637 in other bacteria and which determine resistance to various antimicrobial agents.23 Further characterisations of S. marcescens for epidemiological studies can be made
by serotyping24 and bacteriocin susceptibility typing.25 Antibiograms may also be helpful in epidemiological work. S. marcescens contributes substantially to morbidity and mortality in hospital practice.2-4 Proper management will depend on isolation of the organism, identification, and antibiotic-sensitivity testing. Extra time spent on this will be rewarded.
ASPERGILLOMA cavities in the lung colonised by Aspergillus species, usually A. fumigatus. The fungus grows on the wall of the cavity, tending to peel off to form a fungus ball, and the typical X-ray shows a cavity with irregular central density and surrounding halo.’1 Aspergillomas nearly always arise in diseased lung; residual tuberculous cavities are a common site,’ and other underlying conditions include sarcoidosis, lung abscess, pulmonary infarction, lung cyst, pneumoconiosis, histoplasmosis, carcinoma of the lung, and the apical fibrosis seen in ankylosing spondylitis.l-s Whether aspergilloma can arise in a normal lung is uncertain. The great majority of aspergillomas are in the upper lobes; they may be multiple and bilateral. In 1964-65 the British Tuberculosis Associationy reviewed 544 patients with healed pulmonary tuberculosis who had residual cavitites of 2.5 cm or more in diameter. The patients were then examined after a further 3-4 years.In the first survey 11 % had a definite aspergilloma and a further 4% a probable aspergilloma. On follow-up the percentages were 17% and 3%. The diagnosis is made by X-ray and confirmed by tests for precipitating antibodies to A. fiimigatus in the serum. Precipitins were positive in 72/75 of the B.T.T.A. patients with aspergilloma and 43 of them had 5 or more precipitin lines on gel diffusion plates.’ Bronchopulmonary aspergillosis (asthma and pulmonary eosinophilia) is also characterised by positive precipitins but 1-3 lines is usual. A few patients are precipitin-negative to A. fumigatus but precipitin-positive to A. niger,Y-u nidulans,Y and flavus.IJ-1l An occasional patient with obvious aspergilloma has no demonstrable precipitins, even when tested with multiple Aspergillus antigens.1 ConAsPERGlLLOMAs
are
versely, some have positive precipitins but
no
aspergillo-
ma-10% in the first B.T.T.A. survey.9 These patients were
twice
as
likely
to
acquire
an
aspergilloma
in the
Rodriguez-Lemoine, V., Datta, N. J. gen. Microbiol. 1975, 86, 88. 24. Wilfert, J. N., Barrett, F. F., Ewing, W. H., Finland, M., Kass, E. H. Appl. Microbiol, 1970,19, 345. 25 Traub, W. H., Raymond, E. A. ibid. 1971, 22, 1058. 1 British Thoracic and Tuberculosis Association, Tubercle, 1970, 51, 227. 2. Israel, H. L., Ostrow, A. Am. J. Med. 1969, 47, 243. 3 Solit, R. W., McKeown, J. J., Smullens, S., Fraimow, W. J. thorac. cardio-
23. Hedges, R. W.,
vasc. Surg. 1971, 62, 411. 4. Aslam, P. A., Eastndge, C. E., Hughes, F. A. Chest, 1971, 59, 28. 5. Mays, E. E., Hawkins, J. A. Am. Rev. resp. Dis. 1967, 95, 1056. 6. Villar, T. G., Pimental, J. C., Costa, M. F. E. Thorax, 1962, 17, 22. 7. Campbell, M. J., Clayton, Y. M. Am Rev. resp. Dis. 1964, 89, 186. 8. Varkey, B., Rose, H. D. Am. J. Med. 1976, 61, 626. 9. British Tuberculosis Association, Tubercle, 1968, 49, 1. 10. Finegold, S. M., Will, D., Murray, J. F. Am. J. Med. 1959, 27, 463. 11 Naji, A.F. Archs Path. 1959, 68, 282.
those without precipitins, though their precipitins between the surlost nearly quarter Records of chronic veys. cough, haemoptysis, wheeze, deterioration in health, hospital admisssion, and death were compared in those with and without aspergilloma in the initial survey. Patients with aspergilloma were more likely to have haemoptysis and chronic cough, but were otherwise unexceptional. The death-rate was 18% in both groups -about three times that expected. 4% of the aspergilloma patients died of haemoptysis and a further 5% required resection because of haemoptysis. Other groups3 12 report life-threatening haemoptysis in about 20%. In about 10% of patients the aspergilloma next
3-4 years
as
a
disappears spontaneously.’ 8 13 Surgery has been advocated, particularly in the U.S.A., for all patients who are a reasonable operative risk.3 4 12 14 Postoperatively, precipitins usually fall, but some precipitating antibody often remains, suggesting, residual aspergilli. The overall mortality of operation is 7%.14 Some patients need further surgery for postoperative troubles and end up with pneumonectomy.3 4 12 14 In patients who have underlying lung disease this is likely to subtract considerably from their exercise tolerance and their quality of life. Varkey and Rose8 question the need for routine surgical treatment. In non-randomly selected patients operation had no long-term advantage over no operation. Massive hxmoptysis clearly does call for treatment, and most surgeons would opt for lobectomy in a patient who is a reasonable operative risk. In patients with poor lung function medical treatment has been tried. Intravenous amphotericin has not generally proved helpful,8 though one group claimed some success in an uncontrolled survery There are occasional reports of success when amphotericin and sodium iodide are given via an endobronchial catheter.4 16 Some patients are systemically ill with fever, weight-loss, and malaise.’? This is probably caused by a type-III allergic reaction within the lung.’" Two such patients treated with prednisone were substantially improved although their aspergillomas remained.1Y Two further patients with systemic symptoms had immediate prick-test reactions to A. fiimigatus and possessed IgE and IgG cytophilic antibody, like patients with bronchopulmonary aspergillosis. These antibodies were absent in two patients with aspergilloma without systemic symptoms.20 Villar et al. have studied resected specimens and suggest that there is an initial stage when the fungus is alive, but that the fungus then dies and may degenerate. Antifungal treatment at this stage is unlikely to help. Haemoptysis is more common in longstanding aspergilloma,’ when dead aspergilli and calcification are likely to be present. The treatment of uncomplicated aspergilloma, is still uncertain: a trial of operation against no treatment, in randomly selected patients, would supply the answer. Karas, A., Hankins, J. R., Attar, S., Miller, J. E., McLaughlin, J. S. Ann. thorac. Surg. 1976, 22, 1. 13. Hammerman, K. J., Christianson, C. S., Huntingdon, I., Hurst, G. A., Zelman, M., Tosh, F. E. Chest, 1973, 64, 697. 14. Kilman, J. W., Changwoo, A., Andrews, N. C., Klassen, K. J. thorac. cardiovasc. Surg. 1969, 57, 642. 15. Reddy, P. A., Christianson, C. S., Brasher, C. A., Larsh, H., Sutaria, M. Am. Rev. resp. Dis. 1970, 101, 928. 16. Rairez, R. J. New Engl. J. Med. 1964, 271, 1281 17. Hilvering, C., Stevens, E. A. M., One, N. G. M. Thorax, 1970, 25, 19. 18. Stevens, E. A. M., Hilvering, C., One, N. G. M. ibid. p. 11. 19. Davies, D., Somner, A. R. ibid. 1972, 27, 156. 20. Assem, E. S. K., Turner-Warwick, M. Clin. exp. Immun. 1976, 26, 67.
12.
by serotyping24 and bacteriocin susceptibility typing.25 Antibiograms may also be helpful in epidemiological work. S. marcescens contributes substantially to morbidity and mortality in hospital practice.2-4 Proper management will depend on isolation of the organism, identification, and antibiotic-sensitivity testing. Extra time spent on this will be rewarded.
ASPERGILLOMA cavities in the lung colonised by Aspergillus species, usually A. fumigatus. The fungus grows on the wall of the cavity, tending to peel off to form a fungus ball, and the typical X-ray shows a cavity with irregular central density and surrounding halo.’1 Aspergillomas nearly always arise in diseased lung; residual tuberculous cavities are a common site,’ and other underlying conditions include sarcoidosis, lung abscess, pulmonary infarction, lung cyst, pneumoconiosis, histoplasmosis, carcinoma of the lung, and the apical fibrosis seen in ankylosing spondylitis.l-s Whether aspergilloma can arise in a normal lung is uncertain. The great majority of aspergillomas are in the upper lobes; they may be multiple and bilateral. In 1964-65 the British Tuberculosis Associationy reviewed 544 patients with healed pulmonary tuberculosis who had residual cavitites of 2.5 cm or more in diameter. The patients were then examined after a further 3-4 years.In the first survey 11 % had a definite aspergilloma and a further 4% a probable aspergilloma. On follow-up the percentages were 17% and 3%. The diagnosis is made by X-ray and confirmed by tests for precipitating antibodies to A. fiimigatus in the serum. Precipitins were positive in 72/75 of the B.T.T.A. patients with aspergilloma and 43 of them had 5 or more precipitin lines on gel diffusion plates.’ Bronchopulmonary aspergillosis (asthma and pulmonary eosinophilia) is also characterised by positive precipitins but 1-3 lines is usual. A few patients are precipitin-negative to A. fumigatus but precipitin-positive to A. niger,Y-u nidulans,Y and flavus.IJ-1l An occasional patient with obvious aspergilloma has no demonstrable precipitins, even when tested with multiple Aspergillus antigens.1 ConAsPERGlLLOMAs
are
versely, some have positive precipitins but
no
aspergillo-
ma-10% in the first B.T.T.A. survey.9 These patients were
twice
as
likely
to
acquire
an
aspergilloma
in the
Rodriguez-Lemoine, V., Datta, N. J. gen. Microbiol. 1975, 86, 88. 24. Wilfert, J. N., Barrett, F. F., Ewing, W. H., Finland, M., Kass, E. H. Appl. Microbiol, 1970,19, 345. 25 Traub, W. H., Raymond, E. A. ibid. 1971, 22, 1058. 1 British Thoracic and Tuberculosis Association, Tubercle, 1970, 51, 227. 2. Israel, H. L., Ostrow, A. Am. J. Med. 1969, 47, 243. 3 Solit, R. W., McKeown, J. J., Smullens, S., Fraimow, W. J. thorac. cardio-
23. Hedges, R. W.,
vasc. Surg. 1971, 62, 411. 4. Aslam, P. A., Eastndge, C. E., Hughes, F. A. Chest, 1971, 59, 28. 5. Mays, E. E., Hawkins, J. A. Am. Rev. resp. Dis. 1967, 95, 1056. 6. Villar, T. G., Pimental, J. C., Costa, M. F. E. Thorax, 1962, 17, 22. 7. Campbell, M. J., Clayton, Y. M. Am Rev. resp. Dis. 1964, 89, 186. 8. Varkey, B., Rose, H. D. Am. J. Med. 1976, 61, 626. 9. British Tuberculosis Association, Tubercle, 1968, 49, 1. 10. Finegold, S. M., Will, D., Murray, J. F. Am. J. Med. 1959, 27, 463. 11 Naji, A.F. Archs Path. 1959, 68, 282.
those without precipitins, though their precipitins between the surlost nearly quarter Records of chronic veys. cough, haemoptysis, wheeze, deterioration in health, hospital admisssion, and death were compared in those with and without aspergilloma in the initial survey. Patients with aspergilloma were more likely to have haemoptysis and chronic cough, but were otherwise unexceptional. The death-rate was 18% in both groups -about three times that expected. 4% of the aspergilloma patients died of haemoptysis and a further 5% required resection because of haemoptysis. Other groups3 12 report life-threatening haemoptysis in about 20%. In about 10% of patients the aspergilloma next
3-4 years
as
a
disappears spontaneously.’ 8 13 Surgery has been advocated, particularly in the U.S.A., for all patients who are a reasonable operative risk.3 4 12 14 Postoperatively, precipitins usually fall, but some precipitating antibody often remains, suggesting, residual aspergilli. The overall mortality of operation is 7%.14 Some patients need further surgery for postoperative troubles and end up with pneumonectomy.3 4 12 14 In patients who have underlying lung disease this is likely to subtract considerably from their exercise tolerance and their quality of life. Varkey and Rose8 question the need for routine surgical treatment. In non-randomly selected patients operation had no long-term advantage over no operation. Massive hxmoptysis clearly does call for treatment, and most surgeons would opt for lobectomy in a patient who is a reasonable operative risk. In patients with poor lung function medical treatment has been tried. Intravenous amphotericin has not generally proved helpful,8 though one group claimed some success in an uncontrolled survery There are occasional reports of success when amphotericin and sodium iodide are given via an endobronchial catheter.4 16 Some patients are systemically ill with fever, weight-loss, and malaise.’? This is probably caused by a type-III allergic reaction within the lung.’" Two such patients treated with prednisone were substantially improved although their aspergillomas remained.1Y Two further patients with systemic symptoms had immediate prick-test reactions to A. fiimigatus and possessed IgE and IgG cytophilic antibody, like patients with bronchopulmonary aspergillosis. These antibodies were absent in two patients with aspergilloma without systemic symptoms.20 Villar et al. have studied resected specimens and suggest that there is an initial stage when the fungus is alive, but that the fungus then dies and may degenerate. Antifungal treatment at this stage is unlikely to help. Haemoptysis is more common in longstanding aspergilloma,’ when dead aspergilli and calcification are likely to be present. The treatment of uncomplicated aspergilloma, is still uncertain: a trial of operation against no treatment, in randomly selected patients, would supply the answer. Karas, A., Hankins, J. R., Attar, S., Miller, J. E., McLaughlin, J. S. Ann. thorac. Surg. 1976, 22, 1. 13. Hammerman, K. J., Christianson, C. S., Huntingdon, I., Hurst, G. A., Zelman, M., Tosh, F. E. Chest, 1973, 64, 697. 14. Kilman, J. W., Changwoo, A., Andrews, N. C., Klassen, K. J. thorac. cardiovasc. Surg. 1969, 57, 642. 15. Reddy, P. A., Christianson, C. S., Brasher, C. A., Larsh, H., Sutaria, M. Am. Rev. resp. Dis. 1970, 101, 928. 16. Rairez, R. J. New Engl. J. Med. 1964, 271, 1281 17. Hilvering, C., Stevens, E. A. M., One, N. G. M. Thorax, 1970, 25, 19. 18. Stevens, E. A. M., Hilvering, C., One, N. G. M. ibid. p. 11. 19. Davies, D., Somner, A. R. ibid. 1972, 27, 156. 20. Assem, E. S. K., Turner-Warwick, M. Clin. exp. Immun. 1976, 26, 67.
12.
