A 36-year-old man from Andacollo, who always lived in the Region of Coquimbo, grew up in adobe and worked as a folklorist.
Some of his relatives had a history of Chagas' disease with mega-viscera.
He remembered that in his childhood he had played with vinchucas.
She reported having had an inoculation chagoma, using intravenous drugs, or having received blood transfusions.
Three months prior to hospitalization, the patient presented with progressive weight loss, chronic diarrhea, dysphagia and prostration, which led to HIV serology, which was positive and confirmed by the ISP.
One week before hospitalization, fever, severe headache, seizures, memory impairment and loss of sphincter control were added.
Physical examination revealed emaciation, fever, memory impairment, preserved osteotendinous reflexes and doubtful neck stiffness.
There was no focal neurological deficit.
The general laboratory study showed only mild anemia.
The fundus examination revealed abnormalities consistent with HIV infection.
Upper endoscopy showed lesions suggestive of esophageal candidiasis.
IgM and IgG serology for Toxoplasma gondii were negative.
The CSF study showed the presence of trypanostes, determinations of Chinese ink, adenosine deaminase (ADA), current culture and VDRL cells in CSF were negative.
No study panel was available for other etiologies of encephalitis.
Electroencephalogram was not performed.
Chagas serology by ELISA and IFI were positive, the latter in IgG titers 1/160.
Compromise of usual target organs for megaviscera was ruled out.
Computed axial tomography (CAT) of the brain showed hypodense lesions in the white matter in both cerebral hemispheres.
Based on all these findings, meningoencephalitis was diagnosed by reactivation of Chagas disease.
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Nifurtimox 200 mg was started every eight hours together with phenytoin and was evaluated fortnightly with blood count, creatinine and liver function tests.
The onset of antiretroviral therapy (HAART) was delayed in two weeks to avoid reconstitution syndrome.
On the third day of initiating HAART with zidovudine/ lamivudine in coformulated form and efavirenz, she developed an acute psychotic episode with visual and auditory manifestations that reverted when efavirenz was replaced by nevira.
Two weeks after HAART initiation, viral load tests of 44,000 copies of viral RNA/ml could be performed (N = 135 measurements of HIV-1 QT, BioméCDrieux) and count.
After one month of treatment, short- and medium-term memory was preserved. Mild dysmetria and paresis of the right lower limb was observed.
At the fifth month, the patient presented mild hepatomegaly, mild elevation of transaminases, and mild persistence of the disease.
At 7 months of therapy for both conditions, the patient had a CD4+ TL count of 256 cleavage/detectable and an undetectable viral load.
Molecular biology techniques for the detection of T. cruzi were not available during nifurtimox treatment.
Once paresis and dysmetria were overcome, and when LTCD4 levels were above 200 cc/mm3, it was decided to discontinue antiparasitic therapy.
One year later, a qualitative polymerase chain reaction (PCR) was performed in blood for T. cruzi, which was negative, so no new treatment with nifurtimox was given.
Brain CT showed remission of white matter lesions, appearance of multiple calcifications in the right occipital region, remaining with phenytoin.
Neurology assessment ruled out other causes of CNS calcifications.
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Currently, she is on successful ART and has no neurological symptoms.
At the time of the parasitic meningeal compromise, the patient develops a normal life similar to the previous one.
