Doris M Salgado1, Rocío Vega2, Jairo Antonio Rodríguez2, Ángela Niño2, Rocío Rodríguez2, Ángela Ortiz2, Isabel DeLaura3, Irene Bosch4, Carlos F Narváez5. 1. Programa de Medicina, Facultad de Salud, Universidad Surcolombiana, Neiva, Huila, Colombia; Departamento de Pediatría, Hospital Universitario de Neiva, Neiva, Huila, Colombia; Especialización Médica en Pediatría, Postgrados Clínicos, Facultad de Salud, Universidad Surcolombiana, Neiva, Huila, Colombia. Electronic address: dpanqueba@gmail.com. 2. Programa de Medicina, Facultad de Salud, Universidad Surcolombiana, Neiva, Huila, Colombia; Departamento de Pediatría, Hospital Universitario de Neiva, Neiva, Huila, Colombia; Especialización Médica en Pediatría, Postgrados Clínicos, Facultad de Salud, Universidad Surcolombiana, Neiva, Huila, Colombia. 3. Programa de Medicina, Facultad de Salud, Universidad Surcolombiana, Neiva, Huila, Colombia; Harvard College, Cambridge, MA 02138, USA. 4. E25Bio Inc., The Engine of MIT, 501 Massachusetts Ave., Cambridge, MA 02139, USA; Mount Sinai School of Medicine, Department of Medicine, New York, NY 10029-6500, USA. 5. Programa de Medicina, Facultad de Salud, Universidad Surcolombiana, Neiva, Huila, Colombia; Especialización Médica en Pediatría, Postgrados Clínicos, Facultad de Salud, Universidad Surcolombiana, Neiva, Huila, Colombia. Electronic address: cfnarvaez@usco.edu.co.
Abstract
OBJECTIVE: To evaluate the clinical, laboratory, and immune characteristics of Zika virus (ZIKV)-associated encephalitis in pediatric patients after the epidemic in Huila, southern Colombia. METHODS: A pediatric neuro-surveillance hospital study was conducted in a referral health center in southern Colombia, from October 2016 to October 2017. Cases of encephalitis were confirmed by nucleic acid amplification tests and serological methods in cerebrospinal fluid (CSF), plasma, and/or urine. Levels of six cytokines were evaluated by flow cytometry. Patients underwent daily clinical and laboratory follow-up. RESULTS: Twenty children with probable encephalitis were included for further studies and 16 of them were confirmed. Four cases of bacterial meningoencephalitis (Streptococcus pneumoniae, group B Streptococcus, Staphylococcus epidermidis, and Escherichia coli) and 12 cases of viral encephalitis were identified, six of them associated with ZIKV infection. Other viral encephalitis cases were caused by herpes viruses (n=3), enterovirus (n=2), and dengue virus type 2 (DENV-2; n=1) infections. ZIKV-associated encephalitis symptoms subsided faster than those of patients with encephalitis caused by other agents. CSF analysis revealed lymphocytic pleocytosis. Compared to healthy controls, children with ZIKV-associated encephalitis presented modest plasma interleukin (IL)-10 but not IL-2, IL-4, IL-6, interferon gamma (IFN-γ), or tumor necrosis factor alpha (TNF-α). Cytokine expression was differentially regulated, as dramatically elevated IL-6, IL-10, and IFN-γ levels were observed in CSF but not in paired plasma samples in one of the patients with ZIKV detectable in CSF. CONCLUSIONS: This study provides evidence that ZIKV is responsible for pediatric encephalitis in endemic areas, and the local presence of the virus may induce cephalic but not systemic expression of cytokines.
OBJECTIVE: To evaluate the clinical, laboratory, and immune characteristics of Zika virus (ZIKV)-associated encephalitis in pediatric patients after the epidemic in Huila, southern Colombia. METHODS: A pediatric neuro-surveillance hospital study was conducted in a referral health center in southern Colombia, from October 2016 to October 2017. Cases of encephalitis were confirmed by nucleic acid amplification tests and serological methods in cerebrospinal fluid (CSF), plasma, and/or urine. Levels of six cytokines were evaluated by flow cytometry. Patients underwent daily clinical and laboratory follow-up. RESULTS: Twenty children with probable encephalitis were included for further studies and 16 of them were confirmed. Four cases of bacterial meningoencephalitis (Streptococcus pneumoniae, group B Streptococcus, Staphylococcus epidermidis, and Escherichia coli) and 12 cases of viral encephalitis were identified, six of them associated with ZIKV infection. Other viral encephalitis cases were caused by herpes viruses (n=3), enterovirus (n=2), and dengue virus type 2 (DENV-2; n=1) infections. ZIKV-associated encephalitis symptoms subsided faster than those of patients with encephalitis caused by other agents. CSF analysis revealed lymphocytic pleocytosis. Compared to healthy controls, children with ZIKV-associated encephalitis presented modest plasma interleukin (IL)-10 but not IL-2, IL-4, IL-6, interferon gamma (IFN-γ), or tumor necrosis factor alpha (TNF-α). Cytokine expression was differentially regulated, as dramatically elevated IL-6, IL-10, and IFN-γ levels were observed in CSF but not in paired plasma samples in one of the patients with ZIKV detectable in CSF. CONCLUSIONS: This study provides evidence that ZIKV is responsible for pediatric encephalitis in endemic areas, and the local presence of the virus may induce cephalic but not systemic expression of cytokines.
Authors: Jill F Lebov; Stephen R Hooper; Norma Pugh; Sylvia Becker-Dreps; Natalie M Bowman; Linda M Brown; Pia D M MacDonald; Premkumar Lakshmanane; Ramesh Jadi; Filemon Bucardo; Tatiana Chevez; Andrés Herrera Rodriguez; Teresa de Jesús Aleman Rivera Journal: Rev Panam Salud Publica Date: 2022-07-20