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Ramsay Hunt syndrome (RHS) is characterized by varicella zoster virus (VZV) infection in the geniculate ganglion of the facial nerve. It typically presents with ipsilateral facial palsy and vesicles in the external auditory canal [1] . Recognizing atypical clinical manifestations of RHS, though not frequently reported, is of clinical importance for clinicians. For instance, RHS without vesicles, condition known as zoster sine herpete [2] , is difficult to distinguish itself from Bell's palsy. Although the vestibulocochlear nerve is frequently co-involved during the course of RHS, multiple lower cranial nerve involvement has rarely been described in the literature [5] [6] [7] [8] [9] [10] [11] [12] . Additionally, laryngitis due to VZV associated with RHS is not a well-recognized clinical entity. We herein report a case of Ramsay Hunt syndrome with zoster pharyngitis involving multiple lower cranial nerves. A 66-year-old woman with a history of hypertension was hospitalized because of progressive dizziness, right-side facial weakness and dysphagia. The patient was in her usual state of health until 6 days before admission, when sore throat and odynophagia developed, associated with subjective fevers and anorexia. Two days before admission, the patient reported dizziness, right-side facial weakness associated with pain radiating to the right ear, and dysphagia. The patient denied headache, photophobia, neck stiffness, nausea or vomiting. On the morning of admission, the patient developed right-side tinnitus, unsteady gait and inability to close the right eye. On physical examination, the patient appeared to be in mild distress. The temperature was 101.8 8F, blood pressure 176/93 mm Hg, pulse 102 beats per minute, respirations 20 breaths per minute and oxygen saturation 97% on room air. Her heart sounds were regular without murmurs and her lungs were clear to auscultation. On otologic examination, a few vesicles were observed in the external auditory canal of the right ear with a normal tympanic membrane. Neurological examination revealed peripheral facial nerve palsy (VII), with involvement of the left vestibulocochlear nerve (VIII), glossopharyngeal nerve (IX) and vagus nerve (X) ( Table 1) . Spinal accessory nerve (XI) and hypoglossal nerve (XII) were intact. Flexible laryngoscopic examination revealed erythema and erosive lesions on the right side of the epiglottis and arytenoid. There was an asymmetry of the soft palate. A biopsy of the erosive lesions was not performed. A non-contrast computed tomography of the head and temporal bone revealed no abnormalities. Ramsay Hunt syndrome with laryngitis due to varicella zoster virus was suspected and the patient was started on acyclovir and steroid therapy. After the completion of a 7-day course of the combination therapy, the patient's neurological symptoms improved except for the facial nerve palsy. Healed erosions on the IDCases 2 (2015) 47-48 A B S T R A C T Ramsay Hunt syndrome is characterized by varicella zoster virus infection affecting the geniculate ganglion of the facial nerve. It typically presents with vesicles in the external auditory canal associated with auricular pain and peripheral facial nerve paralysis. Although vestibulocochlear nerve is frequently co-involved during the course of Ramsay Hunt syndrome, multiple lower cranial nerve involvement has rarely been described in the literature. In addition, laryngitis due to varicella zoster virus is a diagnostic challenge due to its unfamiliarity among clinicians. We report a case of Ramsay Hunt syndrome with laryngitis involving multiple lower cranial nerves.
Ramsay Hunt syndrome and zoster laryngitis with multiple cranial nerve involvement-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)

Background: Kawasaki disease (KD) becomes one of the common diseases in Korea. Changes in clinical features and laboratory findings of KD were evaluated over a period of 10 years. Methods: We reviewed the medical records of KD patients and compared the clinical and laboratory features of two KD patient groups: those admitted from 2000 to 2004 (group A, 284 cases) and those admitted from 2010 to 2014 (group B, 331 cases). Results: There were a total of 615 KD patients (mean age: 29.7 months; male-to-female ratio = 1.6:1), including 228 incomplete KD patients. Incomplete KD patients had milder values in some laboratory indices. The preadmission and total fever durations were longer in group A than in group B. The proportion of incomplete KD was higher in group B, but incidence of coronary artery lesions (CALs) was lower. For laboratory indices, the C-reactive protein and follow-up platelet values were lower, and the hemoglobin and albumin values were higher in group B. The same clinical and laboratory findings were confirmed in the KD subgroups; those with the same fever duration of 5 or 6 days and same ages, those with complete KD, and those with incomplete KD in the two different time periods. Conclusions: Our findings suggest that clinical features of KD tend to be milder over time and manifest in a higher incidence of incomplete KD, lower incidence of CALs, and less severe laboratory findings in recent KD patients in Korea compared with their historic counterparts.
Changes in clinical and laboratory features of Kawasaki disease noted over time in Daejeon, Korea

Based on available metabolomic studies, influenza infection affects a variety of cellular metabolic pathways to ensure an optimal environment for its replication and production of viral particles. Following infection, glucose uptake and aerobic glycolysis increase in infected cells continually, which results in higher glucose consumption. The pentose phosphate shunt, as another glucose-consuming pathway, is enhanced by influenza infection to help produce more nucleotides, especially ATP. Regarding lipid species, following infection, levels of triglycerides, phospholipids, and several lipid derivatives undergo perturbations, some of which are associated with inflammatory responses. Also, mitochondrial fatty acid βoxidation decreases significantly simultaneously with an increase in biosynthesis of fatty acids and membrane lipids. Moreover, essential amino acids are demonstrated to decline in infected tissues due to the production of large amounts of viral and cellular proteins. Immune responses against influenza infection, on the other hand, could significantly affect metabolic pathways. Mainly, interferon (IFN) production following viral infection affects cell function via alteration in amino acid synthesis, membrane composition, and lipid metabolism. Understanding metabolic alterations required for influenza virus replication has revealed novel therapeutic methods based on targeted inhibition of these cellular metabolic pathways.

Metabolic host response and therapeutic approaches to influenza infection