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Late recrudescence of Plasmodium falciparum malaria in pregnancy
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Late recrudescence of Plasmodium falciparum malaria in pregnancy
Letters to the Editor Conflict of interest: No conflict of interest to declare.
References Your recent report of a pregnancy-related late recrudescence of Plasmodium falciparum malaria in a Ghanaian woman,1 four years after her last visit to a parasite transmission area, may constitute an illustrative example of how naturally acquired immunity to this parasite works. Individuals growing up in areas with continuous transmission of P. falciparum parasites — such as Ghana — develop substantial clinical immunity to malaria during childhood, and clinical episodes are an exception in adults (reviewed in Hviid2). However, low-grade and asymptomatic parasitemia is probably present in a large proportion of adults, where it can be maintained for extended periods in the absence of infection — the evidence suggests several years. Importantly, such infections, which are controlled at very low levels by immunity, seem to be important for the maintenance of clinical protection.3 The woman in the report by Giobbia and colleagues1 probably carried such an asymptomatic infection when she arrived in Italy. If this hypothesis is correct, why did she become ill from her previously silent infection only when she became pregnant? The authors suggest pregnancy-associated immunosuppression. The fact that previously immune women become highly susceptible to P. falciparum malaria when becoming pregnant makes this explanation seem plausible. Nevertheless, it is almost certainly incorrect. In endemic areas, pregnancy-related P. falciparum malaria is concentrated among primigravidae, and susceptibility rapidly decreases with increasing parity. The immunosuppression hypothesis cannot adequately explain this. Instead, it now seems evident that the placenta creates opportunities for P. falciparum infection not available in non-pregnant hosts.4 Furthermore, placenta-dwelling parasites express antigens on the infected erythrocyte surface that are distinct from those expressed by other P. falciparum, and these antigens are major targets of acquired protective immunity to pregnancy-associated malaria.5—7 Because the antigens expressed by placental parasites are distinct, a woman is completely susceptible to such an infection when she becomes pregnant for the first time, even if her pre-existing acquired immunity can control non-placental parasitemia at low levels (reviewed in Hviid8). The parasites can switch between different surface antigens and therefore no new infection is needed to initiate placental infection in an individual parasitemic at the time of pregnancy.9,10 Apart from providing an exciting piece of evidence in favor of this hypothesis, the report by Giobbia et al.1 suggests that physicians should consider the risk of pregnancy-associated malaria in women who have grown up in endemic areas, even if they have not visited such areas for long periods prior to pregnancy.
1. Giobbia M, Tonon E, Zanatta A, Cesaris L, Vaglia A. Late recrudescence of Plasmodium falciparum malaria in a pregnant woman: a case report. Int J Infect Dis 2005;9:234—5. 2. Hviid L. Naturally acquired immunity to Plasmodium falciparum malaria in Africa. Acta Trop 2005;95:270—5. 3. Staalsoe T, Hviid L. The role of variant-specific immunity in asymptomatic infections: maintaining a fine balance. Parasitol Today 1998;14:177—8. 4. Fried M, Duffy PE. Adherence of Plasmodium falciparum to chondroitin sulphate A in the human placenta. Science 1996; 272:1502—4. 5. Fried M, Nosten F, Brockman A, Brabin BT, Duffy PE. Maternal antibodies block malaria. Nature 1998;395:851—2. 6. Ricke CH, Staalsoe T, Koram K, Akanmori BD, Riley EM, Theander TG, et al. Plasma antibodies from malaria-exposed pregnant women recognize variant surface antigens on Plasmodium falciparum-infected erythrocytes in a parity-dependent manner and block parasite adhesion to chondroitin sulphate A. J Immunol 2000;165:3309—16. 7. Staalsoe T, Shulman CE, Bulmer JN, Kawuondo K, Marsh K, Hviid L. Variant surface antigen-specific IgG and protection against the clinical consequences of pregnancy-associated Plasmodium falciparum malaria. Lancet 2004;363: 283—9. 8. Hviid L. The immuno-epidemiology of pregnancy-associated malaria: a variant surface antigen-specific perspective. Parasite Immunol 2004;26:477—86. 9. Roberts DJ, Craig AG, Berendt AR, Pinches R, Nash G, Marsh K, et al. Rapid switching to multiple antigenic and adhesive phenotypes in malaria. Nature 1992;357:689—92. 10. Staalsoe T, Hamad AA, Hviid L, Elhassan IM, Arnot DE, Theander TG. In vivo switching between variant surface antigens in human Plasmodium falciparum infection. J Infect Dis 2002;186: 719—22.
Lars Hviid* Trine Staalsoe Department of Infectious Diseases M7641, Centre for Medical Parasitology at Rigshospitalet and University of Copenhagen, Blegdamsvej 9, 2100 Copenhagen, Denmark *Corresponding author. Tel.: +45 35 45 79 57; fax: +45 35 45 76 44 E-mail address: [email protected] (L. Hviid) Corresponding Editor: Jonathan Cohen, Brighton, UK 26 July 2005 doi:10.1016/j.ijid.2005.10.013
Late recrudescence of Plasmodium falciparum malaria in pregnancy
Letters to the Editor Conflict of interest: No conflict of interest to declare.
References Your recent report of a pregnancy-related late recrudescence of Plasmodium falciparum malaria in a Ghanaian woman,1 four years after her last visit to a parasite transmission area, may constitute an illustrative example of how naturally acquired immunity to this parasite works. Individuals growing up in areas with continuous transmission of P. falciparum parasites — such as Ghana — develop substantial clinical immunity to malaria during childhood, and clinical episodes are an exception in adults (reviewed in Hviid2). However, low-grade and asymptomatic parasitemia is probably present in a large proportion of adults, where it can be maintained for extended periods in the absence of infection — the evidence suggests several years. Importantly, such infections, which are controlled at very low levels by immunity, seem to be important for the maintenance of clinical protection.3 The woman in the report by Giobbia and colleagues1 probably carried such an asymptomatic infection when she arrived in Italy. If this hypothesis is correct, why did she become ill from her previously silent infection only when she became pregnant? The authors suggest pregnancy-associated immunosuppression. The fact that previously immune women become highly susceptible to P. falciparum malaria when becoming pregnant makes this explanation seem plausible. Nevertheless, it is almost certainly incorrect. In endemic areas, pregnancy-related P. falciparum malaria is concentrated among primigravidae, and susceptibility rapidly decreases with increasing parity. The immunosuppression hypothesis cannot adequately explain this. Instead, it now seems evident that the placenta creates opportunities for P. falciparum infection not available in non-pregnant hosts.4 Furthermore, placenta-dwelling parasites express antigens on the infected erythrocyte surface that are distinct from those expressed by other P. falciparum, and these antigens are major targets of acquired protective immunity to pregnancy-associated malaria.5—7 Because the antigens expressed by placental parasites are distinct, a woman is completely susceptible to such an infection when she becomes pregnant for the first time, even if her pre-existing acquired immunity can control non-placental parasitemia at low levels (reviewed in Hviid8). The parasites can switch between different surface antigens and therefore no new infection is needed to initiate placental infection in an individual parasitemic at the time of pregnancy.9,10 Apart from providing an exciting piece of evidence in favor of this hypothesis, the report by Giobbia et al.1 suggests that physicians should consider the risk of pregnancy-associated malaria in women who have grown up in endemic areas, even if they have not visited such areas for long periods prior to pregnancy.
1. Giobbia M, Tonon E, Zanatta A, Cesaris L, Vaglia A. Late recrudescence of Plasmodium falciparum malaria in a pregnant woman: a case report. Int J Infect Dis 2005;9:234—5. 2. Hviid L. Naturally acquired immunity to Plasmodium falciparum malaria in Africa. Acta Trop 2005;95:270—5. 3. Staalsoe T, Hviid L. The role of variant-specific immunity in asymptomatic infections: maintaining a fine balance. Parasitol Today 1998;14:177—8. 4. Fried M, Duffy PE. Adherence of Plasmodium falciparum to chondroitin sulphate A in the human placenta. Science 1996; 272:1502—4. 5. Fried M, Nosten F, Brockman A, Brabin BT, Duffy PE. Maternal antibodies block malaria. Nature 1998;395:851—2. 6. Ricke CH, Staalsoe T, Koram K, Akanmori BD, Riley EM, Theander TG, et al. Plasma antibodies from malaria-exposed pregnant women recognize variant surface antigens on Plasmodium falciparum-infected erythrocytes in a parity-dependent manner and block parasite adhesion to chondroitin sulphate A. J Immunol 2000;165:3309—16. 7. Staalsoe T, Shulman CE, Bulmer JN, Kawuondo K, Marsh K, Hviid L. Variant surface antigen-specific IgG and protection against the clinical consequences of pregnancy-associated Plasmodium falciparum malaria. Lancet 2004;363: 283—9. 8. Hviid L. The immuno-epidemiology of pregnancy-associated malaria: a variant surface antigen-specific perspective. Parasite Immunol 2004;26:477—86. 9. Roberts DJ, Craig AG, Berendt AR, Pinches R, Nash G, Marsh K, et al. Rapid switching to multiple antigenic and adhesive phenotypes in malaria. Nature 1992;357:689—92. 10. Staalsoe T, Hamad AA, Hviid L, Elhassan IM, Arnot DE, Theander TG. In vivo switching between variant surface antigens in human Plasmodium falciparum infection. J Infect Dis 2002;186: 719—22.
Lars Hviid* Trine Staalsoe Department of Infectious Diseases M7641, Centre for Medical Parasitology at Rigshospitalet and University of Copenhagen, Blegdamsvej 9, 2100 Copenhagen, Denmark *Corresponding author. Tel.: +45 35 45 79 57; fax: +45 35 45 76 44 E-mail address: [email protected] (L. Hviid) Corresponding Editor: Jonathan Cohen, Brighton, UK 26 July 2005 doi:10.1016/j.ijid.2005.10.013