763 the analysis of amniotic fluid is a different matter, since amniocentesis is usually done electively and a much more crucial decision depends on its result. Shelley et al. have specifically excluded from their study amnioticfluid analysis from immature infants, although they have included as controls amniotic-fluid results indicating mature lungs. It is to be hoped that they will be reporting further on this aspect of their valuable work.
WATER SUPPLY HYGIENE THE last waterborne outbreak of typhoid fever in the U.K., the Croydon outbreak of 1937, was due to contamination of a major piped supply. It was attributed to contamination by a chronic typhoid carrier who was one of several sewage workers who had volunteered to assist with the repair of a well. After this outbreak, recommendations were issued on safeguards to be adopted by water undertakings to protect the quality of water supplies.2,3 In the reorganisation of the water industry in 1974, the previously separate water supply and sewage disposal services were amalgamated under the new water authorities, and the National Water Council have lately issued a revised code of hygienic practice4 covering all aspects of these services. This sensible document gives guidance on hygiene, the segregation of staff and plant used in the water-supply and sewage-disposal div-
isions, the protection of sources of supply, and the treatment, testing, and distribution of water supplies. A major change of policy, which will be welcomed by is the abandonment of the recommendascreening of employees by Widal and Vi tests for carriage of typhoid and paraagglutination typhoid organisms. In earlier advice much emphasis was placed on these tests but, for all the thousands of tests done each year since 1937, there is not a single report of a carrier being detected. At present, only about 200 cases of typhoid are notified each year in the U.K. (excluding Scotland), and most of these infections are acquired abroad.5 The number of carriers in the community must therefore now be small, and the chances of finding one among waterworks employees will be almost nil. Moreover, some chronic typhoid carriers have no relevant demonstrable antibodies, and positive results may be due to vaccination, or to infection with antigenically related salmonellas. The reproducibility of the Vi agglutination test in non-specialist laboratories is poor,5 and even if the screening of employees for typhoid carriage were a useful precaution, culture of faeces and urine would be more efficient tests. The current advice therefore stresses the value of stringent medical assessment of employees rather than reliance on Widal tests. Any suspicion that a person might be excreting a pathogenic organism transmissible by drinking-water should be thoroughly investigated. Indications for laboratory tests would include a history of
bacteriologists,
tion for routine
1
Holden, O.M Publ.Hlth, Lond. 1939, 52, 135.
2 Ministry to
of Health. Memorandum on the Safeguards to be Adopted of Water Undertakings. H.M. Stationery
Day Administration
Day Office,
in
1939.
3 Ministry of Housing
and Local Government. Safeguards to be Adopted in the Operation and Management of Waterworks. H.M. Stationery Office, 1967 4 National Water Council. Water Supply Hygiene: Safeguards in the Operation and Management of Public Waterworks in England and Wales. National Water Council (Queen Anne’s Gate, London SW1H 9BT), 1979.
of intestinal upset or prolonged pyrexia during after a visit abroad, or of previous residence in a country where the incidence of enteric fever is high. Adequate chlorination would probably have prevented the Croydon typhoid outbreak, ’despite the contamination, and all the minor waterborne outbreaks that have occurred in recent years have been due to consumption of untreated, or inadequately treated, polluted water. Effective water treatment and the integrity of the distribution system remain therefore the most important factors in the provision of safe water.
typhoid, or
GUT REACTION TO ANTIGEN WHY does antigen stimulate IgA antibody when given by mouth but not when injected? It may have a lot to do with the peculiar anatomical distribution of the T lymphocytes which control the IgA response.1 The idea that T cells regulate antibody productionsome helping, some suppressing-achieved respectin ability studies of IgM, IgG, and IgE responses. And concanavalin A at mitogenic concentrations was found to stimulate T cells to suppress IgM and IgG synthesis. Elson et al.l looked at the ability of con-A stimulated T cells from different anatomical sites in the mouse to stop B lymphocytes from the same site synthesising IgA, IgG, and IgM. T cells from the gut-associated lymphoid tissue (Peyer’s patches) suppressed IgM and IgG synthesis readily enough but would not suppress IgA synthesis - in fact considerably enhanced it. Spleen T cells, by contrast, reduced the synthesis of all three immunoglobulin classes. There seem to be T cells specifically concerned with helping and suppressing IgA responses which are quite distinct from the T cells which regulate production of other classes of antibody. The gut-associated lymphoid tissue contains the IgG and IgM suppressor cells found elsewhere in lymphoid tissue but it is also a haven for IgA helper cells. So oral immunisation would be expected not only to stimulate a brisk IgA response but also simultaneously to suppress the appearance of antibody of other classes. Swarbrick et aI.2 have confirmed this prediction. Mice which had eaten ovalbumin made much less antibody when subsequently injected with ovalbumin than did mice which had not. Antigen-fed mice also had much less ovalbumin in the circulation after intragastric challenge-not because they eliminated it faster but because they absorbed less of it. The T-cell response to an oral antigen seems to have two important functions. It aids the formation of IgA antibody which acts locally to reduce the subsequent absorption of antigen from the gut. And by suppressing the formation of other classes of circulating antibody it ensures that the small quantities of antigen which are absorbed across the mucosa do not provoke possibly damaging systemic responses. A defect in the way that T cells perform these tasks may underlie the altered immune responsiveness characteristic of coeliac and inflammatory bowel disease. 5. Public Health Laboratory Serv ice Standing Committee on the Bacteriological Examination of W ater Supplies. J. Hyg , Camb. 1978, 81, 139 1.Elson, C O., Heck, J. A., Strober, W J. exp Med. 1979, 149, 632. 2 Swarbrick, E. T., Stokes, C.R.,Soothill, J.F.Gut, 1979, 20, 121
WATER SUPPLY HYGIENE THE last waterborne outbreak of typhoid fever in the U.K., the Croydon outbreak of 1937, was due to contamination of a major piped supply. It was attributed to contamination by a chronic typhoid carrier who was one of several sewage workers who had volunteered to assist with the repair of a well. After this outbreak, recommendations were issued on safeguards to be adopted by water undertakings to protect the quality of water supplies.2,3 In the reorganisation of the water industry in 1974, the previously separate water supply and sewage disposal services were amalgamated under the new water authorities, and the National Water Council have lately issued a revised code of hygienic practice4 covering all aspects of these services. This sensible document gives guidance on hygiene, the segregation of staff and plant used in the water-supply and sewage-disposal div-
isions, the protection of sources of supply, and the treatment, testing, and distribution of water supplies. A major change of policy, which will be welcomed by is the abandonment of the recommendascreening of employees by Widal and Vi tests for carriage of typhoid and paraagglutination typhoid organisms. In earlier advice much emphasis was placed on these tests but, for all the thousands of tests done each year since 1937, there is not a single report of a carrier being detected. At present, only about 200 cases of typhoid are notified each year in the U.K. (excluding Scotland), and most of these infections are acquired abroad.5 The number of carriers in the community must therefore now be small, and the chances of finding one among waterworks employees will be almost nil. Moreover, some chronic typhoid carriers have no relevant demonstrable antibodies, and positive results may be due to vaccination, or to infection with antigenically related salmonellas. The reproducibility of the Vi agglutination test in non-specialist laboratories is poor,5 and even if the screening of employees for typhoid carriage were a useful precaution, culture of faeces and urine would be more efficient tests. The current advice therefore stresses the value of stringent medical assessment of employees rather than reliance on Widal tests. Any suspicion that a person might be excreting a pathogenic organism transmissible by drinking-water should be thoroughly investigated. Indications for laboratory tests would include a history of
bacteriologists,
tion for routine
1
Holden, O.M Publ.Hlth, Lond. 1939, 52, 135.
2 Ministry to
of Health. Memorandum on the Safeguards to be Adopted of Water Undertakings. H.M. Stationery
Day Administration
Day Office,
in
1939.
3 Ministry of Housing
and Local Government. Safeguards to be Adopted in the Operation and Management of Waterworks. H.M. Stationery Office, 1967 4 National Water Council. Water Supply Hygiene: Safeguards in the Operation and Management of Public Waterworks in England and Wales. National Water Council (Queen Anne’s Gate, London SW1H 9BT), 1979.
of intestinal upset or prolonged pyrexia during after a visit abroad, or of previous residence in a country where the incidence of enteric fever is high. Adequate chlorination would probably have prevented the Croydon typhoid outbreak, ’despite the contamination, and all the minor waterborne outbreaks that have occurred in recent years have been due to consumption of untreated, or inadequately treated, polluted water. Effective water treatment and the integrity of the distribution system remain therefore the most important factors in the provision of safe water.
typhoid, or
GUT REACTION TO ANTIGEN WHY does antigen stimulate IgA antibody when given by mouth but not when injected? It may have a lot to do with the peculiar anatomical distribution of the T lymphocytes which control the IgA response.1 The idea that T cells regulate antibody productionsome helping, some suppressing-achieved respectin ability studies of IgM, IgG, and IgE responses. And concanavalin A at mitogenic concentrations was found to stimulate T cells to suppress IgM and IgG synthesis. Elson et al.l looked at the ability of con-A stimulated T cells from different anatomical sites in the mouse to stop B lymphocytes from the same site synthesising IgA, IgG, and IgM. T cells from the gut-associated lymphoid tissue (Peyer’s patches) suppressed IgM and IgG synthesis readily enough but would not suppress IgA synthesis - in fact considerably enhanced it. Spleen T cells, by contrast, reduced the synthesis of all three immunoglobulin classes. There seem to be T cells specifically concerned with helping and suppressing IgA responses which are quite distinct from the T cells which regulate production of other classes of antibody. The gut-associated lymphoid tissue contains the IgG and IgM suppressor cells found elsewhere in lymphoid tissue but it is also a haven for IgA helper cells. So oral immunisation would be expected not only to stimulate a brisk IgA response but also simultaneously to suppress the appearance of antibody of other classes. Swarbrick et aI.2 have confirmed this prediction. Mice which had eaten ovalbumin made much less antibody when subsequently injected with ovalbumin than did mice which had not. Antigen-fed mice also had much less ovalbumin in the circulation after intragastric challenge-not because they eliminated it faster but because they absorbed less of it. The T-cell response to an oral antigen seems to have two important functions. It aids the formation of IgA antibody which acts locally to reduce the subsequent absorption of antigen from the gut. And by suppressing the formation of other classes of circulating antibody it ensures that the small quantities of antigen which are absorbed across the mucosa do not provoke possibly damaging systemic responses. A defect in the way that T cells perform these tasks may underlie the altered immune responsiveness characteristic of coeliac and inflammatory bowel disease. 5. Public Health Laboratory Serv ice Standing Committee on the Bacteriological Examination of W ater Supplies. J. Hyg , Camb. 1978, 81, 139 1.Elson, C O., Heck, J. A., Strober, W J. exp Med. 1979, 149, 632. 2 Swarbrick, E. T., Stokes, C.R.,Soothill, J.F.Gut, 1979, 20, 121
