Mycoplasma Pneumoniae and the Aetiology of Lobar Pneumonia in Northern Nigeria
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Thorax: first published as 10.1136/thx.34.6.713 on 1 December 1979. Downloaded from Thorax, 1979, 34, 713-719 Mycoplasma pneumoniae and the aetiology of lobar pneumonia in northern Nigeria J T MACFARLANE,' D S ADEGBOYE,2 AND M J WARRELL3 From the Departments of Medicine' and Veterinary Pathology and Microbiology,2 Ahmadu Bello University, Zaria, Nigeria, and the Department of Virology,3 Churchill Hospital, Oxford UK ABSTRACT Over a six-month period we studied 74 adult Nigerians who presented consecutively to Ahmadu Bello University Teaching Hospital, Zaria, with lobar or segmental pneumonia. Pneumococcal infection was diagnosed in 50% by the detection of pneumococcal polysaccharide antigen in serum or purulent sputum: 24% had pneumococcal antigenaemia. Twelve patients had evidence of Mycoplasma pneumoniae infection and half of these also had pneumococcal infection. The suggestion that M pneumoniae respiratory infection may predispose to serious bacterial pneumonia is discussed. The initial clinical and radiological features were similar in the pneumococcal and M pneumoniae groups. Raised cold agglutinin titres were not a reliable indication of M pneumoniae infection, perhaps due to altered autoantibody production in Nigerians. Pneumonia was commoner in the dry season, probably related to depressed nasopharyngeal defences caused by drying. Less common causes of lobar pneumonia that were copyright. found are also discussed and no cases of legionnaires' disease were identified. Lobar pneumonia continues to be one of the most et al, 1975). It is also common among Chinese important illnesses encountered in developing (Tai and Wei, 1976). Although M pneumoniae in- countries, being the commonest cause of hospital fection has been reported from South Africa http://thorax.bmj.com/ admissions in Zaria, Nigeria (Warrell, 1975), and (Joosting et al, 1975) and Egypt (Hassan et al, in New Guinea (Douglas and Devitt, 1973). Nearly 1972), there are no clinical studies of its importance 700 000 cases of pneumonia were reported to the as a cause of lobar pneumonia in tropical Africa. National Research Council Survey in 1957, 50% In an environment where treatment and follow- coming from Africa alone (National Academy of up are difficult, it is vital to know the likely Science, 1962). A death rate of 20% has been re- aetiology of common infections. Thus we have ported from Nigeria despite antibiotics (Sofowara performed a prospective clinical and laboratory and Onadeko, 1973). study of the cause of lobar pneumonia in Zaria in on September 27, 2021 by guest. Protected Streptococcus pneumoniae is the usual cause of northern Nigeria, with particular emphasis on lobar pneumonia in Africa (Tugwell and Green- pneumococcal and M pneumoniae infection. wood, 1975). However, the fact that between 10% (Douglas and Riley, 1970; Sutton et al, 1970) and Methods 31% (Tugwell and Greenwood, 1975) of patients with lobar pneumonia in the tropics do not Seventy-four Nigerian patients presenting con- respond promptly to penicillin suggests that other secutively to Ahmadu Bello University Teaching micro-organisms may also be implicated. Hospital between August 1977 and January 1978 Mycoplasma pneumoniae is recognised as a sig- with clinical and radiological features of lobar or nificant cause of lower respiratory tract infections, segmental pneumonia were seen by one of us. accounting for 10% (Chanock, 1965) to 15% (Foy There were 60 men and 14 women, mean age et al, 1970) of such infections in American civilian 28 5 years (:4 12.6 SD). Two patients with acute populations. Mycoplasma pneumoniae has a wide respiratory illnesses and pleural effusions were geographical distribution (Chanock et al, 1967) included. A full history was taken, all patients causing 28% of atypical pneumonias in Tokyo were examined, and after other investigations (Kitamoto et al, 1966) and 15% in India (Gupta most patients received parenteral penicillin. 713 Thorax: first published as 10.1136/thx.34.6.713 on 1 December 1979. Downloaded from 714 J T Macfarlane, D S Adegboye, and M J Warrell Twenty-six patients had received antibiotics before was performed on all sera using the method of being seen. Patients attended a special follow-up Bradstreet and Taylor (1962) adapted to micro- clinic two to four weeks after initial presentation. titre apparatus. Specific M pneumoniae IgM was Investigations on all patients included a postero- measured by a fluorescent antibody test (FAT) by anterior and lateral chest radiograph and Dr BE Andrews at the Mycoplasma Reference haemoglobin and white cell count by standard Laboratory, Norwich (Sillis and Andrews, 1978). methods. Haemoglobin electrophoresis showed no This test was performed on all sera from patients patients with sickle cell disease (SS) but 13 patients who had: (a) a four-fold or greater rise in CF with sickle cell trait (AS). titre, (b) a single CF titre of >1/64, (c) M pneu- A specimen of purulent sputum and all serum moniae isolated from the throat swab, or (d) a samples were tested for pneumococcal polysac- cold agglutinin titre of >1/32. The diagnosis of charide antigen by the countercurrent immuno- current M pneumoniae infection was accepted if electrophoresis (CIE) method using pneumococcal the CF antibody titre rose four-fold during con- omniserum (Tugwell and Greenwood, 1975). valescence, or if the M pneumonia-specific IgM Pneumococcal antigen typing was carried out on FAT was > 1/8 (Andrews, personal communica- positive specimens using group-specific and mono- tion). The isolation of M pneumoniae in the ab- specific pneumococcal antisera (Statens Serum sence of serological changes was taken to indicate Institute, Copenhagen). Sputum specimens nega- recent infection, although not necessarily implicat- tive to pneumococcal antigen were then tested for ing M pneumoniae as the primary cause of the antigen to Neisseria meningitidis group Y by CIE current pneumonia. Sera from 13 patients, thought using Difco antiserum. Percutaneous lung aspir- clinically to have a viral type of infection, were ations were obtained in 11 patients by rapidly in- tested for antibody to influenza A and B, adeno- serting a 19-gauge needle into the consolidated virus, parainfluenza, Q fever, and psittacosis area of the lung during suspended respiration antigens by the CF test. Serological evidence indi- while exerting negative pressure on the attached cating influenza A infection was confirmed bycopyright. 5 ml syringe. detecting influenza A-specific IgM by FAT Standard laboratory methods identified bacterial (Urquhart, 1974). The latest specimen of serum isolates from sputum, pleural fluid, and lung from each patient was examined for evidence of aspirates. The diagnosis of significant pneumo- legionnaires' disease by testing for specific IgM coccal infection was based on the finding of and IgG by FAT using a sero group l-Legionella pneumococcal antigen in purulent sputum or pneumophila antigen. http://thorax.bmj.com/ serum or the isolation of pneumococci from lung Specific IgM tests were considered valid only if aspirates. the latex slide agglutination test for rheumatoid factor was negative. ISOLATION OF M PNEUMONIAE Throat swabs from 70 patients were placed in COLD AGGLUTININS complete M pneumoniae broth and stored at A cold agglutinin screening test (CAST) (Garrow, -200C for up to one week before titration and 1958) was performed immediately on each blood incubation in liquid mycoplasma broth and subse- sample; a positive result was recorded only if on September 27, 2021 by guest. Protected quent subculture on to similar solid medium agglutination was obvious. Fifty fit adult Nigerians (Chanock et al, 1962). (35 men and 15 women) awaiting elective surgery M pneumoniae was identified by: (a) slow were used as controls for cold agglutinin titres growth rate, (b) colonial appearance, and (c) (CAT) and CAST. The CAT were measured in growth inhibition test (Black, 1973) using hyper- one batch in Zaria at the end of the study by a immune anti-M pneumoniae serum (FAO/WHO microtitre method using a 2% suspension of Centre for Animal Mycoplasmas, University of washed fresh group 0 adult red cells containing Aarhus, Denmark). 1% bovine serum albumin. After overnight incu- bation at 40C, the titres were read "blind" by two SEROLOGICAL TESTS observers. Blood was taken from all patients and allowed to clot at 370C before storing the serum at -200C. Results Aliquots of all sera were frozen and transported to Britain by air, but temporary thawing was often An aetiology for the lobar pneumonia was found inevitable. On arrival they were stored at -400C. in 51 out of 74 patients (73%) as summarised in A M pneumoniae complement fixation (CF) test the table. Thorax: first published as 10.1136/thx.34.6.713 on 1 December 1979. Downloaded from Mycoplasma pneumoniae and the aetiology of lobar pneumonia in northern Nigeria 715 Micra-organisms associated with lobar pneumonia in 26 74 patients. (Number with mixed infections in 24 parentheses) 22 Micro-organism No of Micro-organism No of 20 patients patients 4l 18 S pneumoniae 37 (7) Tuberculosis 2 a,n 16 Mpneumoniae 12 (6) Staphylococcus aureus I 14 Diagnosed by 8 (3) Salmonella para- 1 serology typhoid C1 u 12 Diagnosed by 4 (3) Legionella 0 j isolation alone pneumophila E 10 Klebsiella species 3 N meningitidis 0 z 8 group Y Influenza A 3 (2) No aetiology found 23 6 4 2 PNEUMONIAE NU STREPTOCOCCUS O I. l _01 1__, RA\M3 \ 3 Thirty-seven patients (50%) with lobar pneumonia Weeks of year 32-36 41-44 49-52 1977-78 37-40 45-48 1-4 had evidence of pneumococcal infection, and one -Dry - died. Of these, nine (24%) had pneumococcal ---Wet-- season antigenaemia and nine had received prior anti- season biotics. Lung aspirate cultures confirmed pneumo- El All lobor pneumonia cases coccal infection in three patients who had pneumo- C M pneumonia cases ("/lof total cases) coccal antigen in their sputum. Serotyping was E Influenza A cases performed on 17 sputum and eight serum samples Fig 1 Seasonal incidence of lobar pneumonia cases.