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Am. J. Trop. Med. Hyg., 76(1), 2007, pp. 27-32
Copyright © 2007 by The American Society of Tropical Medicine and Hygiene

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OF MAURER’S CLEFTS IN PLASMODIUM FALCIPARUM–INFECTED ERYTHROCYTES

MALIN HAEGGSTRÖM, ANNE VON EULER, FRED KIRONDE, VICTOR FERNANDEZ, AND MATS WAHLGREN*
Department of Microbiology, Tumor- and Cellbiology, Karolinska Institutet, Stockholm, Sweden; Department of Biochemistry, University of Makerere, Kampala, Uganda; Department of Parasitology, Mycology and Environmental Microbiology, Swedish Institute for Infectious Disease Control, Solna, Sweden

In 1902 Georg Maurer was the first to publish a detailed description of Giemsa-stained structures in the cytosol of Plasmodium falciparum–infected erythrocytes, today known as Maurer’s clefts. Later when clefts were seen by electron microscopy, the description was modified to also include these, which has caused disagreement over the composition of Maurer’s clefts. For that reason, Maurer’s clefts were characterized during intraerythrocytic development of P. falciparum by simultaneously staining cytosolic structures with antibodies using indirect immunofluorescence assays and with Giemsa. At least three groups of antigens, P. falciparum erythrocyte membrane protein 1 (PfEMP1)/ RIFIN/SURFIN, P. falciparum histidine-rich protein 2 (PfHRP2), and exported proteins 1 and 2 (Exp1 and Exp2), were detected in distinct Giemsa-stained structures in the cytosol of infected erythrocytes, but PfHRP2 and Exp1/Exp2 were not found in clefts by transmission electron microscopy. Therefore, Maurer’s clefts as defined by staining with Giemsa comprise a number of cytoplasmic structures and antigens not included in structures called clefts and seen by electron microscopy.


Received May 17, 2006. Accepted for publication September 11, 2006.

Acknowledgments: We thank Russell J. Howard (Maxygen, Redwood City, CA) for the MAb 2G12 and Jana S. McBride (University of Edinburgh, Edinburgh, Scotland) for MAbs 5.1 and 7.7. We also thank Berit Schmidt-Aydin for collection and processing of patient blood samples.

Financial support: This study was supported by grants to Mats Wahgren from BioMalPar (LSHP-CT-2004-503578), the Swedish Research Council, and the Swedish International Development Authority (Sida/SAREC).

* Address correspondence to Mats Wahlgren, Department of Microbiology, Tumor- and Cellbiology, Karolinska Institutet, Nobels väg 16, SE-171 77 Stockholm, Sweden. E-mail: mats.wahlgren{at}mtc.ki.se

Authors’ addresses: Malin Haeggström, Anne von Euler, and Mats Wahlgren, Department of Microbiology, Tumor- and Cellbiology, Karolinska Institutet, Nobels väg 16, SE-171 77 Stockholm, Sweden, Telephone: 46-8-457-2510, Fax: 46-8-310-525, E-mails: malin.haeggstrom{at}smi.ki.se, anne.von.euler{at}mtc.ki.se, and mats.wahlgren{at}mtc.ki.se. Fred Kironde, Department of Biochemistry, Mulago Hospital, Kampala, Uganda, Telephone: 256-77-854-590, E-mail: kironde{at}starcom.co.ug. Victor Fernandez, Department of Parasitology, Mycology and Environmental Microbiology, Swedish Institute for Infectious Disease Control, SE-171 82 Solna, Sweden, Telephone: 46-8-457-2553, Fax: 46-8-310-525, E-mail: victor.Fernandez{at}smi.ki.se.







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Copyright © 2007 by the American Society of Tropical Medicine and Hygiene.