1204 POLYUNSATURATED FATTY ACIDS AND THE BRAIN
SIR,--I agree with Professor Dobbing (May 21, p. 1107) that the brain structural lipids are "astonishingly unaffected by quite severe and long-standing modifications of dietary lipid quality". We have made this point ourselves. I,2 Nevertheless, those who have succeeded in changing the brain structural lipids in rats have also demonstrated altered function.3-9 Since Hansen et al.lo have already produced severe signs of
essential-fatty-acid deficiency, demonstrating a qualitative requirement that matters profoundly to the human infant, no one would wish to repeat their experiments on children, before after birth. We have no evidence that the growing human brain can make its own essential fats; it must obtain them, eventually, from the diet. There is increasing evidence of the physiological and structural importance of the long-chain unsaturated derivatives which dietary fats must provide, either because they contain them or because they are converted into them or
metabolically. interested in understanding the role of lipids in human without incurring risk or causing damage, and I believe that efforts to provide it with optimum nutrients will I
am
development, not
be misplaced.
Nuffield Institute of Comparative
Zoological Society of London, London NW1 4RY
Medicine,
M. A. CRAWFORD
SIR,-We thank Dr Crawford for his interest (April 30, p. 953) in our letter (April 2, p. 751). However, we did not state that "higher essential fatty acids are absent from plants" but that "long-chain polyunsaturated fatty acids are absent from higher plants". We are aware that long-chain polyunsaturated fatty acids (L.C.P.), with 20-22 carbon atoms, are found in some lower plants (e.g., ferns and alga :) but these are not common dietarv items. As far as we could ascertain no L.C.P. were present in the diets of our vegans. Neither did we conclude that "the high arachidonate and low docosahexaenoate levels in vegans were due to to increased synthesis of arachidonate from linoleate"; differences in fatty-acid composition were reported and not concentrations as implied by Dr Crawford. We concluded that the high ratio of linoleate/a-linolenate in the vegan diet suppressed L.C.P. production from at-linolenate, which raises the question as to whether the long-chain derivatives of oc-linoleriate perform any physiologically essential functions. We assume Dr Crawford now agrees that there is no evidence, as yet, to suggest that L.c.p. are necessary in the human diet for normal brain development. Department of Pathology, Kingston Hospital, Kingston-upon-Thames, Surrey
T. A. B. SANDERS F. R. ELLIS
Nutrition Division,
Department of Biochemistry, University of Surrey, Guildford, Surrey GU2 5XH
J. W. T. DICKERSON
us he has nothing to add except to that Dr Sanders and his colleagues were not study-
***Dr Crawford tells
emphasise
Crawford, M. A., Casperd, N. M., Sinclair, A. J. Comp. Biochem. Physiol. 1976, 54B, 395. 2. Crawford, M. A. Biochem. Soc. Trans. 1976, 4, 231. 3. Caldwell, D. F., Churchill, J. A. Psychol. Rep. 1966, 19, 99. 4. Galli, C. in The Essential Fatty Acids; p. 59. Miles Laboratories Ltd., Ontario, 1976. 5. Sinclair, A. J., Crawford, M. A. Br. J. Nutr. 1973, 29, 127. 6. Sun, G. Y., Sun, A. Y. J. Neurochem. 1974, 22, 15. 7. Lamptey, M. G., Walker, B. L. J. Nutr. 1976, 106, 86. 8. Wheeler, T. G., Benolken, R. M., Anderson, R. E. Science, 1975, 188, 1312. 9. Clausen, J., Moller, J. Acta neurol. scand. 1967, 43, 375. 10. Hansen, A. E., and others. Pediatrics, 1963, 31, suppl. 1, part 2, p. 171. 1.
ing the brain; also, he has found that the seaweeds vegans eat contain even higher proportions of their fatty acids as arachidonate (3-14%) than does meat.’ Seaweeds are algx.-ED.L. HOUSE PETS AND MULTIPLE SCLEROSIS
SIR,-Dr Cook and Dr Dowling (May 7,
p. 980) reported statistically significant association between exposure to house pets and multiple sclerosis (M.S.). They found that in multiplecase families in New Jersey a significantly greater proportion of M.S. patients than a carefully matched control group had exposure to small indoor dogs and cats. The association was especially strong for pet exposure five and ten years before onset of the first symptom of M.S. They also report a specific instance in which three sisters living in the same home developed symptoms of M.S. at about the same time and subsequent to the development of acute encephalopathy in an aged family dog. The probability of this cluster arising by chance is very small. In our study of M.S. in the Orkney and Shetland Islands of Scotland, which have the highest rates of M.S. reported anywhere (309/100 000 and 184/100 000, respectively) we examined animal exposure at different ages among M.S. patients and two groups of age and sex-matched controls. We found no significant differences in degree of contact among M.S. patients a
and controls to over a dozen domestic farm animals and comhouse pets at ages 0-14, 15-21, or 22 to the time of study. At the request of Dr Cook and Dr Dowling we determined the proportion of M.S. patients and controls exposed to an indoor house pet (dog or cat) five years before the onset of M.S. and found the proportions to be comparable among the two groups (74% and 71%, respectively). Although our study did not inquire about dog size, it is our general impression that most dogs in Orkney and Shetland are small (<25 lb, -11 .4 kg), We are, therefore, unable to confirm the association between exposure to small indoor pets and M.S. Nevertheless, the association found by Dr Cook and Dr Dowling is of interest and requires further investigation in light of the postulated role of a common viral agent in the aetiology of M.S.2.3 mon
Harvard Medical School and Massachusetts General Hospital, Boston, Massachusetts 02114, U.S.A.
DAVID C. POSKANZER L. BRADFORD PRENNEY JEAN L. SHERIDAN
PREGNANCY HEPATITIS IN LIBYA
SIR,-My experience at Tripoli Central Hospital, Libya, during 1968-70 was similar to that described by Christie et a1.4 From January to August 1970, 16 of 62 (26%) pregnant women with jaundice died in hepatic coma, while only 1 of 35 jaundiced, non-pregnant women, aged 15-45 years died. An additional 8 pregnant or puerperal women and 1 non-pregnant woman showed signs of impending or fully developed hepatic coma but recovered. I did liver biopsies on 6 of these 8 women 1-3 weeks after admission. 5 showed vacuolation of liver cells and mononuclear cell infiltration which varied from slight to heavy; bile pigment was present in all 5 biopsy specimens and 2 showed bile thrombi. The sixth biopsy specimen showed marked fatty degeneration only. 10 pregnant women with jaundice and neurological changes were tested for HBsAg by immunoelectrophoresis, and 1 was positive. This compared with 26 out of 84 (31%) of other patients with acute hepatitis and 6 out of 200 (3%) of blooddonors. 6 pregnant women with jaundice and neurological changes had a mean serum-protein of 5.6g/dl (S.D. 0.61 g), while the serum-protein in Iwomen in the last trimester of pregnancy 1. Hitchcock, C., Nichols, B. W. in Plant Lipid Biochemistry. London, 1971. 2. Schapira, K., Poskanzer, D. C., Miller, H. Brain, 1963, 86, 315. 3. Poskanzer, D. C., Schapira, K., Miller, H. Lancet, 1963, ii, 917. 4. Christie, A. B., Allam, A. A., Aref, M. K., El Muntasser, I. H., El-Nageh, M. Lancet, 1976, ii, 827.
1205
jaundice but no neurological changes was 6-2±0-35 g/dl. A t test shows that the difference does not quite reach statistical significance. I agree that the most likely cause of this severe syndrome is some form of non-B viral hepatitis, but no convincing reason for the severity of the disease in Libya has yet been suggested. Severe hepatitis in pregnancy is rare in Papua New Guinea, despite widespread circulation of hepatitis viruses and marginal protein intakes.
lated from a urethral swab taken from this patient 4 months after primary infection. Disc sensitivity testing showed resistance to 1 and 10 units of benzylpenicillin, tetracycline (10 jg), streptomycin (10 g), co-trimoxazole, and erythromycin
I thank Dr G. C. Turner for the for reporting on the liver biopsies.
gonorrhcsce is present
with
Department of Community Medicine, University of Papua New Guinea, Port Moresby, Papua New Guinea
HBaAG tests
and Dr S. A. Wassef
G. B. WYATT
PENICILUNASE-PRODUCING NEISSERIA GONORRHŒÆ FROM SOUTH AFRICA the first African country from which penicillinase-producing Neisseria gonorrhaeae was reported.’ Since then a case has been described from South Africa,2 this patient, a White, also having been intected in West Africa. Investigation of the penicillin sensitivity of gonococci isolated from the indigenous Black population of Durban has shown two isolates to be penicillinase producing. The first was trom a 26-year-old African male who presented with a urethral discharge and who had not been out of South Africa. A swab was taken for culture and the patient given a single intramuscular injection of 1.2 megaunits benzathine penicillin. After 24 h N. gonorrhcece was isolated, being identified by Gram’s stain, a positive oxidase reaction, and fermentation of glucose but not sucrose or maltose. Complete resistance to benzylpenicillin was shown by the three-disc method;4 resistance was also shown to a 10 unit disc. The test for p-lactamase production using a chromogenic cephalosporin3500 p,g!ml was positive. Minimum inhibitory concentrations (M.l.c.s) in g/ml, using the agar dilution technique with inocula of 107 organisms/ml, were: benzylpenicillin 25, spectinomycin 2.5, cefamandole 0-14, and cephaloridine 3.12. Using standard discs, sensitivity was demonstrated to erythromycin (5 (ig), tetracycline (10 p.g), and streptomycin (10 fLg), and resistance to co-trimoxazole .5 The patient was traced 36 days later and still had symptoms. A smear from urethral pus yielded gram-negative diplococci but the culture failed to grow. He was then given a single intramuscular injection of 2 g spectinomycin which resulted in symptomatic and bacteriological cure, confirmed 7 days later. The female contact who infected this patient was then traced. She also had symptoms of gonorrhoea despite treatment by several general practitioners. Although a urethral swab showed gram-negative diplococci, N. gonorrhaeae was not cultured. 4 g spectinomycin was given by two intramuscular injections and cure was confirmed on follow-up. This patient claimed to have been intected by an African male who worked on a ship. This man was traced and found to have a urethral discharge. He worked as a seaman and had lately been to Japan. He denied having sexual intercourse there, but on the return journey to South Africa the ship called at Ghana, where he claimed to have been infected. On arrival home he had sexual intercourse with several women. N. gonorrhcece was iso-
S!R,—The Ivory Coast
was
1. Piot, P. Lancet, 1977, i, 857.
2. Robins-Browne, R. M., Gaillard, M. C., Koornhof, H. J., Mauff, A. C. S. Afr. med. J. 1977, 51, 568. 3. O’Callaghan, C. H., Morris, A., Kirby, S. M., Shingler, A. H. Antimicrob. Ag. Chemother. 1972, 1, 283. 4. Wilkinson, A. E., Turner, G. C., Rycroft, J. A. in Laboratory Diagnosis of Venereal Disease (Publ. Hlth. Sere. Monogr. Ser. no. 1) (edited by A. T. Willis and C. H. Collins); p. 38. London, 1972. 5. Stokes, E. J. Clinical Bacteriology; p. 216. London, 1975.
(5 g). M.i.c.s in (Åglml were: penicillin >100, spectinomycin 25, and cefamandole 0.8. The patient was given a single intramuscular injection of 2 g spectinomycin, but did not return for
follow-up. This investigation -
confirms that penicillinase-producing N. in the indigenous Black population of South Africa. The first case seems to have been infected in Ghana. The organism was resistant to several antibiotics in the original patient, with a fairly high M.t.c. to spectinomycin (25 (Åglml). Both the isolates were very sensitive to cefamandole, which may be an alternative antibiotic to spectinomycin for the treatment of penicillinase-producing N. gonorrhaeae. A. F. HALLETT P. C. APPELBAUM ROSEMARY COOPER S. MOKGOKONG D. MONALE
Department of Microbiology, Faculty of Medicine, University of Natal, Durban, South Africa
PENICILLIN-TOLERANT STAPHYLOCOCCUS
AUREUS Sabath and his colleagues (Feb. 26, p. 443) describe a new type of penicillin resistance of Staphylococcus aureus-namely, "penicillin tolerance" in which the minimum inhibitory concentration (M.iC.) of penicillins for the tolerant organisms is low but the minimum bactericidal concentration (M.B.c.) is high. We can confirm their observations with a case of our own. A 59-year-old White woman with non-tropical sprue since 1975 had multiple gastrointestinal complaints for which she underwent laparotomy, liver biopsy, cholecystectomy, and pyloroplasty in October, 1976. Shortly afterwards right-lower-
SIR,-Professor
M.I.C. AND M.B.C.S OF
PENICILLIN, METHICILLIN, AND
CEPHALOTHIN FOR STAPH. AUREUSI AND II
lobe (R.L.L.) pneumonia developed. Sputum culture grew Staph. aureus. The patient was treated with rifampin 600 mg daily and tetracycline Ig daily orally for 14 days with complete improvement. A week later the pneumonia recurred at the same site. Again, sputum culture showed heavy growth of Staph. aureus, plus a moderate growth of Pseudomonas ceruginosa. Intravenous cephalothin was repeated. She was admitted to our hospital with her third recurrence of the R.L.L. pneumonia with a sputum culture of Staph. aureus and Ps. ceruginosa and was treated with gentamicin and erythromycin. 13 days later R.L.L. pneumonia developed yet again. Sputum culture showed heavy growth of two strains of Staph. aureus and moderate growth of Ps. ceruginosa. Sensitivity tests carried out by the Kirby-Bauer disc diffusion method showed one strain of Staph. aureus to be sensitive to penicillin, methicillin, and cephalosporins, and other strain to be resistant to penicillin but sensitive to methicillin and cephalosporins. These sensitivities were retested by the tube-dilution method for M.LC. and M.B.C. Both organisms (table) showed a striking difference between their M.i.c. levels and the M.B.c. levels for the antibiotics tested, thus revealing them to be penicillin-tolerant Staph. aureus.The patient was treated with rifampin 600 mg daily and tetracycline lg daily orally for 14 days with complete