FLOODS AND RESISTANT MALARIA
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1367 I think that the Bamako initiative will seriously undermine efforts elsewhere to give substance to what community participation is all about-giving villagers a say in how to improve their own health. The initiative fails to address a fundamental issue in drug pricing. Is it justified to accept high local prices for drugs (very often not "essential") and take them as the starting-point for the pricing of essential drugs in this cost recovery scheme, as UNICEF proposes? The "essential drugs" policy is aimed at reducing drug costs. Since the Bamako initiative does not address the responsibility of national governments (and ministries of health in particular), it is likely to be received with considerable enthusiasm by national policy makers. However, rather than building self-reliance, it will make rural populations more dependent on the basic health service and will make the national government dependent on external donors and the pharmaceutical industry. I urge national governments and multilateral agencies (donors and technical advisors) to react cautiously to the Bamako initiative. The disruptive effect of this initiative may be much greater than UNICEF has foreseen. PHC Unit, Royal Tropical Institute, 1092AD Amsterdam, Netherlands JARL CHABOT 1. Chabot HTJ, Bremmers J Government health services versus community: conflict or harmony. Soc Sci Med 1988; 26: 957-62. 2. Chabot HTJ, Savage F. A community based health project in West Africa. St Albans, Herts, UK: Teaching Aids at Low Cost, 1983. FLOODS AND RESISTANT MALARIA SIR,-Professor Homeida and colleagues (Oct 15, p 912) express concern at the possible spread of chloroquine-resistant malaria in the Sudan, in the wake of the extensive floods of August, 1988. Many Sudanese work in the Gulf State of Qatar, retuming home once a year with their families. Between Sept 1 and Nov 1, 1988, 15 cases of Plasmodiumfalciparum infection were identified in children of Sudanese families who had recently returned to Qatar for the start of the new school year. There were 6 boys and 9 girls having a mean age of 6-7 years (range 1-5-12). None had taken chemoprophylaxis although 6 had been given a 3-day course of chloroquine for fever in the Sudan. All the children had returned to Qatar less than 3 weeks (mean 10-7 days) before presenting to the paediatric services here. In 4 cases other members of the family had malaria too. The children were treated at Hamad General Hospital with a 3-day course of chloroquine (25 mg/kg), 14 as inpatients. Chloroquine resistance (R2 or R3) was recognised in 11 patients (73%) after failure to clear the parasitaemia by day 6 or 7. A more precise classification of resistance" was not possible because parasite density was assessed semiquantitatively. When treatment failure was noted the patients were given quinine 25 mg/kg daily for 3 days plus either a single dose of ’Fansidar’ or 7 days of tetracycline. All recovered and their parasitaemia cleared. Complications from the disease were mild and included anaemia (< 9 g/dl) in 7 patients, thrombocytopenia in 6, intravascular haemolysis in 3, and coexistent typhoid fever and hepatitis in 1. Chloroquine-resistant P falciparum malaria has not, hitherto, been a major problem in the Sudan, although it is prevalent elsewhere in East Mrica.2 In Qatar in 1987, no Sudanese children were admitted to the paediatric wards with falciparum malaria between Sep 1 and Nov 1. It seems that non-immune individuals or those with lapsed immunity, who are visiting the Sudan, are at risk of chloroquine-resistant malaria. This risk may well have arisen as a result of the catastrophic floods, with the inevitable increase in the mosquito population. Efforts in the Sudan should now be concentrated at vector control and implementation of a rational antimalarial drug policy. Department of Paediatrics, Hamad General Hospital, PO Box 3050, Doha-Qatar VALERIO M. NOVELLI TOHAMI A. EL-TOHAMI VINCENT M. OSUNDWA FREDERICK ASHONG 1. Bruce-Chwatt LJ. Chemotherapy of malaria. 2nd ed. WHO Monogr Ser 1981, no 27. 2. WHO Expert Committee on Malaria. Eighteenth report. Tech Rep Ser WHO 1986, no 735. SIR,-In 1987 continuous heavy rainfall resulted in a major epidemic of malaria in Mvumi, central Tanzania. On average 600-700 children are admitted to Mvumi Hospital in the high malaria transmission period of January to April, about 200 of whom may have malaria. In the same period in 1987, there was a tenfold increase in admissions and 86% were due to malaria, which caused a major strain on medical services. The management of malaria was complicated by a high prevalence of chloroquine resistance. Children attending outpatients with fever usually have a blood smear for malaria parasites and borrelia (tick-bome relapsing fever), and a haemoglobin estimation. The decision to admit a child with malaria depends on several factors, including the ability to take oral drugs and the presence of severe anaemia or suspected cerebral malaria. Chloroquine resistance was presumed if there was a good history of the child having received chloroquine within the previous 7-10 days (for many this could be confirmed from their clinic card), if, in inpatients, there was at 48 hours no response to chloroquine (eg no fall in parasite count and either no improvement clinically or deterioration); and, if at 72 hours or later, pyrexia with parasitaemia (any degree) persisted. Chloroquine resistance was treated with quinine, usually followed by a single dose of ’Fansidar’ on discharge. Between January and June, 1987, 2806 children aged up to 15 years were admitted, of whom 2427 (86-5%) had positive blood smears for malaria, the peak being in April/May. 75% of the children were aged 6 months to 3 years of age. 688 cases (283%) were considered to have chloroquine resistance, and the frequency tended to increase as the epidemic proceeded. Suprisingly, only 125 (5-1%) had cerebral malaria. 246 children (10-1%) died. The haemoglobin was 4 g/dl or less in 1707 (77-6%) of 2199 children, 142 (8-3%) of whom died. The chloroquine resistance, which has been recognised at Mvumi since 1982, not only required alternative drugs therapy but also increased the admission rate. Many patients had RIII resistance. The true incidence of RII and RI was probably underestimated, especially since some severely ill patients were initially given quinine and less severely ill patients treated with chloroquine were discharged early and not followed up. The major cause of admission and death was severe anaemia which usually followed an intermittent fever for 2-3 weeks, in many cases despite the administration of chloroquine. In many patients the lack of response to chloroquine prompted them to seek traditional medicines before taking their children to hospital. This epidemic, particularly associated with chloroquine resistance, had a devastating impact on the child population. In epidemics such as this, especially in villages with limited access to medical services, contingency plans are essential to supply adequate amounts of appropriate drugs; and health education is important to encourage patients to attend early for treatment and to return if it fails. Mvumi Hospital, Mvumi, Dodoma, Tanzania Department of Tropical Paediatrics and International Child Health, Liverpool School of Tropical Medicine, Liverpool L3 5QA A. J. G. BARCLAY J. B. S. COULTER ANGIOSTRONGYLUS CANTONENSIS AND EOSINOPHILIC MENINGITIS SiR,—Your Aug 6 editorial (p 320) discussed the background to the recognition of angiostrongyliasis as the cause of epidemic eosinophilic meningitis in Micronesia, New Caledonia, and Tahiti in 1948—57. In early 1961, Rosen et al2 speculated that this disease was caused by an unspecified worm parasite of the skipjack tuna (or related fish) eaten raw in Tahiti. On April 5, 1961, I wrote to Dr Leon Rosen telling him that I strongly suspected the rat lungworm, Angiostrongylus cantonensis, and suggesting a joint project. The basis for the lungworm theory was a 1955 report from M. J. Mackerras and D. F. Sandars3 that the larvae of this parasite migrated to the brain of the rat host, producing a considerable inflammatory reaction before migrating to the lungs, and my
Transcript of FLOODS AND RESISTANT MALARIA
1367
I think that the Bamako initiative will seriously undermine effortselsewhere to give substance to what community participation is allabout-giving villagers a say in how to improve their own health.The initiative fails to address a fundamental issue in drug pricing.
Is it justified to accept high local prices for drugs (very often not"essential") and take them as the starting-point for the pricing ofessential drugs in this cost recovery scheme, as UNICEF proposes?The "essential drugs" policy is aimed at reducing drug costs.
Since the Bamako initiative does not address the responsibility ofnational governments (and ministries of health in particular), it islikely to be received with considerable enthusiasm by nationalpolicy makers. However, rather than building self-reliance, it willmake rural populations more dependent on the basic health serviceand will make the national government dependent on externaldonors and the pharmaceutical industry.
I urge national governments and multilateral agencies (donorsand technical advisors) to react cautiously to the Bamako initiative.The disruptive effect of this initiative may be much greater thanUNICEF has foreseen.
PHC Unit,Royal Tropical Institute,1092AD Amsterdam, Netherlands JARL CHABOT
1. Chabot HTJ, Bremmers J Government health services versus community: conflict orharmony. Soc Sci Med 1988; 26: 957-62.
2. Chabot HTJ, Savage F. A community based health project in West Africa. St Albans,Herts, UK: Teaching Aids at Low Cost, 1983.
FLOODS AND RESISTANT MALARIA
SIR,-Professor Homeida and colleagues (Oct 15, p 912) expressconcern at the possible spread of chloroquine-resistant malaria inthe Sudan, in the wake of the extensive floods of August, 1988.Many Sudanese work in the Gulf State of Qatar, retuming homeonce a year with their families. Between Sept 1 and Nov 1, 1988, 15cases of Plasmodiumfalciparum infection were identified in childrenof Sudanese families who had recently returned to Qatar for the startof the new school year. There were 6 boys and 9 girls having a meanage of 6-7 years (range 1-5-12). None had taken chemoprophylaxisalthough 6 had been given a 3-day course of chloroquine for fever inthe Sudan. All the children had returned to Qatar less than 3 weeks(mean 10-7 days) before presenting to the paediatric services here.In 4 cases other members of the family had malaria too.The children were treated at Hamad General Hospital with a
3-day course of chloroquine (25 mg/kg), 14 as inpatients.Chloroquine resistance (R2 or R3) was recognised in 11 patients(73%) after failure to clear the parasitaemia by day 6 or 7. A moreprecise classification of resistance" was not possible because parasitedensity was assessed semiquantitatively. When treatment failurewas noted the patients were given quinine 25 mg/kg daily for 3 daysplus either a single dose of ’Fansidar’ or 7 days of tetracycline. Allrecovered and their parasitaemia cleared. Complications from thedisease were mild and included anaemia (< 9 g/dl) in 7 patients,thrombocytopenia in 6, intravascular haemolysis in 3, andcoexistent typhoid fever and hepatitis in 1.
Chloroquine-resistant P falciparum malaria has not, hitherto,been a major problem in the Sudan, although it is prevalentelsewhere in East Mrica.2 In Qatar in 1987, no Sudanese childrenwere admitted to the paediatric wards with falciparum malariabetween Sep 1 and Nov 1. It seems that non-immune individuals orthose with lapsed immunity, who are visiting the Sudan, are at riskof chloroquine-resistant malaria. This risk may well have arisen as aresult of the catastrophic floods, with the inevitable increase in themosquito population. Efforts in the Sudan should now beconcentrated at vector control and implementation of a rationalantimalarial drug policy.
Department of Paediatrics,Hamad General Hospital,PO Box 3050,Doha-Qatar
VALERIO M. NOVELLITOHAMI A. EL-TOHAMIVINCENT M. OSUNDWAFREDERICK ASHONG
1. Bruce-Chwatt LJ. Chemotherapy of malaria. 2nd ed. WHO Monogr Ser 1981, no 27.2. WHO Expert Committee on Malaria. Eighteenth report. Tech Rep Ser WHO 1986,
no 735.
SIR,-In 1987 continuous heavy rainfall resulted in a majorepidemic of malaria in Mvumi, central Tanzania. On average600-700 children are admitted to Mvumi Hospital in the highmalaria transmission period of January to April, about 200 of whommay have malaria. In the same period in 1987, there was a tenfoldincrease in admissions and 86% were due to malaria, which caused amajor strain on medical services. The management of malaria wascomplicated by a high prevalence of chloroquine resistance.
Children attending outpatients with fever usually have a bloodsmear for malaria parasites and borrelia (tick-bome relapsing fever),and a haemoglobin estimation. The decision to admit a child withmalaria depends on several factors, including the ability to take oraldrugs and the presence of severe anaemia or suspected cerebralmalaria.
Chloroquine resistance was presumed if there was a good historyof the child having received chloroquine within the previous 7-10days (for many this could be confirmed from their clinic card), if, ininpatients, there was at 48 hours no response to chloroquine (eg nofall in parasite count and either no improvement clinically ordeterioration); and, if at 72 hours or later, pyrexia with parasitaemia(any degree) persisted. Chloroquine resistance was treated withquinine, usually followed by a single dose of ’Fansidar’ ondischarge.
Between January and June, 1987, 2806 children aged up to 15years were admitted, of whom 2427 (86-5%) had positive bloodsmears for malaria, the peak being in April/May. 75% of thechildren were aged 6 months to 3 years of age. 688 cases (283%)were considered to have chloroquine resistance, and the frequencytended to increase as the epidemic proceeded. Suprisingly, only 125(5-1%) had cerebral malaria. 246 children (10-1%) died. Thehaemoglobin was 4 g/dl or less in 1707 (77-6%) of 2199 children,142 (8-3%) of whom died.The chloroquine resistance, which has been recognised at
Mvumi since 1982, not only required alternative drugs therapy butalso increased the admission rate. Many patients had RIIIresistance. The true incidence of RII and RI was probablyunderestimated, especially since some severely ill patients wereinitially given quinine and less severely ill patients treated withchloroquine were discharged early and not followed up.The major cause of admission and death was severe anaemia
which usually followed an intermittent fever for 2-3 weeks, in manycases despite the administration of chloroquine. In many patientsthe lack of response to chloroquine prompted them to seektraditional medicines before taking their children to hospital. Thisepidemic, particularly associated with chloroquine resistance, had adevastating impact on the child population.
In epidemics such as this, especially in villages with limited accessto medical services, contingency plans are essential to supplyadequate amounts of appropriate drugs; and health education isimportant to encourage patients to attend early for treatment and toreturn if it fails.
Mvumi Hospital,Mvumi, Dodoma, Tanzania
Department of Tropical Paediatricsand International Child Health,
Liverpool School of Tropical Medicine,Liverpool L3 5QA
A. J. G. BARCLAY
J. B. S. COULTER
ANGIOSTRONGYLUS CANTONENSIS ANDEOSINOPHILIC MENINGITIS
SiR,—Your Aug 6 editorial (p 320) discussed the background tothe recognition of angiostrongyliasis as the cause of epidemiceosinophilic meningitis in Micronesia, New Caledonia, and Tahitiin 1948—57. In early 1961, Rosen et al2 speculated that this diseasewas caused by an unspecified worm parasite of the skipjack tuna (orrelated fish) eaten raw in Tahiti. On April 5, 1961, I wrote to DrLeon Rosen telling him that I strongly suspected the rat lungworm,Angiostrongylus cantonensis, and suggesting a joint project. Thebasis for the lungworm theory was a 1955 report from M. J.Mackerras and D. F. Sandars3 that the larvae of this parasitemigrated to the brain of the rat host, producing a considerableinflammatory reaction before migrating to the lungs, and my
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