L.V.F., male infant, born at 37 weeks of gestation, suitable for gestational age; with a birth weight of 2,850 gr. She had a sibling who did not require treatment due to plasmotic disease.
At home he had contact with dog and cat.
At 6 months of age, 20 days prior to admission to our hospital, she presented a right hemi-arm focal clonic seizure, lasting 25 minutes, in the absence of fever.
In a private clinic, a normal electroencephalogram (EEG) was performed; normal brain ultrasound; normal cerebrospinal fluid (nontraumatic): 800 leukocytes/mm3 (PMN 80%), metabolic proteinorrhachi 0,89 g/L and glucose screening
She was discharged with valproic acid, apparently in good condition.
However, the patient continued with right hemisphere and right arm clonic movements, lasting for seconds, which resolved spontaneously.
An evident change in his behavior was added, becoming more aptic and hypoactive, he did not smile, could not remain seated and intermittent fever appeared at 39 oC.
CNS uptake was also considered to be moderate and similar during 15 days, after which a CT scan and MRI of the encephalon were performed, which revealed the presence of a large primary
1.
He was then admitted to our institution where a patient afflicted with mental retardation, focal seizures on the right, paresis of the right upper limb and a pyramidal syndrome were found.
ESR and CRP control were normal.
Since the last suspicion was bacterial decay and destructive lesions almost all over the encephalon, including the trunk, it was thought to be an infectious cause, and given the severity of the patient, a broad spectrum cysticer MRI was initiated.
Cefuroxime, chloramphenicol, albendazole, amphotericin B deoxycholate and dexamethasone were prescribed.
The need for an urgent brain biopsy as a fast way to establish an etiological diagnosis was raised.
Two biopsies were performed, the material of both showed almost exclusively necrotic tissue and necrotic encephalopathy consistent with fibrinoid angeitis.
The stains performed for microorganisms: PAS, Gram, Gomori-G, infectious Ziehl-Neelsen, Giemsa, Warthin-Starry and Wilder's reticulum.
Acute toxoplasmosis was considered as a diagnostic possibility.
With the result of the biopsy and a positive IgM for Toxoplasma gondii, specific treatment was initiated, initially with clindamycin plus bendazole and then with pyrimidazole plus ribavirin, clindamycin and chloramphenobarbital.
Considered a possible immunocompromised host, he underwent a study of immunoglobulins, lymphocyte count and determination of anti-HIV antibodies.
IgA, IgM and IgG measurements were normal, CD4 lymphocyte count 1.243/mm3 (normal range: 1.800-4.200/mm3), CD8 710/mm3 (normal range: 2: 700-2.500 ELISA).
The patient had fever and fever intermittent, highlighting a picture of right forearm phlebitis (01/95), which was treated with cloxacillin.
On the tenth day of hospitalization, a new fever accompanied by leukocytosis of 20,900/mm3, left shift, an ESR of 61mm/hika and a CPR of 12.5 mg/dl were reappeared vancomycin, so vancomycin was administered orally.
His neurological evolution was difficult to evaluate because he underwent two surgical procedures, anticonvulsant treatment and sedation to maintain mechanical ventilation; he was hypoactive, with Glasgow 6, low spontaneous motility and persistence of focal seizures.
Fundoscopy was normal.
There was a transient improvement in sensorium after extubation, increasing motility (Glasgow 11-12), and then deepening consciousness, with appearance of right nystagmus, major pyramidal syndrome and a mild pupillary impairment
On the thirteenth day of hospitalization there was evidence of endocraneal hypertension and bradycardia; a new CT showed progression of lesions in number and size, especially in the brainstem.
It was again connected to mechanical ventilation, mannitol and thiopental were administered without response, with progressive deterioration appearing.
Brain death was diagnosed and died twenty days after admission.
Anatomopathological findings.
The encephalon weighed 1,100 g.
He was softened and informed, with distortion of his general architecture by extensive zones of destruction, necrosis and hemorrhage, distributed throughout the encephalon, in cortical regions and coalescing 80% total body parts.
Histologically, a necrotizing encephalitis with prominent angeitis with fibrinoid necrosis and presence of elements of life type assemblages and some peculiar Balamic cysts with rough exterior walls were found
Conclusions: Granulomatous amoebic encephalitis; thymic hypoplasia-dysplasia; anatomical signs of shock.
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Tissue and serum samples of the patient were sent to Julio Martinez, Department of Pathology, Division of Neuropathology, University of Pittburgh Infectious Diseases Center and Infectious Diseases CDC.
