- Email: [email protected]
SUXAMETHONIUM APNŒA
156
the inconstancy of the i.Q. as measured by tests, Vernon1 made the point that this inconstancy is most likely to be found in the very children for whom intelligence is assayed diagnostically-because they have become retarded and appear to be educationally subnormal. Wherever there is a big discrepancy between the educational quotient and the intelligence quotient, the attempt to measure an attainment quotient in terms of a ratio between the other two, I.Q. and E.Q., will tend to lower the I.Q. score artificially. The subject has lately been raised again by Stott, in the Medical Officer.2 From his own researches he reports on the use of a new set of tests, or rather of observational judgments, which he calls the " Scale of Real-Life Ability ", or colloquially the native-wit form. More accurately, he experimented with assessment of native wit, as we all know it, and from this developed a more organised scheme, which he now persuasively puts forward as worth a trial on larger numbers and by a variety of testers.3 It is important, however, to be clear about the meaning and use of such a test. The aim of this experimental scale of social competence is to measure " native wit ", which is assumed to be concealed in the great majority of backward children, by maturational or " motivational " impairment. But what is meant by motivational impairment " is not altogether clear; for mention is made both "of conative impairment on a psychological level and of damage to the neural mechanisms ", with implications of organic change. Nor are Stott’s views of the cause of high-grade mental subnormality likely to be universally acceptable. He has a strong belief in the prenatal effects of maternal stress4 5; and, although he acknowledges the heterogeneous origin of higher-grade defect, he does not seem to take account of the classical evidence of Penroseon the mental grades of relatives of mentally subnormal patients. Nobody, however, will deny the importance of environmental factors in mental subnormality. As long ago as 1908, A. F. Tredgold pointed out that many so-called defectives can get along quite well provided not too much is asked of them. Clarke and Clarke89 made this even clearer when they selected a group of imbeciles for training in simple factory procedures. Indeed, one of the complexities of the latter part of the 20th century is that, while social adaptation calls for an ever greater capacity to move with the times-if only to cross the road in safety-much of the work by which money is earned demands no great skill. In other words, the test of ability of function is a social rather than an intellectual one. Equally important, of course, is our growing ability, with subtler diagnostic tools, to recognise biochemical and structural deviations which do not in themselves cause measurable disorders of neurological function. Since an increasing proportion of the mentally handicapped are coming into the range of physically disordered cerebral function, is it not likely that others only mildly handicapped will also be found to belong to the organic group ? This may call for changes of method both in diagnosis and in special re-education. Into any reappraisal must come the means whereby defect is " ascertained ".
Writing
"
1. Vernon, P. E. Educ. Res. 1958, 1, 3. 2. Stott, D. H. Med. Offr, 1963, 110, 235. 3. Forms and directions will be supplied, free of 4. 5. 6. 7. 8.
9.
SUXAMETHONIUM APNŒA
on
charge,
on
application
to
Dr. Stott, Psychology Department, University of Glasgow. Stott, D. H. Lancet, 1957, i, 1006. Stott, D. H. Vita humana, 1959, 2, 125. Penrose, L. S. Spec. Rep. med. Res. Coun., Lond. no. 229. 1938. Tredgold, A. F. Textbook of Mental Deficiency, 1908. (See 10th edition, edited by R. F. Tredgold and K. Soddy, London, 1963.) Clarke, A. D. B., Clarke, A. M. Mental Deficiency, the Changing Outlook. London, 1958. Clarke, A. D. B. Lancet, 1962, i, 40.
THE muscle relaxant suxamethonium had
not
been
long in use before there were reports of unexplained prolongation of its action from the usual few minutes to several hours. Presently it was appreciated that this drug was destroyed in the body by the enzyme pseudocholinesterase,l and it was also discovered that many patients on whom the drug acted for an unexpectedly long time had a lowered serum-cholinesterase.23 Further it seemed that there was a reciprocal relation between the activity of this enzyme and the duration of the apnoea5 For a time the matter seemed fully explained, though Foldes and others, as early as 1955, were able to show
that, even in patients whose serum-cholinesterase was greatly reduced by disease, the duration of action of a reasonable dose of suxamethonium was little more than 10 minutes. From other quarters came reports 6of apparent prolongation of the action of suxamethonium in patients whose serum-cholinesterase was seemingly normal. The first step in the further elucidation of the causes of prolongation of suxamethonium apnoea came from Kalow and Gunn .89 They not only demonstrated that the sera of patients in whom the action of suxamethonium was prolonged was depleted in total pseudocholinesterase but also that there was an essential difference between the enzyme in those who responded normally or, if the serum level of the enzyme was lowered, by comparatively short apncea, and the enzyme in those who had the typical prolonged apnoea. Kalow went on to show that where the enzyme was abnormal the proportion of it inhibited by cinchocaine was reduced from a normal of about 80% to something like 25-30%.9 Moreover, this abnormality of the pseudocholinesterase was a hereditary defect. Further work indicated that the nature of the serum-cholinesterase was determined by a pair of genes The vast majority of people were homozygous for the genes which produced normal serum pseudocholinesterase. A very small minority, of the order of 1 in 3000,7 were homozygous for the genes which favoured atypical serum-cholinesterase, and these people tended to have prolonged apnoeas when given suxamethonium. An intermediate group who were heterozygous for the two types of gene were liable to have varying amounts of atypical pseudocholinesterase in their serum, and in them the action of suxamethonium was less prolonged. It was only in this group that there was a clear reciprocal relation between the duration of apnoea and the total concentration of pseudocholinesterase in the serum Presently, however, it became apparent that this pattern of inheritance would not wholly explain all the cases of this kind. It also seemed possible for a silent " gene to occupy the place normally occupied by the gene which determined the type of pseudocholinesterase." When the patient was homozygous for this " silent " gene, virtually no cholinesterase at all would be found in the serum, and a considerable degree of sensitivitv to suxamethonium must exist in them too. "
Bourne, J. G., Collier, H. O. J., Somers, G. F. Lancet, 1952, i, 1225. Evans, F. T., Gray, P. W. S., Lehmann, H., Silk, E. ibid. p. 1229. Evans, F. T., Gray, P. W. S., Lehmann, H., Silk, E. Brit. med. J. 1953, i, 136. 4. Lehmann, H., Ryan, E. Lancet, 1956, ii, 124. 5. Hamer Hodges, R. J., Harkness, J. Brit. med. J. 1954, ii, 18. 6. Foldes, F. F , Swerdlow, M., Lipschitz, E., van Hees, G. R., Shannor, S. P. Anesthesiology, 1956, 17, 559. 7. Argent, D. E., Dinnick, O. P., Hobbiger, F. Brit. J. Anœsth. 1955, 27, 1. 2. 3.
24.
8. 9. 10.
Kalow, W., Gunn, D. R. J. Pharmacol. 1957, 120, 203. Kalow, W., Staron, N. Canad. J. Biochem. Physiol. 1957, 35, 1305. Harris, H., Whittaker, M., Lehmann, H., Silk, E. Acta genet. 1960,
11.
10, 1. Lehmann, H., Silk, E., Harris, H., Whittaker, M. ibid. p. 241.
157
Prolonged apnoea has arisen in patients under treatfor malignant disease with AB-132 or ethyl-N-[bis (2,2-dimethylenamido) phosphoro] carbamate. 12 Like other organophosphorous compounds, this substance inhibits serum-cholinesterase. But only two cases have been reported so far: in them the apnceas lasted a very long time, unlike those noted in other circumstances of severe reduction of serum-enzyme concentration by disease. One of these patients had lung cancer; so there was the possibility of an associated myasthenic syndrome. Disturbance of serum-cholinesterase unfortunately does not explain the many cases of apncea which have
agement of suxamethonium apnoea is simply the continuation of artificial ventilation of the lungs until adequate spontaneous respiration is restored. Certainly, blind administration of neostigmine without information about the nature of the block at any stage of the paralysis is to be condemned. The only question is whether this drug may possibly accelerate the final stages of recovery. It has been suggested that this degree of recovery may be recognised by the fact that intravenous injection of 10 mg. of edrophonium temporarily restores normal breathing; but a case has been recorded where a small dose of neostigmine produced an improvement but a second dose
been described in which the serum-cholinesterase was apparently normal. It is true that in very few of these was the dibucaine number also determined, and some of them may well be heterozygotes with a relatively normal serum-level but a high proportion of the atypical enzyme. The question, however, inevitably arises, particularly in those in whom spontaneous respiration of a normal depth returned suddenly, whether the relaxant was in fact responsible for the apnoea, and in very few of these patients was a muscle-nerve stimulator 13 used to demonstrate whether myoneural block was really present. The principles underlying the management of suxamethonium apnoea have become more clearly defined. Unfortunately the obvious remedy of injecting additional pseudocholinesterase intravenously is of very doubtful value, and there are few documented cases in which this move has promptly restored normal breathing. Pseudocholinesterase is readily available in the form of blood for transfusion, or (better still) concentrated plasma, and the administration of a safe amount of either can certainly do no harm. But the basic remedy is artificial respiration, and this must be continued until normal breathing is restored. The place of antidote drugs in these cases is, at the moment, confused. It is clear from the work of ChurchillDavidson,14 Payne and Holmdahl,l5 and Brennan 16 that when the action of suxamethonium is prolonged for an appreciable period the myoneural block ceases to be depolarising in type and takes on most of the features of paralysis produced by d-tubocurarine-dual block. Two important points must be noted, however. Firstly, Payne and Holmdahl,15 studying this change in the action of suxamethonium, could demonstrate its presence only in some two-thirds of their patients. In the remaining third the block retained its depolarising character even after a long period of suxamethonium administration. Assumptions that within 20 minutes or so the block produced by suxamethonium will have become depolarising in every patient are therefore very unwise. Secondly, a more serious problem arises in the management of the patient in whom the application of a stimulator has clearly indicated that dual block has developed. Those who believe that all types of non-depolarising block are neostigminereversible feel that the change in the character of the block is an indication for giving this antidote." In fact, however, cases have been recorded where the use of neostigmine, so far from improving matters, has actually made them worse.18-20 It seems, therefore, that the best man-
intensified respiratory depression.
ment
12. 13. 14.
15. 16. 17. 18. 19. 20.
Wang, R. I. H., Ross, C.A. Anesthesiology, 1963,24, 363. Christie, T. H., Churchill-Davidson, H. C. Lancet, 1958, i, 776. Churchill-Davidson, H. C., Richardson, A. T. Proc. R. Soc. Med. 1952, 45, 179. Payne,J. P., Holmdahl, M. H. Brit. J. Anœsth. 1958, 31, 341. Brennan, H. J. ibid. 1956, 28, 159. Churchill-Davidson, H. C. Recent Advances in Anesthesia and Analgesia (edited by C. L. Hewer); p. 107. London, 1962. Vickers, M. D. A. Brit. J. Anœsth. 1963, 35, 260. Hunter, A. R. Surv. Anesth. 1963, 7, 319. Vickers, M. D.Brit. J. Anœsth. 1963, 35, 528.
TERMINOLOGY OF MALARIA AND OF MALARIA ERADICATION
A
science quickly acquires its own jargon, and its exponents stand in need of precise definitions. In malariology this need is especially acute: the subject is as hybrid as its name, and in its pursuit the practitioner has to be both doctor and engineer, entomologist and parasitologist, chemist and sociologist-a jack of all trades, who uses a technical vocabulary derived from all these callings. The very word " malaria " is " based on an illusion, for the condition is not caused by bad air " but by a protozoon parasite carried by mosquitoes; these insects often breed in swamps, and the French name paludisme is thus more appropriate. Glossaries of terms used in malariology were prepared by the Health Organisation of the League of Nations1 and by the World Health Organisation.2 Each was preceded by a text giving the gist of the subject, the details of which are well set out in the latest edition of Practical Malariology.3 The terminology now published by W.H.O.4 has a wider scope: the concept of malaria eradication has been added, and with this a vocabulary of epidemiological technicalities at least as formidable as those used in the past. This work was prepared after the wave of enthusiasm for world-wide malaria eradication had passed its crest, when it was no longer considered heretical to question the idea that the abolition of malaria was just round the corner-though few doubt the ultimate feasibility of this. At the International Congress of Tropical Medicine and Malaria, held in Rio de Janeiro in September,5 the view was widely expressed that, whereas malaria eradication is relatively easy in developed countries, it is much more difficult in places where the general administration of the territory and its health services are weaker; in continents such as Africa, infected with the most dangerous carrier of all mosquitoes-Anopheles gambiae-or in South America, where the disease is often transmitted out of doors and the application of dicophane (D.D.T.) to houses may have little effect, no final solution has yet been found despite phenomenal successes in, for instance, Venezuela and British Guiana. The latest terminology includes not only residual insecticides but older methods such as the application of Paris-green as a larvicide, and new ideas on the determination of the age NEW
1. League of Nations, Malaria Commission. Bull. Hlth Org. L.o.N. 1940, 9, 133. 2. Covell, G., Russell, P. F., Swellengrebel, N. H. Malaria Terminology. World Health Organisation, monograph series, 1953, no. 13. 3. Russell, P. F., West, L. S., Manwell, R. D., Macdonald, G. Practical Malariology. London, 1963. 4. Gabaldon, A., Garnham, P. C. C., Macdonald, G., Pampana, E. J. Terminology of Malaria and of Malaria Eradication. World Health Organisation, Geneva, 1963. Obtainable from H.M. Stationery Office, P.O. Box 569, London, S.E.1. Pp. 127. £1. 5. 7th International Congresses on Tropical Medicine and Malaria, Rio de Janeiro, Sept. 1-11, 1963. Abstracts.
the inconstancy of the i.Q. as measured by tests, Vernon1 made the point that this inconstancy is most likely to be found in the very children for whom intelligence is assayed diagnostically-because they have become retarded and appear to be educationally subnormal. Wherever there is a big discrepancy between the educational quotient and the intelligence quotient, the attempt to measure an attainment quotient in terms of a ratio between the other two, I.Q. and E.Q., will tend to lower the I.Q. score artificially. The subject has lately been raised again by Stott, in the Medical Officer.2 From his own researches he reports on the use of a new set of tests, or rather of observational judgments, which he calls the " Scale of Real-Life Ability ", or colloquially the native-wit form. More accurately, he experimented with assessment of native wit, as we all know it, and from this developed a more organised scheme, which he now persuasively puts forward as worth a trial on larger numbers and by a variety of testers.3 It is important, however, to be clear about the meaning and use of such a test. The aim of this experimental scale of social competence is to measure " native wit ", which is assumed to be concealed in the great majority of backward children, by maturational or " motivational " impairment. But what is meant by motivational impairment " is not altogether clear; for mention is made both "of conative impairment on a psychological level and of damage to the neural mechanisms ", with implications of organic change. Nor are Stott’s views of the cause of high-grade mental subnormality likely to be universally acceptable. He has a strong belief in the prenatal effects of maternal stress4 5; and, although he acknowledges the heterogeneous origin of higher-grade defect, he does not seem to take account of the classical evidence of Penroseon the mental grades of relatives of mentally subnormal patients. Nobody, however, will deny the importance of environmental factors in mental subnormality. As long ago as 1908, A. F. Tredgold pointed out that many so-called defectives can get along quite well provided not too much is asked of them. Clarke and Clarke89 made this even clearer when they selected a group of imbeciles for training in simple factory procedures. Indeed, one of the complexities of the latter part of the 20th century is that, while social adaptation calls for an ever greater capacity to move with the times-if only to cross the road in safety-much of the work by which money is earned demands no great skill. In other words, the test of ability of function is a social rather than an intellectual one. Equally important, of course, is our growing ability, with subtler diagnostic tools, to recognise biochemical and structural deviations which do not in themselves cause measurable disorders of neurological function. Since an increasing proportion of the mentally handicapped are coming into the range of physically disordered cerebral function, is it not likely that others only mildly handicapped will also be found to belong to the organic group ? This may call for changes of method both in diagnosis and in special re-education. Into any reappraisal must come the means whereby defect is " ascertained ".
Writing
"
1. Vernon, P. E. Educ. Res. 1958, 1, 3. 2. Stott, D. H. Med. Offr, 1963, 110, 235. 3. Forms and directions will be supplied, free of 4. 5. 6. 7. 8.
9.
SUXAMETHONIUM APNŒA
on
charge,
on
application
to
Dr. Stott, Psychology Department, University of Glasgow. Stott, D. H. Lancet, 1957, i, 1006. Stott, D. H. Vita humana, 1959, 2, 125. Penrose, L. S. Spec. Rep. med. Res. Coun., Lond. no. 229. 1938. Tredgold, A. F. Textbook of Mental Deficiency, 1908. (See 10th edition, edited by R. F. Tredgold and K. Soddy, London, 1963.) Clarke, A. D. B., Clarke, A. M. Mental Deficiency, the Changing Outlook. London, 1958. Clarke, A. D. B. Lancet, 1962, i, 40.
THE muscle relaxant suxamethonium had
not
been
long in use before there were reports of unexplained prolongation of its action from the usual few minutes to several hours. Presently it was appreciated that this drug was destroyed in the body by the enzyme pseudocholinesterase,l and it was also discovered that many patients on whom the drug acted for an unexpectedly long time had a lowered serum-cholinesterase.23 Further it seemed that there was a reciprocal relation between the activity of this enzyme and the duration of the apnoea5 For a time the matter seemed fully explained, though Foldes and others, as early as 1955, were able to show
that, even in patients whose serum-cholinesterase was greatly reduced by disease, the duration of action of a reasonable dose of suxamethonium was little more than 10 minutes. From other quarters came reports 6of apparent prolongation of the action of suxamethonium in patients whose serum-cholinesterase was seemingly normal. The first step in the further elucidation of the causes of prolongation of suxamethonium apnoea came from Kalow and Gunn .89 They not only demonstrated that the sera of patients in whom the action of suxamethonium was prolonged was depleted in total pseudocholinesterase but also that there was an essential difference between the enzyme in those who responded normally or, if the serum level of the enzyme was lowered, by comparatively short apncea, and the enzyme in those who had the typical prolonged apnoea. Kalow went on to show that where the enzyme was abnormal the proportion of it inhibited by cinchocaine was reduced from a normal of about 80% to something like 25-30%.9 Moreover, this abnormality of the pseudocholinesterase was a hereditary defect. Further work indicated that the nature of the serum-cholinesterase was determined by a pair of genes The vast majority of people were homozygous for the genes which produced normal serum pseudocholinesterase. A very small minority, of the order of 1 in 3000,7 were homozygous for the genes which favoured atypical serum-cholinesterase, and these people tended to have prolonged apnoeas when given suxamethonium. An intermediate group who were heterozygous for the two types of gene were liable to have varying amounts of atypical pseudocholinesterase in their serum, and in them the action of suxamethonium was less prolonged. It was only in this group that there was a clear reciprocal relation between the duration of apnoea and the total concentration of pseudocholinesterase in the serum Presently, however, it became apparent that this pattern of inheritance would not wholly explain all the cases of this kind. It also seemed possible for a silent " gene to occupy the place normally occupied by the gene which determined the type of pseudocholinesterase." When the patient was homozygous for this " silent " gene, virtually no cholinesterase at all would be found in the serum, and a considerable degree of sensitivitv to suxamethonium must exist in them too. "
Bourne, J. G., Collier, H. O. J., Somers, G. F. Lancet, 1952, i, 1225. Evans, F. T., Gray, P. W. S., Lehmann, H., Silk, E. ibid. p. 1229. Evans, F. T., Gray, P. W. S., Lehmann, H., Silk, E. Brit. med. J. 1953, i, 136. 4. Lehmann, H., Ryan, E. Lancet, 1956, ii, 124. 5. Hamer Hodges, R. J., Harkness, J. Brit. med. J. 1954, ii, 18. 6. Foldes, F. F , Swerdlow, M., Lipschitz, E., van Hees, G. R., Shannor, S. P. Anesthesiology, 1956, 17, 559. 7. Argent, D. E., Dinnick, O. P., Hobbiger, F. Brit. J. Anœsth. 1955, 27, 1. 2. 3.
24.
8. 9. 10.
Kalow, W., Gunn, D. R. J. Pharmacol. 1957, 120, 203. Kalow, W., Staron, N. Canad. J. Biochem. Physiol. 1957, 35, 1305. Harris, H., Whittaker, M., Lehmann, H., Silk, E. Acta genet. 1960,
11.
10, 1. Lehmann, H., Silk, E., Harris, H., Whittaker, M. ibid. p. 241.
157
Prolonged apnoea has arisen in patients under treatfor malignant disease with AB-132 or ethyl-N-[bis (2,2-dimethylenamido) phosphoro] carbamate. 12 Like other organophosphorous compounds, this substance inhibits serum-cholinesterase. But only two cases have been reported so far: in them the apnceas lasted a very long time, unlike those noted in other circumstances of severe reduction of serum-enzyme concentration by disease. One of these patients had lung cancer; so there was the possibility of an associated myasthenic syndrome. Disturbance of serum-cholinesterase unfortunately does not explain the many cases of apncea which have
agement of suxamethonium apnoea is simply the continuation of artificial ventilation of the lungs until adequate spontaneous respiration is restored. Certainly, blind administration of neostigmine without information about the nature of the block at any stage of the paralysis is to be condemned. The only question is whether this drug may possibly accelerate the final stages of recovery. It has been suggested that this degree of recovery may be recognised by the fact that intravenous injection of 10 mg. of edrophonium temporarily restores normal breathing; but a case has been recorded where a small dose of neostigmine produced an improvement but a second dose
been described in which the serum-cholinesterase was apparently normal. It is true that in very few of these was the dibucaine number also determined, and some of them may well be heterozygotes with a relatively normal serum-level but a high proportion of the atypical enzyme. The question, however, inevitably arises, particularly in those in whom spontaneous respiration of a normal depth returned suddenly, whether the relaxant was in fact responsible for the apnoea, and in very few of these patients was a muscle-nerve stimulator 13 used to demonstrate whether myoneural block was really present. The principles underlying the management of suxamethonium apnoea have become more clearly defined. Unfortunately the obvious remedy of injecting additional pseudocholinesterase intravenously is of very doubtful value, and there are few documented cases in which this move has promptly restored normal breathing. Pseudocholinesterase is readily available in the form of blood for transfusion, or (better still) concentrated plasma, and the administration of a safe amount of either can certainly do no harm. But the basic remedy is artificial respiration, and this must be continued until normal breathing is restored. The place of antidote drugs in these cases is, at the moment, confused. It is clear from the work of ChurchillDavidson,14 Payne and Holmdahl,l5 and Brennan 16 that when the action of suxamethonium is prolonged for an appreciable period the myoneural block ceases to be depolarising in type and takes on most of the features of paralysis produced by d-tubocurarine-dual block. Two important points must be noted, however. Firstly, Payne and Holmdahl,15 studying this change in the action of suxamethonium, could demonstrate its presence only in some two-thirds of their patients. In the remaining third the block retained its depolarising character even after a long period of suxamethonium administration. Assumptions that within 20 minutes or so the block produced by suxamethonium will have become depolarising in every patient are therefore very unwise. Secondly, a more serious problem arises in the management of the patient in whom the application of a stimulator has clearly indicated that dual block has developed. Those who believe that all types of non-depolarising block are neostigminereversible feel that the change in the character of the block is an indication for giving this antidote." In fact, however, cases have been recorded where the use of neostigmine, so far from improving matters, has actually made them worse.18-20 It seems, therefore, that the best man-
intensified respiratory depression.
ment
12. 13. 14.
15. 16. 17. 18. 19. 20.
Wang, R. I. H., Ross, C.A. Anesthesiology, 1963,24, 363. Christie, T. H., Churchill-Davidson, H. C. Lancet, 1958, i, 776. Churchill-Davidson, H. C., Richardson, A. T. Proc. R. Soc. Med. 1952, 45, 179. Payne,J. P., Holmdahl, M. H. Brit. J. Anœsth. 1958, 31, 341. Brennan, H. J. ibid. 1956, 28, 159. Churchill-Davidson, H. C. Recent Advances in Anesthesia and Analgesia (edited by C. L. Hewer); p. 107. London, 1962. Vickers, M. D. A. Brit. J. Anœsth. 1963, 35, 260. Hunter, A. R. Surv. Anesth. 1963, 7, 319. Vickers, M. D.Brit. J. Anœsth. 1963, 35, 528.
TERMINOLOGY OF MALARIA AND OF MALARIA ERADICATION
A
science quickly acquires its own jargon, and its exponents stand in need of precise definitions. In malariology this need is especially acute: the subject is as hybrid as its name, and in its pursuit the practitioner has to be both doctor and engineer, entomologist and parasitologist, chemist and sociologist-a jack of all trades, who uses a technical vocabulary derived from all these callings. The very word " malaria " is " based on an illusion, for the condition is not caused by bad air " but by a protozoon parasite carried by mosquitoes; these insects often breed in swamps, and the French name paludisme is thus more appropriate. Glossaries of terms used in malariology were prepared by the Health Organisation of the League of Nations1 and by the World Health Organisation.2 Each was preceded by a text giving the gist of the subject, the details of which are well set out in the latest edition of Practical Malariology.3 The terminology now published by W.H.O.4 has a wider scope: the concept of malaria eradication has been added, and with this a vocabulary of epidemiological technicalities at least as formidable as those used in the past. This work was prepared after the wave of enthusiasm for world-wide malaria eradication had passed its crest, when it was no longer considered heretical to question the idea that the abolition of malaria was just round the corner-though few doubt the ultimate feasibility of this. At the International Congress of Tropical Medicine and Malaria, held in Rio de Janeiro in September,5 the view was widely expressed that, whereas malaria eradication is relatively easy in developed countries, it is much more difficult in places where the general administration of the territory and its health services are weaker; in continents such as Africa, infected with the most dangerous carrier of all mosquitoes-Anopheles gambiae-or in South America, where the disease is often transmitted out of doors and the application of dicophane (D.D.T.) to houses may have little effect, no final solution has yet been found despite phenomenal successes in, for instance, Venezuela and British Guiana. The latest terminology includes not only residual insecticides but older methods such as the application of Paris-green as a larvicide, and new ideas on the determination of the age NEW
1. League of Nations, Malaria Commission. Bull. Hlth Org. L.o.N. 1940, 9, 133. 2. Covell, G., Russell, P. F., Swellengrebel, N. H. Malaria Terminology. World Health Organisation, monograph series, 1953, no. 13. 3. Russell, P. F., West, L. S., Manwell, R. D., Macdonald, G. Practical Malariology. London, 1963. 4. Gabaldon, A., Garnham, P. C. C., Macdonald, G., Pampana, E. J. Terminology of Malaria and of Malaria Eradication. World Health Organisation, Geneva, 1963. Obtainable from H.M. Stationery Office, P.O. Box 569, London, S.E.1. Pp. 127. £1. 5. 7th International Congresses on Tropical Medicine and Malaria, Rio de Janeiro, Sept. 1-11, 1963. Abstracts.