Neurological manifestations of Chagas’ disease

Ezequiel Córdova*{, Elena Maiolo*{, Marcelo Corti* and Tomás Orduña*

*Infectious Diseases ‘Francisco J. Muñiz’ Hospital, Buenos Aires, Argentina
{
‘Cosme Argerich’ Hospital, Buenos Aires, Argentina

Objectives: To review the neurological manifestations of Chagas’ disease, including its clinical presentation,
diagnosis, management, treatment and follow-up.
Methods: A systematic review of the literature found in MEDLINE, EMBASE, LILACS and SCIELO was
performed to search for relevant references on Chagas’ disease and neurological manifestations.
Results: The involvement of the nervous system in Chagas’ disease is well established. The acute phase is
described as a meningoencephalitis that more frequently affects children under 2 years old and is almost
always fatal in those with coexistent myocarditis and cardiac insufficiency. In the chronic phase, it presents
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as neuritis that results in altered tendon reflexes and sensory impairment, and is reported in up to 10% of
the patients. Isolated cases of central nervous system involvement can also include dementia, confusion,
chronic encephalopathy and sensitive and motor deficits. Concurrent immunosuppression, such as that
related to human immunodeficiency virus and organ transplantation, can result in the reactivation of the
Trypanosoma cruzi infection. In these patients meningoencephalitis and brain abscesses may occur with a
high mortality rate despite specific treatment.
Discussion: Although neurological involvement is infrequent, it has a high mortality and morbidity rate when
is not well diagnosed and treated on time.
Keywords: Chagas’ disease, nervous system, meningoencephalitis, Latin America, trypanosoma cruzi

Introduction The disease consists of an acute and chronic phase.

Chagas’ disease or American trypanosomiasis is a
zoonotic disease caused by the flagellated kinetoplas-
tid protozoan named as Trypanosoma cruzi. This
parasitic disease causes more deaths in the Americas
than any other parasitic disease1.The endemic area
extends from the southern USA to the south of South
America. T. cruzi is transmitted mainly by vectors
(triatomine bugs) more common in rural areas with
poor sanitation conditions. Other mechanisms of
transmission include transfusions of infected blood,
transplacental route, organ transplantation from an
infected donor, and rarely, oral route and laboratory
accidents2. Sharing intravenous needles with an
infected person is another possible way of transmis-
sion in these populations3,4.
In Latin America, 16–18 million people are infected,
and y100 million are at high risk of infection5.
Following urban migration, Chagas’ disease has
become a health problem in previously non-endemic
cities and countries2. In the USA, approximately
50,000–100,000 immigrants have evidence of chronic
T. cruzi infection6, and the estimated seroprevalence
for T. cruzi antibodies is one in 4655 blood donations7.
In recent years, non-vector-associated cases have been
diagnosed in the USA, Canada and Europe1,4,8.
Correspondence and reprint requests to: Ezequiel Cordova, MD, Clinical
Microbiology – Infectious Diseases ‘Francisco J. Muñiz’ Hospital, Moreno
1026 Quilmes, 1878 Buenos Aires, Argentina. [dr_ecordova@hotmail.com]
238 Neurological Research 2010 VOL 32 NO 3 DOI 10.1179/016164110X12644252260637
The acute phase is generally asymptomatic or with
mild and non-specific symptoms, such as fever,
malaise, swelling at the site of inoculation (chagoma),
lymphadenopathy, mild splenomegaly and edema.
Severe myocarditis and meningoencephalitis can also
occur in a small proportion of patients and is a
particular concern in children under 2 years old.
However, in the majority of patients, the acute phase
goes unperceived by not being recognized due to the
scarcity or absence of clinical manifestations. The
acute phase usually resolves spontaneously in 2–4
months. However, 5–10% of symptomatic patients
die during this phase. These deaths usually occur in
children younger than 2 years2.
Following the acute phase, the chronic phase is
established. In this phase, a period of clinical latency,
called indeterminate form, which could last years or
throughout life, is described. However, in ,30% of
patients, signs of myocardiopathy, megaesophagus or
megacolon and/or more rarely, involvement of the
nervous system develop after this period. This
constellation of signs and symptoms is known as
chronic symptomatic Chagas’ disease2,3,9.
States of immunodeficiency, such as human immu-
nodeficiency virus infection, hematological malignan-
cies, organ transplantation or prolonged corticosteroid
therapy, can result in the reactivation of the T. cruzi
infection in chronically infected patients, which is
named as acute Chagas’ disease reactivation. This is
characterized by a high parasite proliferation and a
ß W. S. Maney & Son Ltd 2010

clinical syndrome that resembles the acute phase.
Cutaneous lesions, myocarditis, meningoencephalitis
and brain abscesses also may occur.
Since the first description of the disease by Carlos
Chagas and the clinical studies performed by
Salvador Mazza, the involvement of the nervous
system in Chagas’ disease has been well established in
acute phase as a form of meningoencephalitis and in
the chronic phase, as neuritis and isolated cases of
central nervous system involvement. However, there
are very few studies and articles in the medical
literature about the neurological manifestations of
Chagas’ disease. The aim of this review is to update
the current knowledge and give an overview of the
neurological manifestations of Chagas’ disease, hav-
ing a special emphasis in Latin American countries
where the disease is endemic.
Pathogenesis of the neurological
manifestations
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The triatomine bug becomes infected when it ingests
blood from an infected mammal (including humans)
that has circulating T. cruzi trypomastigotes. The
parasite enters the midgut of the insect and trans-
forms into an epimastigote form. It subsequently
undergoes multiplication and becomes an infective
form known as the metacyclic trypomastigote.
After having a blood meal, triatomine bugs
deposit T. cruzi trypomastigotes in skin breaks or
in the mucosa. After initial multiplication at the
inoculation site, trypomastigotes enter the blood-
stream and spread systemically. This acute phase
is characterized by a high parasitemia with trypo-
mastigote forms and is followed by invasion of
the liver, gut, spleen, lymphatic ganglia, central
nervous system and skeletal and cardiac muscles.
On these tissues, the parasite transforms into an
amastigote, a rounded form that lacks a flagellum
and measures y3 mm in diameter. These
amastigotes are the dividing form found in host
tissues, and they unleash a local inflammatory
reaction and formation of pseudocysts10,11. This
inflammatory reaction (mainly lymphocytes T
CD4z, CD8z, and cytokines interleukin-2 and -4)
leads to muscle (acute myocarditis) and neuronal
destruction (encephalitis).
During this acute phase, amastigotes are rarely
found in the central nervous system. However,
inflammatory infiltrates are scattered throughout
central nervous tissue, suggesting the participation
of the immune system in the genesis of these neural
lesions. Individuals with asymptomatic or mild
symptomatic acute forms of the disease probably
have no central nervous system infection. Some
patients may have discrete encephalitis in sparse foci,
which would explain the frequent finding of trypo-
mastigote forms in cerebrospinal fluid during the
acute phase even in patients without neurological
symptoms12. Encephalitis generally resolves during
the acute phase, and residual paucicellular inflamma-
tory nodules without parasites may persist13.
The initial inoculum and/or the strain of T. cruzi
influence on the severity of disease, on tissue tropism
E. Córdova et al. Neurological manifestations of Chagas’ disease
and its clinical form and on treatment response2,10,11.
The presence of amastigotes forms, their fragments or
parasite deoxyribonucleic acid serves to maintain a
late hypersensitivity reaction after the infammatory
reaction of the acute phase has passed10. Transient
and low-level parasitemias could be detected by
indirect laboratory methods14. The indeterminate
form of the chronic phase (asymptomatic) has
practically no histopathological findings.
In the chronic phase, a combination of direct
inflammatory phenomena and autoimmunity response
induces chronic myocardiopathy, arrhythmias, mega-
esophagus and/or megacolon10. Although neuropa-
thies are a common finding, mild inflammatory
infiltrates are rarely detected in the central nervous
system of chronic chagasic patients, suggesting that
these may represent residual lesions from an acute
phase13,15.
The immune system is responsible for maintaining
low levels of parasites in cases of chronic infection.
States of immunodeficiency, such as hematological
malignancies, organ transplantation, advanced
human immmunodeficiency virus disease or pro-
longed corticosteroid therapy, can lead to parasite
proliferation. This proliferation could reactivate
residual lesions in central nervous system or incre-
ment T. cruzi parasitemia resulting in the invasion of
central nervous tissue and the development of new
lesions.
Neurological manifestations
Acute phase
Central nervous involvement is rare and is more
frequent in children under 2 years of age. In this
population, acute neurological manifestations include
confusion, headache, hypertonia, seizures and menin-
gismus. Occasionally, focal neurological deficits may
be clinically indistinguishable from another form of
meningoencephalitis. The overall frequency of this
presentation is 0.8%16. In these patients, central
nervous system compromise presents as an isolated
clinical manifestation in 60%17. Manifestations of this
involvement include headaches, meningoencephalitis,
seizures, lethargy or mood changes16,17. Prognosis
depends on the patient’s age, as well as on the severity
and location of the lesions. In general, meningoence-
phalitis is very severe among children under 2 years
of age, and it is almost always fatal in those with
myocarditis and cardiac insufficiency10.
Congenital Chagas’ disease is produced by trans-
mission of T. cruzi from the infected mother to the
child. Fetal infection can occur at any time during
pregnancy. The incidence of congenital transmission
varies from 1 to 10% in different geographical zones18.
The acute congenital phase may be asymptomatic2 or
may be associated with seizures, meningoencephalitis,
microcephaly and brain calcifications19–21. A study
from Argentina evaluated 102 newborns with a
diagnosis of congenital Chagas’ disease and found
that four of them (3.9%) had trypomastigotes in the
cerebrospinal fluid. One of the patients had a con-
comitant diagnosis of human immunodeficiency
virus and developed neurological signs with a fatal
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 E. Córdova et al.
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240
Neurological manifestations of Chagas’ disease
outcome22. In another study, six of the nine sympto-
matic newborns presenting with neurological symp-
toms were found to have an altered cerebrospinal fluid
examination. However, cerebrospinal fluid abnormal-
ities were found in one patient with no neurological
findings23.
In the acute form, the most common histopatho-
logical findings is an encephalitis with multiple foci of
glial and microglial nodules resembling granulomas.
Parasites in the form of amastigotes are identified
within the inflammatory foci and/or inside glia,
macrophages, histiocytes or endothelial cells. The
number of parasites is inversely proportional to the
intensity of the inflammatory process. It is contro-
versial whether there is direct neuronal invasion by
amastigotes, but degenerative changes may occur in
those neurons close to inflammatory foci12.
Chronic phase
Central nervous system manifestations
The involvement of the central nervous system in
chronic Chagas’ disease is controversial. There are
rare reports of dementia, confusion, chronic ence-
phalopathy and sensorial and motor deficits. An
increased latency of P300 evoked potency and altered
electroencephalography may be present in 20% of the
patients. These findings did not correlate with cardiac
involvement24. Other authors have reported a discrete
and unspecific functional cortical disorder and
possible white matter lesions25 as well as changes in
impairment in cognitive function17. Computerized
tomography images showing cerebral atrophy are
also described26. However, these reports are not
sufficient to define clearly whether these neurological
findings represent a true clinical manifestation of the
chronic phase of the disease.
Histopathology may show granulomatous ence-
phalitis in multiple non-systematized foci in up to
10% of the patients; in some of them, a recent active
process is involved, with the presence of parasites.
Neuronal loss and ischemic cerebral changes are also
described and may be the consequence of the
hypoxemia resulting from congestive heart failure
and cardiac arrhythmias12. Demyelination of the
spinocerebellar tracts and posterior columns, a
reduction in the Purkinje cells number, extensive
cell loss of the substantia nigra and locus coeruleus
and lacunar state in the basal nuclei were also
reported27.
Peripheral nervous system
Neuritis may result in paresthesias and diminished or
absent muscle stretch reflexes. Impairment of vibra-
tional and positional sense may also be found.
Muscle weakness is not usually observed28. In a
study of 511 patients with chronic Chagas’ disease,
excluding other causes of neurological impairment,
10% had signs and symptoms of mixed peripheral
neuropathy. Histopathology shows segmental and
paranodal demyelination and axonal loss with mono-
nuclear cell infiltrates with predominancy of CD4z
or CD8z T lymphocytes29.
Neurological Research 2010 VOL 32 NO 3
Reactivation of Chagas’ disease in
immunocompromised hosts
Human immunodeficiency virus coinfection
Since the first report of Chagas’ disease reactivation
in a patient infected with the human immunodefi-
ciency virus30, many more cases have been published
in the literature. While most of these cases have
occurred in Latin America, others have been found in
non-endemic countries3. In patients infected with the
human immunodeficiency virus, Chagas’ disease most
often reactivates when the patient’s CD4z T cell
count is ,200 cells/ml, and may have a high mortality
rate. This syndrome tends to present with cerebral
mass lesions or acute diffuse meningoencephalitis in
75–90%31 and with acute myocarditis in 30–45% of
these patients3,32. Neurological symptoms depend
largely on the number, size and location of the
lesions33. Neuroimaging findings are indistinguish-
able from Toxoplasma gondii encephalitis. In a study
of 15 patients infected with human immunodeficiency
virus who had a confirmed diagnosis of Chagas’
disease with central nervous system involvement,
headache, focal neurological deficits, fever, menin-
gismus, seizures and altered mental status were the
most common clinical manifestations. Median CD4
T-cell count was 64 cells/ml (range: 1–240 cells/ml).
None of these patients were receiving highly active
antiretroviral treatment at the time of the onset of
neurological symptoms. Risk factors for transmission
of T. cruzi included a previous history of residence in
an endemic area and sharing intravenous needles.
Concomitant corticosteroid therapy was also pro-
posed as a risk factor for the reactivation of T. cruzi
infection in some of those patients. Positive serolo-
gical tests for T. cruzi were present in 86% of the
patients, but intravenous drug users had a lower
frequency (71%)3. In this study, the white blood cell
count in the cerebrospinal fluid was normal or mildly
elevated, with lymphocytic predominance2,3. Direct
cerebrospinal fluid examination for T. cruzi trypo-
mastigotes was positive in 85% of the cases3, and
parasitemia could be sometimes detected by direct
microscopic examination3,32,34–37. A cerebral biopsy
may be necessary to confirm the presumptive
diagnosis when trypomastigotes cannot be demon-
strated in the cerebrospinal fluid31. Almost all of
these patients had abnormal neuroimaging results,
and the most frequent is the presence of a single
supratentorial hypodense lesion compatible with
abscess in 50% of the cases. These lesions predomi-
nantly involve the white matter of brain lobes,
generally located in the frontal lobe (83%)
(Figure 1)3,31–33,38. Other localizations such as basal
ganglia/thalamus, brainstem, cerebellum lobes and
spinal cord were also reported3,39. However, up to
15% of patients may have normal neuroimaging
studies3.
The mortality rate reaches 85% even in treated
patients. This high mortality rate may be related to a
delayed diagnosis (probably due to the clinical and
radiographic similarities to toxoplasmic encephalitis)
and the profound immunosuppression present in

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Figure 1 Computed tomographic imaging showing a sin-
gle frontal white matter lesion, with contrast
enhancement and perilesional edema corre-
sponding with cerebral chagoma
these patients3,31. Histopathology in this population
shows a multifocal encephalitis, which tends to
develop a necrohemorrhagic component. This lesion
can sometimes evolve further into a tumoral form
(single or multiple), with numerous amastigotes of T.
cruzi always present within the glial cells and
macrophages or free around microglial nodules12,15.
These lesions are found in the white matter but may
have occasional extension into the cortex40.
Leptomeningeal inflammation and the presence of
amastigote forms of the parasite in the leptomeninges
may explain the high frequency of trypomastigote
forms in cerebrospinal fluid3,40.
Organ transplant recipients
The growing use of immunosuppressive drugs for
transplanted solid organs and bone marrow has
increased risk of Chagas’ disease reactivation or T.
cruzi infection through infected grafts or bone
marrow donation28. Pharmacological immunosup-
pression may promote the reactivation of Chagas’
disease before the first year post-transplant, when
there is a profound compromise of the cell-mediated
immunity41,42. The most frequent clinical manifesta-
tions associated with the reactivation of T. cruzi
infection in these patients include panniculitis, brain
lesions, meningoencephalitis and myocarditis. The
incidence of parasitemia and panniculitis among solid
organs recipients is quite similar, but myocarditis is
more frequent in cardiac transplant recipients. The
incidence of Chagas’ disease in mycophenolate-
treated patients is higher than those treated with
cyclosporine, azatioprine and corticosteroids as
immunosuppressive therapy43,44. Contrary to the
E. Córdova et al. Neurological manifestations of Chagas’ disease
reactivation in patients infected with the human
immunodeficiency virus, chagasic involvement of the
central nervous system in solid organ transplant
recipients is infrequent but has a high mortality
rate45. In a cohort of patients with kidney transplant
in Argentina, reactivation of chronic Chagas’ disease
was found in 16% of the chagasic recipients, and
transmission of T. cruzi infection through the kidney
was demonstrated in 15% of non-infected recipients.
The most frequent presentation was parasitemia
(56%), cutaneous lesions (33%) and central nervous
system involvement (11%) (Maiolo et al., unpub-
lished data). Central nervous system compromise
may include meningoencephalitis and/or brain
masses. Histopathology examination of biopsy
smears reveals necrotic lesions with infiltrates of
macrophages, perivascular lymphocytes and pseudo-
cysts of amastigotes. The prognosis depends on early
diagnosis and the level of immunosupression.
Diagnosis and management
Acute disease
The cornerstone of the diagnosis of acute Chagas’
disease is the detection of motile trypanosome forms
through direct examinations, such as wet prepara-
tions of anticoagulated blood. Blood concentration
techniques, such as the Strout method46 and micro-
hematocrit test, can improve the diagnostic sensitivity
(Table 1)47. Repeated examinations should be per-
formed in case of negative results. Microhematocrit is
indicated for newborns because a low amount of
blood (0.3–0.6 ml) is needed for this test. Testing for
anti-T. cruzi immunoglobulin M is not useful9,48. In
patients with signs and symptoms of meningoence-
phalitis, a lumbar puncture should be performed.
Cerebrospinal fluid examination shows mild pleocy-
tosis with a predominance of lymphocytes and
increased protein levels. The presence of motile
trypomastigote forms after centrifugation of cere-
brospinal fluid could be demonstrated in a low
frequency in these patients47. The parasites can also
be seen in Giemsa-stained smears (Figure 2). This
same procedure is recommended for symptomatic
newborns from mothers with risk factors for Chagas’
disease. An electrocardiogram and/or echocardiogram
should be performed in all cases in order to evaluate
cardiac involvement.
Table 1 Sensitivity of different tests for the detection of
T. cruzi in blood in the acute phase
Direct microscopic examination*
Wet preparations of blood 68.6%
Microhematocrit (capillary centrifugation) 97.6%
Strout method 99.2%
Indirect microscopic examination{
Xenodiagnostic{ 100%
*Might take 30–60 minutes. In the case of negative result, repeat
at least three times in a week.
{
Might take 2–8 weeks to become positive. They are useful in the
chronic stages of T. cruzi infection, when the level of parasitemia
is low.
{
Recovering the organism after inoculation of laboratory-raised
insect vectors.
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 E. Córdova et al.
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242
Neurological manifestations of Chagas’ disease
Figure 2 Trypanosoma cruzi trypomastigote in a smear
of cerebrospinal fluid (Giemsa)
Patients in the acute phase should be treated orally
with nifurtimox (LampitH; Bayer, Leverkusen,
Germany) or with benznidazoleH (Rochagan and
Radanil; Hoffman-LaRoche, Basel, Switzerland, now
available at LAFEPE, Recife, Brazil). However, these
drugs are not available in all countries, even in
endemic areas. The daily dose for benznidazole is 5–
7 mg/kg body weight and 8–10 mg for nifurtimox
divided into two daily doses, during 60–90 days2,48.
Side adverse effects include gastrointestinal intoler-
ance, hypersensitivity, bone marrow depression
(neutropenia, thrombocytopenic and purpura) and
peripheral polyneuropathy. No information is
available on the penetration of these drugs into the
central nervous system. With treatment, there is
improvement of symptoms, and the parasites dis-
appear from peripheral blood after the fifth day of
treatment. Serology could become negative in up
to 30–80% of cases2. Higher doses are recommended
(up to 25 mg/kg day) for patients with meningoence-
phalitis and/or myocarditis48. Management with
anticonvulsants, such as phenobarbital, and benzo-
diazepines are indicated if seizures are present.
Mannitol should be added when signs of critically
elevated intracranial pressure are present. With
appropriate therapy, the rate of cure in patients with
isolated central nervous system involvement is nearly
50%47. In severe acute cases, combined treatment
with corticosteroids and parasitological treatment
should be attempted28. In these patients, a high
mortality rate is reported.
Chronic disease
Chronic T. cruzi infection is usually diagnosed by
detecting immunoglobulin G antibodies. The tests
used include indirect hemagglutination, direct agglu-
tination, complement fixation, indirect immuno-
fluorescence, enzyme-linked immunoassays and
radioimmunoprecipitation assays. Two different
positive tests are required to confirm the diagnosis.
Parasites could be detected in blood by indirect
methods, such as blood cultures or xenodiagnosis.
Nerve conduction studies or electroencephalograms
are not recommended in patients with no signs or
symptoms of neurological compromise. The
Neurological Research 2010 VOL 32 NO 3
Figure 3 A magnetic resonance image showing a single
temporoparietoccipital white matter lesion with
perilesional edema corresponding with cerebral
chagoma. Proton magnetic resonance spectro-
scopy acquired from this lesion demonstrates a
choline (Cho) peak and presence of lipids
management of individuals with neurological mani-
festations consists of supportive measures and
symptomatic relief. Patients with chronic T. cruzi
infection should be treated with benznidazole or
nifurtimox, but there is no consensus regarding the
treatment of persons with long-standing asympto-
matic T. cruzi infection9,48,49.
Patients infected with the human immunodeficiency virus
Chagas’ disease should be included in the differential
diagnosis of central nervous system mass lesions and
acute cardiac disease among patients infected with
the human immmunodeficiency virus with the appro-
priate risk factors3,50. Serological tests should always
be performed in all these patients. The absence of T.
cruzi antibodies makes a diagnosis of Chagas’ disease
unlikely, especially in those patients with no history
of intravenous drugs user. The imaging pattern of
brain is similar to that of cerebral toxoplasmosis,
although lesions due to the reactivation of Chagas’
disease tend to be single, affecting mainly supraten-
torial white matter of brain lobes (Figure 3)3.
Whenever possible, a lumbar puncture should be
performed because of its high sensitivity for detecting
trypomastigote forms. Serial samples of blood for
direct examinations should be also performed in
order to identify parasites. When T. cruzi trypomas-
tigotes cannot be demonstrated in the cerebrospinal
fluid, a cerebral biopsy of focal brain lesions may be
needed to establish a definitive diagnosis (Figure 4).
Polymerase chain reaction of peripheral blood is not
helpful for diagnosis of reactivation, as it is often
positive even in the absence of reactivation. However,
polymerase chain reaction testing of cerebrospinal
fluid has been successfully used to diagnose reactiva-
tion in the central nervous system50. No commercial
polymerase chain reaction tests are available. All
patients should also be systematically evaluated for
cardiac involvement with an electrocardiogram and/
or echocardiogram3. Antiparasitic therapy with
benznidazole, 5–7 mg/kg day for 60–90 days, should

Figure 4 Brain (anatomical piece): left parietal cavitated
lesion with destruction of left corpus callosum
in a human immmunodeficiency virus (HIV)-
infected patient with confirmed diagnosis of
Chagas’ disease reactivation. Histopathology
Published by Maney Publishing (c) W. S. Maney & Son Limited
showed numerous amastigotes of T. cruzi (with
permission from Dr Mario Valerga)
be initiated as soon as possible to improve the
prognosis in these patients. Nifurtimox, at doses of
8–10 mg/kg body weight/day, given for 90–120 days,
is a therapeutic alternative in those countries where
this drug is available48,50. Adverse side events have
been described up to 50% of the patients, mainly
hematological disorders and rash3. Anticonvulsant
therapy should not be given routinely; it should be
administered only to patients with seizures.
Adjunctive corticosteroids (intravenous dexametha-
sone 16 mg/day) should be used for patients with
clinical or radiographic evidence of critically elevated
intracranial pressure. Once the acute phase of the
disease has passed, highly active antiretroviral
therapy should be initiated. Secondary prophylaxis
with benznidazole (5 mg/kg three times a week) is
recommended until CD4z T cell count reaches
levels .200 cells/ml. Primary prophylaxis is not
indicated48,50.
Organ transplant recipients
Individuals who are seropositive for T. cruzi should
be accepted as organ transplant recipients but may or
may not be eligible for organ donation depending on
the particular organ to be donated. The use of both
living and cadaveric donors with positive serology for
negative recipients is accepted for kidney transplants
in endemic areas28, and infected donors could be
accepted in the case of bone marrow transplants.
Livers should be accepted from infected donors only
in extreme cases, but hearts from seropositive donors
should never be accepted for transplantation.
Antiparasitic treatment could be administered when
positive donors are used in order to prevent the
infection28. A particular concern in transplant
patients include the potential negative reversal of T.
cruzi serologies due to immunosuppression related to
a renal and a bone marrow transplant28,41,51.
However, reactivations can and do occur in these
patients. Thus, screening for parasites in blood or
E. Córdova et al. Neurological manifestations of Chagas’ disease
other tissues is preferable for the diagnosis of Chagas’
disease reactivation in this population. It is recom-
mended to perform two Strout tests per week, the
first 3 months and then once a month during a year48.
The diagnosis and treatment of central nervous
system involvement in the organ transplant recipient
are not different than in patients infected with the
human immunodeficiency virus. Judicious adjust-
ment of immunosuppressive drugs may be necessary
in the treatment of the infection, especially when
there are no signs of rejection. Secondary prophylaxis
could be necessary.
Conclusion
It is well known that T. cruzi infection is a major
cause of morbidity and mortality in endemic coun-
tries, but now, it is becoming a worldwide health
problem as a result of urban and international
migration. The involvement of the nervous system
is infrequent; however, it has a high mortality and
morbidity rate especially when it is not well diag-
nosed and treatment is not quickly initiated.
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