1101
vasculitis. A firmer diagnosis of KS can be established when the patient also has other clinical and/or laboratory criteria of KS not seen in group A streptococcal infection. This work was supported by NIH Biomedical Research Support Grant 2 S07 RR 05655-20 from Children’s Hospital and Medical Center.
Department of Pediatrics, University of Washington, and Divisions of Rheumatology, Infectious Diseases, and Cardiology, Children’s Hospital and Medical Center, Seattle, WA 98105, USA
LISA G. RIDER PAUL M. MENDELMAN JAMES FRENCH DAVID D. SHERRY
significance is very different. Misdiagnosis may also be a common and serious problem in certain cases of bacterial meningitis.’ The commercial availability of alternative serological tests may eventually solve many of these difficulties but most tests have been evaluated on sera from respiratory cases only. Results on patients with extrapuhnonary symptoms should be interpreted cautiously until further specificity studies have been done. Public Health Laboratory, Norwich NR2 3TX, UK
MARGARET SILLIS
Foy H, Grayston J, Kenny G, Alexander E, McMahan R. Epidemiology of Mycoplasma pneumoniae infection in families. JAMA 1966; 197: 859-66. 2. Biberfeld G. A study of Mycoplasma pneumoniae infections in families. Scand J Infect Dis 1969; 1: 39-46. 3. Sillis M. The limitations of IgM assays in the serological diagnosis of Mycoplasma pneumoniae infections. J Med Microbiol 1990; 33: 253-58. 4. Ali N, Sillis M, Andrews B, Jenkins P, Harrison B. The clinical spectrum and diagnosis of Mycoplasma pneumoniae infection. Q J Med 1986; 227: 241-51. 5. Grady G, Gilfillan R. Relation of Mycoplasma pneumoniae seroactivity immunosuppression and chronic disease to legionnaires disease. Ann Intern Med 1979; 90: 607-10. 6. Barton K, Nicholls D, Stanford C, Connolly J, Wilson T. Which atypical pneumonia? J Infect 1989; 19: 294-96. 7. Kleemola M, Kayhty H. Increase in titres of antibodies to M pneumoniae in patients with purulent meningitis. J Infect Dis 1982; 146: 284-88. 1.
1. Melish ME, Hicks RV. Kawasaki syndrome: clinical features, pathophysiology, etiology and therapy. J Rheumatol 1990; 17 (suppl 24): 2-10. 2. Hokonohara M, Yoshinaga M, Baba Y. Study of antibody response to 4 streptococcal antigens in rheumatic fever and Kawasaki disease with or without cardiovascular
lesions. Jpn Circ J 1957; 51: 1353-56 3. Fnter BS, Lucky AW. The perineal eruption of Kawasaki syndrome. Arch Dermatol 1988; 124: 1805-10. 4. Burns JC, Newburger JW. Clinical and laboratory characteristics of patients referred for evaluation of possible Kawasaki disease (October, 1991, 30th ICAAC, American Society for Microbiology, Atlanta, GA) p 87, abstract 3. 5. Reller M, DeCristofaro J, Schwartz DC. Coronary aneurysms in a patient with atypical Kawasaki syndrome and a streptococcal infection. Pediatr Cardiol 1984; 5: 205-08. 6. Levy M, Koren G. Atypical Kawasaki disease analysis of clinical presentation and diagnostic clues. Pediatr Infect Dis J 1990; 9: 122-26.
Community-acquired pneumonia
Mycoplasma pneumoniae SIR,—I read with interest
your March
16 editorial
SIR,-Your editorial (March 16,
on
Mycoplasma pneumoniae, highlighting the current epidemic. Factors that govern M pneumoniae epidemic cycles are not well known although communicability and transmission of infection and host immunity have been widely studied. Case-to-case transmission is estimated at 20 days,l and attack rates in close communities range from 17% to 66%,1,2 lower in adults. Susceptible individuals without demonstrable specific antibody are reported to escape infection, even when in contact within confirmed family outbreaks.2 Reinfections do occur but the evidence you cite3is tentative and 14 patients were over 45 years of age. The statement that "reinfection accounts for most cases in patients over 45 years" is surprising since an unpublished investigation into the immunity of the symptomless population in the LTK over a five-year period has indicated that 43-83% of those aged 25-40 remain susceptible to M pneumoniae infection. That "25% of infections are symptomless" is not supported by the reference given or by the findings of others.2Truly asymptomatic infection is uncommon (15-4% of cases). About 90% of patients have a history of cough. Some extrapulmonary symptoms (eg, neurological manifestations and haemolytic anaemia) can be serious. In one study4 haemolytic anaemia was the most common extrapulmonary feature, and it dominated the clinical picture in one patient whose haemoglobin fell to 3-6 g/dl. Respiratory symptoms had occurred 3 weeks earlier. Another patient (Hb 6-9 g/dl) died. Haemolytic anaemia was a feature in several post-mortem cases referred to the Mycoplasma Reference Laboratory between 1976 and 1982. Although it is unlikely that anaemia causes death, it may, in association with hypoxia, contribute substantially to morbidity. Close liaison between the haematologist and microbiologist should be encouraged during M pneumoniae epidemics. 8% of our confirmed cases were detected initially by observation of cold agglutinins on blood films by haematology and by follow-up in the microbiology
only 4 of the
department. Neurological manifestations, including meningitis, encephalitis, and Guillain-Barré syndrome, accompany 4-7% of M pneumoniae infections. There is usually a history of respiratory symptoms preceding the neurological episode by 2-3 weeks. Neurological damage is thought to be mediated by autoantibodies, and plasmapheresis may be helpful. Serology remains the main diagnostic tool, and specific IgM is detectable in 86% of patients at admission.4 The complement fixation test may lead to misdiagnosis because of non-specificity. There is
a
risk, albeit
uncommon, of cross-reactions between
Legianella, Mycoplasma,
and
Chlamydia
Spp:5,6 although
management will be the same in all three infections the public health
p 651) recommends either alone in or erythromycin combination with a penicilllin for initial therapy of community-acquired pneumonia in view of the expected increase in frequency of mycoplasma infection in the next twelve months. In the British Thoracic Society/Public Health Laboratory Service study, 27% of all deaths were due to pneumococcal infection compared with 15% that were due to mycoplasma infection.’ Other surveys of community-acquired pneumonia have shown that Streptococcus pneumoniae accounted for 11-36% of all cases,z,3 A study of 325 patients with pneumococcal bacteraemia showed an overall mortality of 28%, although this figure fell to 11 % if the patient had received 24 h antibiotic therapy.4 Mortality approached 50% in the elderly and those with predisposing conditions such as cirrhosis. Although it is right to focus attention on the expected increase in mycoplasma infections, physicians should remember that pneumococci are the most common cause of both infection and death in patients with
community-acquired pneumonia. Penicillin remains the best choice of therapy for pneumococcal infection, although other measures have been suggested.5 One way of reducing mortality associated with pneumococcal infection might be to suggest that general practitioners should treat patients who may have pneumonia empirically with penicillin. This approach may reduce the laboratory yield of pneumococci but could help reduce the high early mortality from pneumococcal infection. Erythromycin-resistant pneumococcaemia has been described,6 and in Belgium 6% of pneumococci were resistant to erythromycin.7 Erythromycin should not be given as the only treatment for community-acquired pneumonia in case pneumococcal infection is inadequately treated. Sandwell District General Hospital, West Bromwich, West Midlands B71 4HJ, UK
A. J. DAVIES A. JOLLEY
Society Research Committee and Public Health Laboratory Service. Community-acquired pneumonia in adults in British hospitals in 1982-83: a survey of aetiology, mortality, prognostic factors and outcome. Q J Med 1987, 62: 195-220. 2. Woodhead MA, Macfarlane JT, McCracken JS, Rose DS, Finch RG. Prospective outcome of the aetiology and outcome of pneumonia in the community. Lancet 1. British Thoracic
1987; i: 671-74. 3. White DJ, Blainey AD, Harrison KJ, Clarke SKR. Cause of pneumonia presenting to a district general hospital. Thorax 1981; 36: 566-70. 4. Gransden WR, Eykyn SJ, Phillips I. Pneumococcal bacteraemia: 325 cases diagnosed at St Thomas’s Hospital. Br Med J 1985; 290: 505-08. 5. Davies AJ, Kumaratne DS. The continuing problem of pneumococcal infection. J Antimicrob Chemother 1988; 21: 387-91. 6. Eykyn SJ. Pneumococcaemia caused by erythromycin-resistant Streptococcus pneumoniae type 14. Lancet 1988; ii: 1086. 7. Verhaegen J, Gaubau P, Verbist L, Glupcznski J, Blogie M, Yourassowsky E. Erythromycin-resistant Streptococcus pneumoniae. Lancet 1988; ii: 1432-33.
vasculitis. A firmer diagnosis of KS can be established when the patient also has other clinical and/or laboratory criteria of KS not seen in group A streptococcal infection. This work was supported by NIH Biomedical Research Support Grant 2 S07 RR 05655-20 from Children’s Hospital and Medical Center.
Department of Pediatrics, University of Washington, and Divisions of Rheumatology, Infectious Diseases, and Cardiology, Children’s Hospital and Medical Center, Seattle, WA 98105, USA
LISA G. RIDER PAUL M. MENDELMAN JAMES FRENCH DAVID D. SHERRY
significance is very different. Misdiagnosis may also be a common and serious problem in certain cases of bacterial meningitis.’ The commercial availability of alternative serological tests may eventually solve many of these difficulties but most tests have been evaluated on sera from respiratory cases only. Results on patients with extrapuhnonary symptoms should be interpreted cautiously until further specificity studies have been done. Public Health Laboratory, Norwich NR2 3TX, UK
MARGARET SILLIS
Foy H, Grayston J, Kenny G, Alexander E, McMahan R. Epidemiology of Mycoplasma pneumoniae infection in families. JAMA 1966; 197: 859-66. 2. Biberfeld G. A study of Mycoplasma pneumoniae infections in families. Scand J Infect Dis 1969; 1: 39-46. 3. Sillis M. The limitations of IgM assays in the serological diagnosis of Mycoplasma pneumoniae infections. J Med Microbiol 1990; 33: 253-58. 4. Ali N, Sillis M, Andrews B, Jenkins P, Harrison B. The clinical spectrum and diagnosis of Mycoplasma pneumoniae infection. Q J Med 1986; 227: 241-51. 5. Grady G, Gilfillan R. Relation of Mycoplasma pneumoniae seroactivity immunosuppression and chronic disease to legionnaires disease. Ann Intern Med 1979; 90: 607-10. 6. Barton K, Nicholls D, Stanford C, Connolly J, Wilson T. Which atypical pneumonia? J Infect 1989; 19: 294-96. 7. Kleemola M, Kayhty H. Increase in titres of antibodies to M pneumoniae in patients with purulent meningitis. J Infect Dis 1982; 146: 284-88. 1.
1. Melish ME, Hicks RV. Kawasaki syndrome: clinical features, pathophysiology, etiology and therapy. J Rheumatol 1990; 17 (suppl 24): 2-10. 2. Hokonohara M, Yoshinaga M, Baba Y. Study of antibody response to 4 streptococcal antigens in rheumatic fever and Kawasaki disease with or without cardiovascular
lesions. Jpn Circ J 1957; 51: 1353-56 3. Fnter BS, Lucky AW. The perineal eruption of Kawasaki syndrome. Arch Dermatol 1988; 124: 1805-10. 4. Burns JC, Newburger JW. Clinical and laboratory characteristics of patients referred for evaluation of possible Kawasaki disease (October, 1991, 30th ICAAC, American Society for Microbiology, Atlanta, GA) p 87, abstract 3. 5. Reller M, DeCristofaro J, Schwartz DC. Coronary aneurysms in a patient with atypical Kawasaki syndrome and a streptococcal infection. Pediatr Cardiol 1984; 5: 205-08. 6. Levy M, Koren G. Atypical Kawasaki disease analysis of clinical presentation and diagnostic clues. Pediatr Infect Dis J 1990; 9: 122-26.
Community-acquired pneumonia
Mycoplasma pneumoniae SIR,—I read with interest
your March
16 editorial
SIR,-Your editorial (March 16,
on
Mycoplasma pneumoniae, highlighting the current epidemic. Factors that govern M pneumoniae epidemic cycles are not well known although communicability and transmission of infection and host immunity have been widely studied. Case-to-case transmission is estimated at 20 days,l and attack rates in close communities range from 17% to 66%,1,2 lower in adults. Susceptible individuals without demonstrable specific antibody are reported to escape infection, even when in contact within confirmed family outbreaks.2 Reinfections do occur but the evidence you cite3is tentative and 14 patients were over 45 years of age. The statement that "reinfection accounts for most cases in patients over 45 years" is surprising since an unpublished investigation into the immunity of the symptomless population in the LTK over a five-year period has indicated that 43-83% of those aged 25-40 remain susceptible to M pneumoniae infection. That "25% of infections are symptomless" is not supported by the reference given or by the findings of others.2Truly asymptomatic infection is uncommon (15-4% of cases). About 90% of patients have a history of cough. Some extrapulmonary symptoms (eg, neurological manifestations and haemolytic anaemia) can be serious. In one study4 haemolytic anaemia was the most common extrapulmonary feature, and it dominated the clinical picture in one patient whose haemoglobin fell to 3-6 g/dl. Respiratory symptoms had occurred 3 weeks earlier. Another patient (Hb 6-9 g/dl) died. Haemolytic anaemia was a feature in several post-mortem cases referred to the Mycoplasma Reference Laboratory between 1976 and 1982. Although it is unlikely that anaemia causes death, it may, in association with hypoxia, contribute substantially to morbidity. Close liaison between the haematologist and microbiologist should be encouraged during M pneumoniae epidemics. 8% of our confirmed cases were detected initially by observation of cold agglutinins on blood films by haematology and by follow-up in the microbiology
only 4 of the
department. Neurological manifestations, including meningitis, encephalitis, and Guillain-Barré syndrome, accompany 4-7% of M pneumoniae infections. There is usually a history of respiratory symptoms preceding the neurological episode by 2-3 weeks. Neurological damage is thought to be mediated by autoantibodies, and plasmapheresis may be helpful. Serology remains the main diagnostic tool, and specific IgM is detectable in 86% of patients at admission.4 The complement fixation test may lead to misdiagnosis because of non-specificity. There is
a
risk, albeit
uncommon, of cross-reactions between
Legianella, Mycoplasma,
and
Chlamydia
Spp:5,6 although
management will be the same in all three infections the public health
p 651) recommends either alone in or erythromycin combination with a penicilllin for initial therapy of community-acquired pneumonia in view of the expected increase in frequency of mycoplasma infection in the next twelve months. In the British Thoracic Society/Public Health Laboratory Service study, 27% of all deaths were due to pneumococcal infection compared with 15% that were due to mycoplasma infection.’ Other surveys of community-acquired pneumonia have shown that Streptococcus pneumoniae accounted for 11-36% of all cases,z,3 A study of 325 patients with pneumococcal bacteraemia showed an overall mortality of 28%, although this figure fell to 11 % if the patient had received 24 h antibiotic therapy.4 Mortality approached 50% in the elderly and those with predisposing conditions such as cirrhosis. Although it is right to focus attention on the expected increase in mycoplasma infections, physicians should remember that pneumococci are the most common cause of both infection and death in patients with
community-acquired pneumonia. Penicillin remains the best choice of therapy for pneumococcal infection, although other measures have been suggested.5 One way of reducing mortality associated with pneumococcal infection might be to suggest that general practitioners should treat patients who may have pneumonia empirically with penicillin. This approach may reduce the laboratory yield of pneumococci but could help reduce the high early mortality from pneumococcal infection. Erythromycin-resistant pneumococcaemia has been described,6 and in Belgium 6% of pneumococci were resistant to erythromycin.7 Erythromycin should not be given as the only treatment for community-acquired pneumonia in case pneumococcal infection is inadequately treated. Sandwell District General Hospital, West Bromwich, West Midlands B71 4HJ, UK
A. J. DAVIES A. JOLLEY
Society Research Committee and Public Health Laboratory Service. Community-acquired pneumonia in adults in British hospitals in 1982-83: a survey of aetiology, mortality, prognostic factors and outcome. Q J Med 1987, 62: 195-220. 2. Woodhead MA, Macfarlane JT, McCracken JS, Rose DS, Finch RG. Prospective outcome of the aetiology and outcome of pneumonia in the community. Lancet 1. British Thoracic
1987; i: 671-74. 3. White DJ, Blainey AD, Harrison KJ, Clarke SKR. Cause of pneumonia presenting to a district general hospital. Thorax 1981; 36: 566-70. 4. Gransden WR, Eykyn SJ, Phillips I. Pneumococcal bacteraemia: 325 cases diagnosed at St Thomas’s Hospital. Br Med J 1985; 290: 505-08. 5. Davies AJ, Kumaratne DS. The continuing problem of pneumococcal infection. J Antimicrob Chemother 1988; 21: 387-91. 6. Eykyn SJ. Pneumococcaemia caused by erythromycin-resistant Streptococcus pneumoniae type 14. Lancet 1988; ii: 1086. 7. Verhaegen J, Gaubau P, Verbist L, Glupcznski J, Blogie M, Yourassowsky E. Erythromycin-resistant Streptococcus pneumoniae. Lancet 1988; ii: 1432-33.
