Case Report A Dual Case of Peritonitis and Central Nervous System Infection Caused by Nutritionally Variant Streptococcal Species Sussi Vivar, 1 Jennifer E. Girotto, 1,2 and Thomas S. Murray 1,3 1 Connecticut Children’s Medical Center, Hartford, CT, USA 2 School of Pharmacy, University of Connecticut, Storrs, CT, USA 3 Frank H. Netter MD School of Medicine, Quinnipiac University, Hamden, CT, USA Correspondence should be addressed to omas S. Murray; tmurray@connecticutchildrens.org Received 25 July 2016; Accepted 4 January 2017; Published 23 January 2017 Academic Editor: Paola Di Carlo Copyright © 2017 Sussi Vivar et al. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Nutritional variant streptococci (NVS) are difficult to identify bacteria that can cause invasive infections such as endocarditis and meningitis. NVS as a cause of peritonitis has not been routinely described. is case of NVS as the etiology of peritonitis associated with previous neurosurgery and ventriculoperitoneal (VP) shunt revision demonstrates its potential role as a significant pathogen in patients with peritonitis and VP shunts. erapy consists of vancomycin plus a second agent but since there are no standards for susceptibility testing, clinical response remains the standard for determining the efficacy of treatment. When there is central nervous system (CNS) involvement it is important to include drugs with appropriate CNS penetration. 1. Introduction Nutritionally variant streptococci (NVS) comprise the Abiotrophia sp. and Granulicatella sp. and are normal residents of the oral cavity, gastrointestinal, and urogenital tracts [1, 2]. Given that NVS are fastidious, grow slowly, and can be pleiomorphic on Gram stain, these bacteria may be misidentified [1]. NVS causes a variety of invasive infections, most commonly endocarditis as a result of bacteremia [2]. Other reported infections include osteomyelitis, otitis media, wound infections, septic arthritis, and pancreatic abscesses and infections of the CNS [2–4]. Here we describe a case of CNS shunt associated peritonitis where the cultures from the CNS grew pure NVS. While peritonitis is a well-known complication of VP shunt infections, this organism as a pathogen in significant abdominal infections in children is rarely reported. 2. Case Presentation A 13-year-old girl with hydrocephalus managed with bilateral ventriculoperitoneal (VP) shunts presented to the Emergency Department (ED) with 24 hours of worsening generalized abdominal pain, headaches, dizziness, and lethargy without fever. She was born prematurely at 27 weeks of gestation resulting in developmental delay and her adoptive parents provided the history. Her parents reported she had decreased oral intake for four days prior to presentation with chills but no fever, emesis, or urinary symptoms. She had 20 VP shunt revisions in her lifetime, the most recent being completed two months prior to presentation. Her additional past medical history was significant for epilepsy, chronic headaches, cere- bral palsy, systemic lupus erythematosus, constipation, and gastroesophageal reflux disease. Her medication list included Fioricet, eletriptan, prednisone, hydrochloroquine, lansopra- zole, ranitidine, phenobarbital, and polyethylene glycol. In the ED she was ill-appearing, uncomfortable, and actively complaining of abdominal pain. Her vital signs were as follows: blood pressure 123/93, heart rate 126 beats/min, temperature 37.6 ∘ C, respiratory rate of 24/min, and pulse oximetry of 100% on room air. Her physical exam showed that her lung sounds were clear to auscultation and the heart rate was sinus tachycardia with regular rhythm without murmur on auscultation. Her abdomen was distended and diffusely tender without guarding or rebound. Initial laboratory values were as follows: white blood cell count 10,000 cells/uL (normal 4.5–13 × 10 3 /uL) with 78.5% Hindawi Case Reports in Infectious Diseases Volume 2017, Article ID 6012964, 4 pages https://doi.org/10.1155/2017/6012964