Isolation of Kawasaki disease-associated with bacterial sequence from peripheral blood leukocytes

The clinical and epidemiologic features of Kawasaki disease [KD] suggest an infectious etiology; however, the agent[s] remain unknown. Our purpose was to isolate the causative bacterial gene from peripheral blood leukocytes of patients with acute KD, by Universal polymerase chain reaction [UPCR], in Tehran Children's Medical Center. Universal polymerase chain reaction [UPCR] assay was used to amplify the bacterial 16S ribosomal RNA gene [rDNA]. Forty three [28 boys and 15 girls] were diagnosed with acute Kawasaki disease included in this study. The median age at diagnosis was 3.5 years [range: 0.5-9 years]. Twenty Nine [29] cases had typical KD criteria and 14 patients had atypical KD at diagnosis. Two of the 43 KD patients were positive for the Universal PCR assay for 16S rRNA, prior to intravenous g-globulin therapy [IVGT], while all specimens were negative by conventional blood culture. In our study, there was fever in 100%, conjunctivitis in 62.7%, rash in 83.72%, oral mucosal changes in 76.74%, peripheral changes in 37.20%, and cervical lymphadenopathy in 39.53% cases. The 16S rDNA sequence was positive in 4.65% of acute KD patients; this data shows that an infectious KD agent is traced in peripheral leukocytes. The question remains as to what true frequency of the16S rDNA sequence in KD is

Long-term antibody response and immunologic memory in children immunized with hepatitis B vaccine at birth

To evaluate the long-term immunity and immunologic memory provided by universal hepatitis B vaccination program at birth, and to evaluate the booster effects of different dosages of hepatitis B vaccine on children, who lost protective antibody titers to hepatitis B surface antigen [HBs -Ag], this study was conducted. Community-based sero-epidemiologic study was done on 453 healthy 10.5 years old Iranian children, one decade after implementation of a mass hepatitis B vaccination program. A booster vaccination with different dosages was given for children who did not have protective level of anti-hepatitis B surface antigen antibody [anti-HBs]. Quantitative serologic responses to different dosages of vaccine were compared using X[2] statistical test. A total of 42% children [191 of 453] children had low concentration [<10IU/L] of anti HBs antibody, 18.5% [84 of 453] were susceptible [antibody titer <2IU/L]. 87.2% of 165 nonprotected-boostered vaccines showed immunologic memory to different doses of booster, and developed protective antibody titer two weeks later. The differences between pre- [3.48 +/- 3.39; mean +/- SD] and post- [153 +/- 163.84] vaccination antibody titers were significant [p=0.000]. Antibody titers achieved by different doses of vaccine had significant proportion to vaccine doses. No hepatitis B infection markers were detected in those children who were not sero-protected and did not respond to booster dose of vaccination. According to these findings, universal hepatitis B vaccination program at birth provides adequate protection against hepatitis B virus infection at least for 10 years. It might suggest that booster vaccination is not recommended, but further follow-up studies at adulthood age group are recommended