Medication Summary
Oral erythromycin or one of the newer macrolides such as azithromycin or clarithromycin have long been the DOC for mycoplasmal respiratory tract infections. Tetracycline and its analogues also are active. Clindamycin is effective in vitro, but limited reports suggest it may not be active in vivo and thus is not considered a first-line treatment. Fluoroquinolones such as levofloxacin or moxifloxacin exhibit bactericidal antimycoplasmal activity but generally are less potent in vitro than macrolides against M pneumoniae. Their advantage lies in the fact that they are active against all classes of bacteria that produce clinically similar respiratory tract infections, including macrolide-resistant S pneumoniae. As would be predicted by the lack of a cell wall, none of the beta-lactams is effective in vitro or in vivo against M pneumoniae, and neither are the sulfonamides or trimethoprim. [1]
Mycoplasma species are slow-growing organisms that have the capacity to reside intracellularly; thus, respiratory tract infections are expected to respond better to longer treatment courses than might be offered for other types of infections. Although physicians typically prescribe most treatment regimens (ie, both oral and parenteral) for 7-10 days, a 14- to 21-day course of oral therapy with most agents is also appropriate. A 5-day course of oral azithromycin is approved for the treatment of community-acquired M pneumoniae pneumonia. Clinical data indicate that this duration of treatment is of comparable efficacy to a 10-day course of erythromycin. Other drugs, including fluoroquinolones, have been approved for the treatment of mycoplasmal respiratory infections with shorter courses because of their favorable pharmacokinetics and tolerability.
In addition to the administration of antimicrobials for the management of M pneumoniae infections, other measures (eg, cough suppressants, antipyretics, analgesics) should be administered as needed to relieve headaches and other systemic symptoms. Because extrapulmonary manifestations often are diagnosed late in the course of disease, the benefit of early treatment is unknown.
Since 2000, macrolide-resistant M pneumoniae caused by point mutations in domain V of 23S ribosomal RNA has emerged in Asia and has now been reported in Europe and North America. Surveillance conducted primarily in pediatric populations has documented resistance rates of 46%-93% in Japan, 69%-97% in China, 12.3%-23% in Taiwan, 61.3% in South Korea, 30% in Israel, and 9.8% in France. A nationwide survey of macrolide resistance performed in the United States between 2016 and 2018 revealed a macrolide resistance rate of 7.5% overall. Prevalence of resistance was significantly higher in the South and East (18.3%) than in the West (2.1%). [22]
Macrolide resistance has also been documented in adults, but to a lesser extent. Selection of resistance during macrolide therapy has been documented in children in France, Italy, and Israel.
While there are no apparent differences in initial presentation to distinguish a patient with macrolide-resistant M pneumoniae, when such infections occur, they often are clinically significant, resulting in prolonged fever, coughing, longer hospital stays, or worsening findings on chest radiographs compared with persons with infections caused by susceptible strains. [23, 24, 25, 26]
The spread of macrolide resistance has led to development of real-time PCR-based assays to detect resistance genes directly in clinical specimens since cultures and conventional susceptibility tests require much longer time and culture may be falsely negative. [24, 25, 26] None of these tests are FDA-cleared for use in the United States, but macrolide resistance testing is available through specialized reference laboratories using lab-developed PCR assays. In view of the increasing spread of macrolide resistance, clinicians are advised to monitor patient outcomes and to consider using alternative antimicrobial agents (eg, minocycline, doxycycline, fluoroquinolones) if an initial treatment with a macrolide is unsuccessful. [27]
Antibiotics
Class Summary
Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.
Erythromycin (E-Mycin, Ery-Tab, E.E.S.)
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections.
In children, age, weight, and severity of infection determine proper dosage. When bid dosing desired, half-total daily dose may be taken q12h. For more severe infections, double the dose.
Clarithromycin (Biaxin, Biaxin XL)
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Azithromycin (Zithromax)
Semisynthetic antibiotic belonging to the macrolide subgroup of azalides and is similar in structure to erythromycin. Inhibits protein synthesis in bacterial cells by binding to the 50S subunit of bacterial ribosomes. Action generally is bacteriostatic but can be bactericidal in high concentrations or against susceptible organisms.
Doxycycline (Vibramycin)
Inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.
Minocycline (Minocin)
Inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.
Levofloxacin (Levaquin)
Inhibits A subunits of DNA gyrase, resulting in inhibition of bacterial DNA replication and transcription.
Moxifloxacin (Avelox)
Inhibits A subunits of DNA gyrase, resulting in inhibition of bacterial DNA replication and transcription.
