Pediatric Mycoplasma Infections Medication
- Author: Archana Chatterjee, MD, PhD; Chief Editor: Russell W Steele, MD more...
Medication Summary
As a result of the lack of a cell wall, beta-lactams are ineffective; neither is the combined therapy of trimethoprim and sulfamethoxazole effective. Aminoglycosides are effective in vitro, but efficacy is unknown in vivo.
Ketolides are in development and show effective activity against mycoplasmal organisms. Telithromycin, a recently-licensed ketolide, has been shown to be active against M pneumoniae. It is approved for treatment of community-acquired pneumonia. Because of the risk of hepatotoxicity associated with telithromycin, the US Food and Drug Administration (FDA) removed previously approved indications for sinusitis and acute bacterial exacerbations of chronic bronchitis.
Streptogramins (ie, quinupristin-dalfopristin) are available only as a parenteral formulation; therefore, they are not practical for use in patients with Mycoplasma diseases.
Macrolides are the agents of choice. Alternatively, tetracyclines may be used in patients older than 8 years. Fluoroquinolones may be considered if macrolides or tetracyclines are not suitable choices; however, most fluoroquinolones are not approved by the FDA for use in patients younger than 18 years.[2, 3, 8, 60]
Antibiotics
Class Summary
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. Because of reports of macrolide resistance, whenever feasible, guide antibiotic selection using culture sensitivity.[2, 3, 8]
Erythromycin (E.E.S., E-Mycin, Eryc)
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl transfer RNA (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.
Clarithromycin (Biaxin)
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, arresting RNA-dependent protein synthesis.
Azithromycin (Zithromax)
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, arresting RNA-dependent protein synthesis.
Tetracycline (Sumycin)
Treats gram-positive and gram-negative organisms, as well as mycoplasmal, chlamydial, and rickettsial infections. Inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunits.
Doxycycline (Vibramycin)
Inhibits protein synthesis and thus bacterial growth by binding to 30S and, possibly, 50S ribosomal subunits of susceptible bacteria.
Levofloxacin (Levaquin)
Of the fluoroquinolones (eg, ciprofloxacin, ofloxacin, levofloxacin, sparfloxacin, grepafloxacin), drug of choice (DOC) to treat community-acquired pneumonia in adults. Use in children and pregnant women restricted because of concern regarding cartilage toxicity, but several clinical trials ongoing, and such use may be indicated in the future.
Telithromycin (Ketec)
First antibiotic in new ketolides class. Combats resistant bacteria by inhibiting protein synthesis necessary for bacterial reproduction, binding 10 times tighter than macrolides at 2 sites on bacterial ribosomes. Blocks protein synthesis by binding to 50S ribosomal subunit (23S rRNA at domains II and V). Binding at domain II retains activity against gram-positive cocci (eg, Streptococcus pneumoniae), eliminating resistance mediated by methylases (erm genes) that alter domain V binding site. May also inhibit the assembly of nascent ribosomal units. Resistance and cross resistance have not been observed.
Active against S pneumoniae, Streptococcus pyogenes, Staphylococcus aureus, Haemophilus influenzae, and Moraxella catarrhalis; as well as atypical bacteria such as Chlamydia pneumoniae, M pneumoniae, and Legionella pneumoniae. Indicated to treat mild-to-moderate community-acquired pneumonia, including infections caused by multidrug resistant S pneumoniae).
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