We have shown that vertical transmission from to infant is the principal means of E. coli Kl infection of healthy neonates. There was a greater than 80% likelihood that the same serotype of E. coli Kl found in the neonate would be identified in the maternal rectal culture also. On the other hand, at least 10% of colonised full-term infants were born to Kl-negative mothers, and these babies acquired the Kl organisms later than did neonates born to Klpositive mothers. E. coli Kl strains in rectal swabs of nursery staff had identical 0 and H serotypes as Kl organisms obtained from babies under their care. Infant-to-infant cross-infection via the hands of nursery staff is likely to be common enough to maintain one or more E. coli serotypes within a nursery for 11 long time. For example, two serotypes (O1: Kl : H-and 018ac : Kl :H-) accounted for 52 % of all E. coli Kl strains obtained from healthy full-term babies for 6 months. During the same time period, two different E. coli serotypes (016 : K1: H6 and 07 : K1: H - ) colonised 57% of premature infants in a separate nursery of Parkland Memorial Hospital. The role of nursery staff in cross-infection is more convincingly demonstrated in the premature unit. Of 71 premature babies with E. coli Kl strains, 39 (55 %) acquired the organism after the first week of life. 50% of nursery staff attending to these infants had Kl strains with identical 0 and H antigens. Although maternal rectal cultures were not done routinely in this phase of the study, the mothers had virtually no contact with their babies from delivery to discharge from the nursery. Thus, acquisition of Kl strains primarily of two specific serotypes after the first week of life in infants without detectable Kl organisms in the first 7 days argues strongly for a non-maternal source of infection. Most babies who develop E. coli Kl disease during the first months of life obtain the pathogen from their mother. This route of infection was documented in approximately 70% of infants with meningitis. This percentage may actually have been greater because we did not select more than one halo-producing colony In addition, rectal on antiserum-agar for serotyping. cultures from sick neonates yielded organisms identical to those causing disease in approximately 65% of cases, suggesting that these organisms were most likely acquired by aspiration of infected material at delivery or by the faecal-oral route during the early days of life. Bloodstream invasion with subsequent involvement of the central nervous system probably occurred from the gastrointestinal tract. The high prevalence-rate of E. coli Kl of similar capsular content and fermentation reactions in diseased patients and among healthy infants, children, and adults suggests that host immune factors are critical in the pathogenesis of neonatal E. coli Kl meningitis. We thank the Cooperative Neonatal Meningitis Study Group participants 12 for providing rectal swab cultures from healthy mother

coli strains isolated from blood and c.s.F. of We also acknowledge the assistance of N. Threlkeld and N. Davis in these studies. L. D. S. and G. H. M. are supported by grants from the United Cerebral Palsy Foundation and the John A. Hartford Foundation Inc. Requests for reprints should be addressed to G. H. M., Department of Pediatrics, 5323 Harry Hines Blvd, Dallas, neonates and E. sick neonates.

Texas 75235. U.S.A.



Endocrine Unit, Royal Postgraduate Medical School, Hammersmith Hospital, London W12 0HS

Serum-lipid concentrations and their relationship to blood-glucose and serum-insulin were examined in non-insulin-requiring diabetics, 62 with and 45 without retinopathy. The age, sex, body-weight, and duration of known diabetes was comparable in the two groups. All were treated by diet only or diet and oral hypoglycæmic agents. Patients with retinopathy had higher fasting serumtriglyceride and serum-cholesterol levels than those without. Compared with a non-diabetic population, significantly more diabetics with retinopathy had raised serum-lipids. The lipid concentrations did not correlate with body-weight, serum-thyroid-stimulating-hormone levels, renal involvement, or fasting blood-sugar. While the blood-sugar concentrations Summary

similar in the two groups the absolute insulin increment and the relative insulin response to a 50 g



Present address: London W2.


Mary’s Hospital Medical School;

DR SARFF AND OTHERS: REFERENCES 1. Smith, T., Bryant, G. J. exp. Med. 1927, 46, 133. 2. Kauffman, F. The Bacteriology of Enterobacteriaceæ. Copenhagen 1966. 3. Ørskov, I., Ørskov, F., Jann, B., Jann, K. Nature, 1963, 200, 144 4. Ørskov, F., Ørskov, I., Jann, B., Jann, K. Acta path. microbiol scand. B, 1971, 79, 142. 5. Ørskov, F., Ørskov, I., Jann, B., Jann, K. ibid. 1971, 80, 905. 6. Heidelberger, M., Jann, B., Jann, K., Ørskov, F., Ørskov, I., Westphal, O. J. Bact. 1968, 95, 2415. 7. Kasper, D. L., Winkelhake, J. L., Zollinger, W. D., Brandt, B., Artenstein, M. S. J. Immun. 1973, 110, 262. 8. Schneerson, R., Bradshaw, M., Whisnant, J. K., Parke, J. C., Robbins, J. B. ibid. 1972, 108, 1551. 9. Robbins, J. B., Myerowitz, R. L., Whisnant, J. K., Argaman, M., Schneerson, R., Handzel, Z. T., Gotschlich, E. C. Infect. Immun. 1973, 6, 651. 10. Kaijser, B. J. infect. Dis. 1973, 121, 670. 11. Robbins, J. B., McCracken, G. H., Jr., Gotschlich, E. C., Ørskov, F., Ørskov, I., Hanson, L. New Engl. J. Med. 1974, 290, 1216. 12. McCracken, G. H., Sarff, L. D., Glode, M. P., Mize, S. G., Schiffer, M. S., Robbins, J. B., Gotschlich, E. C., Ørskov, F., Ørskov, I. and the Cooperative Neonatal Meningitis Study Group. Lancet, 1974, ii, 246. 13. Bukantz, S. E., de Gara, P. F., Bullowa, J. G. M. Archs intern. Med. 1942, 69, 191. 14. Alexander, H. E. J. Pediat. 1944, 25, 517. 15. Hoffman, T. A., Edwards, E. A. J. infect. Dis. 1972, 126, 636. 16. Dorff, G. J., Coonrod, J. D., Ryfel, M. W. Lancet, 1971, i, 578. 17. Ingram, D. L., Anderson, P., Smith, D. H.J. Pediat. 1972, 81, 1156. 18. Mancini, G., Carbonara, A. O., Heremans, J. F. Immunochemistry, 1965, 2, 235. 19. Liu, T. Y., Gotschlich, E. C., Dunne, F. T., Jonsenn, E. K. J. biol. Chem. 1971, 246, 4703. 20. Warren, L. ibid. 1959, 234, 1971. 21. Ørskov, F., Sørensen, K. B. Br. med. J. (in the press). 22. Hanson, L., Kaijser, B. Unpublished. 23. Frasch, C. E., Chapman, S. S. J. infect. Dis. 1973, 127, 149. 24. Gold, R., Winklehake, J. L., Mars, R. S., Artenstein, M. S. ibid 1971, 124, 593. 25. Schnitman, C. A. J. Bact. 1970, 104, 882. 26. Glynn, A. A., Brumfitt, W., Howard, C. J. Lancet, 1971, i, 514. 27. McCabe, W. R., Carling, P. C., Bruins, S., Greely, A. J. infect. Dis

1975, 131, 6.


oral glucose load were significantly lower in those with retinopathy than in those without. The impairment of insulin response correlated significantly with the frequency of hyperlipidæmia. It is suggested that insulin deficiency with secondary hyperlipidæmia is characteristic of diabetic patients with retinopathy.

Introduction DIABETIC retinopathy is the commonest cause of new-blind registration in Britain in the age-group 30-65 years.1 The natural history of this disease is now well described,2-5 but there is no satisfactory explanation for the fact that some patients do not develop this complicationwhile in others it leads to severe visual loss. Several attempts have been made to relate the largevessel disease of diabetes to abnormalities of carbohydrateand/or lipid metabolism.8 That abnormalities of metabolism are related to microangiopathy has also been suggested by Elkeles et al 9 and by Hunt.10 We have compared some of the changes in lipid and carbohydrate metabolism in non-insulin-requiring diabetic patients with and without retinopathy, with similar known duration of diabetes.

Patients and Methods Patients 107 non-insulin-requiring diabetic patients attending the diabetic clinic and the diabetic retinopathy clinic at Hammersmith Hospital were studied. All had proven diabetes for 8 years or more. All were treated by diet alone or diet and oral hypoglycaemic agents (table I). .


* P > 0’05



of the

retinopathy-free with the retinopathy


The presence or absence of retinopathy was determined one of us (E. M. K.) who is experienced in detailed retinal evaluation. 45 patients were without retinopathy; 39 had only a few scattered lesions (mild retinopathy); and 23 had visual impairment from maculopathy or proliferative lesions (severe retinopathy). There were no significant differences between the two retinopathy groups and the non-retinopathy group with respect to age, known duration of diabetes, and per cent ideal body-weight (table i). The per cent ideal body-weight was calculated by comparing the patients’ weight with the standard weight for that sex and height at age 22 in Kemsley’s tables."


Methods Procedure.-Patients attended the outpatient clinic after Venous blood was withdrawn for an overnight fast. estimation of blood sugar and urea and serum insulin, triglyceride, and cholesterol. In 96 patients serum thyroid-stimulating hormone (T.S.H.) was also estimated. 50 g. glucose dissolved in 300 ml. water was taken within Serum-insulin and blood-sugar measure7 minutes. ments were repeated 60 minutes later.

Chemical methods.-Blood-sugar was estimated by the Technicon ferricyanide method, serum-insulin by the

double-antibody technique,12 triglycerides were extracted by the Technicon N-78 method and estimated fluorometrically by the method of Cramp and Robertson,13 cholesterol by the Technicon procedure N24a modified from Levin and Zak,14 T.S.H by a double-antibody radioimmunoassay 15; blood-urea by the method of theAutoAnalyzer ’.16

Analysis.-Patients were subdivided on the basis of their fasting blood-sugar (F.B.S.) into " low " (F.B.S.

insulin relationship in non-insulin-requiring diabetics with and without retinopathy.

1104 We have shown that vertical transmission from to infant is the principal means of E. coli Kl infection of healthy neonates. There was a greater...
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