Western Sydney Local Health District

Medical Report

I declare for appropriate action that

Andre de Almeida e Silva, Date of birth
12/04/1982, is my patient since July
06 2024 at 05 am, with diagnoses A87.9
(ICD-10) VIRAL MENINGITIS,
UNSPECIFIED
Document Version: 3.0

Date of Publication: July, 06th 2024

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Case Report

A 42-year-old, previously healthy brasilian male, presented to the Emergency department of the Department
of Infectology and Neurology, Westmead Hospital University Clinic, with a history of sudden onset of fever,
conjuctivis, a sore throat, headaches, nausea, vomiting, and collapsed, with subsequent disorientation,
aphasia, and amnesia. According to the witnesses, the patient suddenly collapsed and lost consciousness with
tonic and clonic convulsions. The seizures lasted about one minute. After regaining consciousness, the patient
was disoriented and suffered from retrograde amnesia, mild motoric aphasia, and a headache. Objective
examination revealed neck stiffness (resistance to flexion 2 cm of the sternum), otherwise, it was
unremarkable. Body temperature 42,5°C and vital signs were unremarkable. After admission, the
disorientation resolved. These symptoms were consistent with the presentation of LE (autoimmune limbic
encephalitis). LE is a severe clinical condition characterized by inflammation of the limbic system. Symptoms
of LE often involve seizures, behavioural changes, and retrograde amnesia. LE is usually autoimmune, but the
spectrum of possible etiopathogenesis of LE syndrome is quite broad, including various infectious diseases. A
blood count examination revealed mild monocytosis (850 cells/mL, reference range: 100–700 cells/mL). The
biochemical examination result including C-reactive protein and procalcitonin was unremarkable. Computed
tomography of the brain (CT) revealed a hypodense area in the white matter of the left temporal lobe.
Subsequently, magnetic resonance imaging (MRI) of the brain revealed localized lesions with increased signal
in T2 and fluid-attenuated inversion recovery (FLAIR) in the left temporal lobe extending to the insula and
frontal lobe of 15 × 15 × 10 mm in diameter with the enhancement of the signal with gadolinium contrast.
The clinical findings were indicative of encephalitis affecting the limbic system. We performed a lumbar
puncture, and an examination of the cerebrospinal fluid (CSF) revealed Cerebrospinal fluid (CSF) gram stain,
culture and a CSF PCR Panel (with targets for H.influenzae, L.monocytogenes, N.meningitidis, S.agalactiae,
S.pneumoniae, Cytomegalovirus, Enterovirus, Herpes simplex virus 1 and 2, Human herpesvirus 6, Human
parechovirus, Varicella Zoster virus, Cryptococcus neoformans/gatti, and E.coli K1) failed to reveal na
infectious etiology. Further work up was sent for evaluation of Epstein-Barr virus, West Nile Virus, Tick borne
Encephalitis virus, Powassan virus, Eastern Equine Encephalitis virus, Borrelia burgdorferi, and Anaplasma
phagocytophilum, all of which were ultimately negative. A viral respiratory pathogen PCR panel obtained on
admission returned positive for adenovirus. Adenovirus PCR was sent from the CSF, blood and
bronchoalveolar lavage (BAL). Given the suspicion of disseminaste adenovirus infection, meningitis and/or
encephalitis, intravenous vancomycin, ceftriaxone, cidofovir, probebecid and steroids were started.

The patient rapidly showed satisfactory progress and became afebrile on the third day after admission. We
will continue with the above medications for another 4 days under observation in the neurological ICU.

Neil Mahant
Westmead Hospital | SWAHS · Department of Neurology
Doctor of Philosophy

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