established breakpoint and is usually considered when other alternatives are exhausted. [43, 44]

Linezolid has good in vitro activity against M chelonae, and greater than 50% of isolates have susceptible MICs. [25, 29, 45] It has been shown to be successful in treatment, and, similar to tigecycline, it is usually considered when other options have been exhausted owing to the expense and risk of toxicity with long-term therapy. [46, 47] The authors do not recommend linezolid therapy for treatment durations of more than 4 weeks if it can be avoided, owing to unacceptable toxicities.

Other than ocular disease, the fluoroquinolones have limited use for M chelonae infection. Overall, M chelonae isolates have susceptible MICs to moxifloxacin and ciprofloxacin of 25% and 20%, respectively. [29]

Clofazimine also has good in vitro activity against M chelonae and has been shown to have in vitro synergy with amikacin. [48]

Empiric antimicrobial therapy is rarely necessary, and waiting for species identification prior to treatment is prudent. Antibiotics can be tailored or changed based on in vitro susceptibility.

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Antibiotic, Macrolide

Clarithromycin (Biaxin)

Clarithromycin inhibits bacterial growth by binding to the 50S ribosomal subunit and inhibiting protein synthesis. It is recommended to treat in combination with other antibiotics. Clarithromycin is frequently used as a component of oral therapy.

Azithromycin (Zithromax)

Azithromycin inhibits bacterial growth by binding to the 50S ribosomal subunit and inhibiting protein synthesis. It is recommended to treat in combination with other antibiotics. Azithromycin is frequently used as a component of oral therapy.

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Antibiotic, Aminoglycoside

Tobramycin (AKTob, Tobrex)

Tobramycin inhibits bacterial growth by binding to the 30S subunit of bacterial ribosomes and inhibiting protein synthesis. Use the patient's ideal body weight for dosage calculation. Tobramycin is used in combination with other antibiotics.

Amikacin

Amikacin inhibits bacterial growth by binding to the 30S subunit of bacterial ribosomes and inhibiting protein synthesis. Use the patient's ideal body weight for dosage calculation. Amikacin is used in combination with other antibiotics.

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Antibiotic, Carbapenem

Imipenem/cilastatin (Primaxin)

Imipenem/cilastatin combination inhibits bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins (PBPs). Cilastatin prevents renal metabolism of imipenem by competitive inhibition of dehydropeptidase along the brush border of the renal tubules. This combination is used in combination with other antimicrobials.

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Antibiotic, Oxazolidinone

Linezolid (Zyvox)

Linezolid inhibits bacterial protein synthesis by binding to bacterial 23S ribosomal RNA of the 50S subunit.

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Antibiotic, Glycylcycline

Tigecycline (Tygacil)

Tigecycline inhibits bacterial protein by binding to the 30S ribosomal subunit. Tigecycline is used in combination with other antibiotics.

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Antibiotic, Tetracycline Derivative

Doxycycline (Adoxa, Alodox, Doryx, Vibramycin)

Doxycycline inhibits protein synthesis by binding with the 30S subunit.

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Antibiotic, Quinolone

Moxifloxacin (Avelox)

Moxifloxacin inhibits the A subunits of DNA gyrase, resulting in inhibition of bacterial DNA replication and transcription. It is used in combination with other antibiotics. Ensure the organism is susceptible.

Ciprofloxacin (Cipro)

Ciprofloxacin inhibits bacterial DNA synthesis by binding to gyrase.

Ciprofloxacin ophthalmic (Ciloxan)

Ciprofloxacin ophthalmic is used with or without systemic antibiotics (either oral or parenteral). It inhibits bacterial growth by inhibiting DNA gyrase. It is indicated for superficial ocular infections of the conjunctiva or cornea caused by strains susceptible to ciprofloxacin.

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