CASOS CLÍNICOS
Rev Med Chile 2021; 149: 1673-1678

Brain lesions associated with
eosinophilia. A useful clue for
neurotoxocariasis. Report of one case
ALBERTO FICA1,2, MARÍA ISABEL JERCIC3, CLAUDIO NAVARRETE4,5

ABSTRACT
Neurotoxocariasis is uncommon. Its manifestations include events of
meningitis, encephalitis and less frequently vasculitis, which manifest as headache, seizures, focalization, confusion, cognitive alterations and /or fever.
Peripheral eosinophilia with clinical and neurological imaging elements, allow
its early suspicion. We report a 48-year-old agricultural worker, admitted in
our hospital for one week of gastrointestinal complaints, headache, progressive
left hemiparesis and impaired consciousness. He had leukocytosis (13,530/µL)
with peripheral eosinophilia (25%, absolute count 3,400 /µL). CSF analysis
revealed no abnormalities and brain CT showed poorly defined hypodense
lesions on subcortical areas and semioval centers. Magnetic resonance imaging
showed multiple foci with increased signals predominantly in the white matter
in both hemispheres, especially at frontal and occipital regions and at semioval
centers. Lesions reinforced after paramagnetic contrast. Serological studies
found specific IgG antibodies by ELISA against antigens of the genus Toxocara,
which were confirmed by a positive IgG Western Blot. The patient was treated
with albendazole (800 mg/d) for 14 days associated with parenteral and then
oral corticosteroids with a favorable response and gradual complete recovery.
(Rev Med Chile 2021; 149: 1673-1678)
Key words: Adrenal Cortex Hormones; Albendazole; Central Nervous
System Infection; Eosinophilia; Magnetic Resonance Imaging; Toxocariasis.

1
SubDepartamento de Medicina,
Hospital Base de Valdivia,
Valdivia, Chile.
2
Instituto de Medicina, Facultad
de Medicina, Campus Isla Teja,
Universidad Austral de Chile.
Valdivia, Chile.
3
Sección Parasitología, Sub
Departamento de Enfermedades
Infecciosas, Departamento
Laboratorio Biomédico, Instituto
de Salud Pública de Chile.
Santiago, Chile.
4
Servicio de Neurología, Hospital
Base de Valdivia. Valdivia, Chile.
5
Instituto de Neurociencias
Clínicas, Facultad de Medicina,
Campus Isla Teja, Universidad
Austral de Chile. Valdivia, Chile.

Conflicto de Interés: ninguno.
Financiamiento: ninguno.
Recibido el 7 de abril de 2021,
aceptado el 6 de diciembre de
2021.
Correspondencia a:
Dr. Alberto Fica
SubDepartamento de Medicina,
Hospital Base de Valdivia, Chile.
Bueras 1003, Valdivia, Chile.
albertoficacubillos@gmail.com

Lesiones cerebrales asociadas con eosinofilia.
Una clave útil en neurotoxocariasis
La neurotoxocariasis es infrecuente. Sus manifestaciones incluyen eventos
de meningitis, encefalitis y con menor frecuencia vasculitis, que se manifiestan
como cefalea, convulsiones, focalización, confusión, alteraciones cognitivas o
fiebre. La eosinofilia periférica, junto a elementos clínicos e imágenes compatibles, permiten su sospecha. Informamos el caso de un trabajador agrícola de
48 años que ingresó por una semana de molestias gastrointestinales, cefalea,
hemiparesia izquierda progresiva y deterioro de conciencia. Los exámenes
revelaron leucocitosis (13.530/µL) con eosinofilia periférica (25%, recuento
absoluto 3.400/µL). El análisis del LCR sin anomalías y la tomografía computada cerebral mostró lesiones hipodensas mal definidas en áreas subcorticales
y centros semiovales. La resonancia magnética mostró múltiples focos con
aumento de la señal predominantemente en la sustancia blanca en ambos

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Brain lesions and eosinophilia - A. Fica et al

hemisferios. Las lesiones presentaron refuerzo tras contraste paramagnético.
Los estudios serológicos indicaron anticuerpos IgG específicos por ELISA contra
antígenos del género Toxocara. El paciente fue tratado con albendazol (800
mg /día) durante 14 días asociado a corticoides con respuesta favorable y una
recuperación gradual completa.
Palabras clave: Albendazol; Corticosteroides; Eosinofilia; Infecciones del
Sistema Nervioso Central; Imagen por Resonancia Magnética; Toxocariasis.

T

oxocariasis involve several clinical syndromes associated with the migration or
permanence of Toxocora canis larvae or
other rarer species in different human tissues.
The infection is acquired after ingestion of full
mature eggs present in soils, contact with canines,
consumption of vegetables contaminated with
dog feces or consumption of raw or improperly
cooked liver. After their arrival into the intestine, the larvae developed from the eggs, manage
to penetrate the intestinal wall, and migrate to
different tissues1,2. In adults, these syndromes
include asymptomatic forms expressed only by
eosinophilia, ocular migrant larvae (OML), visceral migrant larvae (VML), neurotoxocariasis and
covert toxocariasis1,3,4.
Ocular toxocariasis is an important cause of
ocular morbidity in childhood and explained by
exposure to contaminated soils or contact with
canine pets5. This form accounts for less than 5%
of the causes of uveitis in developing countries
and is only occasionally associated with peripheral
eosinophilia (≤ 20%)6,7. VML characteristically
affects the lung or liver8,9. In the first case, patients
may present nonspecific respiratory symptoms in
about half of cases with peripherally distributed
nodules and/or ground glass infiltrates in CT
imaging. In hepatic toxocariasis, patients present
with single or multiple hypodense lesions with
poorly defined borders along with occasional
symptoms such as right upper quadrant abdominal pain. Cases of visceral pulmonary or hepatic
toxocariasis have few important systemic manifestations or elevation of inflammatory parameters.
However, they are notoriously associated with
mild or moderate peripheral eosinophilia in about
85% of cases, which together with images and
positive serological tests allow the diagnosis1,8,9.
Additionally, an increase in serum IgE titers is
observed1,3,8,9. Another compartmental condition
is neurotoxocariasis, which involves the central
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nervous system (CNS) in the form of transverse
myelitis or cerebral toxocariasis with meningitis,
encephalitis or vasculitis1,3. This infection has also
been invoked as a frequent cause of epilepsy in
developing countries10.
The low frequency of this parasitic infection,
has limited an appropriate clinical experience to
raise an adequate suspicion and study, which is
also surrounded by a broad differential diagnosis.
Chilean literature has adequately described the
extent of carriage in dogs and contamination by
T. canis eggs in public squares and parks, as well as
its seroprevalence in children and adults in urban
or rural areas11-14. However, the description of clinical pictures associated with this microorganism
is very scarce and limited to few publications4,15
confirming the continuous need to communicate
its different clinical forms.
Case Report
A 48-year-old agricultural worker with no
known morbidity was admitted during year 2019
reporting one week of abdominal pain, vomiting,
diarrhea, headache, and dizziness with paresis
in the left lower limb and shortly after in the left
upper limb. On admission he was disoriented
without fever or hemodynamic or respiratory
compromise. Physical examination showed no
abnormalities except for mild diffuse abdominal
tenderness without Blumberg’s sign and a left M3
grade hemiparesis without meningeal signs or
cranial nerve involvement. Exams revealed leukocytosis (13,530/µL) with peripheral eosinophilia
(25%, absolute count 3,400/µL). Neutrophil and
lymphocyte count were normal. He also had
thrombocytopenia (76,000/µL) and the erythrocyte sedimentation rate was 39 mm /h. Renal
function was preserved, and liver biochemical
tests were normal. C-reactive protein was elevated

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Brain lesions and eosinophilia - A. Fica et al

(4.2 mg /dL; normal ≤ 0.5 mg/dL). Rheumatoid
factor, C3 and C4 serum complement levels and
urine sediment showed no abnormalities. IgE
levels were elevated (509.4; IU/ml; reference value
≤ 100 IU/ml). HIV and syphilis serological testing
were non-reactive.
The patient evolved with drowsiness and contralateral hemiparesis. Brain CT showed poorly
defined hypodense lesions on subcortical areas
and semioval centers (Figure 1A). An embolic
vascular event was proposed as an initial working
hypothesis, including a possible event secondary

to infectious endocarditis; tissular parasitosis was
also considered. The cerebrospinal fluid (CSF)
study was normal without pleocytosis and with
normal protein and glucose values. CSF and
blood cultures were negative. The patient worked
in farming activities in a rural area with frequent
but indirect contact with dogs. Besides, pork
consumption together with other family members
3 weeks before admission was retrieved during
anamnesis, however, no trichinosis events were
detected among relatives. Serological samples
for trichinosis and toxocariasis diagnosis were

Figure 1. A: (Upper and lower figures): Brain CT images without contrast media obtained at 2 days post admission. Hypodense
lesions are observed within semioval centers (arrow, upper figure) and in subcortical frontal areas (arrows, lower figure). Minor
hemorrhagic points are also present (arrowhead in upper figure) that were corroborated by GRE T2-weighted MR sequence
(not shown). B: (Upper and lower figures) FLAIR (Fluid-Attenuated Inversion Recovery) MR brain images in axial projection at
7 days post admission. Hypertense signals are observed in semioval centers (arrow, upper figure) and in frontal and occipital
cortical-subcortical areas (arrows, lower figure). C: T1 signal in axial projection of brain MR with gadolinium (Gd, paramagnetic
contrast). Gd-enhanced lesions are observed in semioval centers and in frontal and occipital areas (arrows). Images obtained
at 7 days after admission.

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referred to the National Reference Parasitology
Laboratory.
The patient received empirical therapy with
ceftriaxone and intravenous ampicillin for 48
hours which was suspended after having ruled
out the possibility of infective endocarditis by negative blood cultures, echocardiography without
vegetations and absent minor criteria. The patient
also received acetyl-salicylic acid 100 mg/day with
atorvastatin 80 mg/day due to the possibility of
an acute cerebral vascular event, together with
albendazole 400 mg every 12 hours orally and
intravenous corticosteroids (dexamethasone 10
mg every 6 hours). He was transferred to the Intermediate Care Unit for close monitoring.
Patient evolved satisfactorily with consciousness recovery and complete regression of
his right hemiparesis, and partial improvement
on the left side. A thoracoabdominal-pelvic CT
angiographic study besides a brain and carotid
CT angiography ruled out embolic causes or
vascular abnormalities and a control brain CT
showed a partial regression of the hypodense
lesions. Brain MRI indicated multiple foci with
increased signal predominantly in the white
matter in both hemispheres, especially at frontal
and occipital regions and at semioval centers
(Figure 1B). Lesions presented reinforcement
after paramagnetic contrast (Figure 1C). Incidentally, a venous angioma was observed at the
right fronto-temporal level (not shown).
Parasitic serological study ruled out antibodies
against antigens of the genus Trichinella (ELISA
IgG negative) and confirmed the presence of
specific IgG antibodies by ELISA against antigens of the genus Toxocara that was confirmed
by a positive IgG Western Blot. Corticosteroid
therapy was trespassed to the oral route with
prednisone 60 mg/day and after 2 weeks doses
were gradually reduced. He completed a 14-day
course of albendazole therapy and after 25 days, he
was transferred to other hospital to complete his
rehabilitation. Before discharge, he was evaluated
by ophthalmology, ruling out eye compromise. A
follow-up control at three weeks after discharge
indicated improvement of the left hemiparesis.
A complete recovery at 2 years was registered by
a telephone call. Unfortunately, a brain control
image, IgE levels or eosinophil count could not
be performed due to the COVID pandemic and
patient’s rural condition.

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Discussion
The neurotoxocariasis case presented here, of
which a few hundred cases have been described
in the literature, seems to be well documented by
the presence of compatible brain CT and MRI
images, the double positive serological study
including confirmation by Western Blotting, peripheral eosinophilia, and the associated clinical
picture. Manifestations of cerebral toxocariasis
include events of meningitis, encephalitis and less
frequently vasculitis, which manifest as headache,
seizures, focalization, confusion, cognitive alterations and/or fever1,3. Peripheral eosinophilia with
clinical and neurological imaging elements, permit
early suspicion and requesting of confirmatory
serological studies.
The presence of mild or moderate peripheral
eosinophilia (> 500-5,000/µL) is especially useful for neurotoxocariasis suspicion, since other
causes of neurological pathologies that present
with this feature are much more infrequent to
observe than neurotoxocariasis itself. For example,
Coccidoides inmitis meningitis is an infrequent
form of presentation of this geographic fungal
infection already absent in the temperate climate
of Chile. Likewise, gnathostomiasis, linked to the
consumption of uncooked or raw freshwater fish
rarely affects the CNS and, baylisascariasis, related
to the inadvertent ingestion of parasitic eggs from
raccoon droppings, is rare1. Although Fasciola
hepatica and Trichinella infections are associated with moderate or intense eosinophilia, they
have another clinical profile, and other parasitic
causes with CNS involvement such as neurocysticercosis, have not or just mild eosinophilia16,17.
Finally, other CNS diseases such as tuberculosis
or lymphoma, exceptionally present eosinophilia.
Table 1 shows important parameters observed in
patients with neurotoxocariasis.
The optimal treatment of toxocariasis remains undefined due to the low frequency of
these conditions which has prevented controlled
studies and the self-limited and benign evolution
of most cases18. In animal models, mebendazole
and albendazole have shown to be larvicidal, but
in high doses and for prolonged periods18. The
evidence from the few observational, randomized, or non-randomized comparative studies in
toxocariasis indicates that it is possible to obtain
a favorable clinical and laboratory response using

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Table 1. Relevant features of the reported case and comparison with data available from the literature
Variable

This case

Features previously reported focusing on
neurotoxocariasis

Demographic

Adult, male, 47- year-old, rural condition

Cases concentrate in the middle age of life (40-50
years) and are predominately of the male sex (rate
2-3 to 1)

Zoonotic exposure

Farming worker with indirect contact
with dogs

In adults, contact with dogs, living in rural areas or
consumption of raw of improperly cooked liver. In
children playing in public squares and parks, canine
pet tenure or geophagy (for any kind of toxocariasis:
asymptomatic or symptomatic).
In the region of residence of the patient (South of
Chile), a high prevalence of T. canis in dogs has been
reported (reference 13)

Clinical features

Encephalitis with motor focalization.
Neurotoxocariasis

Compartmental (ocular, lung, liver or CNS toxocariasis) or systemic syndromes with different organs and
systems involvement. Brain toxocariasis is of rare occurrence and it manifest as meningitis, encephalitis,
vasculitis, abscesses or hydrocephalia.

Peripheral eosinophilia

Moderate eosinophilia (3,800/µL)

Near 85% of CNS, lung or liver toxocariasis cases
have mild or moderate eosinophilia that it useful as
a diagnostic clue.

CSF study

Normal

For the 23 brain cases reported in a previous review
with CSF analysis (reference 3) we calculated a median of 20 cells/µL (range 0-1,220;  IQR 0-161/µL);
34.8% has 0 cell count on the CSF.
For the few cases with eosinophil percentage available that have been reported (see reference 3), we
calculated a median of 23% for this parameter (range
0-64%; IQR 9.5-54.7%)

Serological diagnosis

ELISA IgG + for Toxocara genus
Western Blot + for Toxocara genus.
ELISA IgG negative for Trichinella sp.

ELISA yield using larval antigens have a sensitivity of
78% and 92%specificity. Western Blot testing allows
confirm infection and discard cross reactions.
Occasionally, antibody studies from CSF have been
applied either using ELISA and/or Western Blot.

Imaging

Brain CT: ill-defined hypodense lesions in
both hemispheres mainly of subcortical
distribution (contrast media not used).
Brain RMI : multiple hyperintense lesions
on  FLAIR of subcortical distribution. Gadolinium-enhanced lesions on T1 signal.

Brain MR is the preference imaging technique. Neurotoxocariasis cases present hyperintense lesions on
FLAIR or T2 signal, either as single or multiple lesions
distributed in the cortex, subcortical zone or in the
white matter. The use of gadolinium allows in some
cases to demonstrate homogeneous, punctate or
ring reinforcement.

Treatment

Albendazole as 10 mg/Kg /day (oral
route) for 2 weeks and corticosteroids in
high doses.

There are no guidelines for an optimal treatment.
Most of the reported cases of cerebral toxocariasis
have been treated with albendazole and corticosteroids.

Evolution and outcome

Favorable

Favorable in reported cases

antimicrobial regimens in high doses or for prolonged periods19-23. For example, in a randomized
open-label study, about 50% efficacy was observed
with albendazole (10 mg/Kg/d) or thiabendazole

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(50 mg/kg/d) in cases of OML or VML23. The
application of mebendazole at doses of 20-25 mg/
kg/d has a similar efficacy to diethylcarbamezine
in regimens of 3 weeks duration20. The self-limi1677

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ted nature of toxocariasis has been evidenced in
some studies with low dose of mebendazole (1015 mg/kg/d) where it has not been found to be
superior to placebo in accelerating symptomatic
improvement19. Of 34 cases of cerebral toxocariasis reported up to 2015, half of them had been
treated with albendazole and corticosteroids3. Of
the group with cerebral toxocariasis, approximately 76% recovered, 11% worsened, and the rest
remained in stable conditions3. Although there are
no validated guidelines for the management of this
form, the vital prognosis of neurotoxocariasis has
been favorable with no fatal cases in patients with
confirmed infection3.
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Finsterer J, Auer H. Neurotoxocarosis. Rev Inst Med
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