On occasion, outbreaks of infection with adenovirus types 3, 7, and 21 cause severe lower respiratory tract infections (LRTIs) in children. From 1990 to 1998, all cases of LRTI due to adenovirus at the Seoul National University Children's Hospital, Seoul, Korea, were reviewed. Adenoviruses were recovered from nasal aspirate specimens of 87 (5.9%) of 1472 children with LRTI. The principal adenovirus serotypes were type 2 (13 [15%] of 87 strains), type 3 (13 [15%]), and type 7 (36 [41%]). Of the 87 infections, 62 (71%) occurred in children <2 years of age, and 81 (94%) occurred in children <5 years of age. Infections due to types 3 and 7 occurred during epidemics, whereas infections due to type 2 occurred sporadically. For patients who were infected with types 3 and 7, extrapulmonary abnormalities were more common and homogeneous consolidation and pleural effusion were frequently identified on radiographs. The mortality rate was 12% overall and 19% among patients who were infected with type 7. Residual sequelae were identified in 6 (50%) of 12 patients who were infected with type 3 and in 9 (25%) of 36 who were infected with type 7. The data confirm that adenovirus types 3 and 7 can cause epidemics of severe LRTI in young children. Epidemics of LRTIs caused by adenovirus types 3 and 7 in Korea have not been described in reports published elsewhere.

A pilot study was conducted to determine if host genetic factors influence susceptibility and outcomes in human filariasis.Using the candidate gene approach, a well-characterized population in South India was studied using common polymorphisms in six genes (CHIT1, MPO, NRAMP, CYBA, NCF2, and MBL2) . A total of 216 individuals from South India were genotyped; 67 normal (N), 63 asymptomatic microfilaria positive (MF+), 50 with chronic lymphatic dysfunction/elephantiasis (CP), and 36 tropical pulmonary eosinophilia (TPE). An association was observed between the HH variant CHIT1 genotype, which correlates with decreased activity and levels of chitotriosidase and susceptibility to filarial infection (MF+ and CP; P = 0.013). The heterozygosity of CHIT1 gene was over-represented in the normal individuals (P = 0.034). The XX genotype of the promoter region in MBL2 was associated with susceptibility to filariasis (P = 0.0093). Since analysis for MBL-sufficient vs insufficient haplotypes was not informative, it is possible the

CTX-M-14 ␤-lactamase was identified in a stool isolate of Shigella sonnei and in blood isolates of Escherichia coli (one isolate) and Klebsiella pneumoniae (two isolates) from different parts of Korea. The amino acid sequence differed by one amino acid from CTX-M-9 (Ala-2313 Val) and was identical to that of ␤-lactamases recently found in China and Japan.Because resistance is more than locally relevant with increasingly mobile populations and since unique resistance mechanisms may evolve anywhere antibiotics are used, we have investigated several unusually resistant clinical isolates from Korea.One strain of Escherichia coli and two strains of Klebsiella pneumoniae that had high levels of resistance to cefotaxime were isolated from the blood of patients in Seoul National University Children's Hospital in 1995 and 1996. One strain of Shigella sonnei isolated from a pediatric patient on Cheju Island in 2000 also had a high level of cefotaxime resistance. By disk susceptibility testing, the strains were resistant to amoxicillin, cephalothin, and cefotaxime but were susceptible to ceftazidime, cefoxitin, and amoxicillin-clavulanic acid. Isoelectric focusing showed that the four strains produced a ␤-lactamase with an isoelectric point (pI) of 8.0. PCR with SHVspecific primers (3) was negative for all strains. Cefotaxime resistance was transferred by conjugation (9) from K. pneumoniae strain 95151 along with a plasmid of 160 kb to E. coli J53 Azi r (met pro azide resistant) to produce E. coli J53 Azi r / pMG267. The ␤-lactamase gene was cloned from plasmid pMG267 with EcoRI as an 8-kb insert into vector plasmid pBC SK (Stratagene, La Jolla, Calif.) carrying chloramphenicol resistance to produce plasmid pMG268. For sequencing, a Tn7-based transposon carrying a kanamycin resistance gene was inserted into purified pMG268 using the GPS-1 Genome Priming System-1 kit (New England BioLabs, Beverly, Mass.), and the resulting derivative was introduced into E. coli DH10B (Gibco BRL, Rockville, Md.) by electroporation. After selection with 50 g of kanamycin per ml and 30 g of chloramphenicol per ml, colonies were screened for loss of resistance to 100 g of ampicillin per ml. In ampicillin-susceptible colonies, the transposon was assumed to have been inserted into the ␤-lactamase gene. With primers (primerN and primerS) that matched nucleotides at the extremities of the inserted transposon, cycle sequencing (Perkin-Elmer Cetus, Norwalk,

Summary. Inflammatory cytokines and low-affinity Fcg receptor (FcgR) polymorphisms were investigated in 37 children with chronic immune thrombocytopenic purpura (cITP) and 218 controls. Genotype analysis included common variants in the regulatory regions of cytokines, TNF, LTA, IL1RN, IL1A, IL1B, IL4, IL6 and IL10, and structural variants of the low affinity FcgRs, FCGR2A, FCGR3A and FCGR3B. Associations were observed for TNF (P 0´0032), LTA (P 0´019), FCGR3A (P 0´038) and FCGR3B (P 0´0034). Two combinations of genotypes (TNF and FCGR3A; P 0´0003, and LTA and FCGR3B; P 0´011) were significantly associated with cITP. These results provide preliminary evidence that variant genotypes of FcgRs and cytokines contribute to cITP pathogenesis.