BioMed Research International / 2013 / Article / Figbox 1

Review Article

Trypanosoma evansi and Surra: A Review and Perspectives on Origin, History, Distribution, Taxonomy, Morphology, Hosts, and Pathogenic Effects

Box 1

The main characteristics of Trypanosoma evansi.
Trypanosoma evansi is sharing some characteristics with T. brucei brucei and more
generally with the subgenus Trypanozoon, such as the nucleic DNA [27], morphology and
morphometry of the blood stage parasite (especially slender forms: small subterminal
kinetoplast, thin posterior extremity, large undulating membrane, free flagellum, thin and
long parasite, central nucleus, etc.) [1], and ability for peroral and mechanical transmission
[9]. However, the effects of T. b. brucei have not been observed in some hosts due to their
absence from its geographical distribution, limited to the tsetse belt (e.g., the effect
of T. b. brucei on water buffalos is not known); thus, comparison is not always possible.
T. evansi and T. equiperdum are different from T. b. brucei since they suffer from a mutation
leading to the homogenization of their kinetoplastic minicircles, which make them unable
to properly edit their mitochondrial RNA; for this reason, they are unable to transform into
procyclic stage, thus to implement a cycle in tsetse flies; they are consequently locked into
the host as a blood stream form [27]; they are also unable to recombine their DNA since
this event occurs during the implementation of the cycle in the tsetse fly [54].
Distinct from T. equiperdum, T. evansi lost the kinetoplastic maxicircles, although the
extent of the loss is still under discussion since some part of the maxicircle DNA may be
remaining as shown in a Venezuelan strains [72].
Transformation into stumpy form, which is observed in T. brucei spp. when preparing to
the implementation of the cycle in the vector, became useless in T. evansi and T.
equiperdum, which most probably contribute to the rarefaction of the stumpy forms of
these parasites, thus predominantly found under the slender form (only very occasional
stumpy forms have been described [1]). In addition to this modification, the loss of
kinetoplastic DNA can be partial (dyskinetoplastic: Dk) or total (akinetoplastic: Ak).
Finally T. evansi is a parasite derived from T. brucei by deletion of mitochondrial DNA
(kinetoplastic DNA) leading to a strictly blood form parasite, morphologically monotonous,
dividing by binary fission in the blood of numerous hosts. Mechanical vectors most
probably selected the most prolific parasites in given hosts, leading to some divergence
among the strains; however this aspect will be discussed elsewhere, in a paper devoted
more extensively to the transmission of T. evansi. Additionally, distinction between T.
evansi and T. equiperdum would also be discussed based on the tropism of the latter for
genital apparatus, which trapped it in a given host, equines, due to a predominant sexual