Atypical pneumonia - Complications | BMJ Best Practice

Complications

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Complications table
Complication	Timeframe	Likelihood
pleural/parapneumonic effusion	short term	medium
Pleural/parapneumonic effusion is an accumulation of fluid and inflammatory cells caused by adjacent lung infection or due to invasion of the pleural space by the pathogen.[93] It occurs in up to 30% of cases of Legionella pneumophila pneumonia and in rare cases of Mycoplasma pneumoniae pneumonia.[6][94] Appropriate antibiotic treatment is essential. If fluid accumulates or does not resolve, then thoracentesis and drainage may be indicated. In severe nonresolving cases, pleural decortication may be required. Pleural effusion
rash	short term	medium
May occur in up to 25% of M pneumoniae patients and is mainly self-limited maculopapular or vesicular rash.[4] Severe cases may include Stevens-Johnson syndrome and ulcerative stomatitis. The term Mycoplasma-induced rash and mucositis has been used to describe the rash as it can be difficult to classify it as erythema multiforme or Stevens-Johnson syndrome.[95] Because the main cause for the rash is probably systemic spread of the pathogen to the skin, appropriate antibiotic treatment is the treatment of choice.
neurologic complications	short term	low
In up to 7% of patients hospitalized with M pneumoniae, a neurologic complication develops. These occur up to 2 weeks after the onset of infection and may include encephalitis, meningitis, cerebellar syndrome, cranial nerve palsies, and Guillain-Barre syndrome.[4] Because some of these complications have autoimmune features, any treatment for each individual patient should be tailored according to the specific neurologic syndrome.
pericarditis	short term	low
Pericarditis is an accumulation of fluid in the pericardial space that is mainly seen in M pneumoniae and L pneumophila infections.[4][96] If abnormalities do not resolve with antibiotic treatment, then the patient may require pericardiocentesis and drainage. Pericarditis
atherosclerosis	long term	low
For more than a decade, studies have suggested a possible role of atypical pathogens, mainly Chlamydophila pneumoniae, in progression of atherosclerosis. Further study is needed.[97][98][99]

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