Severe Mycoplasma Pneumonia

Thorax: first published as 10.1136/thx.32.1.112 on 1 February 1977. Downloaded from Thorax, 1977, 32, 112-115 Severe mycoplasma pneumonia S. HOLT, W. F. RYAN, AND E. J. EPSTEIN From Liverpool Regional Cardiac Unit, Sefton General Hospital, Smithdown Road, Liverpool 15 Holt, S., Ryan, W. F., and Epstein, E. 1. (1977). Thorax, 32, 112-115. Severe mycoplasma pneumonia. A patient who developed a protracted illness following severe mycoplasma pneumonia is described. The acute phase of the infection was complicated by myocarditis and haemolytic anaemia. The respiratory symptoms abated and lung function tests improved with the administration of systemic and inhaled corticosteroids. Mycoplasma pneumoniae, first isolated in 1944 by was normal. Treatment was started with ampicillin, passage in laboratory animals and chick embryo, 500 mg six-hourly by intramuscular injection. has been implicated as an important cause of On admission the haemoglobulin was 11 5 g/dl, respiratory infection, sometimes producing a wide white cell count 6-2XI109/l with 90% polymorphs variety of non-respiratory syndromes (Eaton et and an ESR of 92. A chest radiograph (Figure) al., 1944; Lambert, 1969). This organism usually demonstrated patchy consolidation in both lower causes mild self-limiting respiratory disease and zones of the lung fields with a small effusion at has been shown by serological studies to have the left base. a wide geographical prevalence (Hayflick and Three days after admission the patient's general Chanock, 1965). condition deteriorated with clinical and radio- Only about 10% of patients with mycoplasma logical evidence of increased consolidation in both infection will develop major respiratory disease, lung fields and extension to the right upper zone. the features of which are not distinct enough to Streptomycin, 0 5 g by intramuscular injection http://thorax.bmj.com/ allow an accurate diagnosis without recourse to twice daily, was added to the treatment with ap- serological studies (Mufson et al., 1961). However, parent slight improvement. Five days after ad- unlike other causes of primary atypical pneu- mission the haemoglobin was recorded at 11 g/dl, monia, untreated mycoplasma pneumonia may white cell count 11 6X 109/1 with 90% polymorphs. give rise to a prolonged respiratory illness with The serum showed a complement fixation anti- persistent radiographic shadows and respiratory body titre of 1 in 1280 against Mycoplasma pneu- symptoms (Mufson et al., 1961). Complications moniae. Cold agglutinins were present and re- of mycoplasma infection tend to be uncommon, ported as follows: on October 1, 2021 by guest. Protected copyright. few severe infections having been described. with adult 0 positive red cells 1 in 1000 A patient with severe mycoplasma pneumonia, with patient's own red cells 1 in 1000 complicated by myocarditis and haemolytic with 0 positive cord red blood cells 1 in 32. anaemia, is described. The infection gave rise to The direct Coombs' test was positive at 1 in 500. prolonged respiratory disability which responded These results indicated mycoplasma pneumonia to treatment with corticosteroids. with cold agglutinin disease of anti-I specificity. Tetracycline was begun in a dose of 1 g orally Case report every six hours, and the ampicillin was discon- tinued on the sixth day after admission. Her A 50-year-old housewife was admitted with a general condition improved over the next 48 three-day history of cough, productive of a small hours, but again deterioration occurred on the amount of mucoid sputum, breathlessness, general eighth day when she developed central cyanosis, malaise, and fever. Examination revealed a tachypnoea, and a pyrexia of 390C. Blood gases pyrexia of 400C, and there were signs of con- were reported as pH 7-42, Pco2 6 5 kPa, and Po, solidation in both lower zones of the lung fields. 5 kPa with a bicarbonate of 29 4 mmol/l. Improve- The pulse was 80 per minute and regular, blood- ment occurred with controlled oxygen therapy. On pressure 120/80 mmHg, and cardiac auscultation the 10th day she complained of bilateral pleuritic 112 Thorax: first published as 10.1136/thx.32.1.112 on 1 February 1977. Downloaded from Severe mycoplasma pneumonia 113 Figure Chest radiograph .showing patchy consolidation at both lung bases with a small effusion at the left base. chest pain and developed a pleural friction rub from hospital she complained of a non-productive over both lung fields. A chest radiograph showed cough and dyspnoea. Examination revealed coarse persistent bilateral lower zone consolidation. How- crepitations over both lower lung fields. Haemo- ever, over the next three days, with continued globin was 13-2 g/dl, white cell count 8-7X109/l, http://thorax.bmj.com/ supportive therapy, she made a good improvement and ESR 20 mm. A further one month's course of with a return of the blood gases to normal. tetracycline, 500 mg every six hours, was pre- Sputum and a throat swab failed to grow any scribed. At her next monthly attendance she organism in a wide range of primary and second- continued to complain of a troublesome cough ary tissue cultures. disturbing her sleep, breathlessness when walking On the 17th day after admission an electro- quickly, and intermittent bouts of wheezing. cardiogram showed sinus rhythm at a rate of 80 Examination demonstrated coarse inspiratory per minute with generalised ST-segment arching crepitations and rhonchi at both lung bases with a on October 1, 2021 by guest. Protected copyright. and T-wave inversion in leads I, II, III, aVL, short wheeze on forced expiration. Respiratory aVF, and VI to V6. These ECG abnormalities had function tests showed a mild restrictive impair- resolved within one week; no pericardial friction ment of ventilatory capacity with a small lung sounds were heard and there was no rise in volume and reduced transfer factor (see Table). transaminase enzymes. On the 25th day, the A chest radiograph revealed fine shadowing in haemogloblin had fallen to 10 g/dl with 3% both lower lung fields and pleural thickening at reticulocytes, and the red cells showed auto- the left base. agglutination. In view of these findings a persistent 'alveolitis' She maintained good progress and was mobilised was suspected and treatment was started with and allowed home after 49 days in hospital. On Becotide inhalations, 2 four times daily, and discharge she still had an irritant non-productive prednisolone, 5 mg once daily. Over the ensuing cough, breathlessness on moderate exertion, and two months the cough and dyspnoea were relieved coarse crepitations in both lower zones of the and lung function tests demonstrated some im- lung fields. provement (see Table). The steroid therapy was gradually tailed off with no recurrence of her FOLLOW-UP STUDIES symptoms. The patient remained well with clear At the outpatient clinic one month after discharge lung fields on examination 12 months after the Thorax: first published as 10.1136/thx.32.1.112 on 1 February 1977. Downloaded from 114 S. Holt, W. F. Ryan, and E. J. Epstein Table Respiratory function tests patients had abnormal radiographs one month after the onset of illness, but these had cleared After onset ofillness within a further six weeks (Mufson et al., 1961). 15 weeks 23 weeks I year Because Mycoplasma pneumoniae infection is rarely fatal, opportunities to study pathological Ventilatory capacity Forced vital capacity (litres) 2-7 2-95 3-0 changes in the lungs have been few. The capacity Forced expiratory volume for producing prolonged respiratory illness, as in (1 s) (litres) 1 95 2-3 2-3 FEVas %ofVC 72% 78% 77% our patient, with impairment of ventilatory Max. voluntary ventilation capacity and gas transfer factor suggests the (1/min) 74 88 83 Lung volumes (litres) presence, in some cases, of a persistent pneumo- Vital capacity 2-6 2-85 nitis. Observed changes in the lungs during Inspiratory capacity 2-0 2-2 infection include lymphocyte and Expiratory reserve volume 0-6 0-65 mycoplasma Functional residual capacity 142 2-6 plasma cell infiltration with purulent exudation Residual volume 0-82 1-95 and microabscess formation of bronchiolar distri- Total lung capacity 3-42 4-8 RV/TLC ratio 24% 41% bution. An alveolitis may also occur with Transfer factor (kPa) 1-73 3-3 desquamation of septal cells, oedema, and hyaline (55'% (107% normal) normal) membrane formation (Jones, 1969) and it may be this which accounts for the protracted illness and disturbed pulmonary function tests in our own onset of the illness. A chest radiograph then patient. demonstrated residual pleural thickening at the Cellular immunity has been implicated in the left costophrenic angle and respiratory function pathogenesis of severe pneumonitis in patients with tests showed further improvement (see Table). mycoplasma pneumonia, and for this reason corticosteroid therapy has been advocated for Discussion patients with severe infection (Noriega et al., 1974). This may provide an explanation for the Mycoplasm,a pneumoniae infection usually gives good therapeutic response that was obtained by rise to a mild respiratory illness and, in many their use in our patient. cases, the attack may be subclinical (Lambert, Haemolytic anaemia and myocarditis are well http://thorax.bmj.com/ 1969). Serological studies have shown a high inci- recognised but uncommon consequences of myco- dence of complement-fixing antibodies against plasma infection (Worlledge and Blajchman, mycoplasma in the population. In one survey it 1972; Lewes et al., 1974). The severity of haemo- was estimated that 19% of the population in lysis may be wide but is clinically apparent in less southern England may possess such antibody than 5% of patients (Jones, 1969). In this patient, (Lambert, 1968). When mycoplasma pneumonia is only a mild asymptomatic haemolytic anaemia complicated by the development of cold agglu- occurred. It is also of interest that myocarditis tinins, as in this patient, then the clinical picture with marked ECG changes was present without tends to be that of major respiratory involvement.

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