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OUTBREAK OF ACUTE HEPATITIS CAUSED BY AFLATOXIN POISONING IN KENYA
1346
Public Health OUTBREAK OF ACUTE HEPATITIS CAUSED BY AFLATOXIN POISONING IN KENYA AUGUSTINE NGINDU PATRICK R. KENYA DAVID M. OCHENG THOMAS N. OMONDI WILLIAM NGARE DAVID GATEI
BRUCE K. JOHNSON JULIUS A. NGIRA HELEN NANDWA ADRIAN J. JANSEN JASON N. KAVITI TIMOTHY ARAP SIONGOK
Division of Disease Control and Epidemiology, Nairobi; Virus Research Centre, Nairobi; Makuerni District Hospital; National Public Health Laboratory Services, Nairobi; Medical Reserch Centre, Nairobi; and Faculty of Medicine, University of Nairobi,
Kenya Between March and early June, 1981, 20 patients with hepatitis, 12 of whom died, were admitted to three hospitals in the Machakos district of Kenya. Two families, from which 8 of 12 sick members, died were eating maize which contained as much as 12 000 parts per billion (p.p.b.) of aflatoxin B1. Liver tissue at necropsy contained up to 89 p.p.b. of this mycotoxin. Probably most or all of the hepatitis cases were caused by acute aflatoxin
Summary
poisoning. INTRODUCTION
AFLATOXINS, a group of metabolic products produced by several
species of saprophytic fungi, particularly Aspergillus flavus, are known to be hepatotoxic in animals, including fowl,rats,2 dogs,3 and lower primates,4,5 causing acute hepatitis, cirrhosis, and hepatoma depending upon concentration and duration of exposure. Acute aflatoxin poisoning in man has been suspected on circumstantial evidence in Uganda6 and in India, where an outbreak of several hundred cases with 10-25% mortality was reported.7,8 Aflatoxins have been suspected on epidemiological grounds9 of causing human disease in Africa and elsewhere, and the prevalence of primary hepatoma has been correlated to the degree of aflatoxin contamination in foodstuffs. 10,11t AREA AND CIRCUMSTANCES OF OUTBREAK
In
April and May, 1981, an increase in the incidence of jaundice noted in patients admitted and referred to the provincial hospital in the Machakos district of Kenya (figure). All patients admitted were deeply jaundiced and had been ill for seven days or was
Most had been referred from Makueni district or Makindu sub-district hospitals about 150 km south east of Nairobi. The patients came from areas of mixed wooded and bushed grassland at an altitude of about 1000 m. The annual rainfall is 255-510 mm12short rains from October to December and long rains from March to May (70% of the annual rainfall). The population, largely Akamba, is dense in the more arable areas. However, most of the hepatitis patients came from marginal agricultural areas with fewer than 20 inhabitants/km2.12 There is mostly mixed farming with some rearing of livestock. Maize is the major crop but millet, sorghum, beans, cowpeas, pigeon peas, and vegetables are frown for home consumption. Cotton is cultivated as a cash crop. The rains were sparse in 1980 and caused food shortages over much of the region, but in 1981 the rains came early and were heavy and prolonged. A good harvest had been anticipated and was underway. On June 3, 1981, a team from the Ministry of Health was sent to the area to investigate the outbreak which was, at that time, suspected of being viral in origin. more.
Map (inset) showing area of hepatitis outbreak. The Athi river flows through the region. Points on inset represent Nairobi, ’
Kitui, and Makindu. Scale=1:2 255 000. CLINICAL FEATURES
Between March 28 and June 3,1981,20 patients (8 women and 12 men aged from 21/2 to 45 years) were admitted to Makueni, Makindu, or Machakos hospitals with jaundice. The early symptoms were abdominal discomfort, anorexia, general malaise, and low grade fever. Jaundice and dark urine appeared after about 7 days. It was at this time that most of the patients sought medical attention. The mean time from onset of symptoms to hospital admission for the 17 patients with complete records was 10 - 2 days. On admission all patients were deeply jaundiced, afebrile or with low grade fevers, and extremely weak. Tachycardia and oedema of the legs and, to a lesser extent, of the face or trunk were features. The liver was tender in all patients but not necessarily enlarged. The spleen was enlarged in 3. Diarrhoea was usually not a feature but some of the patients had melaena stools or frank gastrointestinal bleeding in the terminal stages. Patients were managed conservatively. 8 out of 20 improved with return of appetite, clearing of jaundice, and discharge from hospital within 6-20 days. Hepatic failure developed in the remaining 12 patients and they died between 1 and 12 days after admission. Massive gastrointestinal haemorrhage in the terminal stage was seen in at least 4 patients and massive ascites developed rapidly in another 4. EPIDEMIOLOGICAL FEATURES
The illness tended to occur in family groups. Four families had at least 2 members admitted to hospital. Family clusters accounted for 16 of 20 (80%) cases and 10 of the 12 (83%) fatal cases. The mortality in family groups was significantly higher
1347
glutination (’Hepatest’). Two of these positive sera were from members of the family of 7 in which there were 2 deaths. The third positive serum was from a person who had had no
AFLATOXIN LEVELS IN FOODSTUFFS
contact
with this group.
samples were obtained from 2 patients at necropsy. Aflatoxin levels were measured by thin layer chromatography after methanol extraction.16 The liver samples, which came from 2 of the children of the family in which 6 died, contained 39 and 89 parts per billion (p.p.b. or part per 109) of aflatoxin BI. Histologically, the livers showed evidence of toxic hepatitis-marked centrilobular necrosis with minimal inflammatory reaction. There was only slight fatty infiltration and no proliferation of bile ducts. Aflatoxin levels in foods were measured by thin layer chromatography after chloroform extraction (see table). 16 All of the cereals except finger millet contained high levels of aflatoxin fraction Bl and most had toxic levels of fraction B2. Maize samples from unaffected homesteads also had detectable, even toxic, levels of aflatoxins, but these were considerably lower than those in cereals from the homes where there had been acute illness and death. Maize grains from the two homes where severe and fatal illness had occurred contained 12 000 and 3200 p.p.b. of aflatoxin fraction B1, while maize from the unaffected homes had a maximum of 500 p.p.b. No zearalenone, another mycotoxin, was detected in any sample. Mycological cultures of maize grains containing 3200 p.p.b. of aflatoxin Bl yielded a mixed growth of Aspergillus flavus and Rhizopus and Paecilomyces spp. on groundnut medium. Liver
Levels of aflatoxin fractions expressed in p.p.b. (J,lg/kg). The highest level of aflatoxin B in maize from outside the 500 p.p.b.
epidemic area was
(p 0 - 02 by hypergeometrical distribution for the four-fold table) than that of the isolated cases. This implies that there =
was some
other
cause
for the illness in the isolated
cases.
family of 8 was admitted to Makueni district hospital on June 3, 1981. All were jaundiced except 13-month-old twins who had not yet been weaned. One 5-year-old child died before she could be brought to hospital. Over the next 12 days, all but the twins died. The homestead of this family was visited on June 9, 1981, and neighbours and relatives were interviewed. They told how many of the local "doves" had died in March, 1981, after the rains had begun. Later, dogs in the area were dying after refusing food for a few days. These dogs had been fed essentially the same diet as the people, probably uneaten food from meals. Death in the dogs immediately preceded the illness in man. Foodstuffs-maize, maize flour, cowpeas, sorghum, finger millet, and fresh vegetables-were collected from this homestead and from another, where, of 7 people, 4 were admitted to hospital and 2 died. These foods, and five maize samples from outside the immediate epidemic area, were collected for analysis (see table). The grains were stored by the traditional Akamba method; gourds and clay or woven "pots" inside a granary which was raised above the ground to prevent or retard damage by moisture or vermin. Other grains were stored in containers hanging from the kitchen ceiling, the roof of which leaked. The stored cereals were not only from the previous year but also from the 1979 harvest. The 1981 crop could apparently not be stored until the old One
stocks had been consumed. Some of the old stocks had been given to relatives, in none of whom any illness developed. LABORATORY STUDIES
Liver transaminase levels were measured in 2 patients, of whom survived. Levels were raised in both. The patient who survived had an aspartate aminotransferase (AST) level of 500 IU/1 and an alanine aminotransferase (ALT) level of 480 IU/1 during the second week of illness. The patient who died had AST and ALT levels of 160 IU/1 and 130 IU/1, respectively, during the second week of illness. Virological investigations were done on twenty-nine sera; six from acutely ill patients, four from convalescent patients, and nineteen from contacts or neighbours of the patients. Attempts at virus isolation in intracerebrally inoculated suckling mice and in Vero cells were negative. No antibodies against antigens of Marburg, Ebola, Congo haemorrhagic fever, Rift valley fever, or Lassa viruses were detectable by indirect fluorescence. 14 Vero cell neutralisation tests’5 against 200 plaque-forming units of 17D strain yellowfever virus were negative for antibodies with all sera tested. Three of the twenty-nine sera were positive for hepatitis B surface antigen (HBsAg) when tested by reverse passive haemag-’ one
DISCUSSION
The evidence suggests that aflatoxin poisoning was the of the acute liver disease. The signs and symptoms are remarkably similar to those described in the Indian outbreak where deaths in dogs preceded human illness and unweaned infants were not affected, as in the case of the 13-month-old twins. No recorded outbreaks of a similar nature are known to have occurred previously in Kenya. With the very high mortality of 60% in patients admitted to hospital, had such an outbreak occurred, it would have almost certainly come to the attention of the public health authorities. It is likely that climatic conditions in 1981 favoured the growth of aflatoxinproducing fungi, perhaps over a large area. The previous year was extremely dry and, as a result, the harvest was poor, necessitating the storage of grains that might normally have been discarded as spoiled. Every effort was probably made to conserve stored foods until there was some idea of how successful the current harvest was going to be. When it became apparent that the yield was sufficient, food held from the previous harvest was consumed. The exceptionally prolonged and heavy rains of 1981 may have contributed to the moist environment in the grain stores. Other factors could have contributed to the severity of the illness. The shortage of food before the harvest could have forced some onto a protein-deficient diet. Concurrent low protein intake and aflatoxin ingestion is known to potentiate acute aflatoxin poisoning in monkeys." Pre-existing liver damage, perhaps in fatal cases in the family where two members were HBsAg positive, might also increase the severity of the effects of aflatoxin ingestion. Those who had ingested amounts of contaminated food which caused sublethal or even subclinical liver damage could be at risk from liver disease as a result of this exposure. Cirrhosis is known to develop under certain circumstances after aflatoxin consumption in animalsand in man.18 There is a strong
cause
1348 correlation between aflatoxin levels in food and the prevalence of primary hepatoma. 10,11In fact, the incidence of liver cancer in the Akamba population in Kenya has been found to be twice that of other tribal groups. 19 Investigations to determine the extent of this condition are in progress and help has been given by replacement of contaminated food in the worst affected areas. Correspondence should’ be addressed P.O. Box 20752, Nairobi, Kenya.
to
B. K. J., Virus Research Centre,
REFERENCES 1.
Asplin FD, Carnaham RBA. The toxicity of certain groundnut meals for poultry with special reference to their effect on ducklings and chickens. Vet Rec 1961; 73: 1215-19.
2. Butler WH. Acute toxicity of aflatoxin B1 in rats. Br J Cancer 1964; 18: 756-62. 3. Chaffer VW, Edds GT, Himes TA, Neal FC. Aflatoxicosis in dogs. Am J Vet Sci 1969;
30: 1737-49. 4.
Deo, MG, Dayal Y, Ramalingaswami V. Aflatoxins and liver injury in rhesus monkeys. J Pathol 1970; 101: 47-56. 5. Rao KS, Gehring PJ. Acute toxicity of aflatoxin B1 in monkeys. Toxicol Appl Pharmacol 1971; 19: 169-75. 6. Serck-Hanssen A. Aflatoxin induced fatal hepatitis? A case report from Uganda. Arch Environ Health 1970; 20: 729-31.
Preventive Medicine On July 20 there will be a partial eclipse of the sun visible from the north of North America, Greenland, the arctic regions, northwest Europe (including the British Isles), and the extreme north of Asia. extreme
OVER-EXPOSED FILM AS A PROTECTOR AGAINST SOLAR RETINOPATHIES
COLIN M. KEMP
ROBERT A. WEALE
Department of Visual Science, Institute of Ophthalmology, Judd Street, London WC1H 9QS A filter that protects the retina from burns by ultraviolet light needs to be able to absorb both infrared and visible radiation uniformly and sufficiently and to be widely available and cheap. Overexposed black-and-white photographic film fulfils these
Summary
conditions. INTRODUCTION
DESPITE the oft-repeated warning that the only safe way to view the sun is by imaging it through a pin-hole on a sheet of paper,’ most solar eclipses bring in their wake a spate of chorioretinal burns. That these arise from direct viewing of the sun can sometimes be seen from the shape of the lesion.2 Sun-glasses provide no protection: even a combination of filters3 is likely to be ineffective unless the overall absorption of the incident radiation is reduced by more than what may be achieved by two or three different gelatine filters. It is now thought4 that retinopathies are due not just to infrared radiations, but that the visible part of the spectrum is also responsible,5 so there is a great deal to be said for a protective filter that can also absorb visible radiations, notably those of short wavelengths.6 Since schoolchildren form a high proportion of those affected by chorioretinal burns, since an eclipse may be visible in the United Kingdom next month, and since pin-hole viewing is likely to be carried out only by an obedient minority, it is desirable to produce a filter that is readily obtainable and safe. If the amount of radiation entering the normal young pupil is reduced by a factor of 30 000-i.e., with a filler of neutral density (absorbance) of - 4. 5-the sun remains adequately visible and the eye protected. 4, Amateurs use smoked glass in the erroneous belief that soot particles afford the necessary protection. Both low and high concentrations of soot
7. Krishnamachari
KA, Bhat RV, Nagaragan V, Tilak TB Hepatitis due to aflatoxicosis. An outbreak in West India. Lancet 1975; i: 1061-63. 8. Tandon BH, Krishnamurthy L, Koshy A, Tandon HD, Ramalingaswami V, Bhandari JR, Mathur MM, Mathur PD. Study of an epidemic of jaundice presumably due to toxic hepatitis, in northwest India. Gastroenterology 1977; 72: 488-94. 9. Alpert ME, Davidson CS. Mycotoxins: a possible cause of primary carcinoma of the liver. Am J Med 1969; 46: 325-29. 10. Peers FG, Lmsell CA. Dietary aflatoxins and liver cancer-a population based study in Kenya. Br J Cancer 1973; 27: 473-84. 11. Linsell CA, Peers FG. Aflatoxin and liver cell cancer. Trans Roy Soc Trop Med Hyg 1977; 71: 471-73. 12. National atlas of Kenya, 3rd ed. Kenya Government, 1970. 13. Steenbergen WM van, Kusin JA, Jansen AAJ. Measured food intake of pre-school children in Machakos district. East Afr Med J 1980; 57: 734-44. 14. Wulff H, Lange JV. Indirect immunofluorescence for the diagnosis of Lassa fever infection. Bull WHO 1975; 52: 429-36. 15. Madrid AT de, Porterfield JS. A simple microculture method for the study of group B arboviruses. Bull WHO 1969; 40: 113-20. 16. Horwitz W, ed. Official methods of analysis of the association of official analytical chemists. 12th ed. Washington DC. A.O.F A.C., 1976. 17. Madhaven TV, Suryanarayana R, Tulpule PG. Effect of dietary protein level on susceptibility of monkeys to aflatoxin liver injury. Indian J Med Res 1965; 53:
984-89. 18. Amala I, Kamala CS, Gopolakrishna GS, Jayaraj AP, Screenivasamurthy V, Parpia HA. Cirrhosis in children from peanut meal contaminated by aflatoxin. Am J Clin Nutr 1971; 24: 609-14. 19. Linsell CA. Cancer in Kenya. In Clifford P, Linsell CA, Timms G, eds Cancer in Africa. Nairobi: East Africa Publishing House, 1968: 7-12.
deposits, layed down by the amateur with a smoking candle flame, are unsafe (fig. 1). Their absorbance, measured with a Perkin Elmer spectrophotometer, is not only low at long wave-lengths but also varies significantly with the wavelength.8 It would seem that, for smoked glass to be safe, the solar disc would have to be rendered virtually invisible. Another hazard of smoked glass is that its absorbance is nonuniform (both spectra illustrated in fig. 1 are from the same sample) and that the tendency to view through its more transparent parts is irresistible. Moreover, its susceptibility to disruption by so little as contact with an eye-lash adds to its unsuitability as a protector against photic injury. Layers of over-exposed film may offer much more promise. PREPARATION OF FILM
To be useful, any protection based on photographic emulsions has to fulfil the following conditions: to be safe when processed; to be widely available and, by the same token, not to be special; and to be cheap. We first tested colour-film (’Kodachrome’) because it is now widely used and fogged pieces are available almost everywhere, and found it was unsafe (fig. 1). It is too time-consuming to test the entire film market for the suitability of emulsions for a purpose for which they were not designed, but black-and-white emulsions become very absorbent if sufficiently exposed,
Fig. I-Spectral variation of absorbance (= - loglo transmission) of smoked glass: (-) = densely coated; (———) = thinly coated; and over-exposed ’Kodachrome’ (—’—*—’—).
Public Health OUTBREAK OF ACUTE HEPATITIS CAUSED BY AFLATOXIN POISONING IN KENYA AUGUSTINE NGINDU PATRICK R. KENYA DAVID M. OCHENG THOMAS N. OMONDI WILLIAM NGARE DAVID GATEI
BRUCE K. JOHNSON JULIUS A. NGIRA HELEN NANDWA ADRIAN J. JANSEN JASON N. KAVITI TIMOTHY ARAP SIONGOK
Division of Disease Control and Epidemiology, Nairobi; Virus Research Centre, Nairobi; Makuerni District Hospital; National Public Health Laboratory Services, Nairobi; Medical Reserch Centre, Nairobi; and Faculty of Medicine, University of Nairobi,
Kenya Between March and early June, 1981, 20 patients with hepatitis, 12 of whom died, were admitted to three hospitals in the Machakos district of Kenya. Two families, from which 8 of 12 sick members, died were eating maize which contained as much as 12 000 parts per billion (p.p.b.) of aflatoxin B1. Liver tissue at necropsy contained up to 89 p.p.b. of this mycotoxin. Probably most or all of the hepatitis cases were caused by acute aflatoxin
Summary
poisoning. INTRODUCTION
AFLATOXINS, a group of metabolic products produced by several
species of saprophytic fungi, particularly Aspergillus flavus, are known to be hepatotoxic in animals, including fowl,rats,2 dogs,3 and lower primates,4,5 causing acute hepatitis, cirrhosis, and hepatoma depending upon concentration and duration of exposure. Acute aflatoxin poisoning in man has been suspected on circumstantial evidence in Uganda6 and in India, where an outbreak of several hundred cases with 10-25% mortality was reported.7,8 Aflatoxins have been suspected on epidemiological grounds9 of causing human disease in Africa and elsewhere, and the prevalence of primary hepatoma has been correlated to the degree of aflatoxin contamination in foodstuffs. 10,11t AREA AND CIRCUMSTANCES OF OUTBREAK
In
April and May, 1981, an increase in the incidence of jaundice noted in patients admitted and referred to the provincial hospital in the Machakos district of Kenya (figure). All patients admitted were deeply jaundiced and had been ill for seven days or was
Most had been referred from Makueni district or Makindu sub-district hospitals about 150 km south east of Nairobi. The patients came from areas of mixed wooded and bushed grassland at an altitude of about 1000 m. The annual rainfall is 255-510 mm12short rains from October to December and long rains from March to May (70% of the annual rainfall). The population, largely Akamba, is dense in the more arable areas. However, most of the hepatitis patients came from marginal agricultural areas with fewer than 20 inhabitants/km2.12 There is mostly mixed farming with some rearing of livestock. Maize is the major crop but millet, sorghum, beans, cowpeas, pigeon peas, and vegetables are frown for home consumption. Cotton is cultivated as a cash crop. The rains were sparse in 1980 and caused food shortages over much of the region, but in 1981 the rains came early and were heavy and prolonged. A good harvest had been anticipated and was underway. On June 3, 1981, a team from the Ministry of Health was sent to the area to investigate the outbreak which was, at that time, suspected of being viral in origin. more.
Map (inset) showing area of hepatitis outbreak. The Athi river flows through the region. Points on inset represent Nairobi, ’
Kitui, and Makindu. Scale=1:2 255 000. CLINICAL FEATURES
Between March 28 and June 3,1981,20 patients (8 women and 12 men aged from 21/2 to 45 years) were admitted to Makueni, Makindu, or Machakos hospitals with jaundice. The early symptoms were abdominal discomfort, anorexia, general malaise, and low grade fever. Jaundice and dark urine appeared after about 7 days. It was at this time that most of the patients sought medical attention. The mean time from onset of symptoms to hospital admission for the 17 patients with complete records was 10 - 2 days. On admission all patients were deeply jaundiced, afebrile or with low grade fevers, and extremely weak. Tachycardia and oedema of the legs and, to a lesser extent, of the face or trunk were features. The liver was tender in all patients but not necessarily enlarged. The spleen was enlarged in 3. Diarrhoea was usually not a feature but some of the patients had melaena stools or frank gastrointestinal bleeding in the terminal stages. Patients were managed conservatively. 8 out of 20 improved with return of appetite, clearing of jaundice, and discharge from hospital within 6-20 days. Hepatic failure developed in the remaining 12 patients and they died between 1 and 12 days after admission. Massive gastrointestinal haemorrhage in the terminal stage was seen in at least 4 patients and massive ascites developed rapidly in another 4. EPIDEMIOLOGICAL FEATURES
The illness tended to occur in family groups. Four families had at least 2 members admitted to hospital. Family clusters accounted for 16 of 20 (80%) cases and 10 of the 12 (83%) fatal cases. The mortality in family groups was significantly higher
1347
glutination (’Hepatest’). Two of these positive sera were from members of the family of 7 in which there were 2 deaths. The third positive serum was from a person who had had no
AFLATOXIN LEVELS IN FOODSTUFFS
contact
with this group.
samples were obtained from 2 patients at necropsy. Aflatoxin levels were measured by thin layer chromatography after methanol extraction.16 The liver samples, which came from 2 of the children of the family in which 6 died, contained 39 and 89 parts per billion (p.p.b. or part per 109) of aflatoxin BI. Histologically, the livers showed evidence of toxic hepatitis-marked centrilobular necrosis with minimal inflammatory reaction. There was only slight fatty infiltration and no proliferation of bile ducts. Aflatoxin levels in foods were measured by thin layer chromatography after chloroform extraction (see table). 16 All of the cereals except finger millet contained high levels of aflatoxin fraction Bl and most had toxic levels of fraction B2. Maize samples from unaffected homesteads also had detectable, even toxic, levels of aflatoxins, but these were considerably lower than those in cereals from the homes where there had been acute illness and death. Maize grains from the two homes where severe and fatal illness had occurred contained 12 000 and 3200 p.p.b. of aflatoxin fraction B1, while maize from the unaffected homes had a maximum of 500 p.p.b. No zearalenone, another mycotoxin, was detected in any sample. Mycological cultures of maize grains containing 3200 p.p.b. of aflatoxin Bl yielded a mixed growth of Aspergillus flavus and Rhizopus and Paecilomyces spp. on groundnut medium. Liver
Levels of aflatoxin fractions expressed in p.p.b. (J,lg/kg). The highest level of aflatoxin B in maize from outside the 500 p.p.b.
epidemic area was
(p 0 - 02 by hypergeometrical distribution for the four-fold table) than that of the isolated cases. This implies that there =
was some
other
cause
for the illness in the isolated
cases.
family of 8 was admitted to Makueni district hospital on June 3, 1981. All were jaundiced except 13-month-old twins who had not yet been weaned. One 5-year-old child died before she could be brought to hospital. Over the next 12 days, all but the twins died. The homestead of this family was visited on June 9, 1981, and neighbours and relatives were interviewed. They told how many of the local "doves" had died in March, 1981, after the rains had begun. Later, dogs in the area were dying after refusing food for a few days. These dogs had been fed essentially the same diet as the people, probably uneaten food from meals. Death in the dogs immediately preceded the illness in man. Foodstuffs-maize, maize flour, cowpeas, sorghum, finger millet, and fresh vegetables-were collected from this homestead and from another, where, of 7 people, 4 were admitted to hospital and 2 died. These foods, and five maize samples from outside the immediate epidemic area, were collected for analysis (see table). The grains were stored by the traditional Akamba method; gourds and clay or woven "pots" inside a granary which was raised above the ground to prevent or retard damage by moisture or vermin. Other grains were stored in containers hanging from the kitchen ceiling, the roof of which leaked. The stored cereals were not only from the previous year but also from the 1979 harvest. The 1981 crop could apparently not be stored until the old One
stocks had been consumed. Some of the old stocks had been given to relatives, in none of whom any illness developed. LABORATORY STUDIES
Liver transaminase levels were measured in 2 patients, of whom survived. Levels were raised in both. The patient who survived had an aspartate aminotransferase (AST) level of 500 IU/1 and an alanine aminotransferase (ALT) level of 480 IU/1 during the second week of illness. The patient who died had AST and ALT levels of 160 IU/1 and 130 IU/1, respectively, during the second week of illness. Virological investigations were done on twenty-nine sera; six from acutely ill patients, four from convalescent patients, and nineteen from contacts or neighbours of the patients. Attempts at virus isolation in intracerebrally inoculated suckling mice and in Vero cells were negative. No antibodies against antigens of Marburg, Ebola, Congo haemorrhagic fever, Rift valley fever, or Lassa viruses were detectable by indirect fluorescence. 14 Vero cell neutralisation tests’5 against 200 plaque-forming units of 17D strain yellowfever virus were negative for antibodies with all sera tested. Three of the twenty-nine sera were positive for hepatitis B surface antigen (HBsAg) when tested by reverse passive haemag-’ one
DISCUSSION
The evidence suggests that aflatoxin poisoning was the of the acute liver disease. The signs and symptoms are remarkably similar to those described in the Indian outbreak where deaths in dogs preceded human illness and unweaned infants were not affected, as in the case of the 13-month-old twins. No recorded outbreaks of a similar nature are known to have occurred previously in Kenya. With the very high mortality of 60% in patients admitted to hospital, had such an outbreak occurred, it would have almost certainly come to the attention of the public health authorities. It is likely that climatic conditions in 1981 favoured the growth of aflatoxinproducing fungi, perhaps over a large area. The previous year was extremely dry and, as a result, the harvest was poor, necessitating the storage of grains that might normally have been discarded as spoiled. Every effort was probably made to conserve stored foods until there was some idea of how successful the current harvest was going to be. When it became apparent that the yield was sufficient, food held from the previous harvest was consumed. The exceptionally prolonged and heavy rains of 1981 may have contributed to the moist environment in the grain stores. Other factors could have contributed to the severity of the illness. The shortage of food before the harvest could have forced some onto a protein-deficient diet. Concurrent low protein intake and aflatoxin ingestion is known to potentiate acute aflatoxin poisoning in monkeys." Pre-existing liver damage, perhaps in fatal cases in the family where two members were HBsAg positive, might also increase the severity of the effects of aflatoxin ingestion. Those who had ingested amounts of contaminated food which caused sublethal or even subclinical liver damage could be at risk from liver disease as a result of this exposure. Cirrhosis is known to develop under certain circumstances after aflatoxin consumption in animalsand in man.18 There is a strong
cause
1348 correlation between aflatoxin levels in food and the prevalence of primary hepatoma. 10,11In fact, the incidence of liver cancer in the Akamba population in Kenya has been found to be twice that of other tribal groups. 19 Investigations to determine the extent of this condition are in progress and help has been given by replacement of contaminated food in the worst affected areas. Correspondence should’ be addressed P.O. Box 20752, Nairobi, Kenya.
to
B. K. J., Virus Research Centre,
REFERENCES 1.
Asplin FD, Carnaham RBA. The toxicity of certain groundnut meals for poultry with special reference to their effect on ducklings and chickens. Vet Rec 1961; 73: 1215-19.
2. Butler WH. Acute toxicity of aflatoxin B1 in rats. Br J Cancer 1964; 18: 756-62. 3. Chaffer VW, Edds GT, Himes TA, Neal FC. Aflatoxicosis in dogs. Am J Vet Sci 1969;
30: 1737-49. 4.
Deo, MG, Dayal Y, Ramalingaswami V. Aflatoxins and liver injury in rhesus monkeys. J Pathol 1970; 101: 47-56. 5. Rao KS, Gehring PJ. Acute toxicity of aflatoxin B1 in monkeys. Toxicol Appl Pharmacol 1971; 19: 169-75. 6. Serck-Hanssen A. Aflatoxin induced fatal hepatitis? A case report from Uganda. Arch Environ Health 1970; 20: 729-31.
Preventive Medicine On July 20 there will be a partial eclipse of the sun visible from the north of North America, Greenland, the arctic regions, northwest Europe (including the British Isles), and the extreme north of Asia. extreme
OVER-EXPOSED FILM AS A PROTECTOR AGAINST SOLAR RETINOPATHIES
COLIN M. KEMP
ROBERT A. WEALE
Department of Visual Science, Institute of Ophthalmology, Judd Street, London WC1H 9QS A filter that protects the retina from burns by ultraviolet light needs to be able to absorb both infrared and visible radiation uniformly and sufficiently and to be widely available and cheap. Overexposed black-and-white photographic film fulfils these
Summary
conditions. INTRODUCTION
DESPITE the oft-repeated warning that the only safe way to view the sun is by imaging it through a pin-hole on a sheet of paper,’ most solar eclipses bring in their wake a spate of chorioretinal burns. That these arise from direct viewing of the sun can sometimes be seen from the shape of the lesion.2 Sun-glasses provide no protection: even a combination of filters3 is likely to be ineffective unless the overall absorption of the incident radiation is reduced by more than what may be achieved by two or three different gelatine filters. It is now thought4 that retinopathies are due not just to infrared radiations, but that the visible part of the spectrum is also responsible,5 so there is a great deal to be said for a protective filter that can also absorb visible radiations, notably those of short wavelengths.6 Since schoolchildren form a high proportion of those affected by chorioretinal burns, since an eclipse may be visible in the United Kingdom next month, and since pin-hole viewing is likely to be carried out only by an obedient minority, it is desirable to produce a filter that is readily obtainable and safe. If the amount of radiation entering the normal young pupil is reduced by a factor of 30 000-i.e., with a filler of neutral density (absorbance) of - 4. 5-the sun remains adequately visible and the eye protected. 4, Amateurs use smoked glass in the erroneous belief that soot particles afford the necessary protection. Both low and high concentrations of soot
7. Krishnamachari
KA, Bhat RV, Nagaragan V, Tilak TB Hepatitis due to aflatoxicosis. An outbreak in West India. Lancet 1975; i: 1061-63. 8. Tandon BH, Krishnamurthy L, Koshy A, Tandon HD, Ramalingaswami V, Bhandari JR, Mathur MM, Mathur PD. Study of an epidemic of jaundice presumably due to toxic hepatitis, in northwest India. Gastroenterology 1977; 72: 488-94. 9. Alpert ME, Davidson CS. Mycotoxins: a possible cause of primary carcinoma of the liver. Am J Med 1969; 46: 325-29. 10. Peers FG, Lmsell CA. Dietary aflatoxins and liver cancer-a population based study in Kenya. Br J Cancer 1973; 27: 473-84. 11. Linsell CA, Peers FG. Aflatoxin and liver cell cancer. Trans Roy Soc Trop Med Hyg 1977; 71: 471-73. 12. National atlas of Kenya, 3rd ed. Kenya Government, 1970. 13. Steenbergen WM van, Kusin JA, Jansen AAJ. Measured food intake of pre-school children in Machakos district. East Afr Med J 1980; 57: 734-44. 14. Wulff H, Lange JV. Indirect immunofluorescence for the diagnosis of Lassa fever infection. Bull WHO 1975; 52: 429-36. 15. Madrid AT de, Porterfield JS. A simple microculture method for the study of group B arboviruses. Bull WHO 1969; 40: 113-20. 16. Horwitz W, ed. Official methods of analysis of the association of official analytical chemists. 12th ed. Washington DC. A.O.F A.C., 1976. 17. Madhaven TV, Suryanarayana R, Tulpule PG. Effect of dietary protein level on susceptibility of monkeys to aflatoxin liver injury. Indian J Med Res 1965; 53:
984-89. 18. Amala I, Kamala CS, Gopolakrishna GS, Jayaraj AP, Screenivasamurthy V, Parpia HA. Cirrhosis in children from peanut meal contaminated by aflatoxin. Am J Clin Nutr 1971; 24: 609-14. 19. Linsell CA. Cancer in Kenya. In Clifford P, Linsell CA, Timms G, eds Cancer in Africa. Nairobi: East Africa Publishing House, 1968: 7-12.
deposits, layed down by the amateur with a smoking candle flame, are unsafe (fig. 1). Their absorbance, measured with a Perkin Elmer spectrophotometer, is not only low at long wave-lengths but also varies significantly with the wavelength.8 It would seem that, for smoked glass to be safe, the solar disc would have to be rendered virtually invisible. Another hazard of smoked glass is that its absorbance is nonuniform (both spectra illustrated in fig. 1 are from the same sample) and that the tendency to view through its more transparent parts is irresistible. Moreover, its susceptibility to disruption by so little as contact with an eye-lash adds to its unsuitability as a protector against photic injury. Layers of over-exposed film may offer much more promise. PREPARATION OF FILM
To be useful, any protection based on photographic emulsions has to fulfil the following conditions: to be safe when processed; to be widely available and, by the same token, not to be special; and to be cheap. We first tested colour-film (’Kodachrome’) because it is now widely used and fogged pieces are available almost everywhere, and found it was unsafe (fig. 1). It is too time-consuming to test the entire film market for the suitability of emulsions for a purpose for which they were not designed, but black-and-white emulsions become very absorbent if sufficiently exposed,
Fig. I-Spectral variation of absorbance (= - loglo transmission) of smoked glass: (-) = densely coated; (———) = thinly coated; and over-exposed ’Kodachrome’ (—’—*—’—).