Although human coronavirus (HCoV)‐NL63 was once considered a possible causative agent of Kawasaki disease based on RT‐PCR analyses, subsequent studies could not confirm the result. In this study, this possibility was explored using serological tests. To evaluate the role of HCoV infection in patients with Kawasaki disease, immunofluorescence assays and virus neutralizing tests were performed. Paired serum samples were obtained from patients with Kawasaki disease who had not been treated with γ‐globulin. HCoV‐NL63 and two antigenically different isolates of HCoV‐229E (ATCC‐VR740 and a new isolate, Sendai‐H) were examined as controls. Immunofluorescence assays detected no difference in HCoV‐NL63 antibody positivity between the patients with Kawasaki disease and controls, whereas the rate of HCoV‐229E antibody positivity was higher in the patients with Kawasaki disease than that in controls. The neutralizing tests revealed no difference in seropositivity between the acute and recovery phases of patients with Kawasaki disease for the two HCoV‐229Es. However, the Kawasaki disease specimens obtained from patients in recovery phase displayed significantly higher positivity for Sendai‐H, but not for ATCC‐VR740, as compared to the controls. The serological test supported no involvement of HCoV‐NL63 but suggested the possible involvement of HCoV‐229E in the development of Kawasaki disease. J. Med. Virol. 86:2146–2153, 2014. © 2014 Wiley Periodicals, Inc.
Case: Six-month-old infant with large ventricular septal defect (VSD) who underwent pulmonary artery banding as a part of initial surgery. He had a dying spell due to tracheal compression by dilated right pulmonary artery. Therefore, an emergency VSD repair and aortopexy were performed. Thereafter, peripheral vascular catheter-related blood stream infection due to Methicillin-resistant Staphylococcus aureus (MRSA) occurred andLed to infective endocarditis with vegetation on tricuspid valve. Antimicrobial therapy centering on vancomycin (VCM) was initiated. However, VCM minimum inhibitory concentration of isolates changed from 1 to 2 μg/mL and bacteremia did not improve even though the trough level of VCM was within recommended therapeutic concentrations. We suspected the presence of heterogeneous vancomycin-intermediate Staphylococcus aureus (hVISA), and teicoplanin (TEIC) was started instead of VCM. In addition, albekacin (ABK) and (linezolid) LZD were added on. Thereafter, bacteremia improved and only transient reticulocytopenia and anemia were confirmed as an adverse effect of the therapeutic drug. The multidrug therapy can be an alternative for refractory infective endocarditis due to drug resistant Staphylococcus aureus under adequate therapeutic drug monitoring (TDM).
We defined incomplete Kawasaki disease (KD) as those having less than 5 principal symptoms of KD in this article. Japanese Nationwide KD surveys revealed that the prevalence of coronary artery lesion in incomplete KD is almost the same as that of complete KD. Thus, incomplete KD should not be equated with mild KD. However, there is no royal way to make the correct diagnosis of incomplete KD. We have to remind that incomplete KD is not uncommon (around 15%) and is not mild KD when we work-up patients with few principal symptoms of KD. We have to pay attention also to other significant symptoms or findings of the guideline, especially to the skin changes at the site of BCG inoculation.
BACKGROUND:The aim of the present study was to determine the prevalence of coronary artery abnormality (CAA) and other clinical features in patients with incomplete Kawasaki disease (iKD) using the data from the 17th Japanese nationwide survey of KD.METHODS:iKD was defined as the presence of four or fewer of the principal symptoms of the Japanese diagnostic guidelines, regardless of whether the patient had CAA. A total of 15,857 cases were analyzed.RESULTS:Among 15,857 cases, 83.9% of patients had five to six principal symptoms (complete KD: cKD), and 16.1% had iKD. The prevalence of CAA in cKD was 14.2%, and 18.4% in iKD. The prevalence of CAA in patients with four principal symptoms was 18.1%, which was higher than in cKD cases (14.2%). Although the reliability of the data has some limitations, the prevalence of CAA among patients with one to three symptoms was 19.3%. Among all CAA patients, 14% had four symptoms, and 6% had only one to three symptoms.CONCLUSION:Incomplete KD should not be equated with mild KD. Patients with four principal symptoms were comparable to cKD with respect to CAA occurrence. In patients with one to three symptoms also, especially in those under 1 year and older than 4 years of age, other significant symptoms and laboratory findings of the guidelines are very important in making a correct and early diagnosis of iKD so as to prevent CAA.
Purpose: To clarify the incidence of coronary artery abnormality (CAA) among incomplete (atypical) Kawasaki disease.Method: We defined incomplete cases as follows. The incomplete Kawasaki disease of narrow definition (nd-IKD) consists of cases with 4 items of principal symptoms without CAA, and cases with less than 4 items of principal symptoms regardless of CAA. The broad definition of incomplete Kawasaki disease (bd-IKD) consists of cases with less than 5 items of principal symptoms regardless of CAA. About 48,000 cases of Japanese nationwide Kawasaki disease survey were analyzed using our criteria. The proportion, age distribution and the incidence of CAA of incomplete cases were compared with that of typical cases with 5 to 6 items of principal symptoms. Result: The proportion of typical cases, bd-IKD and nd-IKD were 85.0%, 15.0% and 11.5%, respectively. The frequency of incomplete cases was slightly higher among the age groups of less than 1 year and over 5 year. The incidence of acute phase CAA among typical cases, bd-IKD and nd-IKD were 19%, 20% and 5%, respectively. The incidence of CAA of 30th illness day among typical cases, bd-IKD and nd-IKD were 12%, 11% and 2%, respectively. Discussion: Although the proportion of CAA in nd-IKD was smaller than that of typical cases, the proportion of CAA in bd-IKD was almost same as that of typical cases. Therefore the same treatment is required for the cases with less than 5 items of principal symptoms. The revision of diagnostic guideline may be necessary when the above mentioned evidence is confirmed by precise secondary survey.
The most serious complication of Kawasaki Disease is acute myocardial infraction due to thrombosis in coronary aneurysm. The efficacy of antiplatelet drug is limited especially to those with giant aneurysms. Coronary thrombolysis became one of the standard treatments of choice for acute myocardial infarction in adult patients. The purpose of this study is to evaluate the efficacy of intravenous coronary thrombolysis in Kawasaki Disease. Seven children with intraaneurysmal thrombus not complicated with acute myocardial infarction were studied by two dimensional echocardiography (2DE). Two kinds of thrombolytic agent were infused intravenously. Disappearance of those thrombi was confirmed by :2DE in three patients. Earlier detection of the thrombus seemed to affect the efficacy of the treatment. Among those seven patients thus treated~ no complication associated with this treatment was seen. In conclusion, this treatment seemed to be a promising strategy for coronary thrombosis due to Kawasaki Disease. APPLICATION OF GEA IN CORONARY REVASCULARIZATION OF KAWASAKI DISEASE
Pediatrics InternationalVolume 24, Issue 3 p. 408-409 Studies on Serum Immunoglobulins and Delayed Skin Tests in Patients with MCLS Yoshio Yanase M.D., Yoshio Yanase M.D. Department of Pediatrics, Japanese Red Cross Medical Center, TokyoSearch for more papers by this authorJun Takayama M.D., Jun Takayama M.D. Department of Pediatrics, Japanese Red Cross Medical Center, TokyoSearch for more papers by this authorSeijiro Aso M.D., Seijiro Aso M.D. Department of Pediatrics, Japanese Red Cross Medical Center, TokyoSearch for more papers by this authorYoshio Imada M.D., Yoshio Imada M.D. Department of Pediatrics, Japanese Red Cross Medical Center, TokyoSearch for more papers by this author Yoshio Yanase M.D., Yoshio Yanase M.D. Department of Pediatrics, Japanese Red Cross Medical Center, TokyoSearch for more papers by this authorJun Takayama M.D., Jun Takayama M.D. Department of Pediatrics, Japanese Red Cross Medical Center, TokyoSearch for more papers by this authorSeijiro Aso M.D., Seijiro Aso M.D. Department of Pediatrics, Japanese Red Cross Medical Center, TokyoSearch for more papers by this authorYoshio Imada M.D., Yoshio Imada M.D. Department of Pediatrics, Japanese Red Cross Medical Center, TokyoSearch for more papers by this author First published: September 1980 https://doi.org/10.1111/j.1442-200X.1980.tb00558.xCitations: 2AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume24, Issue3September 1980Pages 408-409 RelatedInformation
AbstractA live varicella vaccine was applied to 13 susceptible children to varicella virus. Three were receiving steroid therapy, and one of them was treated with both steroid and anticancer drugs. Immunosuppressive therapy and anticancer medication were not suspended before and after vaccination. Serological responses were observed in 11 of 13 vaccinated children by fluorescent antibody to membrane antigen (FAMA) test 6 to 7 weeks after Vaccination. Mild rash appeared as only a clinical reaction in 3 of the vaccinated children. However, 3 and a half months later, a vaccinee with acute myeloblastic leukemia, developed herpes zoster. Our observation suggested a possibility of contracting zoster in immune compromised hosts after vaccination with a live varicella vaccine.