Case Report A Case of Early Disseminated Neurological Lyme Disease Followed by Atypical Cutaneous Manifestations Vamsi Kantamaneni, Vikas Sunder, Mohammad Bilal, and Scott Vargo Department of Internal Medicine, Allegheny General Hospital, Allegheny Health Network, Pittsburgh, PA, USA Correspondence should be addressed to Vamsi Kantamaneni; vamsi.847@gmail.com Received 8 February 2017; Revised 26 March 2017; Accepted 3 April 2017; Published 23 April 2017 Academic Editor: Sin´ esio Talhari Copyright © 2017 Vamsi Kantamaneni et al. Tis 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. Lyme disease (LD) is a tick-borne illness caused by Borrelia burgdorferi sensu stricto. An 80-year-old female from Pennsylvania, USA, presented to an outside hospital with fever, confusion, lower extremity weakness, and stool incontinence. CT head and MRI spine were unremarkable. An infectious work-up including lumbar puncture was negative. She was transferred to our tertiary care hospital. Patient was noted to have mild unilateral right-sided facial droop and a difuse macular rash throughout the body. She denied any outdoor activities, tick bites, or previous rash. Intravenous cefriaxone was started for suspected LD. Te patient’s symptoms including facial droop resolved within 24 hours of antibiotic therapy. Polymerase chain reaction of the blood, IgM ELISA, and IgM Western blot testing for LD came back positive a few days afer initiation of therapy. She was treated for a total of 21 days for neurological LD with complete symptom resolution. Not all patients have the classic “targetoid” EM rash on initial presentation, rash could develop afer neurological manifestations, and prompt initiation of antibiotics without awaiting serology is paramount to making a quick and a full recovery. Tere should be a high index of suspicion for early disseminated LD, as presentations can be atypical. 1. Introduction Lyme disease (LD) was originally identifed in Lyme, Con- necticut, when a cluster of patients presented with an appar- ent juvenile rheumatoid arthritis. Previously known as Lyme arthritis, the entity is now called LD because of its wide variety of clinical manifestations including cardiac, dermato- logical, and neurological fndings [1]. LD is the most common tick-borne infection in the northern hemisphere. In North America, LD is predominantly caused by Borrelia burgdorferi sensu stricto. Since it was frst recognized as a clinical entity in 1975, the number of cases in the United States has increased [2]. According to the Center for Disease Control (CDC), the actual number of annual cases is close to 300,000 [3]. Trans- mission occurs secondary to a tick bite containing a spiro- chete in a genetically susceptible host [1]. Prolonged attach- ment allows time for the spirochete to transmit from tick to the human body [4]. LD classically begins with an erythematous rash called erythema migrans (EM). Te rash may have centrally located vesicles or necrotic areas [5]. Although EM lesions may occur anywhere on the body surface, common sites are the groin and axilla and, in children, the head and neck [5]. In children, the lesion can even occur periorbitally [6]. Te rash is classi- cally described as targetoid or bull’s eye appearance, with an area of erythema surrounded by central clearing [7]. Hematogenous dissemination from the initial skin lesion is thought to cause secondary skin lesions and extracutaneous manifestations. Te most common sign of early disseminated infection is multiple, ofen smaller EM lesions. Te time dura- tion at which hematogenous dissemination occurs remains unknown [8]. Approximately 4–8% of patients develop car- diac symptoms and 11% develop neurologic symptoms [1]. Arthritis is usually seen in late disease and occurs in 45–60% of untreated patients [1]. Patients typically present approxi- mately six months afer infection with joint pain and swelling which primarily involves the knees and hips [9]. We present a case of LD at our institution where the patient presented with nonspecifc neurological symptoms Hindawi Case Reports in Infectious Diseases Volume 2017, Article ID 6598043, 5 pages https://doi.org/10.1155/2017/6598043