Author
Michael J Bono, MD, FACEP,
Professor of Emergency Medicine, Associate
Director of Emergency Medicine Residency Program, Department
of Emergency Medicine, Eastern Virginia Medical
School
Nothing to disclose.
Specialty Editor(s)
Francisco Talavera, PharmD, PhD,
Senior Pharmacy Editor,
eMedicine
eMedicine Salary Employment
John D Halamka, MD, MS,
Associate Professor of Medicine, Harvard
Medical School, Beth Israel Deaconess Medical Center; Chief
Information Officer, CareGroup Healthcare System and Harvard
Medical School; Attending Physician, Division of Emergency
Medicine, Beth Israel Deaconess Medical
Center
Nothing to disclose.
Joseph A Salomone III, MD,
EMS Medical Director, Kansas City, Missouri;
Associate Professor and Staff Physician, Truman Medical
Centers/UMKC School of Medicine
Nothing to disclose.
Paul Blackburn, DO, FACOEP, FACEP,
Program Director, Department of Emergency
Medicine, Maricopa Medical Center; Assistant Professor,
Department of Surgery, University of Arizona
Nothing to disclose.
Chief Editor
Robert E O'Connor, MD, MPH,
Professor and Chair, Department of Emergency
Medicine, University of Virginia Health
System
Nothing to disclose.
Background
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 general characteristics of Mycoplasma species are presented in the image below.
View Image | General characteristics of Mycoplasma species. |
Pathophysiology
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. One study reported on an emergence of drug-resistant M pneumoniae infection; however, the study concluded that host immune maturity and not the virulence factor of the organism is a major determinant factor of disease severity.[1] Macrolide-resistant M pneumoniae has emerged in adult community-acquired pneumonia[2] as well as pediatric pneumonia[3] .
Mycoplasma pneumoniae has been identified with an increasing array of illnesses, such as acute hepatitis,[4, 5] immune thrombocytopenic purpura,[6] severe autoimmune hemolytic anemia,[7] Stevens-Johnson syndrome,[8] arthritis,[9] and transverse myelitis[10, 11] .
Epidemiology
Frequency
United States
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 individuals aged 5-20 years. M pneumoniae causes upper and lower respiratory illness in all age groups, particularly in temperate climates, and in summer, may cause as many as 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 is generally 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.
Mortality/Morbidity
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.
Race
No racial predilections are observed in mycoplasmal diseases.
Sex
No difference in disease frequency is observed between males and females, but illnesses are somewhat more severe in males.
Age
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.
History
Mycoplasmal pneumonia is a disease of gradual and insidious onset of several days to weeks. The patient's history may include the following:
Fever
Malaise
Persistent, slowly worsening dry cough; absence of cough makes the diagnosis of M pneumoniae unlikely
Headache
Chills, not rigors
Scratchy sore throat
Sore chest and tracheal tenderness (result of the protracted cough)
Pleuritic chest pain (rare)
Physical
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:
A nontoxic general appearance
Erythematous tympanic membranes or bullous myringitis in patients older than age 2 years, an uncommon but unique sign
Mild pharyngeal injection with minimal or no cervical adenopathy, but no exudate
Normal lung findings with early infection but rhonchi, rales, and/or wheezes several days later
Various exanthems including erythema multiforme and Stevens-Johnson syndrome
Emergency Department Care
Mycoplasmal pneumonia should be considered as a possible etiology in any patient who presents to the ED 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.
Medication Summary
Several antimicrobials are effective in reducing the length of illness due to mycoplasmal pneumonia.
Class Summary
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. Tetracycline and erythromycin compounds are very effective, and the second-generation tetracyclines (doxycycline) and macrolides are the drugs of choice.[14] Penicillins and cephalosporins are ineffective because the organism lacks a cell wall.
Erythromycin (EES, Erythrocin, E-mycin)
Clinical Context:
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.
Azithromycin (Zithromax)
Clinical Context:
Very effective against M pneumoniae. Perhaps the most common agent used to treat M pneumoniae given its ease of administration.
Clarithromycin (Biaxin)
Clinical Context:
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.
Doxycycline (Vibramycin)
Clinical Context:
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.
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