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travellers. It is also felt useful to illustrate something of the burdenof infection experienced in tropical parts so as to put health

problems into a worldwide perspective.At a time when career structures in hospital medicine and general

practice in the U.K. are becoming more stereotyped we agree thatthere is a need for a secure home base for doctors gaining the tropicalexperience necessary to understand and manage importedinfections successfully.Fostering relationships between departments of medicine in the

tropics and departments of infectious diseases in the U.K. cansignificantly assist in this and also provide mutual benefit throughsharing knowledge and experience in the search for better diseasecontrol.

University Department of Infectious Diseases,Ruchill Hospital,Glasgow G20 9NB

ERIC WALKERN. R. GRISTI. W. PINKERTON

MENSA MISUNDERSTANDING?

SIR,-Your note (Feb. 6, p. 349) seems to misunderstand thepurpose and conclusions of our study. The note states that "a causeand effect relationship" between gout and high IQ "cannot beidentified from the Edinburgh study", that "a link between myopiaand intelligence does not need a genetic explanation", and that"Whatever the explanation for the observed associations in Mensamembers, the Edinburgh study provides no evidence for a geneticconnection".Nowhere in our report did we claim to have demonstrated a cause

and effect relationship between gout and high IQ, or a commongenetic basis for gout, myopia or infantile autism and high IQ. Ourclearly stated aim was to try and confirm previously reportedassociations between high IQ and various inherited disorders, notby measuring intelligence in those with the disorders and theirrelatives, as has been done in the past, but rather studying theprevalence of the disorders in a group of highly intelligentindividuals and their relatives. Using this completely differentapproach and looking at a number of disorders at once, instead ofsingle disorders as in previous studies, we were able to demonstratean association of high IQ with gout, myopia, and infantile autism,supporting the suggestions of earlier work.2-4 However, we plainlyacknowledged that such associations can occur for several reasons,and drew attention to the fact that further studies, both

epidemiological and biochemical, are required before a commongenetic basis for any disorder and high IQ can be accepted.Department of Oral Medicineand Oral Pathology,

University of Edinburgh,Old Surgeons Hall,Edinburgh EH1 1NR

University Department of Human Genetics,Western General Hospital,Edinburgh EH4 2XU

J. A. SOFAER

A. E. H. EMERY

COMMUNITY HEALTH COUNCILS

SIR,-My views on community health councils have been mis-quoted in your issue of Jan. 23 (p. 235). I think that communityhealth councils should stay, and I did not compare them

unfavourably (or otherwise) with their French counterparts asstated in your note. I did, however, support Dr David Tod’s viewthat there is a need for some form of hospital inspectorate in theU.K. and I suggested that general practice should be subject to acomparable form of scrutiny.

Hospital of St Cross,Rugby, Warwickshire T. L. DUNN

1. Sofaer JA, Emery AEH. Genes for super-intelligence? J Med Genet 1981; 18: 410-13.2. Anon Uric acid and the psyche. JAMA 1969; 208: 1180.3 Karlsson JL. Influence of the myopia gene on brain development. Clin Genet 1975; 8:

314-18

4 Rimland B Infantile autism. London Methuen, 1965.

1. Horwitz A, Henle W, Henle G, et al. Persistent falsely positive rapid tests for infectiousmononucleosis. Am J Clin Pathol 1979; 72: 807-11

2. Stanček D, Rovensk J. Enhancement of EBV antibody production in SLE patients.Acta Virol 1979; 23: 168-69.

3. Evans AS, Rothfield NF, Niederman JC. Raised antibody titres to EBV in SLE. Lancet1971; i: 167-68.

4. Carter RL, Penman HG. Infectious mononucleosis. Oxford: Blackwell, 1969.

SYSTEMIC LUPUS ERYTHEMATOSUS PRESENTINGAS INFECTIOUS MONONUCLEOSIS WITH A FALSE

POSITIVE MONOSPOT TEST

StR,-The ’Monospot’ test has become well established as a quickand reliable way of confirming the clinical impression of infectiousmononucleosis in patients with atypical lymphocytes in their

peripheral blood. False positive monospot tests are rare, but havebeen reported in rubella, malaria, serum hepatitis, pancreaticcarcinoma, leukaemia, and lymphoma. There is a strongassociation between systemic lupus erythematosus (SLE) and hightitres to Epstein-Barr virus (EBV),2 but so far no positive monospottest has been reported in a patient with SLE.3 We report a case ofSLE presenting with a clinical picture not unlike that of infectiousmononucleosis during its early stages, where infectiousmononucleosis was erroneously diagnosed on the basis of whatturned out to be a false positive monospot test. ,,-

A previously fit 15-year-old girl presented to her generalpractitioner with a sore throat and generalised arthralgia in January,1981. Over the next 2 weeks these symptoms became worse, andfever developed. A monospot test was negative at this time. She wasadmitted to hospital where she was found to have a high remittingfever. There was slight axillary and cervical lymphadenopathy. Apartial ptosis developed, affecting both eyes and lasting 48 h. Arepeat monospot test, done 18 days after her first presentation, waspositive. She was discharged with a diagnosis of infectiousmononucleosis. At home she remained ill, and she was readmitted, 1month after the first onset of symptoms, with arthritis, pleuriticchest pains, and widespread livido reticularis.Her general practitioner found her haemoglobin to be 12 g/dl,

and the white cell count was 5-4 109/1 (82% polymorphs, 15%lymphocytes, 2% monocytes, and 1% eosinophils). The erythrocytesedimentation rate was 55 mm in the first hour. Liver function testswere normal. The antinuclear factor titre was positive at 1/2560dilution, with a DNA antibody titre of 98% in plasma diluted 1/20.Serum C3 and C4 were both reduced. The patient was dischargedbefore the results of these immunological investigations wereavailable. During her second stay in hospital the monospot test wasrepeated, and was again positive, but at no time were there

significant numbers of atypical lymphocytes in her peripheralblood. Three serum samples taken during the first 8 weeks of illnessshowed IgG antibodies to EBV at dilutions greater than 1/2048.This patient clearly had SLE, but it might be argued that she also

had infectious mononucleosis and that the monospot test was not,therefore, falsely positive. This seems unlikely because of thenormal blood film. As Carter and Penman point out,4 the diagnosisof infectious mononucleosis depends on demonstration of atypicallymphocytes in the peripheral blood, so that a positive monospottest, on its own, is not diagnostic.There have been a number of explanations put forward to account

for the high levels of EBV antibody found in SLE, EBV antigenicstimulation might be a cause of SLE or there could be a reawakeningof EBV antibody production after earlier exposure to EBV. It is alsopossible that previous exposure to EBV is not required for theproduction of antibody to EBV in patients with SLE.

It seems likely that, given the random way in which the immunesystem is activated in SLE, it just so happened that in this girlheterophil antibodies and antibodies to EBV were being producedtogether, around the time of her presentation, exactly as if she hadbeen having infectious mononucleosis. Hence there is room fordiagnostic confusion unless due weight is given to the presence orabsence of atypical lymphocytes in the peripheral circulation.Naffield Department of Medicineand Department of Cardiology,

John Radcliffe Hospital, Oxford

B. M. HENDRY*

J. M. LONGMORE*Present address: Physiological Laboratory, University of Cambridge.