This is a 15-year-old male patient, born in Pyedecuesta and residing in the urban area of Florida Budina, secondary student, who consulted for fever 10th April 2008man to asthenia in a clinic.
She had no relevant past medical history.
On general examination, the patient was pale, asthenic, afflicted with cervical tacto, with normal vital signs, erythematous tonsils and whitish plaques, and adenopathy.
His neurological examination was normal.
With the diagnosis of colitis outpatient treatment was prescribed with benzathine penicillin, diclofenac and amoxicillin.
Three days later she consulted again due to persistent fever, nausea, odynophagia and osteomyalgia.
The examination revealed fever (39Â°C), blood pressure 119/70 mm Hg, heart rate 100 beats per minute and respiratory rate 16 per minute.
His pharynx was granular, he had colic pain and the rest of his examination, including the neurological one, was normal.
With the diagnostic impression of dengue or viral pharyngitis, a leukocyte count was performed: 11,400 x mmÂ3 (neutrophils, 80%); hemoglobin, 17 g/dl, and platelets 319.000
Chest radiography, febrile antigens and partial urine antigens were also obtained, which were normal.
Dexamethasone was prescribed.
Three and a half hours later she presented intolerance to fluids due to pharyngeal spasm, which recurred four hours later.
He was alert and had pharyngeal erythema.
Examination of serum electrolytes showed sodium of 129 mmol/L. The diagnostic impression was fever syndrome and hyponatremia.
The next day he was alert, febrile (39Â°C), with osteomyalgias and diffuse muscle weakness, without signs of meningeal irritation and normal pulmonary auscultation.
An internist in the emergency department assessed suspected pneumonia or encephalitis. He reported that he had initially presented pain in the right shoulder, fever was continuous, headache, dysarthria, vomiting.
The patient's mother reported a history of bat bite in her right hand four months earlier.
The patient was found to be in a regular state, sleepless, oriented but with verbal incoherence, decreased strength in the lower limbs and no signs of meningeal irritation.
With the clinical impression of possible viral or rabies encephalitis, computed tomography (CT) of the skull was requested and evaluated by a neurologist.
Twelve hours later she presented agitation, disorientation, dysphagia and paresis of the lower limbs, and was sedated with diazepam.
He was referred to a third level institution, where he was admitted eight hours later, on the eighth day of his affection, of Alliga ́s late evolution, to rule out the possibility of encephalitis, due to a history of bite
The National Institute of Health was informed to send a sample of refrigerated serum to study rabies virus.
However, it was considered unlikely that the case corresponded to rabies given the history of the epidemiological area of exposure (urban area of Floridabla) and the time elapsed since the bite by the bat.
On the day of admission, a CT scan of the head was performed, which showed diminished cerebral ventricles with no areas of hypercaptation.
Lumbar puncture revealed opening pressure of 24 cm of water.
Cerebrospinal fluid cytochemical examination was normal; Gram, KOH, BK and Chinese ink stains, and bacterial antigens were negative.
His heart rate was elevated white blood cells and white blood cells (23,420 x mmÂ3 with 87% segmented), C-reactive protein of 0.3 mg/L (normal, 0.08 to 3.10 mg/L).
She presented psychomotor agitation, episodes of severe drowsiness and isochoric pupils of 3 mm diameter and reactive to light.
Manufacture was caused by endocranean hypertension and sepsis due to the clinical picture suggestive of viral encephalitis.
Orotracheal intubation was performed and mechanical ventilation was given.
However, fever (39.5°C) and hypertension (167/98 mm Hg) persisted.
She received sedation with fentanyl and relaxation with vecuronium.
Hyponatremia and hypokalemia were also found.
Due to her hypertension she was medicated with sodium nitroprusside.
On the ninth day of its evolution, the patient remained febrile (38Â°C), tachycardic (164 beats per minute), and hypertensive (162/108 mm Hg).
The patient was evaluated by the Neurology Department, who considered that the history of bat bites was unlikely to be due to meningitis.
At that time, the patient developed a generalized tonic-clonic seizure that was controlled with midazolam and phenytoin was prescribed.
It was considered that the clinical picture was very suggestive of viral encephalitis, probably herpetiformis, and it was recommended to administer dexamethasone at a dose of 24 mg a day, in addition to the previously established treatment.
On day 12 of evolution, the patient continued with neurological deterioration (Glasgow 4/15), irregular respiratory pattern, with general measures for edema, antiviral therapy and coverage with first-line antibiotics for suspected pulmonary co-infection.
Gadolinium-enhanced magnetic resonance imaging was normal.
When the mother was asked again, she reported that the clinical picture had started with right upper limb weakness and fever, associated with symptoms of foot weakness and dizziness later, dysphagia for liquids, vomiting and drowsiness.
The sedatives were suspended and the patient presented deep coma, feverish, punctiform pupils and absence of brainstem reflexes.
On day 15 of her disease she had several generalized tonic-clonic seizures and continued into a deep comatose state.
Due to the low level of colinesterase, the Neurology Department presented a blockage, insisted on the concept of serum and recommended measuring pesticide levels.
The next day, the patient was dependent on medicaments vasopressin negative shock and also on the mechanical respirator, and with vasopressin supplementation due to diabetes insipidus cerebral death; a Doppler examination of brain death.
Seventeen days after the onset of the disease and in view of its evolution, the Neurology Service considered that the patient had a severe diffuse lesion of the central nervous system of unknown cause and requested the autoimmune catatrophic profile for a possible cause.
However, it was established in the medical board that this could be an uncommon case of human rabies and began coma induction with kerosol, midazolam, pentotal sodium, ribavirin and amantadine.
On day 18 of evolution, a new transcranial Doppler examination revealed absence of flow, compatible with brain death.
That same day, the National Institute of Health confirmed by telephone that the sample sent was negative for equine encephalitis and that they did not receive the biological material sent to study rabies.
On April 26, 2008, a new CT scan of the brain showed severe edema with meningeal reinforcement.
Support measures were withdrawn, the patient presented cardiorespiratory arrest and resuscitation maneuvers were unsuccessful.
He died 19 days after the onset of his clinical condition.
That same day necropsy was performed in the Department of Pathology of the School of Medicine, Universidad Industrial de Santander.
Autopsy study
Internal examination revealed an edematous, highly softened encephalon of 1,300 g, with small subarachnoid hemorrhages and obliteration foci of aplanar hemorrhages.
At the transversal cut and at the level of basal ganglia, collapse of the ventricular system, generalized necrosis of the cerebral cortex, punctiform bleeding in the white matter and extreme distortion of the cerebral stem and cerebellum were observed.
Samples were taken from the frontal, temporal, mesencephalon and C1 segment of the spinal cord, which were referred to the National Institute of Health for confirmatory studies of rabies.
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The microscopic examination of the nervous tissue showed congestion, edema and lymphocyte infiltrates around the small blood vessels, as perivascular cuffs.
Almost all neurons presented loss of their nucleus and were transformed into eosinophilic masses surrounded by lymphocytes, macrophages and glial cells.
Inclusions were identified in the cytoplasm of very few neurons, which corresponded to Negri bodies.
The above findings made it possible to establish the diagnosis of acute necrotizing panencephalitis of possible viral etiology.
The Pathology Group of the National Institute of Health studied the samples sent and confirmed the diagnosis of acute necrotizing panencephalitis, indicative of viral etiology.
The Virology Group of the National Institute of Health carried out a direct immunofluorescence study, which was positive for rabies, with temporal lobe, neutrophil and white stranded antigen, reduced size antimalarial, and polite.
A biological test was also performed with inoculation of the patient's nervous tissue to mice of the IRA strain, with positive results.
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Viral typing showed the 3 antigenic variant, the principal reservoir of which is vampire cholera.
