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MALARIA CHEMOPROPHYLAXIS IN EXPATRIATES IN AFRICA
1046 RAPID ZIEHL-NEELSEN STAINING BY USE OF MICROWAVE OVEN
MALARIA CHEMOPROPHYLAXIS IN EXPATRIATES IN AFRICA
SIR,-I carried out a survey very similar to that of Professor McLarty and colleagues (Sept 22, p 656), on chemoprophylaxis of malaria in non-immune expatriates in Lagos, Nigeria, during the years 1947-49.was, therefore, interested in comparing these two in West Africa and one in East Africa. al studied responses to a questionnaire sent to 1248 residents of Dar es Salaam; 821 replies (66%) were received. Our survey, sent to 1136 non-African residents of Lagos, had a lower response rate (46%), but it was supplemented by another questionnaire sent to 313 medical officers in Nigeria, 40-2% of whom replied; they were responsible for the health of a portion of the non-African population of Lagos and the country. 6 -9% of the expatriates in the Dar es Salaam survey took no antimalarials and McLarty et al are right to express concern about the high (37 . 1%) malaria infection rate of this group. I agree with their surprise at the difference in protective effect of 200 mg and 100 mg proguanil daily (with or without chloroquine) (infection rate with 200 mg 1 -5-20%, with 100 mg 15.7-46.4%). One wonders how the double dose of proguanil alone could show such a remarkable protective effect in conditions where the assumed crossresistance between proguanil and pyrimethamine has been expected in the field. I agree that a fuller study of this finding is needed. The other surprising result is the apparently disappointing effect of chloroquine combined with either ’Maloprim’ (pyrimethamine/ dapsone) or ’Fansidar’ (pyrimethamine/sulfadoxine). The latter combination has been forcefully advocated by a group of American experts3 and is now recommended by the World Health Organisation in areas where resistance of Plasmodium falciparum to4 chloroquine coexists with a significant frequency of P vivax.4 Although the presence of strains of P falciparum resistant to chloroquine is now confirmed in Tanzaniaand other parts of tropical Africa, it is still surprising that the large group of expatriates taking chloroquine (300-600 mg base weekly) fared only slightly better than those who took no antimalarials (31-2% v 37-1%). This brings up another, perhaps major, point in assessing the prophylactic virtues of various drugs on the basis of infection rates derived from information gathered retrospectively. McLarty et al recognised this unavoidable weakness of the survey-the unknown degree of exposure of the various groups to malaria infection. Each of these groups consisted of men, women, and children who travelled in more or less malarious parts of the country; lived in airconditioned, screened, or unscreened houses; and had different habits and patterns of life, such as wearing proper clothing after dark, using mosquito nets or pyrethrum sprays, and6 being more or less compliant with the regular drug prophylaxis. The quoted malaria infection rates must therefore be interpreted with much caution. Thus, table n, showing the statistical significance of differences between the apparent degree of protection by various regimens, indicates association but no direct
studies,
one
McLarty et
large
relation. The same strictures have been applied to our Nigerian survey of 1947-49. Some of its results corroborate the figures produced in Dar es Salaam: the malaria attack rates among a population of 1130 were 22 - 6% in those taking mepacrine, 22% in those taking quinine, and 10% in those taking proguanil; since only 6 people were taking chloroquine (which was then a rare drug) and only 1 had malaria, the rate was of no statistical value. ’
Wellcome Museum of Medical Science, PO Box 129, The Wellcome Building, 183 Euston Road, London NW1 2BP
L. J. BRUCE-CHWATT
1. Bruce-Chwatt
LJ, Bruce-Chwatt JM. Antimalarial drugs in West Africa, with particular reference to proguanil. Results of a survey in Nigeria. Br Med J 1950; ii:
7-12. 2. Rombo L, Hedman 3. 4. 5 6.
P, Kihamia CM, Ramji BD, Björkman A, Bengtsson E. Proguanil for malaria prophylaxis. Lancet 1983; i: 997. Campbell CC, Chin W, Collins WE, Teutsch SM, Moss DM. Chloroquine-resistant Plasmodium falciparum from East Africa. Lancet 1979; ii: 1151-54. Bruce-Chwatt LJ. Chemoprophylaxis of malaria in Africa; the spent "magic bullet". Br Med J 1982; 285: 674-76. Spencer HC, Kariuki DM, Koech DK. Chloroquine resistance in Plasmodium falciparum from Kenyan infants. Am J Trop Med Hyg 1983; 32: 922-25. WHO. Malaria risk in international travel. Wkly Epidemiol Rec 1984; 59: no 30.
SIR,-Ziehl-Neelsen and fluorescent staining for tubercle bacilli well tried and trusted methods but they take 15-20 min of laboratory time. We have speeded up the Ziehl-Neelsen method by using a microwave oven. Smears, made in the normal manner and air-dried, are covered with strong carbol-fuchsin and placed, in a plastic sandwich box, in a domestic microwave oven (Sharp, model 9410E) for 30 s at full power. Slides were decolorised with acid alcohol until no more colour appeared in the washing (about 2 min) and counterstained for 30 s with malachite-green. All stains were prepared according to Cowan. All 30 specimens of tuberculous sputum and all 10 cultures of acid-fast bacteria stained positive by both the microwave method and conventional Ziehl-Neelsen staining; 30 non-tuberculous specimens and 10 cultures of nonacid-fast bacteria were negative by both methods. The slides were cleaner after microwave treatment. This method seems to be as accurate and reliable as the classical Ziehl-Neelsen staining method. It much reduces the time for processing suspected tuberculous specimens in a routine diagnostic laboratory. are
Department of Medical Microbiology, University of Sheffield Medical School,
S. HAFIZ R. C. SPENCER MARGARET LEE HILARY GOOCH
Sheffield S10 2RX
B. I. DUERDEN
1. Cowan ST. Cowan and Steel’s manual for the identification of medical bacteria, 2nd ed
Cambridge: Cambridge University Press, 1974: 161-63.
SUDDEN COLLAPSE AFTER INTRA-AMNIOTIC PROSTAGLANDIN E2 INJECTION
SIR,-Since the report by Karim and Filshie of the use of prostaglandin (PG) F2a and, later, PGE2 for the induction of abortion in the second trimester,1 PGs have become widely used for pregnancy termination. We report a case of sudden collapse after the intra-amniotic injection ofPGE2. A 36-year-old woman with multiple sclerosis was admitted for pregnancy termination after the diagnosis of a mosaic Down’s syndrome fetus on amniocentesis. She was in her third pregnancy; her previous pregnancies had resulted in the vaginal delivery of a girl at term, and a spontaneous abortion at 10 weeks’ gestation. She was well, with no neurological deficit, and the fundal height was compatible with a pregnancy of 20 weeks. The intra-amniotic instillation of 5 mg PGE2 and 40 g urea was planned. An intravenous infusion was set up and 60 ml bloodstained amniotic fluid was removed under local anaesthetic. Within 1 min of injection of a test dose of 1 mg PGE2 the patient collapsed. Her pulse, barely palpable peripherally, increased to 130/min, and her blood pressure dropped to 90/50 mm Hg. She was shivering and her bowels opened. There was no bronchospasm, although she did become tachnypnoeic. 100 mg hydrocortisone and 10 mg chlorpheniramine maleate were administered intravenously and she was given oxygen via a face mask. Within 10 min her blood pressure had returned to 110/68 mm Hg, and after a further 15 min her pulse rate was normal and she had stopped shivering. An ECG at that stage confirmed sinus rhythm, and plasma urea and electrolyte concentrations, measured later that evening, were normal. Her condition remained stable, and on the following day abortion was induced successfully by extra-amniotic PGE2 with supplementary oxytocin. The fetus and placenta were expelled completely after 351f2 hours, and she was allowed home the next day. Follow-up for 6 weeks has revealed no complications. Despite the apparent safety of PGs for abortion induction, severe reactions can occur. Two cases of sudden collapse and death have been reported after intra-amniotic PGF2aand a reaction to extraamniotic PGE2, comprising hypotension, tachycardia, abdominal pain, rigors and difficulty in breathing, attributed to the intravenous injection of the drug, has been described.3 In our case, intra-amniotic administration of PGEz after a bloodstained amniotic tap (the placenta had been located anteriorly by an ultrasound scan at 17 weeks) had probably resulted in some
MALARIA CHEMOPROPHYLAXIS IN EXPATRIATES IN AFRICA
SIR,-I carried out a survey very similar to that of Professor McLarty and colleagues (Sept 22, p 656), on chemoprophylaxis of malaria in non-immune expatriates in Lagos, Nigeria, during the years 1947-49.was, therefore, interested in comparing these two in West Africa and one in East Africa. al studied responses to a questionnaire sent to 1248 residents of Dar es Salaam; 821 replies (66%) were received. Our survey, sent to 1136 non-African residents of Lagos, had a lower response rate (46%), but it was supplemented by another questionnaire sent to 313 medical officers in Nigeria, 40-2% of whom replied; they were responsible for the health of a portion of the non-African population of Lagos and the country. 6 -9% of the expatriates in the Dar es Salaam survey took no antimalarials and McLarty et al are right to express concern about the high (37 . 1%) malaria infection rate of this group. I agree with their surprise at the difference in protective effect of 200 mg and 100 mg proguanil daily (with or without chloroquine) (infection rate with 200 mg 1 -5-20%, with 100 mg 15.7-46.4%). One wonders how the double dose of proguanil alone could show such a remarkable protective effect in conditions where the assumed crossresistance between proguanil and pyrimethamine has been expected in the field. I agree that a fuller study of this finding is needed. The other surprising result is the apparently disappointing effect of chloroquine combined with either ’Maloprim’ (pyrimethamine/ dapsone) or ’Fansidar’ (pyrimethamine/sulfadoxine). The latter combination has been forcefully advocated by a group of American experts3 and is now recommended by the World Health Organisation in areas where resistance of Plasmodium falciparum to4 chloroquine coexists with a significant frequency of P vivax.4 Although the presence of strains of P falciparum resistant to chloroquine is now confirmed in Tanzaniaand other parts of tropical Africa, it is still surprising that the large group of expatriates taking chloroquine (300-600 mg base weekly) fared only slightly better than those who took no antimalarials (31-2% v 37-1%). This brings up another, perhaps major, point in assessing the prophylactic virtues of various drugs on the basis of infection rates derived from information gathered retrospectively. McLarty et al recognised this unavoidable weakness of the survey-the unknown degree of exposure of the various groups to malaria infection. Each of these groups consisted of men, women, and children who travelled in more or less malarious parts of the country; lived in airconditioned, screened, or unscreened houses; and had different habits and patterns of life, such as wearing proper clothing after dark, using mosquito nets or pyrethrum sprays, and6 being more or less compliant with the regular drug prophylaxis. The quoted malaria infection rates must therefore be interpreted with much caution. Thus, table n, showing the statistical significance of differences between the apparent degree of protection by various regimens, indicates association but no direct
studies,
one
McLarty et
large
relation. The same strictures have been applied to our Nigerian survey of 1947-49. Some of its results corroborate the figures produced in Dar es Salaam: the malaria attack rates among a population of 1130 were 22 - 6% in those taking mepacrine, 22% in those taking quinine, and 10% in those taking proguanil; since only 6 people were taking chloroquine (which was then a rare drug) and only 1 had malaria, the rate was of no statistical value. ’
Wellcome Museum of Medical Science, PO Box 129, The Wellcome Building, 183 Euston Road, London NW1 2BP
L. J. BRUCE-CHWATT
1. Bruce-Chwatt
LJ, Bruce-Chwatt JM. Antimalarial drugs in West Africa, with particular reference to proguanil. Results of a survey in Nigeria. Br Med J 1950; ii:
7-12. 2. Rombo L, Hedman 3. 4. 5 6.
P, Kihamia CM, Ramji BD, Björkman A, Bengtsson E. Proguanil for malaria prophylaxis. Lancet 1983; i: 997. Campbell CC, Chin W, Collins WE, Teutsch SM, Moss DM. Chloroquine-resistant Plasmodium falciparum from East Africa. Lancet 1979; ii: 1151-54. Bruce-Chwatt LJ. Chemoprophylaxis of malaria in Africa; the spent "magic bullet". Br Med J 1982; 285: 674-76. Spencer HC, Kariuki DM, Koech DK. Chloroquine resistance in Plasmodium falciparum from Kenyan infants. Am J Trop Med Hyg 1983; 32: 922-25. WHO. Malaria risk in international travel. Wkly Epidemiol Rec 1984; 59: no 30.
SIR,-Ziehl-Neelsen and fluorescent staining for tubercle bacilli well tried and trusted methods but they take 15-20 min of laboratory time. We have speeded up the Ziehl-Neelsen method by using a microwave oven. Smears, made in the normal manner and air-dried, are covered with strong carbol-fuchsin and placed, in a plastic sandwich box, in a domestic microwave oven (Sharp, model 9410E) for 30 s at full power. Slides were decolorised with acid alcohol until no more colour appeared in the washing (about 2 min) and counterstained for 30 s with malachite-green. All stains were prepared according to Cowan. All 30 specimens of tuberculous sputum and all 10 cultures of acid-fast bacteria stained positive by both the microwave method and conventional Ziehl-Neelsen staining; 30 non-tuberculous specimens and 10 cultures of nonacid-fast bacteria were negative by both methods. The slides were cleaner after microwave treatment. This method seems to be as accurate and reliable as the classical Ziehl-Neelsen staining method. It much reduces the time for processing suspected tuberculous specimens in a routine diagnostic laboratory. are
Department of Medical Microbiology, University of Sheffield Medical School,
S. HAFIZ R. C. SPENCER MARGARET LEE HILARY GOOCH
Sheffield S10 2RX
B. I. DUERDEN
1. Cowan ST. Cowan and Steel’s manual for the identification of medical bacteria, 2nd ed
Cambridge: Cambridge University Press, 1974: 161-63.
SUDDEN COLLAPSE AFTER INTRA-AMNIOTIC PROSTAGLANDIN E2 INJECTION
SIR,-Since the report by Karim and Filshie of the use of prostaglandin (PG) F2a and, later, PGE2 for the induction of abortion in the second trimester,1 PGs have become widely used for pregnancy termination. We report a case of sudden collapse after the intra-amniotic injection ofPGE2. A 36-year-old woman with multiple sclerosis was admitted for pregnancy termination after the diagnosis of a mosaic Down’s syndrome fetus on amniocentesis. She was in her third pregnancy; her previous pregnancies had resulted in the vaginal delivery of a girl at term, and a spontaneous abortion at 10 weeks’ gestation. She was well, with no neurological deficit, and the fundal height was compatible with a pregnancy of 20 weeks. The intra-amniotic instillation of 5 mg PGE2 and 40 g urea was planned. An intravenous infusion was set up and 60 ml bloodstained amniotic fluid was removed under local anaesthetic. Within 1 min of injection of a test dose of 1 mg PGE2 the patient collapsed. Her pulse, barely palpable peripherally, increased to 130/min, and her blood pressure dropped to 90/50 mm Hg. She was shivering and her bowels opened. There was no bronchospasm, although she did become tachnypnoeic. 100 mg hydrocortisone and 10 mg chlorpheniramine maleate were administered intravenously and she was given oxygen via a face mask. Within 10 min her blood pressure had returned to 110/68 mm Hg, and after a further 15 min her pulse rate was normal and she had stopped shivering. An ECG at that stage confirmed sinus rhythm, and plasma urea and electrolyte concentrations, measured later that evening, were normal. Her condition remained stable, and on the following day abortion was induced successfully by extra-amniotic PGE2 with supplementary oxytocin. The fetus and placenta were expelled completely after 351f2 hours, and she was allowed home the next day. Follow-up for 6 weeks has revealed no complications. Despite the apparent safety of PGs for abortion induction, severe reactions can occur. Two cases of sudden collapse and death have been reported after intra-amniotic PGF2aand a reaction to extraamniotic PGE2, comprising hypotension, tachycardia, abdominal pain, rigors and difficulty in breathing, attributed to the intravenous injection of the drug, has been described.3 In our case, intra-amniotic administration of PGEz after a bloodstained amniotic tap (the placenta had been located anteriorly by an ultrasound scan at 17 weeks) had probably resulted in some