1129
may well be an important cause of the decreased gluconeogenesis, as suggested by Dr Wardle. We now have plasma glucagon results from the same children. Interestingly glucagon results were appropriately elevated in hypoglycaemic compared with normoglycaemic children (181 [28] vs 58 [4] pg/ml; p < 0 001). Values were also significantly higher in those who died (124 [21] vs 58 [5] pg/ml) and in comatose cases (81 [9] vs 59 [6] pg/ml). However, for the group as a whole and for all subanalyses there were no differences between malaria and non-malaria cases. For all patients glucagon levels correlated negatively with admission glucose (p=0’01) and positively with duration since last meal (p 0-002), lactate (p 0-001), and alanine aminotransferase (p = 0-022). These data support the concept that there is defective hepatic glucose production in the face of a strong =
counter-regulatory drive. Brewster and colleagues
=
state
that "The
implication that
hypoglycaemia is as common a feature of other infections is not justified". Their evidence for this statement is not clear. The prevalence of hypoglycaemia in their control group of conscious children was similar to that in our children with pneumonia. Their control group did not contain children in coma. It would therefore be of interest to know how common hypoglycaemia would be in a control group of Gambian children in coma due to serious illness other than malaria. The primary purpose of our study was nonetheless to establish whether hypoglycaemia occurs in severely ill children who do not have malaria, and we feel that our data demonstrate that this is so.
Muhimbili Medical Centre, University of Dar es Salaam, Tanzania
N. G. KAWO A. E. MSENGI A. B. M. SWAI L. M. CHUWA
Department of Medicine, University of Newcastle upon Tyne, Newcastle upon Tyne NE2 4HH, UK
K. G. M. M. ALBERTI
Muhimbili Medical Centre
D.G.MCLARTY
Aarhus University, Aarhus, Denmark
H. ORSKOV
previously reported decreased urinary inorganic sulphate excretion, indicating a low sulphur aminoacid intake, in children from this area.6 The hallucinogenic properties of DMT have been well documented and 5-MeO-DMT is the main component of intoxicating snuffs used by South American Indians.7 One of the side-effects of levodopa in patients treated for Parkinson’s disease is a toxic confusional state. We have not been able to find previous reports of toxic psychosis associated with the consumption of M pruriens, although in India the seeds are used as a famine food33 and they have also been used experimentally in the treatment of Parkinson’s diseased
Nampula, Mozambique
MARIA E. INFANTE ALFREDO M. PEREZ MANUEL R. SIMAO FRANCISCO MANDA
National Laboratory of Water and Food Hygiene, Mozambique
EVARISTO F. BAQUETE ANGELA M. FERNANDES
Provincial Health Directorate,
Office of
Outbreak of acute toxic psychosis attributed to Mucuna pruriens S!R,—We record an outbreak of acute toxic psychosis attributed to legume Mucuna pruriens, known as feijão macaco in Mozambique and as cowitch, cowhage, kaunch, and pica-pica in other countries. The outbreak was first reported in November, 1989, in the remote district of Memba, Nampula Province. In 1981, the same area had been affected by an epidemic of spastic paraparesis, associated with consumption of cassava containing high concentrations of cyanogenic glycosides under drought
the
conditions.’ Earlier in 1989, the district had suffered a severe famine with 5200 reported deaths, owing to drought and the depredations of the RENAMO rebels. Food shortages continued through 1989, as rebel attacks interfered with farming and impeded food distribution. Agriculture was further disrupted by a plague of rats and an invasion of lions, the latter causing 53 deaths. People subsisted on bitter cassava and wild plants. District authorities reported 203 cases of acute toxic psychosis over a six-week period. The outbreak primarily affected women of childbearing age; 62% of reported cases were women aged 14-44. A further 23% were in girls between 7 and 14 years of age; no cases were reported in younger children. Patients complained of severe headache and palpitations. They were confused and agitated, displaying hallucinations and paranoid delusions. All patients recovered within two weeks, more rapidly after administration of intravenous
other countries have detected levodopa yields of 3.1-6.1 1 % of the mature seeds In this area, Mpruriens is a common famine food, and its toxicity is well known; the seed is usually detoxified by repeated boiling in water which is thrown away. In the spastic paraparesis epidemic, people were well aware of the toxicity of insufficiently detoxified cassava, but preferred the risk of disease to dying of starvation. Shortage of water may have contributed to insufficient detoxification in both epidemics. The predominance in women in both epidemics may result from women reserving better foods for men and eating food during preparation. Also, women of childbearing age and children are usually more nutritionally deficient than men. We have
chlorpromazine.
Patients attributed the disease to the consumption of the seeds of a wild
variety of Mpruriens, a legume widely distributed throughout the tropics. Contact causes an intense itchy dermatitis due to mucunain.2 The seeds contain levodopa, N, N-dimethyltryptamine
(DMT), bufotenine, 5-methoxy-N, N-dimethyltryptamine (5MeO-DMT), and other alkaloids.3,4 Assays of Mucuna spp from
Epidemiology, Ministry of Health, CP 264, Maputo, Mozambique
JULIE L. CLIFF
of Health, Mozambique. Mantakassa: an epidemic of spastic paraparesis associated with chronic cyanide intoxication in a cassava staple area of Mozambique 2: nutritional factors and hydrocyanic acid content of cassava products. Bull WHO 1984; 62: 48592 2. Anon Mucuna pruriens-associated pruritus: New Jersey. MMWR 1985; 34: 732-34. 3. Council of Scientific and Industrial Research, New Delhi Raw materials In: The wealth of India: a dictionary of Indian raw materials and industrial products. New Delhi. CSIR, 1962. 4. Ghosal S, Singh S, Battacharya SK. Alkaloids of Mucuna pruriens: chemistry and pharmacology Planta Med 1971; 19: 280-84. 5. Daxenbichler ME, VanEtten CH, Earle FR, Tallent WH. L-dopa recovery from Mucuna seed. J Agr Food Chem 1972; 20: 1046-48. 6 Cliff J, Lundquist P, Martensson J, Rosling H, Sorbo B. Association of high cyanide and low sulphur intake in cassava-induced spastic paraparesis Lancet 1985; ii: 1211-13. 7. Ahlborg U, Holmstedt B, Lindgren J-E. Fate and metabolism of some hallucinogenic indolealkylamines. In: Garattini S, Shore PA, eds. Advances in pharmacology, vol 6, part B. New York: Academic Press, 1968: 213-29. 8. Vaidya AB, Rajagopalan TG, Mankodi NA, et al Treatment of Parkinson’s disease with the cowhage plant-Mucuna pruriens Bak. Neurology India 1978; 26: 171-76. 1.
Ministry
Community-based approach to pneumonia SIR,-Dr Bang and colleagues (July 28, p 201) assume that baseline infant and childhood mortality rates in the control and the intervention areas were similar. Table I showed that the proportion of the population aged 04 years was 11-32% and 12-72% in the control and intervention areas, respectively. This difference of 1 -45 % is significant (p < 0-001) yet there is no significant difference in birth rates, suggesting that baseline mortality in the intervention area was less. In the selection of sample for the morbidity study, which was started in July, 1989 (see Subjects and Methods section), 1 ’years after the December, 1987,survey,outof731 selected only 39(5 5%) were in the 32 + age group at the time of the 1987 survey. In the under-5s the 3,1+ age group constitute 30% (1’/5 x 100). From the 30% only 55% children were included. In a random selection this is unexpected. Probably the morbidity study began in July, 1988 (see Results section). The different dates are confusing. Before
may well be an important cause of the decreased gluconeogenesis, as suggested by Dr Wardle. We now have plasma glucagon results from the same children. Interestingly glucagon results were appropriately elevated in hypoglycaemic compared with normoglycaemic children (181 [28] vs 58 [4] pg/ml; p < 0 001). Values were also significantly higher in those who died (124 [21] vs 58 [5] pg/ml) and in comatose cases (81 [9] vs 59 [6] pg/ml). However, for the group as a whole and for all subanalyses there were no differences between malaria and non-malaria cases. For all patients glucagon levels correlated negatively with admission glucose (p=0’01) and positively with duration since last meal (p 0-002), lactate (p 0-001), and alanine aminotransferase (p = 0-022). These data support the concept that there is defective hepatic glucose production in the face of a strong =
counter-regulatory drive. Brewster and colleagues
=
state
that "The
implication that
hypoglycaemia is as common a feature of other infections is not justified". Their evidence for this statement is not clear. The prevalence of hypoglycaemia in their control group of conscious children was similar to that in our children with pneumonia. Their control group did not contain children in coma. It would therefore be of interest to know how common hypoglycaemia would be in a control group of Gambian children in coma due to serious illness other than malaria. The primary purpose of our study was nonetheless to establish whether hypoglycaemia occurs in severely ill children who do not have malaria, and we feel that our data demonstrate that this is so.
Muhimbili Medical Centre, University of Dar es Salaam, Tanzania
N. G. KAWO A. E. MSENGI A. B. M. SWAI L. M. CHUWA
Department of Medicine, University of Newcastle upon Tyne, Newcastle upon Tyne NE2 4HH, UK
K. G. M. M. ALBERTI
Muhimbili Medical Centre
D.G.MCLARTY
Aarhus University, Aarhus, Denmark
H. ORSKOV
previously reported decreased urinary inorganic sulphate excretion, indicating a low sulphur aminoacid intake, in children from this area.6 The hallucinogenic properties of DMT have been well documented and 5-MeO-DMT is the main component of intoxicating snuffs used by South American Indians.7 One of the side-effects of levodopa in patients treated for Parkinson’s disease is a toxic confusional state. We have not been able to find previous reports of toxic psychosis associated with the consumption of M pruriens, although in India the seeds are used as a famine food33 and they have also been used experimentally in the treatment of Parkinson’s diseased
Nampula, Mozambique
MARIA E. INFANTE ALFREDO M. PEREZ MANUEL R. SIMAO FRANCISCO MANDA
National Laboratory of Water and Food Hygiene, Mozambique
EVARISTO F. BAQUETE ANGELA M. FERNANDES
Provincial Health Directorate,
Office of
Outbreak of acute toxic psychosis attributed to Mucuna pruriens S!R,—We record an outbreak of acute toxic psychosis attributed to legume Mucuna pruriens, known as feijão macaco in Mozambique and as cowitch, cowhage, kaunch, and pica-pica in other countries. The outbreak was first reported in November, 1989, in the remote district of Memba, Nampula Province. In 1981, the same area had been affected by an epidemic of spastic paraparesis, associated with consumption of cassava containing high concentrations of cyanogenic glycosides under drought
the
conditions.’ Earlier in 1989, the district had suffered a severe famine with 5200 reported deaths, owing to drought and the depredations of the RENAMO rebels. Food shortages continued through 1989, as rebel attacks interfered with farming and impeded food distribution. Agriculture was further disrupted by a plague of rats and an invasion of lions, the latter causing 53 deaths. People subsisted on bitter cassava and wild plants. District authorities reported 203 cases of acute toxic psychosis over a six-week period. The outbreak primarily affected women of childbearing age; 62% of reported cases were women aged 14-44. A further 23% were in girls between 7 and 14 years of age; no cases were reported in younger children. Patients complained of severe headache and palpitations. They were confused and agitated, displaying hallucinations and paranoid delusions. All patients recovered within two weeks, more rapidly after administration of intravenous
other countries have detected levodopa yields of 3.1-6.1 1 % of the mature seeds In this area, Mpruriens is a common famine food, and its toxicity is well known; the seed is usually detoxified by repeated boiling in water which is thrown away. In the spastic paraparesis epidemic, people were well aware of the toxicity of insufficiently detoxified cassava, but preferred the risk of disease to dying of starvation. Shortage of water may have contributed to insufficient detoxification in both epidemics. The predominance in women in both epidemics may result from women reserving better foods for men and eating food during preparation. Also, women of childbearing age and children are usually more nutritionally deficient than men. We have
chlorpromazine.
Patients attributed the disease to the consumption of the seeds of a wild
variety of Mpruriens, a legume widely distributed throughout the tropics. Contact causes an intense itchy dermatitis due to mucunain.2 The seeds contain levodopa, N, N-dimethyltryptamine
(DMT), bufotenine, 5-methoxy-N, N-dimethyltryptamine (5MeO-DMT), and other alkaloids.3,4 Assays of Mucuna spp from
Epidemiology, Ministry of Health, CP 264, Maputo, Mozambique
JULIE L. CLIFF
of Health, Mozambique. Mantakassa: an epidemic of spastic paraparesis associated with chronic cyanide intoxication in a cassava staple area of Mozambique 2: nutritional factors and hydrocyanic acid content of cassava products. Bull WHO 1984; 62: 48592 2. Anon Mucuna pruriens-associated pruritus: New Jersey. MMWR 1985; 34: 732-34. 3. Council of Scientific and Industrial Research, New Delhi Raw materials In: The wealth of India: a dictionary of Indian raw materials and industrial products. New Delhi. CSIR, 1962. 4. Ghosal S, Singh S, Battacharya SK. Alkaloids of Mucuna pruriens: chemistry and pharmacology Planta Med 1971; 19: 280-84. 5. Daxenbichler ME, VanEtten CH, Earle FR, Tallent WH. L-dopa recovery from Mucuna seed. J Agr Food Chem 1972; 20: 1046-48. 6 Cliff J, Lundquist P, Martensson J, Rosling H, Sorbo B. Association of high cyanide and low sulphur intake in cassava-induced spastic paraparesis Lancet 1985; ii: 1211-13. 7. Ahlborg U, Holmstedt B, Lindgren J-E. Fate and metabolism of some hallucinogenic indolealkylamines. In: Garattini S, Shore PA, eds. Advances in pharmacology, vol 6, part B. New York: Academic Press, 1968: 213-29. 8. Vaidya AB, Rajagopalan TG, Mankodi NA, et al Treatment of Parkinson’s disease with the cowhage plant-Mucuna pruriens Bak. Neurology India 1978; 26: 171-76. 1.
Ministry
Community-based approach to pneumonia SIR,-Dr Bang and colleagues (July 28, p 201) assume that baseline infant and childhood mortality rates in the control and the intervention areas were similar. Table I showed that the proportion of the population aged 04 years was 11-32% and 12-72% in the control and intervention areas, respectively. This difference of 1 -45 % is significant (p < 0-001) yet there is no significant difference in birth rates, suggesting that baseline mortality in the intervention area was less. In the selection of sample for the morbidity study, which was started in July, 1989 (see Subjects and Methods section), 1 ’years after the December, 1987,survey,outof731 selected only 39(5 5%) were in the 32 + age group at the time of the 1987 survey. In the under-5s the 3,1+ age group constitute 30% (1’/5 x 100). From the 30% only 55% children were included. In a random selection this is unexpected. Probably the morbidity study began in July, 1988 (see Results section). The different dates are confusing. Before
