There is limited microbiological and virological knowledge of MERS-CoV infection among healthcare personnel in the southern region of Saudi Arabia, although the clinical aspects are known.

Introduction: The pathway of glycogen metabolism is regulated by many hormones such as insulin, glucagon, and corticosteroids. Glycogen storage diseases (GSD) most commonly affect muscles, liver, or both and occur in each 20000 to 43000 live birth. They are classified into 12 subtypes, but types I, II, and IX are the most common. Methodology: We conducted this review using a comprehensive search of MEDLINE, PubMed, and EMBASE, from January 2001, through February 2017. The following search terms were used: glycogen storage diseases, Von Gierke disease, Pompe's disease, Cori Disease, Forbes disease, Andersen's disease, McArdle disease, neonatal hypoglycemia, neonatal hepatomegaly. Aim: In this review, we aim to study the genetic basis, diagnosis, presentation, and different management approach to various common types of glycogen storage diseases prevalent in pediatric population. Conclusion: There are no cures for any type of glycogen storage diseases presently. Most treatments are designed to control signs and symptoms. The overall goals are primarily avoiding hypoglycemia, hyperlactatemia, hyperuricemia, and hyperlipidemia. Liver transplantation should be deliberated for patients with GSD type IV and for other progressive hepatic types of GSDs in order to avoid hepatic failure or malignancy. More research must be carried out to develop newer and more effective ways of management.

PRUNE 1- related disorder, is a neurodevelopmental problem characterized by microcephaly, hypotonia, and variable central nervous system abnormalities, it is a unique uncommon autosomal recessive disease caused by a homozygous or compound heterozygous mutation in the PRUNE1 gene on chromosome 1q21.4. Here we report a 15 months old girl who presented with characteristic features compatible with Prune syndrome informed of severe developmental delay, progressive microcephaly, hypertelorism, micrognathia and low set ears. The neurological evaluation revealed profound central hypotonia and spastic limbs with increased deep tendon reflexes. At the age of 15 months, she became more flaccid, with multiple hospitalizations because of recurrent aspiration, refractory seizure and severe gastroesophageal reflux disease. Eye examination showed severe optic atrophy. Further molecular genetic analysis revealed a homozygous variant c.383G>A – P(Arg128Gln)-chr1:150997134.