Updated: Aug 5, 2008
Mycoplasma pneumoniae is a common cause of community-acquired pneumonia, and, usually, the disease has a prolonged, gradual onset. M pneumoniae was first isolated in cattle with pleuropneumonia in 1898. In 1938, Reimann described the first cases of mycoplasmal pneumonia in man. Reimann coined the term "primary atypical pneumonia" after observing 7 patients in Philadelphia with marked constitutional symptoms, upper and lower respiratory tract symptoms, and a protracted course with gradual resolution. Peterson discovered the phenomenon of cold agglutinin in 1943, and high titers of cold agglutinins in patients with this type of pneumonia were discovered accidentally. In 1944, Eaton was credited with discovering a specific agent, coined Eaton's agent, as the principal cause of primary atypical pneumonia. First thought to be a virus, Eaton's agent was proved to be a Mycoplasma species in 1961.
The responsible organism, M pneumoniae, is a pleomorphic organism that, unlike bacteria, lacks a cell wall, and unlike viruses do not need a host cell for replication. The prolonged paroxysmal cough seen in this disease is thought to be due to the inhibition of ciliary movement. The organism has a remarkable gliding motility and specialized filamentous tips end that allows it to burrow between cilia within the respiratory epithelium, eventually causing sloughing of the respiratory epithelial cells.
The organism has two properties that seem to correlate well with its pathogenicity in humans. The first is a selective affinity for respiratory epithelial cells, and the second is the ability to produce hydrogen peroxide, which is thought to be responsible for much of the initial cell disruption in the respiratory tract and for damage to erythrocyte membranes.
The pathogenicity of M pneumoniae has been linked to the activation of inflammatory mediators, including cytokines.
M pneumoniae is now recognized as one of the most common causes of community-acquired pneumonia in otherwise healthy patients younger than 40 years, with the highest rate in 5- to 20-year olds. M pneumoniae causes upper and lower respiratory illness in all age groups, particularly in temperate climates, and in summer, may cause up to 50% of all pneumonias.
Mycoplasmal pneumonia can occur at any time of the year, but large outbreaks tend to occur in the late summer and fall. The incubation period tends to be smoldering and averages 3 weeks, in contrast to that of influenza and other viral pneumonias, which generally is a few days. Epidemics of mycoplasmal pneumonia tend to occur every 4-8 years in the general population and tend to be more frequent within closed populations, such as in military and prison populations. Although M pneumoniae is a common cause of pneumonia, only 5-10% of infected patients actually develop pneumonia.
In almost all patients, the pneumonia resolves without any serious complications. M pneumoniae can cause severe pneumonia in children and has recently been associated with acute chest syndrome in patients with sickle cell anemia.
No racial predilections exist in mycoplasmal diseases.
No difference in disease frequency exists between males and females, but illnesses are somewhat more severe in males.
Mycoplasmal pneumonia is common in all age groups; however, it is most common in the first 2 decades of life and is rare in children younger than 5 years.
Mycoplasmal pneumonia is a disease of gradual and insidious onset of several days to weeks. The patient's history may include the following:
Most cases of pneumonia due to M pneumoniae resolve after several weeks, although a dry cough can be present for as long as a month; some patients can have a protracted illness lasting as long as 6 weeks. Other findings may also include the following:
Pediatrics, Pneumonia
Pneumonia, Aspiration
Pneumonia, Bacterial
Pneumonia, Empyema and Abscess
Pneumonia, Immunocompromised
Pneumonia, Viral
Chlamydia pneumoniae
Legionella pneumophila
Chlamydia psittaci
Chlamydia trachomatis
Coxiella burnetii (Q fever)
Mycoplasmal pneumonia should be considered as a possible etiology in any emergency department patient presenting with 3 weeks of a steadily progressive cough. Patients are usually not critically ill, but seek relief from the persistent, worsening cough. Occasionally, various pulmonary and extrapulmonary complications may occur and may require emergent attention.
Several antimicrobials are effective in reducing the length of illness due to mycoplasmal pneumonia.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. In the treatment of mycoplasmal pneumonia, antimicrobials against M pneumoniae are bacteriostatic, not bactericidal.
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes and causing RNA-dependent protein synthesis to arrest; for treatment of staphylococcal and streptococcal infections.
500 mg PO qid for 7-10 d
7.5-12.5 mg/kg/dose PO qid for 7-10 d
Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis
Documented hypersensitivity; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur
Very effective against M pneumoniae. Perhaps the most common agent used to treat M pneumoniae given its ease of administration.
Day 1: 500 mg PO
Days 2-5: 250 mg/d PO
<6 months: Not established
>6 months: day 1: 10 mg/kg PO once; not to exceed 500 mg/d; days 2-5: 5 mg/kg/d PO; not to exceed 250 mg/d
May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine
Documented hypersensitivity; hepatic impairment; do not administer with pimozide
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Site reactions can occur with IV route; bacterial or fungal overgrowth may result with prolonged antibiotic use; may increase hepatic enzymes and cholestatic jaundice; caution in patients with impaired hepatic function, prolonged QT intervals, or pneumonia; caution in hospitalized, geriatric, or debilitated patients
Reversibly binds to the P site of the 50S ribosomal subunit of susceptible organisms and may inhibit RNA-dependent protein synthesis by stimulating the dissociation of peptidyl tRNA from ribosomes; result is bacterial growth inhibition.
500 mg PO bid for 7-14 d
<6 months: Not established
>6 months: 7.5 mg/kg/dose PO bid for 10 d
Toxicity increases with coadministration of fluconazole and pimozide; effects decrease and GI adverse effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, HMG CoA-reductase inhibitors; plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmias and increase in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both
Documented hypersensitivity; coadministration of pimozide
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Coadministration with ranitidine or bismuth citrate is not recommended with CrCl <25 mL/min; give half dose or increase dosing interval if CrCl <30 mL/min; diarrhea may be sign of pseudomembranous colitis; superinfections may occur with prolonged or repeated antibiotic therapies
Treats susceptible bacterial infections of both gram-positive and gram-negative organisms, as well as infections caused by Mycoplasma, Chlamydophilia, and Rickettsia organisms; inhibits bacterial protein synthesis by binding with the 30S subunit and possibly the 50S ribosomal subunit of susceptible bacteria; as effective as erythromycin and other macrolides in the treatment of M pneumoniae infection.
100 mg PO bid for 1-4 wk
<8 years: Not recommended
>8 years: 2-4 mg/kg/d up to 200 mg/d PO divided bid
Do not give with dairy products or with any divalent cations (eg, Fe++, Ca++, Mg++); can increase hypoprothrombinemic effects of anticoagulants (monitor PT in patients taking both medications); coadministration can decrease the pharmacologic effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider determining drug serum levels in prolonged therapy; doxycycline use during tooth development (last half of gestation through age 8 y) can cause permanent discoloration of teeth; fluids should be liberally consumed to reduce the risk of esophageal irritation and ulceration
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mycoplasma pneumonia, mycoplasmal pneumonia, Mycoplasma pneumoniae, M pneumoniae, CAP, community-acquired pneumonia, atypical pneumonia, sore chest, tracheal tenderness, dry cough, bullous myringitis, pharyngeal erythema, scratchy sore throat
Michael J Bono, MD, FACEP, Professor of Emergency Medicine, Associate Director of Emergency Medicine Residency Program, Department of Emergency Medicine, Eastern Virginia Medical School
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