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distinctive cerebral lesions closed to humans, cerebral vessels
obstruction is monocytes predominant by adhesion to vessels
walls (
12
). Moreover, PbA cerebral malaria lacks the systemic
involvement such as hypoglycaemia and the liver damage
observed in
falciparum
malaria (
13
). Another difference com-
monly found in the literature is that over 80% of susceptible
mice infected with PbA died with cerebral symptoms and BBB
breakdown (
14
), whereas very few humans develop cerebral
complications leading to death. This statement could be
explained by the experiment homogeneity: animals (sex, age,
and genetic background), clone of
Plasmodium
, and treatment.
Such conditions are not applicable to humans. Experimental
models cannot reproduce exactly the brain pathology observed
in humans, but there is a growing number of similarities
between models and the human disease. In particular, mono-
cytes are also seen in the cerebral vessels of African children
(
15
). The accumulation of platelets in the brain vessel of these
children is also significantly more important than in non cere-
bral malarial patients (
16
). While only slight differences in the
sequestration process were described (
17
), this model has con-
tributed greatly to general understanding of cerebral malaria.
4. Four species and 13 subspecies of rodent
Plasmodium
exist
(
18
), but
P. berghei
and
P.
yoelii
are commonly used for CM
studies.
P. berghei
was first isolated from an infected
Anopheles
dureni
in Congo in 1948 (
19
). Different strains were isolated
in the same region of Congo and four of them,
P. berghei
SP11, ANKA (Anvers-Kasapa) (PbA), NK65, and Kyberg 173
(K173), were used to study CM The extent of experimental
cerebral malaria (ECM) induction is also dependent of the
amount of inoculum (
20
). In (
20
), a 2 × 10
6
inoculum led to
the maximum incidence of ECM in C57BL/6 mice (80-
100%). Changes in the amount of the inoculum could lead to
the release of a different array of lymphokines by activation of
CD4 Th2 cells and could explain this observation. The K173
was also used to study CM because histopathological analysis
of the brains of infected mice showed cerebral involvement
(
21
). Ball et al. (
22
) demonstrated that low inoculum of K173
induces CM-neurological signs. Despite this demonstration,
the PbA strain is the most common strain for cerebral malaria
studies: from 2000 to 2008, only five CM studies used Pb
K173, comparing to 97 for PbA and 10 for
P. yoelii
(Pubmed
“cerebral malaria and
P. berghei
K173 or
P. berghei
ANKA or
P. yoelii
”).
5. PbA in CBA/Ca and C57BL/6 mice and PbK173 in C57BL/6
have been the most studied mouse/parasite combination.
Alternative CM models using
P
.
yoelii yoelii
17XL or YM in
CF1, Swiss and BALB/c mice have also been proposed (
23
),
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