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Sulfadiazine resistance in Toxoplasma gondii: no involvement of overexpression or polymorphisms in genes of therapeutic targets and ABC transporters.
[congenital toxoplasmosis]
Several
treatment
failures
have
been
reported
for
the
treatment
of
toxoplasmic
encephalitis
,
chorioretinitis
,
and
congenital
toxoplasmosis
.
Recently
we
found
three
Toxoplasma
gondii
strains
naturally
resistant
to
sulfadiazine
and
we
developed
in
vitro
two
sulfadiazine
resistant
strains
,
RH-R
(
SDZ
)
and
ME
-
49
-
R
(
SDZ
)
,
by
gradual
pressure
.
In
Plasmodium
,
common
mechanisms
of
drug
resistance
involve
,
among
others
,
mutations
and
/
or
amplification
within
genes
encoding
the
therapeutic
targets
dhps
and
dhfr
and
/
or
the
ABC
transporter
genes
family
.
To
identify
genotypic
and
/
or
phenotypic
markers
of
resistance
in
T
.
gondii
,
we
sequenced
and
analyzed
the
expression
levels
of
therapeutic
targets
dhps
and
dhfr
,
three
ABC
genes
,
two
Pgp
,
TgABC
.
B
1
and
TgABC
.
B
2
,
and
one
MRP
,
TgABC
.
C
1
,
on
sensitive
strains
compared
to
sulfadiazine
resistant
strains
.
Neither
polymorphism
nor
overexpression
was
identified
.
Contrary
to
Plasmodium
,
in
which
mutations
and
/
or
overexpression
within
gene
targets
and
ABC
transporters
are
involved
in
antimalarial
resistance
,
T
.
gondii
sulfadiazine
resistance
is
not
related
to
these
toxoplasmic
genes
studied
.
Diseases
Validation
Diseases presenting
"encephalitis"
symptom
alexander disease
congenital toxoplasmosis
dracunculiasis
locked-in syndrome
malignant atrophic papulosis
pyomyositis
pyruvate dehydrogenase deficiency
scrub typhus
systemic capillary leak syndrome
typhoid
This symptom has already been validated