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J R Soc Med. 2002 March; 95(3): 132–133.
PMCID: PMC1279480

Wheeze and Mycoplasma pneumoniae


There is increasing interest in whether the atypical organisms Mycoplasma pneumoniae and Chlamydia pneumoniae can cause exacerbations of asthma1,2. I describe four previously fit non-asthmatic patients who developed severe wheeze and airways obstruction in association with M. pneumoniae and who made a full recovery. When atypical asthma is associated with systemic symptoms the differential diagnosis should include M. pneumoniae infection.


The four patients were previously fit with no history of asthma and they presented with dyspnoea, chest tightness and malaise. All were wheezy with an obstructive pattern of spirometry (Table 1). Initial white blood cell counts were raised (range 12.6-16.8 × 109 L-1; predominant neutrophilia). They were not anaemic and the initial erythrocyte sedimentation rate was high (range 93-125 mm/h). Chest radiographs (CXR) showed bilateral fine infiltrates. The diagnosis of M. pneumoniae infection was based on raised IgM antibodies and raised or rising titres of complement fixing antibodies against M. pneumoniae (range > 1:256- > 1:512). Symptoms, abnormal investigations and radiographs eventually resolved and no patient has subsequently needed treatment for wheeze or asthma.

Table 1
Spirometry values at time of initial presentation to hospital and after recovery

Case 1

A man of 45 had a one-month history of cough and dyspnoea associated with sore throat, headache and malaise. He looked unwell with bi-basal crackles and wheeze. He was treated with inhaled corticosteroids and oral erythromycin. Over the next two months his wheeze and CXR changes resolved.

Case 2

A woman aged 59 was admitted with a two-week history of dyspnoea, wheeze, non-productive cough and sore throat. She had bilateral inspiratory crackles and loud expiratory ‘squeaks’ and was hypoxic (PaO2 6.8 kPa). She was treated with intravenous (iv) cephradine and clarithromycin with prednisolone 30 mg/day. She was in hospital for ten days and her wheeze slowly improved. Two months after admission she had fully recovered.

Case 3

A man of 53 was admitted with a two-week history of dyspnoea, chest tightness, malaise and aches. He had tachycardia, tachypnoea and hypoxia (PaO2 6.5 kPa). There were bilateral inspiratory crackles with a harsh expiratory wheeze. He was treated with iv cefuroxime and clarithryomycin plus oral prednisolone 40 mg/day. Because he was still unwell after a week, bronchoscopy was performed. Transbronchial biopsies showed normal alveoli and scanty inflammation in the bronchial mucosa. Eleven days after admission he rapidly improved and was discharged on a reducing dose of prednisolone. Three months later he was symptom-free and off all treatment.

Case 4

A 63-year-old man had a one-month history of wheeze and dyspnoea associated with dry cough, malaise and weight loss. On examination he had bi-basal crackles and expiratory wheeze. He was treated with oral erythromycin and prednisolone 30 mg/day. Prednisolone was gradually reduced and two months later he was symptom-free.


These four patients with wheeze, dyspnoea and airways obstruction proved to be infected with M. pneumoniae. Presentation was unusual for community-acquired pneumonia in that wheeze was a prominent feature, the onset was gradual with lack of fever, and the CXR appearances were atypical. M. pneumoniae has a predilection for the respiratory epithelium and a luminal infiltrate can affect bronchi, bronchioles and alveoli3. Sore throat and cough are common and the disease can ‘march’ from the upper to the lower airways3.

In view of its ability to produce airway inflammation it would be understandable if M. pneumoniae infection were to exacerbate preexisting asthma. Gil et al.4 cultured M. pneumoniae from throat swabs in 25% of asthmatics compared with 6% of controls. Airway colonization might increase chronic inflammation and make asthma more difficult to control. Other workers have looked for M. pneumoniae using the polymerase chain reaction in bronchial lavage specimens obtained at bronchoscopy. The organism was detected in 10 out of 18 patients with chronic asthma and in only 1 of 11 controls5. It is increasingly suggested that C. pneumoniae too can exacerbate asthma1,2.

M. pneumoniae infection can cause wheeze in children6 but it is not clear how commonly it causes wheeze in non-asthmatic adults. In a large study comparing features in adult pneumonia caused by different organisms wheeze was not assessed7. However, in keeping with the findings in my four patients, people with M. pneumoniae infection tended to be younger with a longer history and more frequent upper respiratory symptoms7. Although spirometric values were not reported, some authors have noted that in the acute phase of mycoplasma pneumonia a coexisting obstructive and restrictive picture is common and can be slow to resolve8. Another study found evidence of M. pneumoniae infection in only 3 out of 151 admissions for severe asthma9. Mycoplasma infections occur in cyclical epidemics and how commonly they are reported to produce wheeze may depend on whether or not it is an epidemic year. In adults, mycoplasma-associated bronchiolitis without pneumonia has occasionally been reported10. Asthma is probably uncommon in M. pneumoniae infection as a study of 15 adults showed no evidence of airways obstruction11.

It is not possible to say whether resolution of wheeze in these cases was hastened by use of macrolide antibiotics and/or corticosteroids (oral in three, inhaled in one), but this is likely. Macrolides can have anti-inflammatory as well as antibiotic actions12. In light of the current interest in the relationship between M. pneumoniae infection and asthma1,2, it is reassuring to note that severe wheeze caused by this organism can fully resolve.


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Articles from Journal of the Royal Society of Medicine are provided here courtesy of Royal Society of Medicine Press