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disease.9, 12, 14 At the third International Symposium onRickettsiae and Rickettsial Diseases, Kazar and

Schramekl5 reported that, in mice, protection againstexperimental Q fever infection correlated better withdevelopment of delayed hypersensitivity to C burnetithan with antibody, and that protection and delayedhypersensitivity lasted longer after immunisation withwhole cells of C burneti than with antigenic extracts ofthe organism. These workers have also pointed out theimportance of skin test response as an indicator ofimmunity in Q fever convalescents and vaccinees.16 Inagreement with this, Professor Marmion and his

colleagues report that vaccinated abattoir workers wereresistant to experimental infection even in the absenceof antibody, and they did not observe Q fever in anyunvaccinated subjects with a positive skin test,

irrespective of the presence of antibody. Thus, it seemsthat both humoral and cell-mediated immunity areimportant in Q fever, and that skin test conversion is auseful indicator of vaccine efficacy. Investigations ofskin test reactivity" and lymphocyte transformationwith C burneti phase 1 and 2 antigens in human beingsshow a good correlation between these two assays ofcell-mediated immunity, again indicating that markersof cellular immunity may be present in the absence ofantibody.Despite the acceptable reaction rates when small

doses of modern, whole-cell, vaccines are given to pre-tested subjects, the pursuit of immunity withoutreactogenicity continues. Phase 1 antigen can beextracted from C burneti with trichloracetic acid;extracts retain CF antigen activity, stimulate neutral-ising antibody in guineapigs, and protect againstchallenge with live organisms. 19,20 Romanian andCzechoslovakian workers21, 22 have immunised peoplewith C burneti phase 1 trichloracetic acid extracts, andsuch "chemovaccines" have apparently protectedagainst infection in laboratory workers23 (doses were

12 Hinrichs DJ, Jerrells TR In vitro evaluation of immunity to Coxiella burneti. JImmunol 1976; 117: 996-1003

13 Kazár J, Skultetyova E, Brezina R. Phagocytosis of Coxiella burneti by macrophagesActa Virol 1975, 19: 426-31

14. Kishimoto RA, Veltri BJ, Shirey FG, Canonico PG, Walker JS. Fate of Coxiella burnetiiin macrophages from immune guinea pigs Infect Immun 1977; 15: 601-07.

15 Kazár J, Schramek K. Relationship between delayed antigenic hypersensitivityreaction and resistance to virulent challenge in mice immunised with differentCoxiella burnetii antigen preparations In. Kazár J, ed. Proceedings of the thirdinternational symposium on rickettsiae and rickettsial diseases. Bratislava VIDA (inpress)

16 Kazár J, Schramek S, Brezina R. The value of skin test in Q fever convalescents andvaccinees as indicator of antigen exposure and inducer of antibody recall. Acta. Virol1984, 28: 134-40

17. Ascher MS, Berman MA, Ruppanner R Initial clinical and immunologic evaluation ofa new phase 1 Q fever vaccine and skin test in humans J Infect Dis 1983; 148:214-22

18. Jerrells TR, Mallavia LP, Hinrichs DJ Detection of long term cellular immunity toCoxiella burneti as assayed by lymphocyte transformation. Infect Immun 1975; 11:280-86

19 Brezina R, Urvolgyi J Extraction of Coxiella burneti phase 1 antigen by means oftrichloracetic acid. Acta Virol 1961; 5: 193

20 Anacker RL, Lackman DB, Pickens EG, Ribi E Antigenic and skin reactive propertiesof fractions of Coxiella burnetii. J Immunol 1962; 89: 145-53.

21 Cracea E, Dumitrescu S, Botez D, et al. Immunisation in man with a soluble Q fevervaccine Arch Roum Path Exp Microbiol 1973; 32: 45-51.

22 Kazár J, Brezina R, Palanova A, Tvrda B, Schramek S. Immunogenicity andreactogenicity of a Q fever chemovaccine in persons professionally exposed to Qfever in Czechoslovakia Bull WHO 1982; 60: 389-94.

23 Brezina R, Schramek S, Kazár J, Urvolgyi J Q fever chemovaccine for human use ActaVirol 1974, 18: 269

approximately 10-20 times greater than those of wholecell vaccine). Although comparisons of reactogenicityof chemovaccines and whole-cell vaccines are difficultto assess, systemic reactions were also related to pre-existing immunity in the Czechoslovakian studies.Other approaches involve use of chloroform/methanol-extracted C burneti phase 1 cells; such a vaccinestimulates protection in guineapigs challenged withaerosols of living C burneti but a lower antibodyresponse.24The lipopolysaccharide of C burneti is unusual both

in its chemical composition25 and in its potency as animmunogen; these properties may be related in termsof slow elimination of a whole-cell vaccine from thetissues and long-term stimulation of cell-mediatedimmunity. It remains to be seen whether the same lipo-polysaccharide, phase 1 antigen, in its own right will beas effective and as long lasting against natural infectionin man.

Towards Better General Practice

A DECADE after the National Health Service (NHS)began, Geiringer’ wrote of the "decapitation of generalpractice" by a threefold effect of the end of private fee-earning : "bad practice, the utility practitioner, and thehospitalisation of medicine"-by which he meant a"voluntary surrender of responsibility on the part ofGPs [which] becomes an almost irreversible customagainst which individual practitioners hold out at theirperil". His assumption that a cheap and nasty system ofcare for the poor was about to wash away all the

growing points of good clinical work in the morereasonable conditions of middle-class practice, wasshared by others, and almost became the receivedwisdom of the time. Yet, today, general practice is themost popular career choice of British medical students.Half the graduates still become GPs, and Britishgeneral practice has an academic, research, and

undergraduate and postgraduate teaching base at leastequal to any other in north-west Europe. Public

opinion polls consistently show satisfaction with theGP service, and GP morale seems to be good.Geiringer got it wrong because he was looking from thetop end of the market, just as Sir Clifford Allbutt haddone in 1912 when he predicted that the precursor ofthe NHS, the Lloyd-George Insurance Act, wouldcondemn all manual workers to "perfunctory care byperfunctory men and degrade the career of medicine by

24 Votruba D, Popper P, Kazár J, Schramek S. Comparison of protective effects ofdifferent Coxiella burnetii preparations against aerosol challenge in guinea pigs In:Kazár J, ed Proceedings of the third international symposium on rickettsiae andrickettsial diseases Bratislavia: VIDA (in press)

25 Schramek S, Mayer H. Different sugar compositions of lipopolysaccharides isolatedfrom phase I and pure phase II cells of Coxiella burneti. Infect Immun 1982, 38:53-57.

1. Geiringer E. Murder at the crossroads or the decapitation of general practice. Lancet1959; i: 1039-45

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sending every malady of importance to some centralinstitution".2 The chance that any randomly selectedpatient consulting a randomly selected GP will receiveinformed, responsible, and effective care is certainlybetter in 1984 than it was in 1959, just as it was better in1959 than it was in 1912. The quality of generalpractice has, by orders of magnitude, improved; andthis improvement has in part occurred because of,rather than despite, registration of the whole

population for State-funded primary medical care.If, however, we look at the quality of general practice

in absolute rather than relative terms, and above all ifwe look at the care of populations at risk rather than theresponse to individually presented sickness, there is amass of evidence to justify the worst fears of bothGeiringer and Allbutt. Type 2 diabetes and

uncomplicated hypertension are common conditions,so common that management of all cases in hospitaloutpatient clinics is logistically impossible, and theyare undeniably at the core of clinical responsibility atany professional level. Yet, comparing type 2 diabeticsrandomly allocated to continued care at a hospitaldiabetic clinic or returned to the care of their GPs,Hayes and Harries3 found that, over five years’ follow-up, only 14% of patients in the GP group had beenreviewed at least once a year, compared with 100% ofthe hospital group, and three times as many had died.Reviewing twenty-seven consecutive hospitaladmissions for ketoacidotic coma, Pyké found thatfifteen patients were previously undiagnosed diabetics.In twelve of these fifteen urine had never been tested,though they had visited their GPs on a total of forty-oneoccasions. In many studies of GP populations half totwo-thirds of all men over 20 have not had their blood-

pressure recorded in over ten years, nearly half of thosestarted on antihypertensive drugs have had only onemeasurement of blood-pressure, and two-thirds havehad no blood or urine tests of any kind.5-8 Reviewing aconsecutive series of hypertension-related deaths inhospital in patients under 50, Whitfield9 found thathypertension had not been recognised before the finalillness in 27%, had been recognised but not treated in20%, and had been treated but not controlled in 51%.Against this discouraging evidence of what actually

happens, is the news of what can be achieved when GPsorganise their work to search for needs, and stop relyingon the customers to initiate every demand. Singh et apocompared diabetics attending GP mini-clinics with

matched controls attending a hospital clinic; there wasno difference in monitoring or metabolic control, andthere was a smaller default rate in the GP group. Hart"

1

found all the hypertensives in a geographically definedGP population by a combination of screening and case-finding and, reviewing them fifteen years later on anintention-to-treat basis, found that group mean

pressure had been reduced from 199/119 to 152/90mm Hg, the proportion of male cigarette smokers hadbeen reduced from 55% to 25%, and 91% of the grouphad been reviewed within the previous three months attime of audit.’2 Many GPs seem now to be turningtowards this more structured approach to continuinganticipatory care and health conservation for high-riskgroups such as diabetics, hypertensives, epileptics, andasthmatics. During the past five years particularly, theRoyal College of General Practitioners (RCGP) hasemphasised the need for a preventive approach basedon a wider team and better organisation of practice13-18and has launched a "quality initiative plan" to improvestandards by encouraging within-practice audit,measuring what actually is done against what ought tobe done, in defined populations.There is a real risk that, in adopting this brave policy,

the RCGP may isolate itself from those many GPs whoconsider themselves already at full stretch meetingindividually presented demands, without the addedburdens of searching for unmet needs and monitoringblood sugars and blood-pressures. The planning,administration, and implementation of blood-pressurecontrol in a general practice population requiresroughly one 3-hour session of medical time each week,about half of which is face-to-face with patients. Thiscould be reduced by computer-assisted records, andmore imaginative work-sharing with nurses and

receptionists, but if we then go on to include

management on a local population scale of type 2diabetes, airways obstruction, epilepsy, rheumatoiddisease, and chronic psychotic illness-in all of which agood case can be made for community rather thanoutpatient management-there is no way all this can beaccommodated. Individual pioneering GPs have

developed components of this more effective future,but only at a personal and family cost in time andmoney which repels more colleagues than it attracts.The 1966 Charter was a turning point for general

practice in Britain. No randomised trial is necessary toshow that GPs working from their own front parloursor squalid lock-up shops, in isolation, without office or

2. Allbutt TC. Times, Feb 27, 1912.3. Hayes TM, Harries J. Randomised controlled trial of routine hospital clinic care versus

routine general practice care for type II diabetes. Br Med J 1984; 289: 728-30.4. Pyke DA. Diabetic ketoacidosis. J Roy Soc Med 1980; 73: 131-34.5. Kurji KH, Haines AP. Detection and management of hypertension in general practices

in northwest London. Br Med J 1984; 288: 903-06.6. Michael G. Quality of care in managing hypertension by case-finding in northwest

London. Br Med J 1984; 288: 906-08.7. Ritchie LD, Currie AM. Blood pressure recording by general practitioners in northeast

Scotland Br Med J 1983; 286: 107-09.8. Heller RF, Rose GA. Current management of hypertension in general practice. BrMed

J 1977; i: 1442.9. Whitfield AGW. Young medical deaths: their cause and prevention. Update February

1981, 1249-54.10. Singh BM, Holland MR, Thorn PA. Metabolic control of diabetes in general practice

clinics: comparison with a hospital clinic. Br Med J 1984; 289: 726-28.

11. Hart JT. Semicontinuous screening of a whole community for hypertension. Lancet1970; ii: 223-26.

12. Hart JT Prevention of coronary heart death in general practice. Postgrad Med J 1984;60: 42-46.

13. Health and prevention in primary care. Reports from general practice, no 18 London:Royal College of General Practitioners, 1981.

14. Prevention of arterial disease in general practice Reports from general practice no 19.London Royal College of General Practitioners, 1981.

15 Prevention of psychiatric disorders in general practice. Reports from general practiceno. 20. London: Royal College of General Practitioners, 1981.

16 Family planning-an exercise in preventive medicine. Reports from general practiceno. 21. London: Royal College of General Practitioners, 1981.

17. Healthier children-thinking prevention. Reports from general practice no 22.

London: Royal College of General Practitioners, 1982.18. Handbook of preventive care for pre-school children London: BMA General Medical

Services Committee & Royal College of General Practitioners, 1984

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nursing staff, and meeting all the costs of a publicservice from their own pockets, make less effective useof their long and costly training than GPs working ingroups, assisted by secretaries and nurses, in purpose-built premises, with most of the costs met directly bythe State. If hopes for better care from group practiceare still incompletely realised, this is attributable not toa failure of the large public investment in primary careencouraged by the 1966 Charter, but to lack of

accountability: GPs were completely free to continuewithout adequate supporting staff; and quality of caredoes not always go hand in hand with financial

rewards, which began to reach high levels for youngGPs.How might general practice be stimulated to

undertake some of the tasks now performed so

insensitively and wastefully by hospital outpatientdepartments?19 The first requirement would be a

substantial increase in supporting staff, thus a muchbigger public investment in primary care; and thefamily practitioner committee, practice team, and

registered population might reasonably ask forevidence of value for money: Is there forward planningfor defined objectives? What is actually done in relationto what needs to be done? Hart20, 21 has outlined one setof proposals of this kind-whereby a communitygeneral practitioner would act as medical officer ofhealth reporting on these matters, once a year, not onlyto the family practitioner committee but also to his orher registered population: the watchword is

accountability. Similar ideas have been put forward byVarnam22 and the Medical Practitioners’ Union.23Diametrically opposed to these are proposals, fromMaynard and Marinker,24 that GPs should act as

budget-holders for the entire NHS, spending thepractice allocation as they think best, and promotingfashionable competition between hospitaldepartments. The BMA General Medical ServicesCommittee’s proposals for expanded fees-for-service afew years ago foundered as it became apparent to

everyone that they would be both inflationary andunworkable. Robson25 has presented a serious case forsalaried service, drawing attention to experience in theProvince of Quebec, central Oslo, Finland, and somecities in France. The long-delayed Government green-paper on general practice, now due to appear early in1985, will almost certainly favour a cost-sensitive

contract, possibly linked also with performance. Thiswill force the matter onto the medicopolitical agenda.Let us hope that the contract will be fashioned notmerely to save money, but also to secure better publichealth through more effective and accountable generalpractice.

19 Todd JA Wasted resources. Lancet 1984; ii: 1089, 126620. Hart JT. A new kind of doctor J Roy Soc Med 1981, 74: 871-83.21 Hart JT. The community general practitioner Br Med J 1984; 288: 1670-73.22 Varnam MA. Should general practitioners be planners? Br Med J 1982; 285: 479-80.23. Medical Practitioners’ Union. A new charter for general practice? London. Association

of Scientific, Technical & Managerial Staffs, 1984.24. Marinker M. Developments in primary health care In: Teeling-Smith G, ed. A new

NHS Act for 1996? London: Office of Health Economics, 1984: 17-22.25 Robson J Salaried service—a basis for the future? Br Med J 1981; 283: 1225-27

FETAL CHROMOSOME ABNORMALITIES

THE importance of the mother’s age to the risk of a babybeing born with Down’s syndrome was recognised byPenrose in 1934, and this observation has since been foundtrue of other chromosome disorders. Prenatal monitoring andselective termination of pregnancies will distort the incidenceof these conditions at birth and blur the correlation with the

age of the mother. It has been suggested, therefore, that infuture the risks quoted to would-be mothers and pregnantwomen should be obtained by extrapolation from the

frequency of chromosomally abnormal fetuses identified byprenatal diagnostic procedures. Adjustments would have tobe made for the natural fetal loss that occurs when

pregnancies are allowed to continue to spontaneoustermination. With this requirement in mind a collaborativestudy has been undertaken in 58 European centres and wenow have results in 52 965 pregnancies in women over 34years of age.2 Chromosome aberrations were detected in 1200pregnancies and from these data age-specific incidence rateshave been derived. The rates for trisomy 21, the mostcommon abnormality, rise from 0.38% at age 35 to a peak of5 - 75% at age 46. The rates for trisomy 18 rise from 0 .05% to0 - 76% at age 43 and for trisomy 13 from 0 - 0207o to a peak of0.21% at age 42 years. Within these age ranges the rise is

exponential but after the peak age for each trisomy the rateaverages out at 2 .33%, 0 .48%, and 0 .05%, respectively.The authors of the report suggest that the fall-off in rate is dueto an inability of older mothers to maintain a fetus with anautosomal trisomy in utero up to the time of amniocentesis.This explanation is consistent with the earlier change in ratefor the more severe trisomy conditions. There is also thepossibility that the change may reflect different risks formothers of the same age but born in different years. If thereare enough data, this possibility could be investigated by acohort analysis.3 The report provides no information on thetotal number of pregnant women in each age group in theareas served by the contributing centres. Nor does it disclosethe number of babies with chromosome abnormalities born tomothers whose pregnancies were not monitored. The

proportion of amniocenteses presumably rises with maternalage, which would explain the increasing numbers of

pregnancies included in the study for each age up to age 40.Information on pregnancies in the same age range but whichwere not monitored may be available and would be

biologically and clinically valuable.About 10% of infants with chromosome abnormalities at

birth have an unbalanced chromosome structural re-

arrangement. In most of them, the structural rearrange-ment is carried in a balanced form by one of the parents.These carriers are a well-defined group of patients requiringgenetic counselling and prenatal diagnosis. It has long beenrecognised that the frequency of unbalanced rearrangementin offspring falls far short of the theoretically expectednumbers and is strongly influenced by the method ofascertainment of the carrier parent. In a collaborative

European study4 of 1079 families with segregating structuralchromosomal anomalies, 408 were ascertained through aninfant with an unbalanced structural rearrangement and 294

1. Penrose LS The relative etiological importance of birth order and maternal age inmongolism Proc R Soc B 1934; 115: 795.

2 Ferguson-Smith MA, Yates JRW. Maternal age-specific rates for chromosomeaberrations and factors influencing them report of a collaborative European studyon 52,965 amniocenteses. Prenat Diagn 1984; 4: 5-44.

3. Case RAM Cohort analysis in cancer mortality in England and Wales 1911-1954 bysite and sex. Br J Prev Soc Med 1956; 10: 172-99.

4. Boué A, Gallano P A collaborative study of the segregation of inherited chromosomestructural rearrangements in 1,356 prenatal diagnosis Prenat Diag 1984; 4: 45-67