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MERCURIAL POISONING IN LABORATORIES USING VOLUMETRIC GAS ANALYSIS
222
aseptic cellular response (a raising white-cell posed mainly of lymphocytes).
count com-
Two of the children in the paper you cited by Converse and others1 had this picture, and I have recently encountered two adults with these C.S.F. findings together with pyrexia, meningism, and previous antibiotic therapy. No acid/alcohol-fast bacilli were seen on Ziehl-Neelsen staining of c.s.F. deposits. Both patients were treated with streptomycin, p-aminosalicylic acid, and isoniazid. Clinical recovery was prompt and complete. After eight weeks no tuberculous organisms had been grown, and guineapig inoculations were negative. As there was no evidence of past or present tuberculosis in either, antituberculous therapy was stopped, and both have remained well; subsequent lumbar punctures were normal. In retrospect it seems more likely that the high lymphocyte-counts and low c.s.F. sugars were due to a partly treated bacterial meningitis responsive to streptomycin, rather than to tuberculous meningitis. However, one must always consider tuberculous meningitis and also fungal and carcinomatous meningitis under these circumstances. Diagnostic difficulties are increased after Edmond and McKendrick’s2 account of four cases of " aseptic meningitis " who recovered spontaneously, but whose c.s.F. cultures subsequently yielded tuberculous organisms. Clearly, all such doubtful cases, even if not treated, should remain under close review. Department of Neurology, Queen Elizabeth Hospital, Birmingham B15 2TH.
D.
J. THOMAS.
Converse, G. M., Gwaltney, J. M., Strassburg, D. A., Hendley, J. O. J. Pediat. 1973, 83, 220. 2. Edmond, R. T. D., McKendrick, G. D. W. Lancet, 1973, ii, 234. 1.
ground to Staphylococcus aureus as our society has become more sophisticated (in terms of hygiene, antibiotics, and so on). There is certainly evidence in the case of septicaemia for a swing of this sort over the years. Thus James,’ referring to the work of Finland et al. at the Boston City Hospital, comments,
SIR— Dr Harrington (Jan. 19, p. 86) has reported high values for urine mercury in laboratory technicians who were using the Martin apparatus for measuring the carbondioxide content of beer. In about 1951 Dr Van Slyke told me that during the development of his original volumetric gas analysis apparatus (J. biol. Chem. 1917, 30, 347) he detected frequent mercurial poisoning in his staff by the appearance of proteinuria. Department of Chemical Pathology, Royal Free Hospital, London WC1.
D. N. BARON.
BACTERIOLOGICAL FINDINGS IN PNEUMONIA
SIR,-I was most interested in Dr Tugwell and Dr Greenwood’s letter of Jan. 19 (p. 95) in which they agree that sputum culture is of little value in the investigation of suspected pneumococcal pneumonia and then detail a counterimmunoelectrophoretic (C.LE.) method of establishing a diagnosis of pneumococcal infection in cases of lobar pneumonia. I know of no prospective study of this sort in the U.K. Since it is little affected by previous antibiotic therapy, C.LE. could provide a most useful method of establishing whether the pneumococcus is still the chief pathogen in primary pneumonias in this country. Tugwell and Greenwood have found that pneumococcal antigen figured prominently in lobar pneumonia in the context, where pneumonia is the commonest I presume that the acute medical admission. Nigerian community is not nearly so saturated with antibiotics as is ours. This is more reminiscent of the U.K. situation of previous decades. My guess would be, as I said in my previous letter, that the pneumococcus has lost
Nigerian reason
for
In
essence
the antibiotic
era
has witnessed
a
change from pneumococcal and streptococcal to staphylococcal and coliform septicemia." If this is true of septicxmia why should it not also be true of lobar pneumonia-especially since pneumonia is often a source of septicaemia ? Tugwell and Greenwood’s Nigerian work must be repeated here if we are to answer this important question. Meanwhile, it does no harm to include an antistaphylococcal agent in our routine antipneumonic therapy. Gateside Hospital, Greenock PA16 9ER.
H. KINNELL.
1.
James, D. G. in Recent Advances in Medicine; 14th ed. (edited by D. N. Baron, N. Compston, and A. M. Dawson); p. 55. London,
2.
Finland, M., Jones, W. F., Barnes, M. 170, 2188.
1964. W.
J. Am. med. Ass. 1958,
DIAGNOSTIC INDEX FOR PREMYXŒDEMA SIR,—DR Evered and Professor Hall have twice criticised our diagnostic index for premyxoedema (Oct. 27, p. 963, and Jan. 19, p. 99). We should like to reply especially to their second letter, since they had then had the opportunity of seeing the details of the diagnostic index which we had devised. Their first letter surprised us, written as it was without this advantage. The term index has come to mean any measure which combines the values of several variables items into a composite measure. The initial valuation of items may be subjective, but if it proves valid for definite examples of a condition, as in the 25 patients who later progressed to myxoedema, it is equally valid for other patients such as the 75 with premyxoedema who had not progressed to myxoedema. It would be fair to say that an index attempts to give a constant, final, objective, discriminating score. We agree with Dr Evered and Professor Hall that the serum-T.S.H. concentration is the most sensitive indication of any reduction of circulatingblood-hormone levels. This is why this test in our index scores the highest marks. We agree with them that the finding of circulating thyroid antibodies merely reflects the presence of lymphocytic infiltration of the thyroid, and these subjects are apparently normal (if you wish to ignore the lymphocytic infiltration of the thyroid). Since they agree with us that there must be a stage between normal thyroid function and symptomatic hypothyroidism in autoimmune thyroiditis, they can hardly dismiss the finding of circulating thyroid antibodies when most would accept that myxoedema is usually due to autoimmune disease. Unfortunately, clinical experience teaches that no great reliance can be placed on a single test. We know this to be true of serum-T.s.H. estimations, and it is borne out by published results to which we have previously drawn attention.2 We hope that on reflection Dr Evered and Professor Hall may agree that other variables beside the serum-T.s.H. estimation can help in the diagnosis of premyxoedema and that the diagnosis can be made without the great help to be obtained by this test. The diagnosis of pernicious anaemia used to be made with some confidence before serum-B12 levels could be estimated. Dr Evered and Professor Hall point out that, from an epidemiological point of view, subclinical hypothyroidism plays a minor part in influencing the cholesterol level. If the serum-B12 level was estimated in 100 consecutive anaemic patients, not one case of pernicious ansemia might be detected. This does not imply that pernicious anaemia is an unimportant disease. If premyxoedema is or
MERCURIAL POISONING IN LABORATORIES USING VOLUMETRIC GAS ANALYSIS
"
aseptic cellular response (a raising white-cell posed mainly of lymphocytes).
count com-
Two of the children in the paper you cited by Converse and others1 had this picture, and I have recently encountered two adults with these C.S.F. findings together with pyrexia, meningism, and previous antibiotic therapy. No acid/alcohol-fast bacilli were seen on Ziehl-Neelsen staining of c.s.F. deposits. Both patients were treated with streptomycin, p-aminosalicylic acid, and isoniazid. Clinical recovery was prompt and complete. After eight weeks no tuberculous organisms had been grown, and guineapig inoculations were negative. As there was no evidence of past or present tuberculosis in either, antituberculous therapy was stopped, and both have remained well; subsequent lumbar punctures were normal. In retrospect it seems more likely that the high lymphocyte-counts and low c.s.F. sugars were due to a partly treated bacterial meningitis responsive to streptomycin, rather than to tuberculous meningitis. However, one must always consider tuberculous meningitis and also fungal and carcinomatous meningitis under these circumstances. Diagnostic difficulties are increased after Edmond and McKendrick’s2 account of four cases of " aseptic meningitis " who recovered spontaneously, but whose c.s.F. cultures subsequently yielded tuberculous organisms. Clearly, all such doubtful cases, even if not treated, should remain under close review. Department of Neurology, Queen Elizabeth Hospital, Birmingham B15 2TH.
D.
J. THOMAS.
Converse, G. M., Gwaltney, J. M., Strassburg, D. A., Hendley, J. O. J. Pediat. 1973, 83, 220. 2. Edmond, R. T. D., McKendrick, G. D. W. Lancet, 1973, ii, 234. 1.
ground to Staphylococcus aureus as our society has become more sophisticated (in terms of hygiene, antibiotics, and so on). There is certainly evidence in the case of septicaemia for a swing of this sort over the years. Thus James,’ referring to the work of Finland et al. at the Boston City Hospital, comments,
SIR— Dr Harrington (Jan. 19, p. 86) has reported high values for urine mercury in laboratory technicians who were using the Martin apparatus for measuring the carbondioxide content of beer. In about 1951 Dr Van Slyke told me that during the development of his original volumetric gas analysis apparatus (J. biol. Chem. 1917, 30, 347) he detected frequent mercurial poisoning in his staff by the appearance of proteinuria. Department of Chemical Pathology, Royal Free Hospital, London WC1.
D. N. BARON.
BACTERIOLOGICAL FINDINGS IN PNEUMONIA
SIR,-I was most interested in Dr Tugwell and Dr Greenwood’s letter of Jan. 19 (p. 95) in which they agree that sputum culture is of little value in the investigation of suspected pneumococcal pneumonia and then detail a counterimmunoelectrophoretic (C.LE.) method of establishing a diagnosis of pneumococcal infection in cases of lobar pneumonia. I know of no prospective study of this sort in the U.K. Since it is little affected by previous antibiotic therapy, C.LE. could provide a most useful method of establishing whether the pneumococcus is still the chief pathogen in primary pneumonias in this country. Tugwell and Greenwood have found that pneumococcal antigen figured prominently in lobar pneumonia in the context, where pneumonia is the commonest I presume that the acute medical admission. Nigerian community is not nearly so saturated with antibiotics as is ours. This is more reminiscent of the U.K. situation of previous decades. My guess would be, as I said in my previous letter, that the pneumococcus has lost
Nigerian reason
for
In
essence
the antibiotic
era
has witnessed
a
change from pneumococcal and streptococcal to staphylococcal and coliform septicemia." If this is true of septicxmia why should it not also be true of lobar pneumonia-especially since pneumonia is often a source of septicaemia ? Tugwell and Greenwood’s Nigerian work must be repeated here if we are to answer this important question. Meanwhile, it does no harm to include an antistaphylococcal agent in our routine antipneumonic therapy. Gateside Hospital, Greenock PA16 9ER.
H. KINNELL.
1.
James, D. G. in Recent Advances in Medicine; 14th ed. (edited by D. N. Baron, N. Compston, and A. M. Dawson); p. 55. London,
2.
Finland, M., Jones, W. F., Barnes, M. 170, 2188.
1964. W.
J. Am. med. Ass. 1958,
DIAGNOSTIC INDEX FOR PREMYXŒDEMA SIR,—DR Evered and Professor Hall have twice criticised our diagnostic index for premyxoedema (Oct. 27, p. 963, and Jan. 19, p. 99). We should like to reply especially to their second letter, since they had then had the opportunity of seeing the details of the diagnostic index which we had devised. Their first letter surprised us, written as it was without this advantage. The term index has come to mean any measure which combines the values of several variables items into a composite measure. The initial valuation of items may be subjective, but if it proves valid for definite examples of a condition, as in the 25 patients who later progressed to myxoedema, it is equally valid for other patients such as the 75 with premyxoedema who had not progressed to myxoedema. It would be fair to say that an index attempts to give a constant, final, objective, discriminating score. We agree with Dr Evered and Professor Hall that the serum-T.S.H. concentration is the most sensitive indication of any reduction of circulatingblood-hormone levels. This is why this test in our index scores the highest marks. We agree with them that the finding of circulating thyroid antibodies merely reflects the presence of lymphocytic infiltration of the thyroid, and these subjects are apparently normal (if you wish to ignore the lymphocytic infiltration of the thyroid). Since they agree with us that there must be a stage between normal thyroid function and symptomatic hypothyroidism in autoimmune thyroiditis, they can hardly dismiss the finding of circulating thyroid antibodies when most would accept that myxoedema is usually due to autoimmune disease. Unfortunately, clinical experience teaches that no great reliance can be placed on a single test. We know this to be true of serum-T.s.H. estimations, and it is borne out by published results to which we have previously drawn attention.2 We hope that on reflection Dr Evered and Professor Hall may agree that other variables beside the serum-T.s.H. estimation can help in the diagnosis of premyxoedema and that the diagnosis can be made without the great help to be obtained by this test. The diagnosis of pernicious anaemia used to be made with some confidence before serum-B12 levels could be estimated. Dr Evered and Professor Hall point out that, from an epidemiological point of view, subclinical hypothyroidism plays a minor part in influencing the cholesterol level. If the serum-B12 level was estimated in 100 consecutive anaemic patients, not one case of pernicious ansemia might be detected. This does not imply that pernicious anaemia is an unimportant disease. If premyxoedema is or
MERCURIAL POISONING IN LABORATORIES USING VOLUMETRIC GAS ANALYSIS
"