Mycoplasma Infections (Mycoplasma pneumoniae) Clinical Presentation

Updated: Dec 13, 2022
  • Author: Ken B Waites, MD; Chief Editor: Michael Stuart Bronze, MD  more...
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Typical symptoms can develop and persist over weeks to months and include flulike manifestations.

Symptoms may include the following:

  • Generalized aches and pains

  • Fever (usually ≤ 102°F)

  • Cough - Usually nonproductive

  • Sore throat (nonexudative pharyngitis)

  • Headache/myalgias

  • Chills but not rigors

  • Nasal congestion with coryza

  • Earache

  • General malaise

In very young children, upper respiratory tract manifestations may predominate, whereas in older children and adults, lower respiratory tract symptoms are more likely.



Physical findings can be quite variable. Patients typically do not appear toxic or severely ill, but some abnormalities may be apparent in a significant proportion of cases.

Physical findings include the following:

  • Oropharyngeal inflammation

  • Cervical adenopathy - Usually absent

  • Erythematous tympanic membranes

  • Conjunctivitis

  • Maculopapular or urticarial rash

Chest auscultation in patients with pneumonia may demonstrate localized rhonchi and scattered moist rales, generally involving multiple lobes of the lung and sometimes accompanied by wheezes, with no signs of consolidation, egophony, or bronchial breathing.

In many persons, chest auscultative and percussive abnormalities are minimal to absent.

Extrapulmonary manifestations may occur in a minority of persons (see Complications). [1, 6]  



This is a bacterial infection caused by M pneumoniae.



Role in Asthma

M pneumoniae has evolved to create persistent infection and has been associated with development of asthma or atopic disease in persons who appear to have less robust immune responses to respiratory infections. Research in this area has been summarized in a review. [1] Epidemiologic studies have yielded evidence that M pneumoniae infection, diagnosed primarily by serology is associated with the development of asthma. Patients with M pneumoniae infection had a higher risk of developing asthma than matched controls, and this risk was further augmented by comorbidities such as atopic disease.

Studies of acute asthma in hospitalized children or adults revealed an incidence of M pneumoniae ranging from 4.5% to 65%. Other studies have reported a very high prevalence of M pneumoniae in chronic asthma, even in the absence of exacerbation. There have been reports that a course of macrolide antibiotics active against M pneumoniae will shorten the duration of wheezing episodes in children, but it is unclear whether antimicrobial activity of macrolides, anti-inflammatory activity, or a combination is behind the protective effect of this class of medication in asthma and asthma-like diseases. Many children with asthma also receive corticosteroids, which further complicates interpretation of antimicrobial effects on M pneumoniae in reducing severity and/or duration of asthma. Studies using murine animal models suggest that allergic airway inflammation downregulates the host response to M pneumoniae and provides a plausible explanation for reports of increased prevalence of M pneumoniae in chronic asthma as well as a potential role in the pathogenesis and perpetuation of this inflammatory respiratory disease.

Extrapulmonary Manifestations

M pneumoniae is well recognized for producing a broad array of extrapulmonary manifestations that can affect almost every organ in the body. Even though many different extrapulmonary manifestations of M pneumoniae infection have been characterized, they usually are not specific enough to confirm the diagnosis.

Three different mechanisms have been proposed for extrapulmonary complications of M pneumoniae infection. The first is a direct effect of the bacteria that are present at the site of inflammation mediated by cytokine release by the host. The second is through the production of autoimmunity or immune complexes. The third is by the production of vasculitis or thrombosis as a result of cytokines and chemokines such as TNF-α and IL-8 or by immunomodulation through mediators such as complement and fibrin D-dimers.