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genicity and suggested that in some cases it might be a cause of "flagellate dysentery". However, the 1972 edition says "... there is no evidence of pathogenicity."4 In the first patient there was no other microbiological explanation of diarrhoeaEntamaeba coli and small numbers of T. trichiura are very unlikely to cause this-and there was a prompt response to metronidazole. These features suggest that C. mesnili was a pathogen in this case. In the other patients it was considered that diarrhoea with profuse excretion of the flagellates in the absence of any other microbiological explanation deserved treatment with metronidazole. The results of treatment are not known (case 2) or difficult to interpret (case 3, probably an infection superimposed on long-standing diarrhoea of different

aetiology). G. lamblia has for long been known as a cause of diarrhoea in children but it is only lately that it has been recognised as an important parasite in adults, notably travellers. Endemic giardiasis is usually asymptomatic but travellers to endemic areas run a high risk of disease; the reasons for this are not clear.s A comparable situation might exist with C. mesnili which in tropical areas is often found in patients without symptoms: it may be more harmful to the traveller.

PROTECTION AGAINST POLIOMYELITIS

SIR,-During the first half of 1977, 12 cases of poliomyelitis reported in England and Wales. This prompted us to look for evidence of immunity against polio by serological studies on specimens received in this laboratory. 1016 sera sent in during the period May, 1976, to March, 1977, were tested for neutralising antibodies to polio viruses 1, 2, and 3 by a microplate technique with the serum at a dilution of 1/4. Sera from children under 1 year of age were excluded because immunisation is not normally completed until a child is a year old. The only other criteria for inclusion of a specimen were that the age and sex of the patient and the locality from which the specimen was submitted were known and that were

for our purposes remained after the test had been done. 457 (45%) of the 1016 specimens requested examined were submitted by hospitals and general practitioners in Newcastle; most of the others came from Northumberland, Tyne & Wear, Durham, and Cleveland. 539 (53%) of the specimens were from males. sufficient

serum

TABLE I-PRESENCE OF ANTIBODY TO INDIVIDUAL POLIO VIRUSES

I thank Mr H. H. Nixon and Dr 1. Grimble for permission to publish details of patients under their care and Mr P. Sargeaunt of the London School of Hygiene and Tropical Medicine for confirming the identity of the parasites m the first patient.

Department of Bacteriology, St Mary’s Hospital (Harrow Road), London W9 3RL

M. BARNHAM

FREE-LIVING AMŒBÆ IN HOME DIALYSIS UNIT

SIR,-During April and May of this year a 46-year-old man with chronic renal failure had several episodes of pyrexia with rigors. He was on haemodialysis which, since December, 1974, had been done at home on a Dylade III B unit with a multipoint Kiil dialyser. His symptoms seemed to be caused by pyrogenic toxins. Microbiological examination of his dialysis unit revealed high bacterial colony-counts, predominantly of Aeromonas hydrophila at several points, and large numbers of amoebae resembling Acanthamaeba in the Hartmannellida;.6Small numbers of both A. hydrophila and amocbae were found in the mains water supply. Three more filters (25, 2, and 0-2 pm pore size) were placed between the water softener and the dialyser unit. Other measures included allowing several litres of dialysate to run to waste before starting dialysis and draining as much of the tubing as possible afterwards. Despite the use of 4% formalin and the additional filters counts remain high. It may be that the dialysate sterilising bath increases endotoxin levels by heat disruption of cells. However, the patient is now well and has returned to work. The most beneficial measures were, therefore, probably flushing and running to waste of dialysate before dialysis begins. Aeromonads are known to be endotoxic and pathogenic and hartmannellid amoebae have also been shown to be toxigenic’7 and they have been associated with primary amoebic encephalitis,’ chronic brain abscess,9 and destructive eye lesions’o Public Health Laboratory, General Hospital, Middlesbrough, Cleveland

4.

5. 6. 7. 8. 9. 10.

D. P. CASEMORE

Wilcocks, C., Manson-Bahr, P. E. C. Manson’s Tropical Diseases; p. 982. London, 1972. Morbid. Mortal. wkly Rep. 1976, 25, no. 38, p. 307. Center for Disease Control, Atlanta, 1976 Page, F. C. J. Protozool. 1967, 14, 709. McIntosh, A. H., Chang, R. S. ibid. 1971, 18, 632. Carter, R. F. Trans. R. Soc. trop. Med. Hyg. 1972, 66, no. 2. Jager, B. V., Stamm, W. P. Lancet, 1972, ii, 1343. Nagington, J. ibid. 1974, ii, 1537.

TABLE II-DISTRIBUTION BY AGE OF IMMUNE STATE TO POLIO

The age distribution is shown in table I, with the percentage of each age-group with detectable antibodies to the individual polio viruses. Table ii shows the percentage in each age-group who have detectable antibodies to three, two, one, or no polio viruses. 70% of sera had antibodies to polio 1, 75% to polio 2, and 57.5% to polio 3. For all three viruses the percentage of sera with antibodies was higher in the 30-40 year age-group than in any other age-group. This difference was statistically significant for polio 3 (r=0-0005). 49% had antibody to all three viruses, and it is disturbing to see that only 43% of children aged 1-5 and 40% of those aged 5-19 had full immunity. A further 21c’, of the population had antibodies to two of the three viruses.

These results suggest that the immune state against poliovirus of the population examined is unsatisfactory; this is particularly so for those under 20 years of age. There is no indication that a reduction in the numbers receiving primary vaccination has been compensated for by transmission of vaccine virus to unvaccinated contacts of those recently vaccinated. If this level of immunity persists or falls even further, the introduction of wild polio strains, given suitable seasonal and environmental conditions, is likely to lead to outbreaks and an increase in the incidence of paralytic disease. Public Health Laboratory, General Hospital, Newcastle upon Tyne NE4 6BE

A. A. CODD E. WHITE

Protection against poliomyelitis.

1078 genicity and suggested that in some cases it might be a cause of "flagellate dysentery". However, the 1972 edition says "... there is no evidenc...
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