497 EFFECT OF DISINFECTANTS AGAINST ECHOVIRUS
11
(1 min HOLDING - TIME
infection is well recognised, 7,8 unlike congenital rubella where similar clear-cut pathological evidence of pancreatic involvement has been sparse, and yet where diabetes as a complication is well established.9 For these reasons we feel that the congenital cytomegalovirus infection may well be implicated in our case, and we should be interested to learn whether others have seen similar cases either in children or, in adults, where if the experience in congenital rubella were duplicated, such cases might be more common.1,22
megalovirus
Royal
Aberdeen Children’s
K. P. WARD W. H. GALLOWAY
Hospital,
Aberdeen
desirable to use a skin disinfectant with the broadest spectrum of virucidal activity. While a 50% concentration of isopropanol inactivated H.s.v. and would probably be effective against many other ether-labile viruses, it had no virucidal effect against echovirus type 11 even at 95% concentration. The same concentration of ethanol however, was effective. Those responsible for choosing hand disinfectants for hospital use should not forget viruses when deciding which one to order. seem
Virology Laboratory, Churchill Hospital, Oxford OX3 7LJ
J. B. KURTZ
CONGENITAL CYTOMEGALOVIRUS INFECTION AND
DIABETES
SIR The interest in a possible link between viruses and diabetes mellitus has been directed almost entirely towards postnatally acquired infections. Some recent reports, however, have shown a high incidence of diabetes in patients with congenital rubellaI.2 and led to speculation as to whether other congenital infections might be similarly implicated. We have seen a child with congenital cytomegalovirus infection who acquired diabetes mellitus at the age of thirteen months. The patient is a male infant, the second child of healthy unrelated parents in their mid-20s. The maternal grandmother was a maturity-onset diabetic, but there is no other family history of diabetes or of other autoimmune disease. He was born at term, after an apparently normal pregnancy, during which there had been no history of overt infections. The birth-weight was 2.420 kg. Examination showed a light-for-dates infant with a petechial rash and hepatosplenomegaly. Investigations revealed a platelet-count of 40 x 109, and a raised cytomegalovirus titre of 1:128; the titres for rubella and T oxoplasina were not raised. By the age of one month his platelet-count was 110 x 109 and he was discharged. On follow-up he was found to be deaf and to have moderate psychomotor retardation. The hepatosplenomegaly persisted until he was 9 months old, and the cytomegalovirus titre was still 1: 128 at one year. When he was 13 months old he presented with a 2-week history of polydipsia, vomiting, and weight loss, and was found to be severely dehydrated and ketoacidotic with a blood-glucose of 50 mmol/1 (900 mg/dl) and a plasma pH of 7.04. He was treated with fluid replacement and slow insulin infusion and made a satisfactory recovery, but his subsequent insulin requirements have been unusually high with daily requirements of between 25 and 30 units. It is possible that the association in this case is one of chance alone, but diabetes is rare at such an early age3 and leads to a comparison with congenital rubella, where most reported cases of diabetes in childhood have been at a notably early age.4-6 Moreover, pancreatic involvement in congenital cyto-
Department of Child Health, University of Aberdeen
BACTERIURIA AND RENAL TRANSPLANTATION
SIR,-- Dr Byrd and co-workers’° record an interesting association between
early postoperative bacteriuria due to Streptoin fcecalis patients with renal transplants and failure of the graft in the first year. However, they did not note an even more surprising association-that between bacteriuria with organisms other than streptococci and transplant success. Their table I shows that transplant success at one year occurred in 35 out of 63 patients with significant bacteriuria due to E. coli or other non-streptococcal organisms. Of those with no infection, only 34/96 were successful at one year. Thus the patients with non-streptococcal bacteriuria had a significantly higher success rate (P<0.02, by chi-square test) than those with no bacteriuria at all. coccus
Department of Medicine, University of Wisconsin, Madison, Wisconsin 53706,
J. M., Menser, M. A. Lancet, 1971, ii, 332. 2. Menser, M. A., Forrest, J. M., Bransby, R. D. ibid. 1978, i, 57. 3 White, P., Graham, C. A. in Joslin’s Diabetes Mellitus (edited by A. Marble, R. F. Bradley, and L. P. Krall); p. 339. Philadelphia, 1971. 4. Forrest, J. M., Menser, M. A., Harley, J. D. Pediatrics, Springfield, 1969, 44, 445. 5. Plotkin, S. A., Kaye, R. ibid. 1970, 120, 453. 6 Johnson, G. M., Tudor, R. B. Am. J. Dis. Child. 1970, 120, 453.
AVERY R. HARRINGTON
U.S.A.
RENAL TRANSPLANTATION IN DIABETES
SIR,-Dr Deppermann and Professor Ritz (Jan. 6, p. 41 to a Scandinavian report" where patient survival in insu
refer
lin-dependent diabetics was 60% and 50% at one and tw( years, respectively. The results for haemodialysis given in their letter (patient survival 70-90% at one year, and 55-85% al two years) clearly suggest that insulin-dependent diabetic! should not be transplanted. On the other hand, our own ex. perience with diabetics has been much more favourable (set table). PATIENT AND GRAFT SURVIVAL FOR
44
DIABETIC TRANSPLANT
RECIPIENTS
I feel strongly that diabetic patients should be transplanted rather than hxmodialysed; more information is needed to evaluate the role of peritoneal dialysis. Our data support the conclusion that the diabetic patient receiving a cadaver kidney is at no greater risk than the recipient of a living related kidney, although there is a considerable difference in graft survival. It would be of great interest to elucidate the factors responsible for the discrepancy between our results and those reported in the joint Scandinavian report.
Transplant Service, Department ofSurgery, University of Wisconsin Hospital, Madison, Wisconsin 53706, U.S.A. University
1. Forrest,
I. A. AUCHTERLONIE
of
Wisconsin
Hospital,
NEAL R. GLASS
7. Hildebrandt, R. J., Monif, G. R. C. Am. J. Obstet. Gynec. 1969, 105, 349. 8. Gajl-Peczalska, K. Archs Dis. Childh. 1967, 42, 14. 9. Menser, M. A., Reye, R. D. K. Pathology, 1974, 6, 215. 10. Byrd, L. H., Cheigh, J. S., Stenzel, K. H., Tapia, L., Aronian, J., Rubin, A. L. Lancet, 1978, ii, 1167. 11. Joint Scandinavian Report: Lancet, 1978, ii, 915.