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3. Cemacek J. Stabilography in neurology. Agressologie 1980; 21: 25-29.4. Andres RO, Anderson DJ. Designing a better postural measurement system. Am J

Otolaryngol 1980; 1: 197-206.5. Wall C, Black FO. Postural stability of rotational tests: their effectiveness for screening

dizzy patient. Acta Otolaryngol 1983; 95: 235-46.6. Morest DK. Degeneration in the brain following exposure to noise. In: Hamernik RP,

Henderson D, Salvi R, eds. New perspectives on noise-induced hearing loss. NewYork: Raven Press, 1982: 87-102

7. Morest DK, Bohne BA. Noise-induced degeneration in the brain and representationof the inner and outer hair cells. Hear Res 1983; 9: 145-51.

8. Ylikoski J. Impulse noise induced damage m the vestibular end organs of the guineapig Acta Otolaryngol 1987; 103: 415-21.

9. Dickson ED, Chadwick DL. Observations on disturbance of equilibnum and othersymptoms induced by jet-engine noise. J Laryngol Otol 1951; 65: 154-65.

10. Antaglia JR, Cohen A. Extra-auditory effects of noise as a health hazard. Am IndustHyg Ass J 1970; 31: 277-81.

11. Kemink JL, Graham MD. Hearing loss with delayed onset of vertigo. Am J Otol 1985;6: 344-48.

12 Ylikoski J. Delayed endolymphatic hydrops syndrome after heavy exposure to impulsenoise. Am J Otol (in press).

13. Juntunen J. Neurological examination and assessment of the syndromes caused byexposure to neurotoxic agents. Adv Biosci 1983; 6: 3-10.

14. Norre ME, Forrest G. Posture testing (posturography) in the diagnosis of peripheralvestibular pathology. Arch Otorhinolaryngol 1986; 243: 186-89.

15. Skre H. Neurological signs m a normal population. Acta Neurol Scand 1972; 48:575-606.

16. Anderson RG, Meyerhoff WL. Otologic manifestation of aging. Otolaryngol Clin NAm 1982; 15: 353-70.

17. Era P, Heikkinen E. Postural sway during standing and unexpected disturbance ofbalance in random samples of men of different ages. J Gerontol 1985; 40: 287-95

18. Pyykko I, Månsson M, Matsuoka I, Ito S, Hinoki M. Effects of pure-tone sound,impulse noise, and vibration on visual orientation Am J Otol 1982; 3: 104-11.

19. Collins EG. Aural trauma caused by gunfire. J Laryngol Otol 1948, 62: 388-90.20. Hamernik RP, Henderson D, Crosley JJ, Salvi RJ. Interaction of continuous and

impulse noise: audiometric and histological effects. J Acoust Soc Am 1974; 55:117-21.

21. Hamernik RP, Turrentine G, Roberto M, et al. Anatomical correlates of impulsenoise-induced mechanical damage m the cochlea. Hear Res 1984; 13: 229-47.

22. Spoendlin HH. Anatomic changes following various noise exposure. In: HendersonD, Hamernik RP, Dosengsh DS, Mills JH, et al, eds. Effects of noise on hearingNew York: Raven Press, 1976: 69-87.

23. Oosterveld WJ, Polman AR, Schoonhey J. Vestibular implications of noise-inducedhearing loss. Br J Audiol 1982; 16: 227-32.

24. Steel K, Bock GR. Genetic factors affecting hearing development. Acta Otolaryngol1985; Suppl 421: 48-56.

Conference

LYME DISEASE IN EUROPE

LYME disease, though reported from most Europeancountries, is an uncommon zoonosis, and the spectrum ofclinical manifestations is still expanding. The infection,caused by a spirochaete, Borrelia burgdorferi, follows the biteof the hard tick Ixodes ricinus and in some cases

mosquitoes-borreliae may persist in the mouthparts ofmosquitoes for at least 48 h. The principal mammalian hostsare deer. The earliest (stage I) feature is the distinctive skinhallmark, erythema chronicum migrans (ECM),1 whichmay be followed by disease of the central and peripheralnervous systems2 and heart3 (stage II), with acrodermatitischronica atrophicans (ACA),4 solitary or diffuse lymphade-nosis benigna cutis (LBC)5, and, rarely, arthritis arising aslate (stage III) manifestations months or years later. Thestages are often imprecise, and in some patients the stagesmay overlap or be altogether absent. The arbitrary classifi-cation into stages is perhaps best discontinued, and themanifestations should probably be perceived as early andlate phases of the disease.At a conference in Vienna in June, the relationship of

borrelia to a variety of syndromes was discussed. Thosediseases now known definitely to be caused by B burgdorferiinclude the skin disorders ECM, ACA, and LBC; theneurological disease triad meningoencephalitis, cranial neu-ritis, and radiculoneuritis, (Garin-Bujadoux-Bannwarthsyndrome); arthritis, pancarditis, and the more recentlydescribed hepatitis, nephritis, uveitis, and precursors ofACA, such as a Shulman-like myositis6 and atypicalmorphoea. An underlying vasculitis dominates the path-ology. More difficult to determine with respect to borrelialpathogenesis are anetoderma and Sudeck’s atrophy-anill-defined syndrome of chronic neuroborreliosis withfeatures of depression, demyelination, optic atrophy, trans-verse myelitis, and pseudotumor cerebri.The evidence for an association of B burgdorferi with

multiple sclerosis7 and Alzheimer’s disease is unconvinc-ing. Liability to ECM following tick-bite was investigatedby R. Ackermann, who found that the disorder

developed in only 1 of 51 children bitten by ticks proven tobe infected with B burgdorferi. Histocompatibility antigensmay provide a clue to susceptibility. DR2 was less common

in chronic neurological disease than in Lyme arthritis. HLACW3 may be a marker of reduced resistance, whereas HLACW7 may be associated with protection against infection.

This clinical uncertainty arises from the lack of specificdiagnostic tests. Borrelia-derived antigens are heter-

ogeneous. Indirect immunofluorescence and enzyme-linked immunosorbent assay (ELISA)9 are the methodsmost commonly used in the laboratory, but both tests lackspecificity and there is no generally agreed criterion as towhat constitutes a positive test. The confidence limit ofpositivity in a rural area may be very different from thatfound in town.10 Some discrepancies can also be accountedfor by loss of plasmids from the borrelia during passage, butthere are genuine differences between human and tickisolates. Western blots could well become the gold standardin diagnosis.These fmdings highlight the need not only for typing

methods for borrelia but also for the subsequent develop-ment of genus and ultimately species specific antigens. Tothis end, interesting work was presented by Dr K. Hansenand colleagues from Denmark, who identified a recombi-nant clone of Escherichia coli that expressed potential antigencomposed of 30 kD, 21 kD, and 19 kD proteins ofB burgdorferi in E coli. Hansen also found that a 41 kDperiaxial filament protein extracted from B burgdorferiincreased diagnostic sensitivity when used as antigen inELISA and promises to replace the current screening test.The ability of strains to undergo antigenic variation may

further confuse the serology. Genes encoding the outersurface proteins OspA and OspB are located on linearplasmids rather than in the bacterial chromosome." DNAprobe analysis shows that (in the American strain B31) theOspA and OspB genes are located on a 49 kb linear plasmid.It is now thought likely that plasmid variation withinB burgdorferi may influence strain antigenicity.

Borrelia infections are increasingly being recognised, butcaution is needed when interpreting the results of positivetests until better diagnostic tests are available. Whereas thediagnosis may be easy in the presence of a positive history oftick bite and ECM, confirmation of neurological Lymedisease needs not only positive serology but also

cerebrospinal-fluid antibodies. Similarly, in arthritis, speci-fic antibodies in synovial fluid would likewise be required.There may be a delay in the appearance of both serum andCSF IgG antibodies, and these antibodies may persistindefinitely in the CSF after treatment. The finding ofimmunoblasts in the CSF or Reed-Sternberg-like cells in

265

the spleen may account for the persistence of antibodies, andaccumulations of such lymphocytes have led clinicians

mistakenly to diagnose cerebral B-cell lymphomas. Isolationof B burgdorferi from patients with clinical features of Lymedisease has not always been successful but should always beattempted to confirm the diagnosis.12,13

REFERENCES

1 Muhlemann MF. Thirteen British cases of erythemia chronicum migrans in Britain.Br J Dermatol 1984; 111: 335-39.

2. Reik L, Steere AC, Bartenhagen NH, Shope RE, Malawista SE. Neurologicabnormalities of Lyme disease. Medicine 1979; 58: 281-93.

3. Marcus LC, Steere AC, Duray PH, Anderson AE, Mahoney EB Fatal pancarditis in apatient with coexistent Lyme disease and babesiosis. Ann Intern Med 1985; 103:374-76.

4. Asbrink E, Hovmark A, Olsson I. Clinical manifestations of acrodermatitis chronicaatrophicans in 50 Swedish patients. Zbl Bakt Hyg A 1968; 263: 253-61.

5 Wilske B, Schierz G, Preac-Mursic V, Weber K, Pfister H-W, Einhaupl K.Serological diagnosis of erythma migrans and related disorders. Infection 1984; 12:331-37

6. Duray PH. Lyme borreliosis: Histopathology updated. Abstracts of meeting on Lymedisease in Europe, 1987, p 31.

7. Schutzhard E, Pohl P, Stanek G. Failure to demonstrate B burgdorfen as an etiologicagent in multiple sclerosis. Abstracts of meeting on Lyme disease in Europe, 1987,p 38.

8. McDonald AB, Borrelia in the brains of patients dying of early dementia. J AMA 1986;256: 2195-96.

9. Magnerelli LA, Meegan JM, Anderson JF, Chappel WA. Comparison of an indirectfluorescent antibody test with an enzyme linked immunosorbant assay for

serological studies of Lyme disease. J Clin Microbiol 1984; 20: 181-84.10. Cooper C, Muhleann M, Wnght DJM, Hutchmson CA, Armstrong R, Maini RN.

Arthritis as a manifestation of Lyme disease in England. Lancet 1987; i: 1313-14.11. Howe TR, LaQuier MW, Barbour AG. Organisation of genes encoding two outer

surface membrane proteins of the Lyme disease agent Borrelia burgdorfen within asingle transcription unit. Infect Immun 1986; 54: 207-12.

12. Barbour AG. Cultivation of Borrelia: A historical overview. Zbl Bakt Hyg A 1986, 263:11-14.

13. Asbnnk E, Hovmark A. Successful cultivation of spirochaetes from skin lesions ofpatients with erythema chronicum migrans Afzelius and acrodermatitis chronicaatrophicans. Acta Path Microbiol Scand B 1985; 93: 161-63.

Point of View

DUAL MEANING OF MEMBERSHIP

SUCCESS in the demanding and expensive examinationsfor membership (or fellowship) of a Royal College is now arequirement for a consultant post in most specialties. Theseregistrable higher qualifications (MFCM, MRCP, and soon) are regarded as evidence of having met certain

professional standards of knowledge and competence. But itis not that simple. The right to use the qualification maydepend on indefinite annual payments to the College thatawarded it. In the Faculty of Community Medicine, forexample, non-payment of fees for six months leads toremoval from membership of the Faculty and loss of theright to use the designation MFCM. It is bizarre that youshould lose an educational qualification if you choose not toremain a member of the institution that awarded it. It maybe fair to expel members of a club for non-payment of asubscription, but it is wrong to strip them of professionalstatus earned by examination. The two meanings of

"membership"-a mark of achievement and membership ofa club-have become confused.

The Faculty of Community Medicine would doubtlessargue that you are elected to membership under its rules,one of which is that you must first pass the examinations."Election" to membership, however, is merely a blanketacceptance of the latest batch of successful examination

candidates, and it is made conditional upon agreement toabide by the rules, one of which sets out a duty to pay annualfees in order to remain a member. But no-one takes a

membership examination just to join a club. They do it toearn a badge of professional excellence with a worldwidecurrency; many overseas candidates never practise in theUK. Nor do the documents dealing with the examinationmake it clear that if you pass, the right to use the

postgraduate qualification will be conditional on indefiniteannual payments.

Faculty members thus find themselves in an invidiousposition: either they continue paying fees long after theyhave passed the examination or they refuse and are expelled.They could then risk prosecution for deception if they holdthemselves out as having "the membership" when obtaininga post for which such membership is required. It is most

unlikely that a court of law would take the same view ofmembership as the Faculty does, but it cannot be theintention behind the rules under which members are"elected" to place them in this position.One argument might be that continued club membership

is necessary to ensure maintenance of standards throughprofessional contact and continuing education. But annualpayment of membership fees is a poor proxy for themaintenance of standards or commitment to continuingeducation.

The rules should be changed so that the membershipexamination would become like any other examination: a

pass would be recognised by the irreversible award of thequalification and there would be no subsequent financialobligation. Such a change would have several advantages.Paying membership of the Faculty would become a

voluntary act, which it should be. Examination successcould then be followed by an invitation to become a payingmember. Many, perhaps most, doctors would wish tosupport the -body that represents their discipline bybecoming active, paying members and receiving its journal.The Faculty would also be obliged to reflect the views andaspirations of its members. There would be no reason torestrict paying membership to doctors who had passed theexamination (or had been deemed too eminent to take it) andmembers of other professions could join. Medical practice,teaching, and research are no longer the exclusive preserveof medically qualified doctors. Biochemists, physiologists,and statisticians are just a few of the many scientists who playan active part in medicine today, and their contributionmight be as invaluable to the Faculty of CommunityMedicine as it already is in hospitals, medical schools, andresearch institutions.

The situation in other Faculties and Royal Colleges is lessclear but we suspect that the Faculty of CommunityMedicine is not alone in having adopted the dual meaning ofmembership. Diplomas in child health and in tropicalmedicine and hygiene are registrable higher medical

qualifications awarded irreversibly on examination success,and membership of the Royal College of Physicians dependsonly on examination, with no obligation to pay annual fees.How can the Faculty of Community Medicine (or any otherFaculty or Royal College with similar rules) justifyprofessional blackmail?

Radcliffe Infirmary,Oxford OX2 6HE

MICHEL P. COLEMANDAVID MANT