LCVA, 35 yr-old, gave birth in November 24th, 2015 of a male neonate with 3500 g, cephalic perimeter of 34.0 cm and with normal vital signs at Hospital Alianca, a 210 bed tertiary hospital in Salvador, Brazil. Antenatal visits were normal except for reporting that four days before a C-section delivery she experienced a disseminated rash and fever with dengue serology positive for IgG and negative for IgM.
The neonate was doing well until November 28th when the newborn developed a macular erythematous rash, hypoactivity and temperature of 37.9  C. On November 30th, the neonate began presenting generalized seizures that responded to anticonvulsants.
Blood, saliva, urine, and CSF samples were screened for CHIKV, Zika, and Dengue using rt-PCR techniques. Briefly, RNA was extracted using QIAmp Viral RNA mini kit according to manufacturers instructions for CHIKV. The amplification product was 305 bp within the gene that codes for the viral envelope protein E2 of CHIKV. For Zika virus, the amplicon product was 192 bp within the gene that codes for the viral NS5 region. HSV was screened in CSF and Acyclovir was initiated. EEG showed diffuse slowing compatible with the diagnosis of encephalitis.
Brain NMR showed hyperintensity signals on diffusion-weighted imaging (DWI) involving the subcortical white matter of the frontal, parietal, temporal areas, and the corpus callosum as shown in Figs. 1-3 , and were unremarkable in T1 or T2 weighted images with no enhancement in post-contrast T1-weighted NMR imaging (Fig. 4).
NMR imaging of the brain showing no enhancement of the lesions.
CSF results: 0.7 mononuclear cells per mm3, protein 106 mg/dL; glucose 23 mg/dl; immune markers for syphilis (Fta-Abs, VDRL) and toxoplasmosis (indirect immunofluorescence assay) were negative; and aerobic, mycobacterial and fungal cultures were all negative. Rt-PCR for CHIKV was positive in CSF, blood, urine and saliva. Rt-PCR for Zika virus, Dengue virus, and HSV were all negative.
The newborn began to show improvement in neurological parameters, being more active, from December 9th and was discharged home on December 16th. The newborn was more active, less hypotonic, and showing a normal sucking and palmar grasp reflexes.
Geraldin et cols presented cases of CHIKV encephalopathy with a similar pattern of neurological involvement as seen in our case and indicative of an early cytotoxic edema with marked reduction of the apparent diffusion coefficient.
In La Reunion Island CHIKV outbreak during 2005-2006, cases of chikungunya-associated encephalitis contributed to a two-fold increase in the regional overall incidence of all encephalitis.
During an outbreak in India 3 fatal cases in children were documented and were associated with nervous system complications. In the La Reunion epidemic, a similar report of 3 deaths were documented in children under 18 years, and 2 of them were due to encephalitis.
The pathogenic mechanism of the various neurological syndromes during CHIKV infection is largely unknown. Neurological involvement in CHIKV infection may include encephalitis, meningoencephalitis, encephalomyeloradiculitis, among others.