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Benign meningococcaemia: a rash diagnosis?
610
viruses, and organisms. This study confirms the role of B hominis as an intestinal pathogen and suggests the possibility of transmission,
probably via the faecal-oral route, in
closed communities such
as
this. Department of Infectious Diseases, St Anna Hospital, Ferrara, Italy; and Department of Infectious Diseases, General Hospital, Alessandria
MARCO LIBANORE MARIA RITA ROSSI LORENZO SCAGLIONE PIETRO LUIGI GARAVELLI
1. Sheehan
DJ, Raucher BG, McKitrick JC. Association of Blastocystis hominis with signs and symptoms of human disease. J Clin Microbiol 1986, 24: 548-50. 2. Guglielmetti P, Cellesi C, Figura N, Rossolini A. Family outbreak of Blastocystis hominis associated gastroenteritis. Lancet 1989; ii: 1394.
Benign meningococcaemia: diagnosis?
a
rash
SIR,-Dr Riordan and his colleagues’ patient (Dec 8, p 1456) may be unusual for the extent of the rash that they describe, but the presentation of meningococcal infection with a macular or maculopapular rash is well described in standard textbooks of infectious disease,l,2 as is the resolution of infection before bacteriological examination reveals the diagnosis. One book1 includes a photograph of this type of rash. It may well be that the child would have relapsed if not treated, as was noted in an earlier description of five cases of benign meningococcaemia3 (a somewhat different disease presentation from that described by Riordan et al), two of whom relapsed after discharge from hospital without antibiotic therapy. Some patients with meningococcaemia have a mild illness as evidenced by the occasional case of meningococcal arthritis that may resolve without antibiotic therapy, possibly because some have reactive arthritis rather than metastatic sepsis. It may be that the condition is not reported in the UK as often as in the US, as seems to be the case with occult pneumococcaemia.4 Finally, the isolation of a meningococcus from the throat two months after prophylaxis for eradication of the organism should not occasion surprise since not only may prophylaxis fail but also once the nasopharynx has been cleared of meningococci (as far as laboratory tests can show) there is no reason why recolonisation should not take place. Were the meningococci isolated by Riordan et al on the second occasion the same (in genotype as well as phenotype) as those isolated during the infant’s original infection? Meningococcus Reference Laboratory (Scotland), Ruchill Hospital, Glasgow G20 9NB, UK
R. J. FALLON
Apicella MA. Neisseria meningitidis. In: Mandell GL, Douglas RG, Bennet JE, eds. Principles and practice of infectious diseases, 2nd edn. Chichester: John Wiley & Sons, 1985. 2. Hoffman TA. Meningococcemia. In: Braude IA, ed. Medical microbiology and 1.
infectious diseases. London: Saunders, 1981. 3. Olcén P, Eeg-Olofsson O, Frydén A, Kernall A, Ånséhn S. Benign meningococcemia in childhood. Scand J Infect Dis 1978; 10: 107-11. 4. Phillips I, Eykyn SJ. Bacteraemia, septicaemia and arthritis. In: Parker MT, Collier LH, eds. Topley and Wilson’s principles of bacteriology, virology and immunity, 8th edn, vol 3. London: Edward Arnold, 1990.
*** This letter has been shown to Dr Riordan and colleagues, whose reply follows.-ED. L. SIR,-Dr Fallon’s comments on our case report support the fact that meningococcal disease can present with a maculopapular rash. Despite such a rash being well described in standard texts of infectious disease, it is rarely mentioned in most short paediatric textbooks for junior hospital doctors and general practitioners. This presentation has been highlighted,l and, until knowledge of this presentation is well known, deserves re-emphasiseResolution of meningococcaemia, without treatment and before bacteriological examination has revealed the diagnosis, has, as we indicated, been reported. However, it was the combination of meningococcaemia and maculopapular rash arising in one patient that we felt was noteworthy. It has been suggested that meningococcal disease presenting with maculopapular rash has a good prognosis. Although the outcome in our case was favourable this is not invariably so. In a prospective
study of 69 children admitted with meningococcal disease in Mersey region between Novermber, 1988, and November, 1989, the mortality rate for children with a maculopapular rash did not differ from that in children who presented initially with haemorrhagic rashes.’ In the 12 who were not initially treated because the diagnosis of meningococcal disease was not considered there was only one death-a child who had presented with a maculopapular rash that became haemorrhagic eight hours later. Doctors who have first contact with meningococcal disease should have "knowledge out of proportion to their previous experience".2 Only by drawing their attention to the variability of the rash can we hope to make meningococcal disease "a diagnosis be missed" Z Fallon as Finally, points out, the isolation of meningococcus from the throat five months after prophylaxis could result from either failure of prophylaxis or from recolonisation. We do not have the genotype/phenotype of both isolates and therefore cannot answer his question. F. A. I. RIORDAN O. MARZOUK Royal Liverpool Children’s Hospital (Alder Hey), D. C. DAVIDSON Liverpool L12 2AP, UK
not to
1. Carter PE. Meningococcal meningitis. Br Med J 1990; 300: 1584. 2. Welsby PD, Golledge CL. Meningococcal meningitis. Br Med J 1990; 300: 1150-51. 3. Toews WH, Bass JW. Skin manifestations of meningococcal infection. Am J Dis Child
1974; 127: 173-76. O, Thompson APJ, Sills JA, Hart CA, Harris F. Features and outcome in meningococcal disease presenting with maculopapular rash Arch Dis Child (in press).
4. Marzouk
Trial
design
in the thrombolytic age
SiR,—Today’s confusion created by recent thrombolytic trials could have been avoided with proper direction from leaders in cardiology. We still do not know what the best thrombolytic agent is or whether heparin needs to be part of the recombinant tissue plasminogen activator (t-PA) regimen if it is to be better than streptokinase. Better planning might have avoided confusion on these vital issues. In the past five years, large trials of thrombolytic agents seemed the best approach to get statistically significant information, but on the way they became a panacea, paralysing thought processes at a time when clear orchestration was needed. This was illustrated at the American Heart Association meeting in New Orleans, in November, 1989, and at the American College of Cardiology meeting in the same city five months later. GISSI-11 was nearing completion and ISIS-111 was about to get off the ground. In the absence of constructive criticism of the design of ISIS-III, cardiologists in the United States were led to believe that the study was flawless and would give definitive answers. The planning committee for ISIS-III had to answer the concerns of community hospital cardiologists, not their peers in academic institutions. The concerns of community cardiologists focused on the place of alteplase and on the use of subcutaneous heparin 4 hours after the administration of the thrombolytic agent. We wondered whether it was ethical not to give heparin after t-PA but in the absence of informed criticism we were easily persuaded to take part in the study. At the Russek Cardiology Conference (New York, 1989) one leading cardiologist had predicted GISSI-11 would reveal no difference between the two thrombolytic agents, would cause a great deal of confusion, and would be considered flawed because heparin was not given until 12 hours after t-PA. He went on to say that the method of giving heparin in ISIS-111 was acceptable. N0%, however, we are hearing differently from the cardiology conferences-namely, that results of ISIS-111 cannot be believed because the t-PA used was inferior and because subcutaneous heparin cannot be compared with intravenous heparin given at the time of the thrombolytic agent. It seems a shame that our thought processes could not have extracted this information ahead of time so that a better study than ISIS-111 could have been designed. GUSTO is being done. That would have saved a great deal of money and anguish if cardiology leaders had criticised the design of the ISIS-111 long before it recruited 40 000 patients.
viruses, and organisms. This study confirms the role of B hominis as an intestinal pathogen and suggests the possibility of transmission,
probably via the faecal-oral route, in
closed communities such
as
this. Department of Infectious Diseases, St Anna Hospital, Ferrara, Italy; and Department of Infectious Diseases, General Hospital, Alessandria
MARCO LIBANORE MARIA RITA ROSSI LORENZO SCAGLIONE PIETRO LUIGI GARAVELLI
1. Sheehan
DJ, Raucher BG, McKitrick JC. Association of Blastocystis hominis with signs and symptoms of human disease. J Clin Microbiol 1986, 24: 548-50. 2. Guglielmetti P, Cellesi C, Figura N, Rossolini A. Family outbreak of Blastocystis hominis associated gastroenteritis. Lancet 1989; ii: 1394.
Benign meningococcaemia: diagnosis?
a
rash
SIR,-Dr Riordan and his colleagues’ patient (Dec 8, p 1456) may be unusual for the extent of the rash that they describe, but the presentation of meningococcal infection with a macular or maculopapular rash is well described in standard textbooks of infectious disease,l,2 as is the resolution of infection before bacteriological examination reveals the diagnosis. One book1 includes a photograph of this type of rash. It may well be that the child would have relapsed if not treated, as was noted in an earlier description of five cases of benign meningococcaemia3 (a somewhat different disease presentation from that described by Riordan et al), two of whom relapsed after discharge from hospital without antibiotic therapy. Some patients with meningococcaemia have a mild illness as evidenced by the occasional case of meningococcal arthritis that may resolve without antibiotic therapy, possibly because some have reactive arthritis rather than metastatic sepsis. It may be that the condition is not reported in the UK as often as in the US, as seems to be the case with occult pneumococcaemia.4 Finally, the isolation of a meningococcus from the throat two months after prophylaxis for eradication of the organism should not occasion surprise since not only may prophylaxis fail but also once the nasopharynx has been cleared of meningococci (as far as laboratory tests can show) there is no reason why recolonisation should not take place. Were the meningococci isolated by Riordan et al on the second occasion the same (in genotype as well as phenotype) as those isolated during the infant’s original infection? Meningococcus Reference Laboratory (Scotland), Ruchill Hospital, Glasgow G20 9NB, UK
R. J. FALLON
Apicella MA. Neisseria meningitidis. In: Mandell GL, Douglas RG, Bennet JE, eds. Principles and practice of infectious diseases, 2nd edn. Chichester: John Wiley & Sons, 1985. 2. Hoffman TA. Meningococcemia. In: Braude IA, ed. Medical microbiology and 1.
infectious diseases. London: Saunders, 1981. 3. Olcén P, Eeg-Olofsson O, Frydén A, Kernall A, Ånséhn S. Benign meningococcemia in childhood. Scand J Infect Dis 1978; 10: 107-11. 4. Phillips I, Eykyn SJ. Bacteraemia, septicaemia and arthritis. In: Parker MT, Collier LH, eds. Topley and Wilson’s principles of bacteriology, virology and immunity, 8th edn, vol 3. London: Edward Arnold, 1990.
*** This letter has been shown to Dr Riordan and colleagues, whose reply follows.-ED. L. SIR,-Dr Fallon’s comments on our case report support the fact that meningococcal disease can present with a maculopapular rash. Despite such a rash being well described in standard texts of infectious disease, it is rarely mentioned in most short paediatric textbooks for junior hospital doctors and general practitioners. This presentation has been highlighted,l and, until knowledge of this presentation is well known, deserves re-emphasiseResolution of meningococcaemia, without treatment and before bacteriological examination has revealed the diagnosis, has, as we indicated, been reported. However, it was the combination of meningococcaemia and maculopapular rash arising in one patient that we felt was noteworthy. It has been suggested that meningococcal disease presenting with maculopapular rash has a good prognosis. Although the outcome in our case was favourable this is not invariably so. In a prospective
study of 69 children admitted with meningococcal disease in Mersey region between Novermber, 1988, and November, 1989, the mortality rate for children with a maculopapular rash did not differ from that in children who presented initially with haemorrhagic rashes.’ In the 12 who were not initially treated because the diagnosis of meningococcal disease was not considered there was only one death-a child who had presented with a maculopapular rash that became haemorrhagic eight hours later. Doctors who have first contact with meningococcal disease should have "knowledge out of proportion to their previous experience".2 Only by drawing their attention to the variability of the rash can we hope to make meningococcal disease "a diagnosis be missed" Z Fallon as Finally, points out, the isolation of meningococcus from the throat five months after prophylaxis could result from either failure of prophylaxis or from recolonisation. We do not have the genotype/phenotype of both isolates and therefore cannot answer his question. F. A. I. RIORDAN O. MARZOUK Royal Liverpool Children’s Hospital (Alder Hey), D. C. DAVIDSON Liverpool L12 2AP, UK
not to
1. Carter PE. Meningococcal meningitis. Br Med J 1990; 300: 1584. 2. Welsby PD, Golledge CL. Meningococcal meningitis. Br Med J 1990; 300: 1150-51. 3. Toews WH, Bass JW. Skin manifestations of meningococcal infection. Am J Dis Child
1974; 127: 173-76. O, Thompson APJ, Sills JA, Hart CA, Harris F. Features and outcome in meningococcal disease presenting with maculopapular rash Arch Dis Child (in press).
4. Marzouk
Trial
design
in the thrombolytic age
SiR,—Today’s confusion created by recent thrombolytic trials could have been avoided with proper direction from leaders in cardiology. We still do not know what the best thrombolytic agent is or whether heparin needs to be part of the recombinant tissue plasminogen activator (t-PA) regimen if it is to be better than streptokinase. Better planning might have avoided confusion on these vital issues. In the past five years, large trials of thrombolytic agents seemed the best approach to get statistically significant information, but on the way they became a panacea, paralysing thought processes at a time when clear orchestration was needed. This was illustrated at the American Heart Association meeting in New Orleans, in November, 1989, and at the American College of Cardiology meeting in the same city five months later. GISSI-11 was nearing completion and ISIS-111 was about to get off the ground. In the absence of constructive criticism of the design of ISIS-III, cardiologists in the United States were led to believe that the study was flawless and would give definitive answers. The planning committee for ISIS-III had to answer the concerns of community hospital cardiologists, not their peers in academic institutions. The concerns of community cardiologists focused on the place of alteplase and on the use of subcutaneous heparin 4 hours after the administration of the thrombolytic agent. We wondered whether it was ethical not to give heparin after t-PA but in the absence of informed criticism we were easily persuaded to take part in the study. At the Russek Cardiology Conference (New York, 1989) one leading cardiologist had predicted GISSI-11 would reveal no difference between the two thrombolytic agents, would cause a great deal of confusion, and would be considered flawed because heparin was not given until 12 hours after t-PA. He went on to say that the method of giving heparin in ISIS-111 was acceptable. N0%, however, we are hearing differently from the cardiology conferences-namely, that results of ISIS-111 cannot be believed because the t-PA used was inferior and because subcutaneous heparin cannot be compared with intravenous heparin given at the time of the thrombolytic agent. It seems a shame that our thought processes could not have extracted this information ahead of time so that a better study than ISIS-111 could have been designed. GUSTO is being done. That would have saved a great deal of money and anguish if cardiology leaders had criticised the design of the ISIS-111 long before it recruited 40 000 patients.