1314
natural health foods for more than 50 years in eastern countries, especially in Japan and Korea. There it is used as an additional and alternative treatment in diseases such as hypercholesterolaemia, atherosclerosis, ischaemic heart disease, liver disorders, and those affecting the gastrointestinal system. That olive oil helps to prevent restenosis does not surprise me. I suggest that fish oil (EPA), squalene, and corn oil should be compared. Squalene is odourless and tasteless and can be obtained in capsules or as liquid. It does not stick to the mouth and does not freeze at - 20°C. I am confident that squalene would prove better than fish oil and corn oil in such a
study.
to
Department Faculty of Medicine, University of Tarumanagara,
IWAN T. BUDIARSO
1. Reis GJ, Boucher TM,
Sipperly ME, et al. Randomised trial of fish oil for prevention of restenosis after coronary angioplasty. Lancet 1989; ii: 177-81. 2. Riemersma RA, Sargent CA, Abraham RA, Wright RL, Oliver MF. Fish and the heart. Lancet 1989; ii: 1450.
Subacute sclerosing
panencephalitis in the developing world
SiR,—Your Sept 8 editorial on subacute sclerosing panencephalitis (SSPE) draws attention to a grave legacy of the failure to control measles by immunisation in developing countries. The exact pathogenesis of SSPE is unknown but several general observations SSPE referred to in the editorial and by others’ do not accord with South African data accumulated over 7 years of surveillance. Since 1984 details of the 72 cases of SSPE conforming to US Centers for Disease Control criteriaz-ie, a clinical diagnosis supported by cerebrospinal fluid antibodies, a characteristic electroencephalographic pattern, or histological findings in the brain-have been collected by the National Institute for Virology, Johannesburg. The reported age and sex distributions, suggesting that SSPE occurs at between 5 and 15 years of age and with a sex ratio in favour of boys, were not found. The cases ranged in age from 2 to 29 years (median 11); 17 patients (24%) were over the age of 15 (figure). The sex ratio (male to female) was 0 9:1, consistent with earlier South African series.3’ The distribution of cases by race (70% black, 22% white, 7% "coloured" [mixed race], and 1% Asian) corresponded roughly to racial proportions for the population for the country as a whole (74% black, 14% white, 9% coloured, 3% Asian; 1990 projections based on the 1985 census, from Centre for Information Analysis, Development Bank of Southern Africa). In contrast, the notified measles incidence for South African blacks in 1987 was 105 per 100 000 population compared with 14 per 100 000 for whitest Furthermore, whereas the measles incidence rate for white infants less than 1 year was 251 per 100 000, that for black infants was 1592 per 100 000 from 1985 to 1987. However, the corresponding figures for white and black children at 5 to 9 years of age were closer (266 and 398, respectively). Thus, South Africa data do not accord with the hypothesis that your editorial and others1,6suggest-namely, that the development of SSPE is related to the dose of measles virus received at the time of exposure and the high attack rates at an early age of infection. The pathogenesis of SSPE may well be independent of viral dose or immunological status. Thus, although the epidemiology of SSPE in on
Race and age distribution of South African SSPE cases, 1984-90.
be very similar in white and black
B. D. SCHOUB National Institute for Virology, Sandringham 2131, South Africa
of Pathology,
Jakarta Barat, Indonesia 11440
South Africa appears
populations, that of measles differs greatly-the pattern in the black population generally resembles that in third world countries whereas in the white population it corresponds to that found in developed countries. This would suggest that SSPE is more likely to be a fortuitous complication rather than a consequence of intensive exposure or compromised host resistance. Whatever the pathogenesis, however, reduction of circulating wild virus by immunisation will strikingly lower the incidence of SSPE.7,8 S. JOHNSON J. M. McANERNEY
1. Aaby P, Bukh J, Lisse IM, Smits AJ. Risk factors in subacute sclerosing panencephalitis; age and sex-dependent host reactions or intensive exposure. Rev Infect Dis 1984; 6: 239-50. 2. Centers for Disease Control. Subacute sclerosing panencephalitis surveillance— United States. MMWR 1982; 31: 585-88. 3. Moodie JW, MacKenzie DJM, Kipps A. Subacute sclerosing panencephahtis (SSPE) in Southern Africa. S Afr Med J 1980; 58: 964-67. 4. Carman WF, Johnson S. Subacute sclerosing panencephalitis in South Africa Trans R Soc Trop Med Hyg 1989; 83: 117-18. 5 Department of National Health and Population Development. Eight years of measles notifications. Epidemiol Comments 1988; 15(6): 1-31. 6. Grant JP. The state of the world’s children 1990. Oxford: Oxford University Press, 1990. 7. Miller CL. Current impact of measles in the United Kingdom. Rev Infect Dis 1983; 5: 439-44 8. Bloch AB, Orenstein WA, Stetler HC, et al. Health impact of measles vaccination in the United States. Pediatrics 1985; 76: 524-32.
Rotavirus infection and persistent diarrhoea in young children SIR,-Protracted diarrhoea in infants and young children is associated with a variety of infectious and non-infectious disorders.’ Although persistent rotavirus infection has not been incriminated, except in the immunocompromised host,2 it may be an important initiating illness in protracted diarrhoea, especially since rotavirus produces brush-border damage and disaccharides deficiency.3 No prospective studies, however, have been done that show a direct correlation between acute rotavirus infection and persistence of diarrhoea. Patients were selected from children attending the paediatric gastroenterology unit, All India Institute of Medical Sciences, during the 12 months from July, 1986, to June, 1987, and who had had diarrhoea for over 14 days with no intervening non-diarrhoeal day. Other criteria were acute onset of symptoms, recorded weight loss (after correcting dehydration), and no history of antibiotics or diarrhoea in the preceding 6 weeks. Children whose stools contained macroscopic blood were excluded. 55 consecutive patients fulfilling these entry criteria were studied. The median age at onset was 11 -5 months (range 6-22) and the median duration of diarrhoea was 17 days (range 14-30). Patient selection was uniform throughout the year, without significant seasonal variations. 12 age-matched normally nourished children who had no gastrointestinal symptoms and who were attending the immunisation clinic were included as controls. On the day of admission/attendance three stool samples were collected for detection of viruses (rotavirus and enteric adenovirus), protozoa (Giardia intestinalis and Entamoeba histolytica), and bacterial enteric pathogens (Escherichia coli, shigella, salinonella, campylobacter, Vibrio cholerae, and Aeromonas). Where isolated, three morphologically similar colonies of E coli were selected for detection of labile toxin and stable toxin by DNA hybridisation, adherence (localised, diffuse, and aggregative) in a HEp-2 cell assay, invasiveness by Sereny test, and verotoxin assay. E coli were serotyped for enteropathogenic E coli with monovalent antisera by tube agglutination. Rotavirus was sought by use of the WHO ELISA kit.4 For enteric adenovirus, a two-step ELISA was used-a group-specific ELISA for adenovirus and the other specific for enteric adenovirus types 40 and 41. The identification of bacteria was done according to the WHO manual.4 Fresh stool specimens were examined for giardia and entamoeba and for cryptosporidium by the modified Ziehl/Neelsen stain. After informed consent, serum was collected from all patients and controls for rotavirus-specific antibodies (IgM)5 and stored at
natural health foods for more than 50 years in eastern countries, especially in Japan and Korea. There it is used as an additional and alternative treatment in diseases such as hypercholesterolaemia, atherosclerosis, ischaemic heart disease, liver disorders, and those affecting the gastrointestinal system. That olive oil helps to prevent restenosis does not surprise me. I suggest that fish oil (EPA), squalene, and corn oil should be compared. Squalene is odourless and tasteless and can be obtained in capsules or as liquid. It does not stick to the mouth and does not freeze at - 20°C. I am confident that squalene would prove better than fish oil and corn oil in such a
study.
to
Department Faculty of Medicine, University of Tarumanagara,
IWAN T. BUDIARSO
1. Reis GJ, Boucher TM,
Sipperly ME, et al. Randomised trial of fish oil for prevention of restenosis after coronary angioplasty. Lancet 1989; ii: 177-81. 2. Riemersma RA, Sargent CA, Abraham RA, Wright RL, Oliver MF. Fish and the heart. Lancet 1989; ii: 1450.
Subacute sclerosing
panencephalitis in the developing world
SiR,—Your Sept 8 editorial on subacute sclerosing panencephalitis (SSPE) draws attention to a grave legacy of the failure to control measles by immunisation in developing countries. The exact pathogenesis of SSPE is unknown but several general observations SSPE referred to in the editorial and by others’ do not accord with South African data accumulated over 7 years of surveillance. Since 1984 details of the 72 cases of SSPE conforming to US Centers for Disease Control criteriaz-ie, a clinical diagnosis supported by cerebrospinal fluid antibodies, a characteristic electroencephalographic pattern, or histological findings in the brain-have been collected by the National Institute for Virology, Johannesburg. The reported age and sex distributions, suggesting that SSPE occurs at between 5 and 15 years of age and with a sex ratio in favour of boys, were not found. The cases ranged in age from 2 to 29 years (median 11); 17 patients (24%) were over the age of 15 (figure). The sex ratio (male to female) was 0 9:1, consistent with earlier South African series.3’ The distribution of cases by race (70% black, 22% white, 7% "coloured" [mixed race], and 1% Asian) corresponded roughly to racial proportions for the population for the country as a whole (74% black, 14% white, 9% coloured, 3% Asian; 1990 projections based on the 1985 census, from Centre for Information Analysis, Development Bank of Southern Africa). In contrast, the notified measles incidence for South African blacks in 1987 was 105 per 100 000 population compared with 14 per 100 000 for whitest Furthermore, whereas the measles incidence rate for white infants less than 1 year was 251 per 100 000, that for black infants was 1592 per 100 000 from 1985 to 1987. However, the corresponding figures for white and black children at 5 to 9 years of age were closer (266 and 398, respectively). Thus, South Africa data do not accord with the hypothesis that your editorial and others1,6suggest-namely, that the development of SSPE is related to the dose of measles virus received at the time of exposure and the high attack rates at an early age of infection. The pathogenesis of SSPE may well be independent of viral dose or immunological status. Thus, although the epidemiology of SSPE in on
Race and age distribution of South African SSPE cases, 1984-90.
be very similar in white and black
B. D. SCHOUB National Institute for Virology, Sandringham 2131, South Africa
of Pathology,
Jakarta Barat, Indonesia 11440
South Africa appears
populations, that of measles differs greatly-the pattern in the black population generally resembles that in third world countries whereas in the white population it corresponds to that found in developed countries. This would suggest that SSPE is more likely to be a fortuitous complication rather than a consequence of intensive exposure or compromised host resistance. Whatever the pathogenesis, however, reduction of circulating wild virus by immunisation will strikingly lower the incidence of SSPE.7,8 S. JOHNSON J. M. McANERNEY
1. Aaby P, Bukh J, Lisse IM, Smits AJ. Risk factors in subacute sclerosing panencephalitis; age and sex-dependent host reactions or intensive exposure. Rev Infect Dis 1984; 6: 239-50. 2. Centers for Disease Control. Subacute sclerosing panencephalitis surveillance— United States. MMWR 1982; 31: 585-88. 3. Moodie JW, MacKenzie DJM, Kipps A. Subacute sclerosing panencephahtis (SSPE) in Southern Africa. S Afr Med J 1980; 58: 964-67. 4. Carman WF, Johnson S. Subacute sclerosing panencephalitis in South Africa Trans R Soc Trop Med Hyg 1989; 83: 117-18. 5 Department of National Health and Population Development. Eight years of measles notifications. Epidemiol Comments 1988; 15(6): 1-31. 6. Grant JP. The state of the world’s children 1990. Oxford: Oxford University Press, 1990. 7. Miller CL. Current impact of measles in the United Kingdom. Rev Infect Dis 1983; 5: 439-44 8. Bloch AB, Orenstein WA, Stetler HC, et al. Health impact of measles vaccination in the United States. Pediatrics 1985; 76: 524-32.
Rotavirus infection and persistent diarrhoea in young children SIR,-Protracted diarrhoea in infants and young children is associated with a variety of infectious and non-infectious disorders.’ Although persistent rotavirus infection has not been incriminated, except in the immunocompromised host,2 it may be an important initiating illness in protracted diarrhoea, especially since rotavirus produces brush-border damage and disaccharides deficiency.3 No prospective studies, however, have been done that show a direct correlation between acute rotavirus infection and persistence of diarrhoea. Patients were selected from children attending the paediatric gastroenterology unit, All India Institute of Medical Sciences, during the 12 months from July, 1986, to June, 1987, and who had had diarrhoea for over 14 days with no intervening non-diarrhoeal day. Other criteria were acute onset of symptoms, recorded weight loss (after correcting dehydration), and no history of antibiotics or diarrhoea in the preceding 6 weeks. Children whose stools contained macroscopic blood were excluded. 55 consecutive patients fulfilling these entry criteria were studied. The median age at onset was 11 -5 months (range 6-22) and the median duration of diarrhoea was 17 days (range 14-30). Patient selection was uniform throughout the year, without significant seasonal variations. 12 age-matched normally nourished children who had no gastrointestinal symptoms and who were attending the immunisation clinic were included as controls. On the day of admission/attendance three stool samples were collected for detection of viruses (rotavirus and enteric adenovirus), protozoa (Giardia intestinalis and Entamoeba histolytica), and bacterial enteric pathogens (Escherichia coli, shigella, salinonella, campylobacter, Vibrio cholerae, and Aeromonas). Where isolated, three morphologically similar colonies of E coli were selected for detection of labile toxin and stable toxin by DNA hybridisation, adherence (localised, diffuse, and aggregative) in a HEp-2 cell assay, invasiveness by Sereny test, and verotoxin assay. E coli were serotyped for enteropathogenic E coli with monovalent antisera by tube agglutination. Rotavirus was sought by use of the WHO ELISA kit.4 For enteric adenovirus, a two-step ELISA was used-a group-specific ELISA for adenovirus and the other specific for enteric adenovirus types 40 and 41. The identification of bacteria was done according to the WHO manual.4 Fresh stool specimens were examined for giardia and entamoeba and for cryptosporidium by the modified Ziehl/Neelsen stain. After informed consent, serum was collected from all patients and controls for rotavirus-specific antibodies (IgM)5 and stored at
