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POSTGRADUATE TEACHING IN OBSTETRICS
371 results. While these findings are naturally subject to confirmation or the reverse, our limited experience leads us to suggest that the undoubted analgesic pronerties of miadone will find it a place in fields other than those of obstetrical analgesia. G. C. STEEL Hon. Anæsthetist.
EILEEN GUNDERSON Anæsthetic Registrar.
Queen Charlotte’s Maternity Hospital. **Messrs. Burroughs Wellcome & Co. are to issue this product under the trade-name’Physeptone.’-ED. L. ASHRIDGE
SIR,-While fully endorsing the remarks in
your annotation last week, I should like to commend the Ashridge " weekend habit " to medical men. In the
comfortable atmosphere of a house-party one can spend two days in the consideration of various topics of national
importance under the guidance of experts.
It
provides
excellent opportunities both for informal discussions and for learning to speak in public. All opinions are welcome and the Ashridge College is not now linked with any
political party. JOAH BATES.
POSTGRADUATE TEACHING IN OBSTETRICS
SIR,-I read with great interest your Students’ Guide in the issue of Aug. 30, and feel sure that this will be a very great help both to students and to postgraduates. At the
time I was rather surprised and most that the Combined Postgraduate Teaching School in Obstetrics and Gynaecology of Queen Charlotte’s and Chelsea Hospital for Women was not mentioned. This school is running refresher courses and courses for the M.R.C.O.G. and D.R.C.O.G., the deans being Mr. H. G. E. Arthure, F.R.C.S., of Queen Charlotte’s and Mr. C. D. Read, F.R.C.O.G., of Chelsea Hospital, with a teaching staff outstanding either in obstetrics or in gynaecology. The school is recognised by the University of London and the Postgraduate Medical Federation. Further particulars can be obtained from Miss M. E. Taylor, secretary, The Combined School, Chelsea Hospital for Women, Dovehouse Street, S.W.3. same
disappointed
’
A. J. ESPLEY Vice-chairman.
ÆTIOLOGY OF INFANTILE ENTERITIS
SiR,-Your leader of Aug. 23 on the epidemiology of infantile enteritis was welcome, in particular your plea for renewed and more extensive epidemiological study. It is my opinion that valuable setiological information could be obtained by a combined field survey and laboratory investigation of the nutritional aspects of this disease. In support of this I offer the following
paragraphs.
It has been repeatedly found that the main incidence and fatality of infantile diarrhoea falls on the babes of the poorer sections of our urban populations, while the disease seldom attacks the better-off classes. Largely from this, it had been concluded that overcrowding and insanitary conditions of the homes of poor people were responsible for outbreaks of the disease ;’ the assumption being that infantile diarrhoea was a bacterial infection of the gastro-intestinal tract and that adverse housing conditions favoured the spread of bacteria. In an epidemiological survey of infantile diarrhoea in Dublin during 1942 and 1943, my colleague Dr. J. St. L. O’Deashowed that the incidence and fatality of the disease was much the same in the overcrowded slum districts as it was in many newly built well-planned working-class suburbs. The inhabitants of both types of area were of the same income-group (more truthfully, lack of income group), and indeed most of the occupants of the new houses had come from the slum areas. Undoubtedly the slum houses, the " tenements" of Dublin, are overcrowded and often insanitary, but this cannot be said of the houses in the new suburbs. Overcrowding and insanitary conditions are therefore not necessarily associated with the disease, and some other accompaniment of poverty must be concerned. It is 1.
O’Dea, J. St. L. Irish J. med.
Sci.
1944, p. 111.
that malnutrition plays an important r6le. In a survey of the disease in Holland in 1945, Van Creveld agreed with this view. Again, field-surveys have shown that breast-fed infants, even of the poorer classes, tended to escape the disease while the artificially fed had a high incidence. It has been tacitly accepted by some that the protective mechanism of breast-feeding is due to the transfer of bacteria-free milk directly to the infant, and that the high incidence among the artificially fed is related to the contamination of cow’s milk by pathogenic or facultatively pathogenic bacteria. It is now known that maternal milk is commonly contaminated with bacteria, parstaphylococci. Moreover O’Deacould find no difference in incidence or fatality by dividing the artificially fed diarrhoeal infants into two groups-those fed on loose " raw " milk, and those consuming highgrade bottled milk. This does not support the theory that contaminated milk is the source of the disease, nor could I incriminate any bacteria isolated from a number of milk samples.3 Does human milk contain an antiOr is the diarrhoeal factor absent from cow’s milk ? general level of the infants’ nutrition mainly concerned ? Further support that nutritional factors play a part in the causation of infantile diarrhoea comes from autopsy and liver biopsy material. I found4 that the livers of
probable a
ticularly
infants dying of gastroenteritis showed various degrees of degeneration including fatty change and accumulation or deposition of the brown non-iron-containing pigment in and between the liver cells. Similar changes were reported by Debr6 5 in France, in the livers of infantile pellagrins in South Africa by Gillman and Gillman6 and in the tropical nutritional deficiency called kwashiorkor by various writers.7 Bacteriological studies have shown that no common pathogen exists ; although in most epidemics various non-lactose-fermenting gram-negative bacilli were isolated, including B. proteus, B. rnorgani, various types of paracolon bacilli, and in a minority of’ cases organisms In other of the dysentery and salmonella groups. outbreaks no incriminatory organisms were found and a virus infection was postulated. In 1943 I carried out experiments with young kittens in an attempt to reproduce the disease by the oral administration of paracolon bacilli freshly isolated from the fseces of infants suffering from gastroenteritis. Partial success was achieved, particularly with type-A paracolon strains.3 At necropsy the successfully infected animals showed pathological findings similar to those found in human cases. But this feline diarrhoea could not always be produced even with a " kitten-passaged " paracolon strain. Too many kittens were resistant and the results suggested that another factor was involved. As the epidemiological and some of the pathological findings pointed to nutrition, an experiment (unpublished) was later performed to test the combined effect of malnutrition with infection. Twenty-four kittens, 3-5 weeks old and weighing 8-16 oz.,
m
divided into four groups of six animals (A, B, C, and D). A and B were fed adequately with cow’s milk and increased satisfactorily in weight over a test period of two weeks. C and D were fed with diluted skimmed milk in such quantities that they put on very little weight over the same test period. Then the kittens of B and D groups were given 1 c.cm. of an overirght broth culture of a paracolon type A strain.3 Diarrhoea occurred in three groups of animals B, C, and D whilst all the A animals (controls) remained well. Two B kittens (well fed, infected) developed diarrhoea and one died ; one C kitten (semi-starved, not infected) developed diarrhoea but survived : while five of the D animals (semi-starved and’ infected) went down with severe diarrhaea and three of these died. This experiment, although carried out with few animals, supports the hypothesis that the previous nutritional state is important in determining how many
were
Van Creveld, S. (personal communication). Sevitt, S. J. Hyg., Camb. 1945, 44, 37. Sevitt, S. Irish J. med. Sci., 1944, p. 25. Debré, R. Proc. R. Soc. Med. 1945, 38, 447. Gillman, J. Brit med. J. 1944, i, 149; Gillman, T., Gillman, J. J. Amer. med. Ass. 1945, 129, 12. 7. Williams, C. D. Arch. Dis. Childh. 1933, 8, 423; Trowell, H. C. Ibid, 1937, 12, 193.
2. 3. 4. 5. 6.
EILEEN GUNDERSON Anæsthetic Registrar.
Queen Charlotte’s Maternity Hospital. **Messrs. Burroughs Wellcome & Co. are to issue this product under the trade-name’Physeptone.’-ED. L. ASHRIDGE
SIR,-While fully endorsing the remarks in
your annotation last week, I should like to commend the Ashridge " weekend habit " to medical men. In the
comfortable atmosphere of a house-party one can spend two days in the consideration of various topics of national
importance under the guidance of experts.
It
provides
excellent opportunities both for informal discussions and for learning to speak in public. All opinions are welcome and the Ashridge College is not now linked with any
political party. JOAH BATES.
POSTGRADUATE TEACHING IN OBSTETRICS
SIR,-I read with great interest your Students’ Guide in the issue of Aug. 30, and feel sure that this will be a very great help both to students and to postgraduates. At the
time I was rather surprised and most that the Combined Postgraduate Teaching School in Obstetrics and Gynaecology of Queen Charlotte’s and Chelsea Hospital for Women was not mentioned. This school is running refresher courses and courses for the M.R.C.O.G. and D.R.C.O.G., the deans being Mr. H. G. E. Arthure, F.R.C.S., of Queen Charlotte’s and Mr. C. D. Read, F.R.C.O.G., of Chelsea Hospital, with a teaching staff outstanding either in obstetrics or in gynaecology. The school is recognised by the University of London and the Postgraduate Medical Federation. Further particulars can be obtained from Miss M. E. Taylor, secretary, The Combined School, Chelsea Hospital for Women, Dovehouse Street, S.W.3. same
disappointed
’
A. J. ESPLEY Vice-chairman.
ÆTIOLOGY OF INFANTILE ENTERITIS
SiR,-Your leader of Aug. 23 on the epidemiology of infantile enteritis was welcome, in particular your plea for renewed and more extensive epidemiological study. It is my opinion that valuable setiological information could be obtained by a combined field survey and laboratory investigation of the nutritional aspects of this disease. In support of this I offer the following
paragraphs.
It has been repeatedly found that the main incidence and fatality of infantile diarrhoea falls on the babes of the poorer sections of our urban populations, while the disease seldom attacks the better-off classes. Largely from this, it had been concluded that overcrowding and insanitary conditions of the homes of poor people were responsible for outbreaks of the disease ;’ the assumption being that infantile diarrhoea was a bacterial infection of the gastro-intestinal tract and that adverse housing conditions favoured the spread of bacteria. In an epidemiological survey of infantile diarrhoea in Dublin during 1942 and 1943, my colleague Dr. J. St. L. O’Deashowed that the incidence and fatality of the disease was much the same in the overcrowded slum districts as it was in many newly built well-planned working-class suburbs. The inhabitants of both types of area were of the same income-group (more truthfully, lack of income group), and indeed most of the occupants of the new houses had come from the slum areas. Undoubtedly the slum houses, the " tenements" of Dublin, are overcrowded and often insanitary, but this cannot be said of the houses in the new suburbs. Overcrowding and insanitary conditions are therefore not necessarily associated with the disease, and some other accompaniment of poverty must be concerned. It is 1.
O’Dea, J. St. L. Irish J. med.
Sci.
1944, p. 111.
that malnutrition plays an important r6le. In a survey of the disease in Holland in 1945, Van Creveld agreed with this view. Again, field-surveys have shown that breast-fed infants, even of the poorer classes, tended to escape the disease while the artificially fed had a high incidence. It has been tacitly accepted by some that the protective mechanism of breast-feeding is due to the transfer of bacteria-free milk directly to the infant, and that the high incidence among the artificially fed is related to the contamination of cow’s milk by pathogenic or facultatively pathogenic bacteria. It is now known that maternal milk is commonly contaminated with bacteria, parstaphylococci. Moreover O’Deacould find no difference in incidence or fatality by dividing the artificially fed diarrhoeal infants into two groups-those fed on loose " raw " milk, and those consuming highgrade bottled milk. This does not support the theory that contaminated milk is the source of the disease, nor could I incriminate any bacteria isolated from a number of milk samples.3 Does human milk contain an antiOr is the diarrhoeal factor absent from cow’s milk ? general level of the infants’ nutrition mainly concerned ? Further support that nutritional factors play a part in the causation of infantile diarrhoea comes from autopsy and liver biopsy material. I found4 that the livers of
probable a
ticularly
infants dying of gastroenteritis showed various degrees of degeneration including fatty change and accumulation or deposition of the brown non-iron-containing pigment in and between the liver cells. Similar changes were reported by Debr6 5 in France, in the livers of infantile pellagrins in South Africa by Gillman and Gillman6 and in the tropical nutritional deficiency called kwashiorkor by various writers.7 Bacteriological studies have shown that no common pathogen exists ; although in most epidemics various non-lactose-fermenting gram-negative bacilli were isolated, including B. proteus, B. rnorgani, various types of paracolon bacilli, and in a minority of’ cases organisms In other of the dysentery and salmonella groups. outbreaks no incriminatory organisms were found and a virus infection was postulated. In 1943 I carried out experiments with young kittens in an attempt to reproduce the disease by the oral administration of paracolon bacilli freshly isolated from the fseces of infants suffering from gastroenteritis. Partial success was achieved, particularly with type-A paracolon strains.3 At necropsy the successfully infected animals showed pathological findings similar to those found in human cases. But this feline diarrhoea could not always be produced even with a " kitten-passaged " paracolon strain. Too many kittens were resistant and the results suggested that another factor was involved. As the epidemiological and some of the pathological findings pointed to nutrition, an experiment (unpublished) was later performed to test the combined effect of malnutrition with infection. Twenty-four kittens, 3-5 weeks old and weighing 8-16 oz.,
m
divided into four groups of six animals (A, B, C, and D). A and B were fed adequately with cow’s milk and increased satisfactorily in weight over a test period of two weeks. C and D were fed with diluted skimmed milk in such quantities that they put on very little weight over the same test period. Then the kittens of B and D groups were given 1 c.cm. of an overirght broth culture of a paracolon type A strain.3 Diarrhoea occurred in three groups of animals B, C, and D whilst all the A animals (controls) remained well. Two B kittens (well fed, infected) developed diarrhoea and one died ; one C kitten (semi-starved, not infected) developed diarrhoea but survived : while five of the D animals (semi-starved and’ infected) went down with severe diarrhaea and three of these died. This experiment, although carried out with few animals, supports the hypothesis that the previous nutritional state is important in determining how many
were
Van Creveld, S. (personal communication). Sevitt, S. J. Hyg., Camb. 1945, 44, 37. Sevitt, S. Irish J. med. Sci., 1944, p. 25. Debré, R. Proc. R. Soc. Med. 1945, 38, 447. Gillman, J. Brit med. J. 1944, i, 149; Gillman, T., Gillman, J. J. Amer. med. Ass. 1945, 129, 12. 7. Williams, C. D. Arch. Dis. Childh. 1933, 8, 423; Trowell, H. C. Ibid, 1937, 12, 193.
2. 3. 4. 5. 6.