Mycoplasmal Pneumonia

Mycoplasmal Pneumonia

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Mycoplasma pneumoniae is a common cause of community-acquired pneumonia (CAP), and the disease usually has a prolonged, gradual onset. [1]  M pneumoniae was first isolated in cattle with pleuropneumonia in 1898.

In 1938, Reimann described the first cases of mycoplasmal pneumonia in man and 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. [2] Peterson discovered the phenomenon of cold agglutinin in 1943. High titers of cold agglutinins in patients with primary atypical 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. [3] First thought to be a virus, Eaton’s agent was proved to be a Mycoplasma species in 1961.

The breakdown of the Mollicutes class, which includes the Mycoplasma genus, is presented in the image below.

Go to Community-Acquired Pneumonia, Bacterial Pneumonia, Mycoplasma Infections, and Imaging Atypical Bacterial Pneumonia for more information on these topics.

The organism responsible for mycoplasmal pneumonia, M pneumoniae, is a pleomorphic organism that, unlike bacteria, lacks a cell wall, and unlike viruses, does 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. M pneumoniae has a remarkable gliding motility and specialized tip organelles 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. [4] Macrolide-resistant M pneumoniae has emerged in adult community-acquired pneumonia [5] as well as pediatric pneumonia. [6, 7, 8, 9, 10]

Mycoplasma pneumoniae has been identified with an increasing array of illnesses, such as acute hepatitis, [11, 12] immune thrombocytopenic purpura, [13] severe autoimmune hemolytic anemia, [14] Stevens-Johnson syndrome, [15, 16] arthritis, [17] and transverse myelitis. [18, 19]

The causative agent of mycoplasmal pneumonia is M pneumoniae, a bacterium in the shape of a short rod, lacking a cell wall, which belongs to the class Mollicutes, the smallest known free-living microorganisms. The organism can be excreted from the respiratory tract for several weeks after the acute infection; therefore, isolation of the organism may not indicate acute infection. The organism is difficult to grow in the laboratory, requiring not only specialized growth medium, but also long growth times, which limits the clinical utility of culturing the organism.

M pneumoniae is now recognized as one of the most common causes of community-acquired pneumonia in otherwise healthy patients younger than 40 years. Although mycoplasmal pneumonia is common in all age groups, it is most common in the first 2 decades of life, is rare in children younger than five years, and has the highest rate of infection in individuals aged 5-20 years. Although no difference in disease frequency is observed between males and females, illnesses are somewhat more severe in males.

M pneumoniae causes upper and lower respiratory illness in all age groups, particularly in temperate climates, and can occur at any time of the year, but large outbreaks tend to occur in the late summer and fall. Transmission of the organism is person-to-person by infected respiratory droplets. In summer, this organism may cause as many as 50% of all pneumonias.

The incubation of mycoplasmal pneumonia tends to be smoldering and averages a period of 2-3 weeks, in contrast to that of influenza and other viral pneumonias, which generally average 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. Many patients infected with M pneumoniae remain asymptomatic, but patients who become symptomatic develop a respiratory infection which can be lingering and quite bothersome.

With proper treatment, a full recovery is expected. In almost all patients, the pneumonia resolves without any serious complications. However, M pneumoniae can cause severe pneumonia in children and has been associated with acute chest syndrome in patients with sickle cell anemia. [20] Immunity after infection with M pneumoniae is not long lasting.

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Michael Joseph Bono, MD, FACEP Professor of Emergency Medicine, Vice Chair, Emergency Medicine Residency Program, Department of Emergency Medicine, Eastern Virginia Medical School

Michael Joseph Bono, MD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, Medical Society of Virginia, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Paul Blackburn, DO, FACOEP, FACEP Attending Physician, Department of Emergency Medicine, Maricopa Medical Center

Paul Blackburn, DO, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, Arizona Medical Association, American College of Osteopathic Emergency Physicians, American Medical Association

Disclosure: Nothing to disclose.

Guy W Soo Hoo, MD, MPH Clinical Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Director, Medical Intensive Care Unit, Pulmonary and Critical Care Section, West Los Angeles Healthcare Center, Veteran Affairs Greater Los Angeles Healthcare System

Guy W Soo Hoo, MD, MPH is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Thoracic Society, Society of Critical Care Medicine, California Thoracic Society, American Association for Respiratory Care

Disclosure: Nothing to disclose.

Mycoplasmal Pneumonia

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