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DIP-SLIDE DIAGNOSIS OF URINARY-TRACT INFECTION
202
in placenta.3 Further analysis of the purine effect has shown that other purines, notably uric acid, inhibit the activity of the enzyme. With every purine tested there is pronounced phenotype dependence in the degree of enhancement or inhibition. This is shown in the table; enzyme activities relative to the activity in the absence of purine are reported for each phenotype. Evidence that the severity of haemolytic favism4,5and of neonatal jaundice6.7 varies with acid-phosphatase phenotype has been presented by Bottini and coworkers. For both disorders the CA phenotype is at greatest risk and the B phenotype is at the least. These two phenotypes are at opposite extremes with respect to the degree of activity modulation by purines. It is thus possible that the association of acid-phosphatase phenotype with these hsemolytic disorders is in some way linked to the phenotype-dependent modulation of the acid phosphatase activity by purines. We have evidence that the redblood-cell acid phosphatase functions in vivo specifically as flavine mononucleotide phosphohydrolase; the purine effect may, then, be associated with variation in flavine coenzyme levels which in turn affect the activity of flavoenzymes such as glutathione reductase which are vital to the maintenance of red-blood-cell integrity.
phosphatase
Department of Genetics
and School of Public Health,
University of California, Berkeley, California 94720, U.S.A.
E. MANSFIELD G. F. SENSABAUGH
DIP-SLIDE DIAGNOSIS OF URINARY-TRACT INFECTION
SIR,-During a drug trial in which the efficacy of trimetho-. prim alone in the treatment of urinary-tract infection (U.T.I.) in general practice is being compared with that of trimethoprim-suiphamethoxazole (co-trimoxazole) we were suprised to find that 38 (75%) of 51 patients entered into the trial showed a pure growth of the following pathogens: Escherichia coli 23 (61%), Staphylococcus albus 9 (24%), Proteus spp. 3 (8%), Klebsiella 2, Streptococcusfcecalis 1. Mond et al.l showed that 55% of women who presented with symptoms of U.T.I. have no infection-i.e., they had fewer than 100 000 organisms/ml urine. The "urethral syndrome" (symptoms of U.T.I. in the absence of infection) therefore appears to be much less common in Cardiff than in London1 New Zealand.2 Several reasons may be advanced to account
or
for the discrepancy. Participation in a clinical trial may have enhanced the diagnostic acuity of clinicians and bacteriologists DiPietro, D. L., Zengerle, F. S. J. biol. Chem. 1967, 242, 3391. Bottini, E., Lucarelli, P., Agostino, R., Palmarino, R., Businco, L., Antognoni, G. Science, 1971, 171, 409. 5. Bottini, E. J. med. Genet. 1973, 10, 154. 6. Bottini, E., Lucarelli, P., Bastianoni, V., Gloria, F. ibid. 1972, 9, 434. 7. Bottini, E., Scacchi, R., Gloria-Bottini, F., Mortera, J., Palmarino, R., Carapella-DeLuca, E., Lapi, A., Nodari, C. Lancet, 1976, i, 918. 1. Mond, N. C., Percival, A., Williams, J. D., Brumfitt, W. Lancet, 1965, i, 3. 4.
514. 2.
Gallagher, i, 622.
D.
J. A., Montgomerie, J. Z., North, J. D. K.
Br.
med. J. 1965,
alike. Secondly, the belief that the urine must contain more than 100 000 organisms/ml for infection to exist, though widespread, is fallacious. This criterion of infection was introduced to diagnose symptomless infections in apparently healthy populations.3 In the symptomatic patient frequency of micturition may be severe enough to lower bacterial numbers and/or the infection may be due to fastidious pathogens (e.g., Strep. /ccca/!). Colony-counts should not, therefore, play a part in the diagnosis of symptomatic infections. Instead, diagnosis should be based on whether or not a pure or dominant growth of one organism is obtained. 5 of our 38 patients had less than 100 000 organisms/ml urine, and they responded to co-trimoxazole or trimethoprim alone in the same way as did those with counts in excess of 100 000/ml. The number of culture-negative patients who present with symptoms of U.T.I. may be greatly lowered by making dipslides available to general practitioners because on-the-spot inoculation of these slides reduces the diagnostic problem resulting from growth of contaminants in the urine after it is voided. We would repeat the plea of Arneil et a1.4 that dip-slides be made available to general practitioners. This measure may greatly reduce the prevalence of that ill-understood entity the "urethral syndrome" and may so decrease morbidity from frequency and dysuria. K.R.U.F. Institute of Renal Disease,
Royal Infirmary, and General Practice Unit, Welsh National School of Medicine, Cardiff
A. W. ASSCHER R. HARVARD DAVIS R. MACKENZIE
CARDIAC DYSRHYTHMIAS: TREATABLE CAUSE OF TRANSIENT CEREBRAL DYSFUNCTION IN THE ELDERLY
SIR,-We became interested in the possibility that transient cardiac dysrhythmias might be responsible for many of the episodic cerebral symptoms in the elderly for which no other cause can be found. 40 patients (ages 65-90) with recurrent episodes of giddiness, falls, blackouts, or confusional states, and 16 controls (ages 70-88) without these symptoms were studied. A cardiac dysrhythmia monitor (Hewlett-Packard) with a signal storage system, trend recorder, and rapid writer was incorporated into an existing cardiac monitoring system. 19 (48%) of the 40 symptomatic patients had a tachydysrhythmia (more than 150/min for 3 s) or a bradydysrhythmia (less than 45/min for 3 s or asystole longer than 1.5 s) during 24 h continuous monitoring. The other 21 (52%) patients with symptoms had no evidence of these dysrhythmias. Of the 16 control patients without cerebral symptoms 1 had a transient cardiac dysrhythmia (ventricular tachycardia). 12 (63%) of the 19 symptomatic patients with cardiac dysrhythmias on continuous monitoring had normal initial standard electrocardiograms; 4 had carotid-sinus hypersensitivity. 15 (79%) had normal rhythms on repeat 24 h continuous monitoring after treatment (4 with a pacemaker); 1 was unchanged; 3 died before treatment was started. 14 patients whose dysrhythmia was controlled had no further episodes of giddiness, falls, blackouts, or confusion whilst in hospital; 1 was un-
changed. The association of cardiac dysrhythmias with transient cerebral dysfunctionS-9 is often only shown on continuous electrocardiographic monitoring."* The results of our study suggest 3. Kass, E. H. Trans. Ass. Am. Phys, 1956, 69, 56. Arneil, G. C., McAllister, T. A., Kay, P. Lancet, 1973, i,
4. 5. 6. 7.
94.
McAllen, P. M., Marshall, J. Lancet, 1973, i, 1212. Abdon, N. J., Malmcrona, R. Acta med. scand. 1975, 198, 455. Wollner, L., Spalding, J. M. K. in Textbook of Geriatric Medicine and Gerontology (edited by J. C. Brocklehurst); p. 247. Edinburgh 1973. 8. Livesley, B. Age Ageing 1977, 6, suppl. p. 9. 9. Lancet, 1977, i, 27. 10. Goldberg, A. D., Raftery, E. B., Cashman, P. M. M. Br. med. J. 1975, iv, 569.
in placenta.3 Further analysis of the purine effect has shown that other purines, notably uric acid, inhibit the activity of the enzyme. With every purine tested there is pronounced phenotype dependence in the degree of enhancement or inhibition. This is shown in the table; enzyme activities relative to the activity in the absence of purine are reported for each phenotype. Evidence that the severity of haemolytic favism4,5and of neonatal jaundice6.7 varies with acid-phosphatase phenotype has been presented by Bottini and coworkers. For both disorders the CA phenotype is at greatest risk and the B phenotype is at the least. These two phenotypes are at opposite extremes with respect to the degree of activity modulation by purines. It is thus possible that the association of acid-phosphatase phenotype with these hsemolytic disorders is in some way linked to the phenotype-dependent modulation of the acid phosphatase activity by purines. We have evidence that the redblood-cell acid phosphatase functions in vivo specifically as flavine mononucleotide phosphohydrolase; the purine effect may, then, be associated with variation in flavine coenzyme levels which in turn affect the activity of flavoenzymes such as glutathione reductase which are vital to the maintenance of red-blood-cell integrity.
phosphatase
Department of Genetics
and School of Public Health,
University of California, Berkeley, California 94720, U.S.A.
E. MANSFIELD G. F. SENSABAUGH
DIP-SLIDE DIAGNOSIS OF URINARY-TRACT INFECTION
SIR,-During a drug trial in which the efficacy of trimetho-. prim alone in the treatment of urinary-tract infection (U.T.I.) in general practice is being compared with that of trimethoprim-suiphamethoxazole (co-trimoxazole) we were suprised to find that 38 (75%) of 51 patients entered into the trial showed a pure growth of the following pathogens: Escherichia coli 23 (61%), Staphylococcus albus 9 (24%), Proteus spp. 3 (8%), Klebsiella 2, Streptococcusfcecalis 1. Mond et al.l showed that 55% of women who presented with symptoms of U.T.I. have no infection-i.e., they had fewer than 100 000 organisms/ml urine. The "urethral syndrome" (symptoms of U.T.I. in the absence of infection) therefore appears to be much less common in Cardiff than in London1 New Zealand.2 Several reasons may be advanced to account
or
for the discrepancy. Participation in a clinical trial may have enhanced the diagnostic acuity of clinicians and bacteriologists DiPietro, D. L., Zengerle, F. S. J. biol. Chem. 1967, 242, 3391. Bottini, E., Lucarelli, P., Agostino, R., Palmarino, R., Businco, L., Antognoni, G. Science, 1971, 171, 409. 5. Bottini, E. J. med. Genet. 1973, 10, 154. 6. Bottini, E., Lucarelli, P., Bastianoni, V., Gloria, F. ibid. 1972, 9, 434. 7. Bottini, E., Scacchi, R., Gloria-Bottini, F., Mortera, J., Palmarino, R., Carapella-DeLuca, E., Lapi, A., Nodari, C. Lancet, 1976, i, 918. 1. Mond, N. C., Percival, A., Williams, J. D., Brumfitt, W. Lancet, 1965, i, 3. 4.
514. 2.
Gallagher, i, 622.
D.
J. A., Montgomerie, J. Z., North, J. D. K.
Br.
med. J. 1965,
alike. Secondly, the belief that the urine must contain more than 100 000 organisms/ml for infection to exist, though widespread, is fallacious. This criterion of infection was introduced to diagnose symptomless infections in apparently healthy populations.3 In the symptomatic patient frequency of micturition may be severe enough to lower bacterial numbers and/or the infection may be due to fastidious pathogens (e.g., Strep. /ccca/!). Colony-counts should not, therefore, play a part in the diagnosis of symptomatic infections. Instead, diagnosis should be based on whether or not a pure or dominant growth of one organism is obtained. 5 of our 38 patients had less than 100 000 organisms/ml urine, and they responded to co-trimoxazole or trimethoprim alone in the same way as did those with counts in excess of 100 000/ml. The number of culture-negative patients who present with symptoms of U.T.I. may be greatly lowered by making dipslides available to general practitioners because on-the-spot inoculation of these slides reduces the diagnostic problem resulting from growth of contaminants in the urine after it is voided. We would repeat the plea of Arneil et a1.4 that dip-slides be made available to general practitioners. This measure may greatly reduce the prevalence of that ill-understood entity the "urethral syndrome" and may so decrease morbidity from frequency and dysuria. K.R.U.F. Institute of Renal Disease,
Royal Infirmary, and General Practice Unit, Welsh National School of Medicine, Cardiff
A. W. ASSCHER R. HARVARD DAVIS R. MACKENZIE
CARDIAC DYSRHYTHMIAS: TREATABLE CAUSE OF TRANSIENT CEREBRAL DYSFUNCTION IN THE ELDERLY
SIR,-We became interested in the possibility that transient cardiac dysrhythmias might be responsible for many of the episodic cerebral symptoms in the elderly for which no other cause can be found. 40 patients (ages 65-90) with recurrent episodes of giddiness, falls, blackouts, or confusional states, and 16 controls (ages 70-88) without these symptoms were studied. A cardiac dysrhythmia monitor (Hewlett-Packard) with a signal storage system, trend recorder, and rapid writer was incorporated into an existing cardiac monitoring system. 19 (48%) of the 40 symptomatic patients had a tachydysrhythmia (more than 150/min for 3 s) or a bradydysrhythmia (less than 45/min for 3 s or asystole longer than 1.5 s) during 24 h continuous monitoring. The other 21 (52%) patients with symptoms had no evidence of these dysrhythmias. Of the 16 control patients without cerebral symptoms 1 had a transient cardiac dysrhythmia (ventricular tachycardia). 12 (63%) of the 19 symptomatic patients with cardiac dysrhythmias on continuous monitoring had normal initial standard electrocardiograms; 4 had carotid-sinus hypersensitivity. 15 (79%) had normal rhythms on repeat 24 h continuous monitoring after treatment (4 with a pacemaker); 1 was unchanged; 3 died before treatment was started. 14 patients whose dysrhythmia was controlled had no further episodes of giddiness, falls, blackouts, or confusion whilst in hospital; 1 was un-
changed. The association of cardiac dysrhythmias with transient cerebral dysfunctionS-9 is often only shown on continuous electrocardiographic monitoring."* The results of our study suggest 3. Kass, E. H. Trans. Ass. Am. Phys, 1956, 69, 56. Arneil, G. C., McAllister, T. A., Kay, P. Lancet, 1973, i,
4. 5. 6. 7.
94.
McAllen, P. M., Marshall, J. Lancet, 1973, i, 1212. Abdon, N. J., Malmcrona, R. Acta med. scand. 1975, 198, 455. Wollner, L., Spalding, J. M. K. in Textbook of Geriatric Medicine and Gerontology (edited by J. C. Brocklehurst); p. 247. Edinburgh 1973. 8. Livesley, B. Age Ageing 1977, 6, suppl. p. 9. 9. Lancet, 1977, i, 27. 10. Goldberg, A. D., Raftery, E. B., Cashman, P. M. M. Br. med. J. 1975, iv, 569.