Lancet 1966 TB and Immigration

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  • 785LEADING ARTICLES

    Tuberculosis and Immigration

    THE LANCETLONDON 8 OCTOBER 1966

    FOR many years, successive British Governments havebeen urged to take action to prevent or reduce theimport of tuberculosis into Britain by immigrants,particularly by those who come from areas of the worldwhere the disease is common. The Ministry of Healthhas always held that a compulsory medical examinationwith chest X-ray, conducted in the immigrants countryof origin, or compulsory X-ray examination of the cheston arrival in this country, is impracticable. In 1965,the chief medical officer of the Ministry wrote to allgeneral practitioners in the Health Service asking themto look out for immigrants among their patients and toconsider the need to have a chest X-ray.l The Ministryalso encouraged immigrants to register promptly with ageneral practitioner in the area where they settled, andwhere possible the Ministry notified medical officers ofhealth when long-stay immigrants came to their districts.In the same year, X-ray apparatus was installed atLondon Airport for an on-the-spot examination whenthe medical inspectors suspected tuberculosis. Whetherthese activities yield useful results is doubtful. In anyevent there are no powers to examine medically the largenumbers of dependants who continue to arrive each yearto join immigrant relatives already here.The view that tuberculosis is commoner among

    immigrants than among the British-born population isbased on the findings of SPRINGETT 2 in Birmingham,STEVENSON 3 and EDGAR in Bradford, and ASPIN 5 inWolverhampton. After large numbers of immigrantsbegan to arrive from 1955 onwards, these cities hadrapidly rising numbers of tuberculosis notificationsamong the immigrants but fewer notifications amongresidents born in Britain. But these reports came fromthe North and the Midlands, where the great majority ofimmigrants eventually settle, and they were not repre-sentative of the whole country. A survey was obviouslyneeded to discover what proportion of tuberculosisnotifications in Britain as a whole was due to tuberculosisin immigrants, and whether tuberculosis in immigrantswas widespread or confined to a small number of urbancentres. Such a survey 6 has now been carried out by theresearch committee of the British Tuberculosis Associa-tion. Chest physicians were asked about all newnotifications of tuberculosis in England and Walesbetween Feb. 1 and April 30, 1965 (the survey was

    1. See Lancet, 1965, i, 150.2. Springett, V. H. ibid. 1964, i, 1091.3. Stevenson, D. K. Br. med. J. 1962, i, 1382.4. Edgar, W. ibid. 1964, ii, 1565.5. Aspin, J. ibid. 1962, i, 1386.6. Tubercle, Lond. 1966, 47, 145.

    confined to England and Wales because few immigrantssettle in Scotland and Northern Ireland). The objectiveof the survey could be attained only if 90% of chestclinics in England and Wales took part: in fact, 488 chestclinics agreed to do so-99% of the total. Each chestphysician was asked to tell the coordinator of the surveyof the birthplace of each patient newly notified, and forthose born in countries other than Great Britain thedate of entry to England and Wales was recorded.Persons born in countries other than Great Britain andIreland contributed a disproportionate share of thenotifications. Among 3806 cases of tuberculosis, 16-5%were in immigrants (that is, persons born in countriesother than Great Britain and Ireland), who formed onlyabout 4% of the population of England and Wales.Furthermore, 9-6% of the notifications were amongthose born in India and Pakistan, who formed onlyabout 1% of the population in 1965. Further analysisshowed that persons born in India and now living inEngland and Wales had a notification-rate twelve timesgreater than the rate for those born in Britain; and thenotification-rate for those born in Pakistan was twenty-six times greater than that for the British-born popula-tion of England and Wales. The rates of notification forthose born in Ireland, the rest of Europe, the BritishCaribbean area, and Africa were only slightly higher thanfor those born in Great Britain.

    An interesting, but not unexpected, finding was that ahigher proportion of non-respiratory forms of the diseasewas discovered among immigrants from India (33%)and Pakistan (26%) than in those born in Britain(11%). But this excess among Indians and Pakistaniswas insufficient to account for the difference in notifica-tion-rates of tuberculosis as a whole, because the ratesfor respiratory tuberculosis were still considerably higherfor those born in India and Pakistan than for thoseborn in Britain. Unfortunately very little informa-tion is available about the total numbers of personsmoving in and out of England and Wales, although thishas to some extent been corrected since the Common-wealth Immigrants Act of 1962. The survey showedclearly that many notifications applied to those whohad not recently entered England and Wales. But itwas not possible to know whether immigrants arrivedwith active disease, or with quiescent disease whichbroke down a few years later, or whether they camewithout disease and acquired it in England and Wales.A national survey of primary drug resistance in pul-monary tuberculosis in Great Britain, carried out by theMedical Research Council in 1963,7 provides some usefulinformation. Primary drug resistance was commoneramong immigrants than among patients born in Britainor Ireland. Again, drug resistance was seen moreoften among recently arrived immigrants than amongthose who had been living in Britain for five years ormore, or who had lived here since birth. But the num-ber of immigrants in this group was not large and furtherstudy is required.7. Miller, A. B., Tall, R., Wallace, F., Lefford, M. J., Mitchison, D. A.

    ibid. p. 92.

  • 786

    Tuberculosis among immigrants amounts to a medicalproblem only in certain cities and towns in the Northand the Midlands and the London area: 27% of theimmigrants notified in the survey were living in thecounty boroughs of Halifax, Bradford, West Bromwich,Bolton, Wolverhampton, Smethwick, and Birmingham.In these towns immigrants formed at least a third of allthe total notifications. Of the administrative counties ofEngland, only Bedfordshire, Middlesex, and Bucking-hamshire had a significant number of notifications, andin these counties a quarter of the notifications concernedpersons born outside Great Britain and Ireland. To putthe matter into perspective it should be noted that mostof the county boroughs and counties of England andWales rarely encounter tuberculosis in this way becausetheir immigrant population is very small.

    In the light of this survey, what action is called for ?In 1965 the British Medical Association set up a workingPABfty of a senior airport or seaport medical officer, achest physician, a radiologist, and a medical officer ofhealth to investigate the health problems of immigrantsto Great Britain. Their report 8 recommended routinechest radiography before admission to this country forall immigrants over the age of 12 years. Much thoughtwas given to where the medical examination should beconducted and who should do it. Examination in thecountry of origin had several advantages, particularly tothe immigrants themselves, and the report favoured theuse of Government medical officers from this country,aided where necessary by local doctors approved by theUnited Kingdom Government. Other countries haveschemes with built-in safeguards to prevent falsificationof papers. Examination at the ports of entry has severaldisadvantages. It is often impossible to have advanceknowledge of the numbers of immigrants intending toarrive at a particular time. Once immigrants have dis-persed from the ports of entry it is very hard to tracethem to arrange further medical examinations. More-over, examination on entry may mean considerablehardship to the immigrants because those who get anunfavourable medical report may be sent back.SPRINGETT 9 says that " the very high tuberculosisnotification rates recorded for Asian-born groups in thiscountry are due mainly to their bringing with them thehigh rates they would experience in their own country."Many physicians would share his view that if uncon-trolled immigration from areas of high prevalence con-tinues, tuberculosis is likely to be present in Britain fora very long time. If the Ministry of Health does notaccept the B.M.A. report and examine all immigrants,then it would be wise to examine all immigrants fromAsia, particularly those from India and Pakistan.Finally, if no action at all is taken, the Ministry of Healthshould at least show to the country that no appreciableamount of tuberculosis is being imported. How else canthis be done than by some form of compulsory medicalexamination ?8. Medical Examination of Immigrants. British Medical Association, 1965.

    See Lancet, 1965, ii, 1229.9. Springett, V. H. in Immigration: Medical and Social Aspects. Ciba

    Foundation Report. London, 1966.

    Cliac DiseaseSINCE the toxic effect of gluten in the small bowel

    was recognised, the causes and results of creliac diseasehave been under continual scrutiny. BOOTH and hiscolleagues 1 have now studied the intestinal epitheliumhistochemically before and after the patients were givena gluten-free diet. In untreated patients their findingslargely agreed with those of earlier workers 2 whodescribed three zones : a basal crypt region of small ger-minative cells lacking phosphatases, and with low ester-ase and succinic-dehydrogenase activities; an uppercrypt region which corresponded histochemically to thenormal villous region in its high phosphatase, esterase,and succinic-dehydrogenase content; and a surfaceregion of pseudostratified cells deficient in succinic-dehydrogenase, esterase, acid-phosphatase, and adeno-sine-triphosphatase. BOOTH et al. have drawn attentionto some features which suggest to them that the ratesof production of some enzymes-notably alkaline-phosphatase, non-specific acid-phosphatase, and thia-mine-pyrophosphatase-may be raised. The signi-ficance of these changes is uncertain, but the suggestionis that they may reflect an attempt, by increased pro-duction of crypt cells, to compensate for loss of surfacecells. Finally, BOOTH et al. deduce from other resultsthat dispersion of lysosomal hydrolytic activity mayaccount for some of the histological abnormality insurface cells.PITTMAN and POLLITT 4 followed up earlier sugges-

    tions 5-7 that the cells in the small intestine of patientswith coeliac disease might, through lack of peptidase, beunable to degrade peptides derived from wheat protein,They prepared peptic-tryptic digests of gliadin, thealcohol-soluble fraction of wheat gluten; and the resultsof further digestion by homogenates of mucosal cellsof guineapig and by normal human and untreated creliacmucosa were compared by means of multidimensionaldigestion maps using combinations of chromatographyand high-voltage electrophoresis. They found that, incontrast to normal mucosae, homogenates from cceliacpatients failed to liberate proline from gliadin peptides-an interesting result because previous work had sug-gested that the toxic gliadin peptides contain thisaminoacid. This work does not, however, distinguishprimary from secondary peptidase deficiency, andthe findings may be similar to those in secondarydisaccharidase deficiency. 8 ,

    Since the first account of intestinal reticulosis as acomplication of idiopathic steatorrhoea,9 further sugges-tive cases have been recorded 10 11; and LEE,12 trying to1. Riecken, E. O., Stewart, J. S., Booth, C. C., Pearse, A. G. E. Gut,

    1966, 7, 317.2. Padykula, H. A., Stauss, E. W., Ladman, A. J., Gardner, F. H. Gastro-

    enterology, 1961, 40, 735.3. Padykula, H. A. Fedn Proc. Fedn Am. Socs exp. Biol. 1962, 21, 873.4. Pittman, F. E., Pollitt, R. J. Gut, 1966, 7, 368.5. Frazer, A. C. J. Pediat. 1960, 57, 262.6. Rubin, C. E. Gastroenterology, 1960, 39, 260.7. Laster, L., Ingelfinger, F. J. New Engl. J. Med. 1961, 264, 1246.8. See Lancet, Oct. 1, 1966, p. 736.9. Gough, K. R., Read, A. E., Naish, J. M. Gut, 1962, 3, 232.

    10. Spracklen, F. Proc. R. Soc. Med. 1963, 56, 167.11. McCarthy, C. F., Austad, W. I., Evans, K. T., Comes, J. S., Read, A. E.

    Gut, 1966, 7, 104.12. Lee, F. D. ibid. p. 361.