1411 of
ageing. They
could be the result of
a
decline in the func-
tional state of lymphocytes with advancing age, or they may represent a real fall in either total body T-cell numbers or only in
peripheral
T-cell numbers. The explanation remains
to
be
elucidated. These findings of gradual depression of cellular immune function with advancing age are applicable to all studies in clinical immunology. It is apparent that in such studies it is mandatory either to use age-matched controls or to make adequate correction for age differences which may exist between nntrn1 anrl
tpQt
Ql1h,prtc:6
C. TEASDALE J. THATCHER R. H. WHITEHEAD L. E. HUGHES
University Department of Surgery, Welsh National School of Medicine, Heath Park, Cardiff CF4 4XN
EFFECT OF HYPERTRANSFUSIONS ON THE NEONATE
SiR,—The presence of a pool of multipotential stem cells in the bone-marrow has been postulated and has been demonstrated in animal experiments.’ The report by Dr Smith and Dr Ekert (April 10, p. 776), in which hypertransfused leukaemic children showed a more rapid rise in neutrophil-counts than those with low ha:moglobins, seems to support the presence of pluripotential stem cells in man. We have analysed the effects of hypertransfusions on newborn infants. Unlike the investigation by Dr Smith and Dr Ekert, our neonates were less influenced by the effects of
chemotherapy. Sixteen infants with blood-transfusions and 7 control inwere selected for the study from a total of 122 newborn
fants
HAEMOGLOBIN LEVELS AND LEUCOCYTE-COUNTS BEFORE AND AFTER
TRANSFUSION
*In control group, 5-8
days after the initial determination.
tNo significant difference between
pre and post transfusion
leucocyte-counts
(p>O.30).
infants who were admitted to hospital because of respiratorydistress syndrome from October, 1975, to March, 1976. Those who had clinical and radiological evidence of infections or insufficient hospital days or follow-ups were excluded from the study. Haemoglobins and leucocyte-counts were done before blood-transfusion and 5-8 days after the transfusions. They are divided into three groups: group A, whose haemoglobin was maintained between 14 and 16 g/dl during post-transfusion; group B, whose haemoglobin ranged from 11 to 13 g/dl after blood-transfusion; and the control group who did not receive blood-transfusions but whose haemoglobins ranged from 14 to 16g/dl. As shown in the table, no statistically significant difference in leucocyte-counts among the three groups was found. The increase of leucocyte-count in group A from 10-69x 109/1 to 12.17x 109/1 was also not statistically significant. In this preliminary study, we could not detect significantly different leucocyte responses between the low haemoglobin of neonatal infants and hypertransfused infants. Divisions of Clinical Laboratories and Pediatrics, Lutheran General Hospital, Park Ridge, Illinois 60068, U.S.A., and University of Illinois School of Medicine
TAKASHI OKUNO MEENALOCHANI RENGARAJAN
6. Teasdale, C., Newcombe, R. G., Hughes, L. E. Br. 7. Hellman, S., Grate, H. E. Nature, 1967, 216, 65.
J. Surg. 1976, 63,
149.
DIAGNOSIS AND PROGNOSIS IN PYOGENIC MENINGITIS .&.&fWII’
SIR,-Your excellent editorial (June 12, p. 1277) should stimulate many laboratory workers to review their techniques for the rapid recognition of bacterial meningitis. One additional manoeuvre which may be helpful in establishing the aetiology of pyogenic meningitis in which neither bacterial culture nor antigen demonstration is positive, is to take a pernasal or nasopharyngeal swab from the patient on admission to hospital. This may, as has happened in this hospital, reveal meningococci when other manoeuvres have failed and is especially helpful since meningococci may persist in the nasopharynx despite antibiotic therapy, particularly with penicillin aimed at treating the meningitis. The isolation of meningococci from the nasopharynx can then not only provide useful epidemiological information and details of the sulphonamide sensitivity of the organism, which will be valuable in defining how to eradicate the organisms from the patient’s nasopharynx, but also will guide any epidemiological investigations and family surveillance. Department of Laboratory Medicine, Ruchill
Hospital, Glasgow G20 9NB
R.
J. FALLON
ENTEROPATHOGENIC E. COLI
SIR,-Dr Rowe and his colleagues 1have failed
to demonthe production of enterotoxin by strains of Escherichia coli associated with well-documented outbreaks of infantile diarrhcea. They conclude that serotyping remains the most significant test for the identification of enteropathogenic strains at present. However, it has been clearly demonstrated that the excretion of enteropathogenic serotypes-even in an epidemic situation-is not necessarily associated with diarrhrea3-5 and conversely that serotypes of E. coli not normally regarded as with diarrhoea cases and enteropathogenic can be associated 7 enterotoxin in vitro.6 produce In developing countries such as Jamaica, malnourished infants frequently present with acute or acute on chronic diarrhoea that is not necessarily infectious in origin. These infants are liable to colonisation with enteropathogenic serotypes of E. coli, and several different serotypes may be cultured from the stools during a single hospital admission. However, there is usually no epidemiological or clinical evidence that these organisms actually cause diarrhoea in such cases. For example, of 51 infants with acute gastrointestinal symptoms admitted to this hospital, 26% grew enteropathogenic serotypes of E. coli from their stools, but 20% of 32 control patients also grew enteropathogenic serotypes. Thus, this laboratory frequently reports the isolation of an "enteropathogenic" E. coli which has little bearing on the clinical management of the patient. If the production of enterotoxin by human strains of enteropathogenic E. coli is determined by a plasmid, as it is in some animal strains,8 this confusing situation might be explained by the loss or gain of such a plasmid, especially if it were unusually unstable. Plasmids bearing antibiotic resistance factors may be lost on storage, and a similar situation may apply to plasmids responsible for enterotoxin production. Smith and Halls8 considered the Ent plasmid of porcine enteropathogenic E. coli to be stable. However, Taylor et al." noted that some human enterostrate
1. Rowe, B., Gross, R. J., Scotland, S. M. Lancet, 1975, ii, 925. 2. Gross, R. J., Scotland, S. M., Rowe, B. ibid. 1976, i, 629. 3. Payne, A. M. M., Cook, G. T. Br. med. J. 1950, ii, 192. 4. Taylor, J., Charter, R. E. J. Path. Bact. 1952, 64, 715. 5. McDonald, J. C., Charter, R. E. Proc. R. Soc. Med. 1956, 49, 85. 6. Gorbach, S. L., Khurana, C. M. New Engl. J. Med. 1972, 287, 791. 7. Etkin, S., Gorbach, S. L. J. Lab. clin. Med. 1971, 78, 81. 8. Smith, H. W., Halls, S. J. gen. Microbiol. 1968, 52, 319. 9. Taylor, J., Wilkins, P., Payne, J. M. Br. J. exp. Path. 1961, 42, 43.
ageing. They
could be the result of
a
decline in the func-
tional state of lymphocytes with advancing age, or they may represent a real fall in either total body T-cell numbers or only in
peripheral
T-cell numbers. The explanation remains
to
be
elucidated. These findings of gradual depression of cellular immune function with advancing age are applicable to all studies in clinical immunology. It is apparent that in such studies it is mandatory either to use age-matched controls or to make adequate correction for age differences which may exist between nntrn1 anrl
tpQt
Ql1h,prtc:6
C. TEASDALE J. THATCHER R. H. WHITEHEAD L. E. HUGHES
University Department of Surgery, Welsh National School of Medicine, Heath Park, Cardiff CF4 4XN
EFFECT OF HYPERTRANSFUSIONS ON THE NEONATE
SiR,—The presence of a pool of multipotential stem cells in the bone-marrow has been postulated and has been demonstrated in animal experiments.’ The report by Dr Smith and Dr Ekert (April 10, p. 776), in which hypertransfused leukaemic children showed a more rapid rise in neutrophil-counts than those with low ha:moglobins, seems to support the presence of pluripotential stem cells in man. We have analysed the effects of hypertransfusions on newborn infants. Unlike the investigation by Dr Smith and Dr Ekert, our neonates were less influenced by the effects of
chemotherapy. Sixteen infants with blood-transfusions and 7 control inwere selected for the study from a total of 122 newborn
fants
HAEMOGLOBIN LEVELS AND LEUCOCYTE-COUNTS BEFORE AND AFTER
TRANSFUSION
*In control group, 5-8
days after the initial determination.
tNo significant difference between
pre and post transfusion
leucocyte-counts
(p>O.30).
infants who were admitted to hospital because of respiratorydistress syndrome from October, 1975, to March, 1976. Those who had clinical and radiological evidence of infections or insufficient hospital days or follow-ups were excluded from the study. Haemoglobins and leucocyte-counts were done before blood-transfusion and 5-8 days after the transfusions. They are divided into three groups: group A, whose haemoglobin was maintained between 14 and 16 g/dl during post-transfusion; group B, whose haemoglobin ranged from 11 to 13 g/dl after blood-transfusion; and the control group who did not receive blood-transfusions but whose haemoglobins ranged from 14 to 16g/dl. As shown in the table, no statistically significant difference in leucocyte-counts among the three groups was found. The increase of leucocyte-count in group A from 10-69x 109/1 to 12.17x 109/1 was also not statistically significant. In this preliminary study, we could not detect significantly different leucocyte responses between the low haemoglobin of neonatal infants and hypertransfused infants. Divisions of Clinical Laboratories and Pediatrics, Lutheran General Hospital, Park Ridge, Illinois 60068, U.S.A., and University of Illinois School of Medicine
TAKASHI OKUNO MEENALOCHANI RENGARAJAN
6. Teasdale, C., Newcombe, R. G., Hughes, L. E. Br. 7. Hellman, S., Grate, H. E. Nature, 1967, 216, 65.
J. Surg. 1976, 63,
149.
DIAGNOSIS AND PROGNOSIS IN PYOGENIC MENINGITIS .&.&fWII’
SIR,-Your excellent editorial (June 12, p. 1277) should stimulate many laboratory workers to review their techniques for the rapid recognition of bacterial meningitis. One additional manoeuvre which may be helpful in establishing the aetiology of pyogenic meningitis in which neither bacterial culture nor antigen demonstration is positive, is to take a pernasal or nasopharyngeal swab from the patient on admission to hospital. This may, as has happened in this hospital, reveal meningococci when other manoeuvres have failed and is especially helpful since meningococci may persist in the nasopharynx despite antibiotic therapy, particularly with penicillin aimed at treating the meningitis. The isolation of meningococci from the nasopharynx can then not only provide useful epidemiological information and details of the sulphonamide sensitivity of the organism, which will be valuable in defining how to eradicate the organisms from the patient’s nasopharynx, but also will guide any epidemiological investigations and family surveillance. Department of Laboratory Medicine, Ruchill
Hospital, Glasgow G20 9NB
R.
J. FALLON
ENTEROPATHOGENIC E. COLI
SIR,-Dr Rowe and his colleagues 1have failed
to demonthe production of enterotoxin by strains of Escherichia coli associated with well-documented outbreaks of infantile diarrhcea. They conclude that serotyping remains the most significant test for the identification of enteropathogenic strains at present. However, it has been clearly demonstrated that the excretion of enteropathogenic serotypes-even in an epidemic situation-is not necessarily associated with diarrhrea3-5 and conversely that serotypes of E. coli not normally regarded as with diarrhoea cases and enteropathogenic can be associated 7 enterotoxin in vitro.6 produce In developing countries such as Jamaica, malnourished infants frequently present with acute or acute on chronic diarrhoea that is not necessarily infectious in origin. These infants are liable to colonisation with enteropathogenic serotypes of E. coli, and several different serotypes may be cultured from the stools during a single hospital admission. However, there is usually no epidemiological or clinical evidence that these organisms actually cause diarrhoea in such cases. For example, of 51 infants with acute gastrointestinal symptoms admitted to this hospital, 26% grew enteropathogenic serotypes of E. coli from their stools, but 20% of 32 control patients also grew enteropathogenic serotypes. Thus, this laboratory frequently reports the isolation of an "enteropathogenic" E. coli which has little bearing on the clinical management of the patient. If the production of enterotoxin by human strains of enteropathogenic E. coli is determined by a plasmid, as it is in some animal strains,8 this confusing situation might be explained by the loss or gain of such a plasmid, especially if it were unusually unstable. Plasmids bearing antibiotic resistance factors may be lost on storage, and a similar situation may apply to plasmids responsible for enterotoxin production. Smith and Halls8 considered the Ent plasmid of porcine enteropathogenic E. coli to be stable. However, Taylor et al." noted that some human enterostrate
1. Rowe, B., Gross, R. J., Scotland, S. M. Lancet, 1975, ii, 925. 2. Gross, R. J., Scotland, S. M., Rowe, B. ibid. 1976, i, 629. 3. Payne, A. M. M., Cook, G. T. Br. med. J. 1950, ii, 192. 4. Taylor, J., Charter, R. E. J. Path. Bact. 1952, 64, 715. 5. McDonald, J. C., Charter, R. E. Proc. R. Soc. Med. 1956, 49, 85. 6. Gorbach, S. L., Khurana, C. M. New Engl. J. Med. 1972, 287, 791. 7. Etkin, S., Gorbach, S. L. J. Lab. clin. Med. 1971, 78, 81. 8. Smith, H. W., Halls, S. J. gen. Microbiol. 1968, 52, 319. 9. Taylor, J., Wilkins, P., Payne, J. M. Br. J. exp. Path. 1961, 42, 43.
