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How does Trypanosoma equiperdum fit into the Trypanozoon group? A cluster analysis by RAPD and Multiplex-endonuclease genotyping approach

Published online by Cambridge University Press:  07 May 2003

F. CLAES
Affiliation:
Prince Leopold Institute of Tropical Medicine, Department of Parasitology, Nationalestraat 155, Antwerpen, Belgium Faculty of Agriculture and Applied Biological Sciences, K. U. Leuven, Department of Animal Science, Kasteelpark Arenberg 30, 3000 Leuven, Belgium
E. C. AGBO
Affiliation:
Institute for Animal Science and Health (ID-Lelystad), Division of Animal Sciences, Edelhertweg 15, 8200 AB Lelystad, The Netherlands
M. RADWANSKA
Affiliation:
Prince Leopold Institute of Tropical Medicine, Department of Parasitology, Nationalestraat 155, Antwerpen, Belgium
M. F. W. TE PAS
Affiliation:
Institute for Animal Science and Health (ID-Lelystad), Division of Animal Sciences, Edelhertweg 15, 8200 AB Lelystad, The Netherlands
T. BALTZ
Affiliation:
Laboratoire de Parasitologie Moleculaire, Université Victor Ségalen Bordeaux II, 146, Rue Léo Saignat, 33076 Bordeaux, France
D. T. DE WAAL
Affiliation:
Parasitology Division, Onderstepoort Veterinary Institute, Private Bag X05, Onderstepoort 0110, South Africa
B. M. GODDEERIS
Affiliation:
Faculty of Agriculture and Applied Biological Sciences, K. U. Leuven, Department of Animal Science, Kasteelpark Arenberg 30, 3000 Leuven, Belgium
E. CLAASSEN
Affiliation:
Department of Immunology, Erasmus University Rotterdam, Dr Molewaterplein 50, 3015 GE Rotterdam, The Netherlands
P. BÜSCHER
Affiliation:
Prince Leopold Institute of Tropical Medicine, Department of Parasitology, Nationalestraat 155, Antwerpen, Belgium

Abstract

The pathogenic trypanosomes Trypanosoma equiperdum, T. evansi as well as T. brucei are morphologically identical. In horses, these parasites are considered to cause respectively dourine, surra and nagana. Previous molecular attempts to differentiate these species were not successful for T. evansi and T. equiperdum; only T. b. brucei could be differentiated to a certain extent. In this study we analysed 10 T. equiperdum, 8 T. evansi and 4 T. b. brucei using Random Amplified Polymorphic DNA (RAPD) and multiplex-endonuclease fingerprinting, a modified AFLP technique. The results obtained confirm the homogeneity of the T. evansi group tested. The T. b. brucei clustered out in a heterogenous group. For T. equiperdum the situation is more complex: 8 out of 10 T. equiperdum clustered together with the T. evansi group, while 2 T. equiperdum strains were more related to T. b. brucei. Hence, 2 hypotheses can be formulated: (1) only 2 T. equiperdum strains are genuine T. equiperdum causing dourine; all other T. equiperdum strains actually are T. evansi causing surra or (2) T. equiperdum does not exist at all. In that case, the different clinical outcome of horse infections with T. evansi or T. b. brucei is primarily related to the host immune response.

Type
Research Article
Copyright
2003 Cambridge University Press

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