key: cord-255357-oar2pttf authors: Kijima, Emi; Yamamura, Haruka; Okada, Mari; Nagasawa, Masayuki title: Kawasaki Disease and Invasive Pneumococcal Infection date: 2020-06-17 journal: SN Compr Clin Med DOI: 10.1007/s42399-020-00350-9 sha: doc_id: 255357 cord_uid: oar2pttf nan Streptococcus were both negative. Intravenous cefotaxime (CTX) administration was started empirically. In the morning, she developed five out of six major KD symptoms (except for lip findings), and intravenous immunoglobulin (2 g/kg; IVIG) and oral aspirin (30 mg/kg/day) were started according to the definite diagnosis of KD with a Kobayashi score of 4 [2] . The blood culture became positive for GPC in the evening, and intravenous ampicillin (ABPC) was added to cover enterococcus infection, empirically. Both spinal fluid and urine culture were negative. On the next day, fever decreased transiently. However, fever increased again to 39.0°C on the 3rd day after admission and systemic rash and edema became further deteriorated. Blood examination revealed WBC of 11,100/μL, CRP of 7.52 mg/dL, sodium of 136 mEq/L, albumin of 2.4 g/dL, and D-dimer aggravated to 13.7 μg/mL. GPC was determined to be Streptococcus pneumoniae with penicillin susceptibility, and antibiotic treatment was switched to ABPC only. Considering of unresponsiveness to IVIG, prednisolone (2 mg/kg/day; PSL) was added. The follow-up blood culture performed on the same day was found to be negative later. Fever decreased to normal level, and a rash and edema improved dramatically on the 4th day. The pneumococcal serotype was determined as 24B (nonvaccine strain) later. The patient was discharged on oral aspirin after 14 days antibiotic treatment. During the course, the coronary lesion was absent. In our case, KD was unresponsive to IVIG in spite of proper antibiotic treatment for IPD, and KD was well responsive to PSL instead. It is considered that IPD might be a triggering factor of KD and highly elevated D-dimer is a significant risk factor of IVIG unresponsiveness in KD as we have previously reported [3] . Concerning the preceding febrile episode which occurred 10 days before the admission, the likelihood of exanthem subitum was speculated, although it was not confirmed serologically. It is very interesting to speculate that the preceding viral infection might be a prerequisite background of KD which was later triggered by IPD, when considering the unknown immunological pathology of KD [4, 5] . Furthermore, when once induced, KD requires specific treatment for itself, even if the triggering infection such as IPD as in our case is controlled by proper antibiotic therapy. Kawasaki disease associated with pneumococcal infection. SN Comprehensive Clinical Medicine Evaluation of Kawasaki disease risk scoring system in a single center experience from Japan Impact of D-dimer on the resistance to intravenous immunoglobulin therapy in Kawasaki disease GSL Circulating CD3+ HLA-DR+ extracellular vesicles are not increased in the acute phase of Kawasaki disease Soluble Sortilin in elevated in the acute phase of Kawasaki disease An outbreak of severe Kawasaki-like disease at the Italian epicentre of the SARS-CoV-2 epidemic: an observational cohort study Erythema multiforme and Kawasaki disease associated with COVID-19 infection in children Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. SN Compr