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Leishmania infantum as a cause of cutaneous leishmaniasis
898 TRANSACTIONS OF THE ROYAL SOCIETY OF TROPICAL MEDICINE
Lei&mania infanturn as a cause of cutaneous leishmaniasis We read with interest the report by Zeledon et al. (1989: Transactions, 83, 786) of cutaneous leishmaniasis (CL) in Central America caused by Leishmania ‘chagasi’. Similar cases were reported by Oliveira Neto et al. (1982: Pesquisas Brusiliera DoenGa Chagas, 9th meeting, November 1982, Caxambu, Brazil, p. 130 and Memorias do Instituco Oswahfo Cruz, 81, 303) and Oster et al. (1985: American Journal of Tropical Medicine and Hygiene, 34, 856-860). Such reports are not surprising to workers around the Mediterranean basin. Ten years ago, the first 2 cases of CL caused by L. infanturn were reported form France (Rioux et al.. 1980: Comptes Rendus Hebdomonadaire des Seances de l’Academ>e des Sciences, Paris,
series D, 291, 701-703). Subsequently, similar cases were found in Spain, Italy, Malta and Algeria, and more were reported from France. In the European countries of the western Mediterranean, the commonest, possibly sole, causeof CL now seemsto be L. infanturn transmitted by sandflies of the subgenus Larroussius. The distribution of the disease is contiguous with, or superimposed on, that of visceral leishmaniasis (VL) caused by zymodeme MON-1 of the same parasite. In the Old World, although a few casesof CL are also caused by this zymodeme, most parasites isolated from skin lesions are isoenzymatic variants differing from MON-1 bv one to 3 of the 15 enzymes we rou‘tinely examine. There are 3 unusual features of the variants. Firstly, they are seldom or never isolated from human casesof VL and. therefore, are largely restricted to CL cases; secondly, variants can be sympatric; and, thirdly, among the different zymodemes, there are various combinations of electromorphs suggesting genetic exchange. It would be most interesting to know which zymodeme or zymodemes of L. ‘chagasi’ cause CL of man in Latin America. All of 37 stocks of L. ‘chagasi from 6 countries of Latin America (Bolivia, Brazil, Colombia, Honduras, Panama, Venezuela) typed by isoenzyme analysis in our laboratory have been indistinguishable from zymodeme MON-1 of L. infantum. Similarly, Momen et al. (1987: In: Leishmaniasis, Hart, D. T. (editor). New York: Plenum, pp. 911-916) examined up to 16 isoenzymes of over 100 isolates of L. ‘chugasi’ from man, dogs and opossums in Brazil and Honduras and could not distinguish them from zymodeme MON-1 of L. infanturn. The fact that both the uarasites convent&ally considered as causative agents of VL can commonly give rise to CL is another feature supporting the notion that L. infantum and L. ‘chagasi) are conspectic. J&J-E Fact& de Midecine Universite de Montpellier 34000 Montpellier, France
AND HYGIENE (1990) 84, CORRESPONDENCE
Congenital malaria in Papua New Guinea Drs Lehner and Andrews (1988: Transactions, 82, 822-826) noted that infants born with Plasmodium falciparum infection of cord blood were well at birth, but were likely to develop clinical malaria 21 to 96 days after birth. Various mechanisms were suggested,such as transfer of maternal antibodies, to explain this delay of onset. Another example of apparent delayed falciparum parasitaemia in the first 3 months of life is illustrated in my paper on indigenous malaria in the D’Etrecasteaux islands (1988: Papua Nero Guinea MedicalJournal, 31, 45-55). Figures 4 & 5 show low P. falciparum prevalence and density in this agegroup. At the time I attributed this to the effect of foetal haemoglobin (Pasvol et al., 1988; Nature, 270, 171-173). Since then another paper by Pasvol et al. has come to my notice (1980: British Journal of Haematology, 45, 208-295). This paper gives a neat explanation of these observed phenomena, i.e. that reticulocytes and young red cells are more susceptible to invasion by this parasite as compared with metabolically older cell populations and that a few weeks after birth erythopoiesis virtually ceases for 2-3 months, resulting in the presence of relatively few young cells susceptible to invasion. I should be interested in further comment. T. E. T. Spencer 1 George Street, Tenterfield, 2372, Australia (Formerly Assesment Malariologist Department of Health Papua New Guinea)
9 December I989
Vitamin B complex for chloroquine-induced pruritis We have observed that vitamin B complex is effective in preventing chloroquine-induced pruritus, the commonest unwanted reaction to chloroquine, which is experienced by somepredisposed individuals and is commoner among Blacks (Osifo, 1984: Archives of Dermatology, 128, 80-82). Antihistamines are not very helpful in reheving the itch. Personal experience on several occasions(one of us, S. A. A., suffers from chloroquine itch) and the exnerience of various colleaguesindicate that iniection of-vitamin B complex preients development ‘of the itch. The mechanism of chloroauine itch is illunderstood. Further studies on *the efficacy and mechanism of action of vitamin B complex in preventing chloroquine itch might throw more light on the pathogenesis of chloroquine-induced pruritus, apart from the possibility of obtaining a cure for this common distressing drug reaction. S.A. Abdulkadir M. A. Pate
12 March 1990
C60-BDH Ahmadu Bello University Hospital Zaria Nigeria
21 May 1990
Lei&mania infanturn as a cause of cutaneous leishmaniasis We read with interest the report by Zeledon et al. (1989: Transactions, 83, 786) of cutaneous leishmaniasis (CL) in Central America caused by Leishmania ‘chagasi’. Similar cases were reported by Oliveira Neto et al. (1982: Pesquisas Brusiliera DoenGa Chagas, 9th meeting, November 1982, Caxambu, Brazil, p. 130 and Memorias do Instituco Oswahfo Cruz, 81, 303) and Oster et al. (1985: American Journal of Tropical Medicine and Hygiene, 34, 856-860). Such reports are not surprising to workers around the Mediterranean basin. Ten years ago, the first 2 cases of CL caused by L. infanturn were reported form France (Rioux et al.. 1980: Comptes Rendus Hebdomonadaire des Seances de l’Academ>e des Sciences, Paris,
series D, 291, 701-703). Subsequently, similar cases were found in Spain, Italy, Malta and Algeria, and more were reported from France. In the European countries of the western Mediterranean, the commonest, possibly sole, causeof CL now seemsto be L. infanturn transmitted by sandflies of the subgenus Larroussius. The distribution of the disease is contiguous with, or superimposed on, that of visceral leishmaniasis (VL) caused by zymodeme MON-1 of the same parasite. In the Old World, although a few casesof CL are also caused by this zymodeme, most parasites isolated from skin lesions are isoenzymatic variants differing from MON-1 bv one to 3 of the 15 enzymes we rou‘tinely examine. There are 3 unusual features of the variants. Firstly, they are seldom or never isolated from human casesof VL and. therefore, are largely restricted to CL cases; secondly, variants can be sympatric; and, thirdly, among the different zymodemes, there are various combinations of electromorphs suggesting genetic exchange. It would be most interesting to know which zymodeme or zymodemes of L. ‘chagasi’ cause CL of man in Latin America. All of 37 stocks of L. ‘chagasi from 6 countries of Latin America (Bolivia, Brazil, Colombia, Honduras, Panama, Venezuela) typed by isoenzyme analysis in our laboratory have been indistinguishable from zymodeme MON-1 of L. infantum. Similarly, Momen et al. (1987: In: Leishmaniasis, Hart, D. T. (editor). New York: Plenum, pp. 911-916) examined up to 16 isoenzymes of over 100 isolates of L. ‘chugasi’ from man, dogs and opossums in Brazil and Honduras and could not distinguish them from zymodeme MON-1 of L. infanturn. The fact that both the uarasites convent&ally considered as causative agents of VL can commonly give rise to CL is another feature supporting the notion that L. infantum and L. ‘chagasi) are conspectic. J&J-E Fact& de Midecine Universite de Montpellier 34000 Montpellier, France
AND HYGIENE (1990) 84, CORRESPONDENCE
Congenital malaria in Papua New Guinea Drs Lehner and Andrews (1988: Transactions, 82, 822-826) noted that infants born with Plasmodium falciparum infection of cord blood were well at birth, but were likely to develop clinical malaria 21 to 96 days after birth. Various mechanisms were suggested,such as transfer of maternal antibodies, to explain this delay of onset. Another example of apparent delayed falciparum parasitaemia in the first 3 months of life is illustrated in my paper on indigenous malaria in the D’Etrecasteaux islands (1988: Papua Nero Guinea MedicalJournal, 31, 45-55). Figures 4 & 5 show low P. falciparum prevalence and density in this agegroup. At the time I attributed this to the effect of foetal haemoglobin (Pasvol et al., 1988; Nature, 270, 171-173). Since then another paper by Pasvol et al. has come to my notice (1980: British Journal of Haematology, 45, 208-295). This paper gives a neat explanation of these observed phenomena, i.e. that reticulocytes and young red cells are more susceptible to invasion by this parasite as compared with metabolically older cell populations and that a few weeks after birth erythopoiesis virtually ceases for 2-3 months, resulting in the presence of relatively few young cells susceptible to invasion. I should be interested in further comment. T. E. T. Spencer 1 George Street, Tenterfield, 2372, Australia (Formerly Assesment Malariologist Department of Health Papua New Guinea)
9 December I989
Vitamin B complex for chloroquine-induced pruritis We have observed that vitamin B complex is effective in preventing chloroquine-induced pruritus, the commonest unwanted reaction to chloroquine, which is experienced by somepredisposed individuals and is commoner among Blacks (Osifo, 1984: Archives of Dermatology, 128, 80-82). Antihistamines are not very helpful in reheving the itch. Personal experience on several occasions(one of us, S. A. A., suffers from chloroquine itch) and the exnerience of various colleaguesindicate that iniection of-vitamin B complex preients development ‘of the itch. The mechanism of chloroauine itch is illunderstood. Further studies on *the efficacy and mechanism of action of vitamin B complex in preventing chloroquine itch might throw more light on the pathogenesis of chloroquine-induced pruritus, apart from the possibility of obtaining a cure for this common distressing drug reaction. S.A. Abdulkadir M. A. Pate
12 March 1990
C60-BDH Ahmadu Bello University Hospital Zaria Nigeria
21 May 1990