Interaction between Streptococcus pneumoniae and Branhamella catarrhalis obtained from double-colonized, healthy nasopharynx and double-infected, diseased middle ear cavity

Streptococcus pneumoniae and Branhamella catarrhalis were obtained from the double-colonized nasopharynx of 3 healthy carriers and from the double-infected middle ear cavity of 3 patients suffering from acute otitis media. The bacterial strains were isolated and injected both separately and together into brain-heart infusion broth. Separately injected, both S. pneumoniae and B. catarrhalis survived in the broth for at least 48 h. When injected together, B. catarrhalis was completely suppressed after 16-24 h, whereas S. pneumoniae survived for at least 48 h. Thus S. pneumoniae had a remarkable inhibitory growth effect on B. catarrhalis, which can explain why double-infected middle ear cavities so seldom are found during acute otitis media.     

肺炎嗜衣原体临床株的分离鉴定与小鼠接种的初步观察

目的从临床标本中分离培养肺炎嗜衣原体,接种小鼠后对其进行初步观察。方法采用细胞培养法从临床标本中分离培养肺炎嗜衣原体;结合吉姆萨染色、间接免疫荧光、16SrDNA序列同源性和系统发育分析对其进行鉴定;建立动物模型对其毒力进行初步研究。结果从临床标本中分离的菌株NH001和NH002被鉴定为肺炎嗜衣原体,攻击小鼠后均产生明显肺部病理改变。结论成功分离培养出两株毒力较强的肺炎嗜衣原体菌株,为肺炎嗜衣原体相关研究提供了优质菌源。     

Flamingo cadherin: a putative host receptor for Streptococcus pneumoniae

Streptococcus pneumoniae fructose bisphosphate aldolase (FBA) is a cell wall-localized lectin. We demonstrate that recombinant (r) FBA and anti-rFBA antibodies inhibit encapsulated and unencapsulated S. pneumoniae serotype 3 adherence to A549 type II lung carcinoma epithelial cells. A random combinatorial peptide library expressed by filamentous phage was screened with rFBA. Eleven of 30 rFBA-binding phages inhibited 90% of S. pneumoniae adhesion to A549 cells. The insert peptide sequence of 9 of these phages matched the Flamingo cadherin receptor (FCR) when aligned against the human genome. A peptide comprising a putative FBA-binding region of FCR (FCRP) inhibited 2 genetically and capsularly unrelated pairs of encapsulated and unencapsulated S. pneumoniae strains from binding to A549 cells. Moreover, FCRP inhibited S. pneumoniae nasopharyngeal and lung colonization and, possibly, pneumonia development in the mouse intranasal inoculation model system. These data indicate that FBA is an S. pneumoniae adhesin and that FCR is its host receptor.     

The effect that mutations in the conserved capsular polysaccharide biosynthesis genes cpsA, cpsB, and cpsD have on virulence of Streptococcus pneumoniae

Four genes, cpsA-cpsD, at the 5' end of the capsular polysaccharide (CPS) biosynthesis locus are conserved in nearly all of the 90 known serotypes of Streptococcus pneumoniae. In the present study, the impact that mutations in cpsA, cpsB, and cpsD have on CPS production and on virulence in mice infected via systemic and intranasal routes was investigated. Strains exhibiting rough colony morphologies (in which either the cpsB or cpsD gene had been deleted) were avirulent, but a smooth, partially encapsulated strain (in which the cpsA gene had been deleted) was as virulent as the wild-type strain. Interestingly, mucoid strains containing mutations affecting the [YGX](3)-repeat domain of CpsD were unable to cause bacteremia after intranasal challenge of CD1 mice, even though such strains were capable of killing BALB/c mice after intraperitoneal challenge. In our model, the ability of S. pneumoniae to regulate, via CpsD phosphorylation, CPS production was required for its transition from the lung to the bloodstream.     

Role of type 1 T helper cells in the resolution of acute Streptococcus pneumoniae sinusitis: a mouse model

BACKGROUND: We examined the importance of the adaptive and innate immune responses in the resolution of an acute bacterial sinus infection in mice. Methods: Recombinase-activating gene knockout (RAG-1(-/-)) (no lymphocytes) and C57BL/6 (wild-type) mice were infected with Streptococcus pneumoniae. For determination of the cell type involved, lymphocytes from mice were adoptively transferred into RAG-1(-/-), C57BL/6 (all lymphocytes), B cell-deficient, and T cell-deficient mice. The degree of infection and inflammation was determined by quantification of S. pneumoniae from nasal lavage and analysis of sinus tissue, respectively. RESULTS: In C57BL/6 mice, both the infection and inflammation resolved in 21 days, whereas neither resolved in RAG-1(-/-) mice. When C57BL/6 lymphocytes were adoptively transferred into RAG-1(-/-) mice, resolution of the infection and inflammation occurred. Mice without B cells were able to clear the infection, whereas mice without T cells could not clear it. In vitro stimulation of the draining lymph nodes of the infected mice by use of heat-killed S. pneumoniae led to the production of interferon (IFN)- gamma. Flow-cytometric analysis of lymphocytes obtained from sinus mucosa and draining lymph nodes showed an increase in the number of type 1 T helper cell-like cells over that in control mice. CONCLUSIONS: RAG-1(-/-) mice with innate immunity but no lymphocytes contain--but cannot clear--a bacterial sinus infection. Lymphocytes transferred to RAG-1(-/-) mice clear the infection. The sinus mucosa and draining lymph nodes show an increase in T cells generating IFN- gamma. These data demonstrate that T cells are essential in clearing an acute S. pneumoniae bacterial sinus infection.     

2002～2003年中国社区呼吸道感染常见病原菌的耐药性监测

目的　调查 2 0 0 2～ 2 0 0 3年中国社区呼吸道感染常见病原菌的耐药性。方法　收集2 0 0 2年 4月～ 2 0 0 3年 4月全国 5个地区 5家医院社区呼吸道感染患者中分离的 779株肺炎链球菌、流感嗜血杆菌、卡它莫拉菌、A群 β溶血链球菌及苯唑西林敏感的金黄色葡萄球菌 (MSSA) ;同时收集北京市两家幼儿园儿童鼻咽携带的 185株肺炎链球菌、流感嗜血杆菌及卡它莫拉菌。琼脂稀释法测定头孢丙烯等 10种抗生素的最低抑菌浓度 (MICs)。结果　全国 5个地区 ,青霉素中介的肺炎链球菌(PISP)为 2 3 9% ,青霉素耐药 (PRSP)为 2 2 7%。PISP发生率从高至低依次为杭州 (4 4 1% )、武汉(2 6 2 % )、沈阳 (2 1 5 % )、上海 (2 0 8% )、北京 (18 5 % )、北京幼儿园 (12 7% ) ;而PRSP的排序则为北京幼儿园 (34 9% )、上海 (31 9% )、武汉 (2 7 9% )、杭州 (2 2 1% )、沈阳 (13 8% )、北京 (8 6 % )。肺炎链球菌对左氧氟沙星的敏感率为 96 3%。 9 5 %的流感嗜血杆菌和 87 4 %的卡它莫拉菌产生 β内酰胺酶 ,这两种菌对阿莫西林 /克拉维酸、头孢克洛、头孢丙烯、头孢呋辛、头孢曲松、阿奇霉素、左氧氟沙星的敏感率在 96 4 %～ 10 0 %之间。肺炎链球菌、A群 β溶血链球菌、MSSA对阿奇霉素耐药率高于 6 0 %。头孢丙烯对PISP     

肺炎链球菌不同菌株自溶酶基因的克隆、序列分析及重组表达

目的克隆肺炎链球菌自溶酶(LytA)的基因序列，并进行重组表达。方法分别提取不同临床分离株的基因组DNA，根据已知肺炎链球菌野生R6株LytA基因序列设计引物，进行PCR扩增，将获得的目的基因片段克隆人原核表达质粒，然后测序；利用生物信息学方法，对不同临床分离株LytA基因序列进行比较分析，同时进行LytA基因的重组表达。结果从不同临床分离株的基因组中均扩增出完整的LytA基因片段，成功构建了重组质粒pGEX-4T-1-LytA。比较不同临床分离株LytA基因的DNA序列及推测的氨基酸序列，发现各株LytA基因序列及氨基酸序列间存在差异。通过异丙基巯基半乳糖(IPTG)诱导，LytA基因在大肠埃希菌JM109中得到高效表达，十二烷基硫酸钠-聚丙烯酰胺凝胶电泳(SDS-PAGE)结果显示pGEX-4T-1-LytA融合蛋白相对分子质量约62000，与理论预测一致。结论序列分析发现各分离株的LytA基因序列及氨基酸序列间存在差异，但同源性极高，推测LytA基因序列保守，可用于疫苗研发。     

Interleukin-18 protects splenectomized mice from lethal Streptococcus pneumoniae sepsis independent of interferon-gamma by inducing IgM production

The mechanism of the susceptibility of splenectomized mice to Streptococcus pneumoniae infection and the therapeutic effect of interleukin (IL)-18 were investigated. We demonstrated that, although S. pneumoniae challenge induced IL-12 production, it did not induce either interferon (IFN)-gamma or IL-18 production in mice with or without a splenectomy. Liver mononuclear cells stimulated with heat-killed S. pneumoniae but not with viable S. pneumoniae produced IFN- gamma in vitro. However, IL-18 pretreatment recovered the low serum immunoglobulin (Ig) M levels in splenectomized mice and completely inhibited mortality after S. pneumoniae infection without any IFN-gamma up-regulation. Injection of IgM from noninfected control mice into splenectomized mice before infection confirmed the essential role that IgM plays against S. pneumoniae infection. Therefore, low serum IgM levels but not a low IFN-gamma response in splenectomized mice cause lethality in S. pneumoniae infection, and IL-18 pretreatment protects them from infection by increasing IgM levels before infection.     

Mouse lysozyme M is important in pulmonary host defense against Klebsiella pneumoniae infection

Klebsiella pneumoniae is a common virulent causative agent for pneumonia. Lysozyme has previously been shown to play an important role in nonimmune host defense of the airways. This study was undertaken to assess the role of lysozyme M, the major isoform of lysozyme in mouse lung, in the killing of K. pneumoniae in lysozyme M(-/-) mice and transgenic mice with increased expression of lysozyme (lysozyme(tg) mice). The airways of lysozyme M(-/-) mice maintained in a pathogen-free facility were colonized by Lactobacilli, a component of the oropharyngeal flora. No lactobacilli were detected in the lungs of wild-type (WT) or lysozyme(tg) mice. Twenty-four hours after intratracheal infection with K. pneumoniae, bacterial killing was enhanced 9-fold in lysozyme(tg) mice compared with WT mice and 43-fold compared with lysozyme M(-/-) mice. In survival studies, no lysozyme M(-/-) mice survived beyond 72 hours after infection, whereas 75% of lysozyme(tg) (p < 0.01) and 25% of WT mice survived to 120 hours (p < 0.01). Deficiency of lysozyme M in the lungs increased susceptibility to K. pneumoniae infection, whereas increased expression of lysozyme conferred resistance to infection and enhanced survival.     

331株肺炎链球菌的耐药性及基因分型

目的 了解杭州地区肺炎链球菌临床株的耐药性及青霉素耐药株的分子流行病学特征。方法 用Etest法测定菌株对青霉素的最低抑菌浓度(MIC)，用纸片扩散法测定肺炎链球菌对其他8种抗生素的耐药情况。并以盒式聚合酶链反应(PCR)和青霉素结合蛋白(PBP)基因指纹等分子生物学方法分析菌株间的亲缘关系。结果临床分离得到肺炎链球菌331株，Etest法测得55株(16．6％)青霉素高度耐药株(PRSP)，127株(38．4％)青霉素中度耐药株(PISP)。纸片扩散法测得氨苄西林、复方新诺明、红霉素、四环素、利福平、氯霉素的耐药率分别为1．2％、47．7％、90％、84．3％、0．3％及13％。所有菌株对氧氟沙星、万古霉素敏感。保存存活的35株PRSP可分为17种盒式-PCR谱型，PBP2X、PBP2B、PBP1A的指纹各为5种、7种、5种。盒式谱型A、H的菌株其耐药谱、MIC值和PBP基因指纹高度一致。结论杭州地区肺炎链球菌临床株的青霉素耐药率较高，非β-内酰胺类红霉素、四环素、复方新诺明的耐药率亦较高。杭州地区可能有耐药克隆的流行。     

Increase of apoptosis in a murine model for severe pneumococcal pneumonia during influenza A virus infection

The mechanisms of severe pneumonia caused by co-infection of bacteria and influenza A virus (IAV) have not been fully elucidated. We examined apoptosis and inflammatory responses in a murine model for pneumococcal pneumonia during IAV infection. Inflammation, respiratory epithelium apoptosis, and inflammatory-cell infiltration increased in a time dependent manner in the lungs of mice co-infected with Streptococcus pneumoniae and IAV, in comparison with those infected with either S. pneumoniae or IAV. According to appearance of terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling positive cells, caspases-3 and -8 were activated 24 h after S. pneumoniae infection, and caspase-3 activation decreased after 48 h, whereas inflammatory cytokine levels continued to increase in co-infected mice. In contrast, in mice infected with either IAV or S. pneumoniae, apoptosis and activation of factors related to caspase-3 peaked at 48 h. Furthermore, Fas-associated death domain was significantly expressed in the lungs of co-infected mice 24 h after S. pneumoniae infection. These data suggest that early onset of apoptosis and its related factors play important roles in fulminant pneumonia resulting from bacterial pneumonia complicated by co-infection with influenza virus.     

Sequential virus infections, bacterial superinfections, and fibrogenesis

Parainfluenza 1 (Sendai) and influenza A virus pneumonitis cause severe lung damage, which, upon resolution, is followed by persistent alveolitis and parenchymal changes characterized by patchy consolidation and collagen deposition in the affected areas. To determine whether these long-term sequelae of the virus pneumonias are cumulative, mice were infected by aerosol inhalation with Sendai virus, influenza A virus, or Sendai followed 30 days later by influenza virus infection. At 90 days after the initial infection, mice were killed for assay of long-term parenchymal changes as quantitated lung hydroxyproline (Hpr) content, morphometric analysis, and total and differential lavage cell counts. Sendai virus infection did not alter the proliferation of influenza virus in the lungs as quantitated by infectious virus titers on Day 1, 3, 5, 7, 9, and 11 of influenza infection. At Day 90, lung Hpr content was cumulative in dual-infected mice, with a concomitant increase in the persistent alveolitis. To determine whether bacterial infections played a similar role in these long-term pulmonary sequelae, mice were infected by aerosol inhalation with either Staphylococcus aureus or Klebsiella pneumoniae or, during the course of influenza virus infection, superinfected with each of the bacteria. Sixty days after infection with K. pneumoniae alone, lung Hpr levels were significantly increased over those in noninfected control mice. Infection with S. aureus had no effect on the quantitated parameters of long-term lung damage. In influenza-infected mice superinfected with K. pneumoniae, lung Hpr content was significantly increased over that of S. aureus did not elevate any quantitated parameter of lung damage when compared with the virus alone.(ABSTRACT TRUNCATED AT 250 WORDS)     

Improved host defense against pneumococcal pneumonia in platelet-activating factor receptor-deficient mice

Platelet-activating factor (PAF) is a phospholipid with proinflammatory properties that binds to a specific receptor (PAF receptor [PAFR]) that is expressed on many different cell types. PAFR is able to bind phosphorylcholine, which is present in both PAF and the pneumococcal cell wall. Activation of respiratory epithelial cells in vitro results in up-regulation of PAFR, which, in turn, facilitates invasion of Streptococcus pneumoniae. To determine the role of PAFR in host defense against pneumococcal pneumonia, PAFR-deficient (PAFR(-/-)) and wild-type (wt) mice were inoculated intranasally with S. pneumoniae. PAFR(-/-) mice were relatively resistant to pneumococcal pneumonia, as indicated by delayed and reduced mortality, diminished outgrowth of pneumococci in lungs, and reduced dissemination of the infection (all P<.05, vs. wt mice). PAFR(-/-) mice also had less pulmonary inflammation. These data provide evidence that PAFR is used by S. pneumoniae to induce lethal pneumonia.     

Inhibition of the expression of penicillin resistance in Streptococcus pneumoniae by inactivation of cell wall muropeptide branching genes

Penicillin-resistant strains of Streptococcus pneumoniae contain low affinity penicillin-binding proteins and often also produce abnormal indirectly crosslinked cell walls. However the relationship between cell wall abnormality and penicillin resistance has remained obscure. We now show that the genome of S. pneumoniae contains an operon composed of two genes (murM and murN) that encode enzymes involved with the biosynthesis of branched structured cell wall muropeptides. The sequences of murMN were compared in two strains: the penicillin-susceptible strain R36A producing the species-specific pneumococcal cell wall peptidoglycan in which branched stem peptides are rare, and the highly penicillin-resistant transformant strain Pen6, the cell wall of which is enriched for branched-structured stem peptides. The two strains carried different murM alleles: murM of the penicillin-resistant strain Pen6 had a "mosaic" structure encoding a protein that was only 86.5% identical to the product of murM identified in the isogenic penicillin-susceptible strain R36A. Mutants of R36A and Pen6 in which the murMN operon was interrupted by insertion-duplication mutagenesis produced peptidoglycan from which all branched muropeptide components were missing. The insertional mutant of Pen6 carried a pbp2x gene with the same "mosaic" sequence found in Pen6. On the other hand, inactivation of murMN in strain Pen6 and other resistant strains caused a virtually complete loss of penicillin resistance. Our observations indicate that the capacity to produce branched cell wall precursors plays a critical role in the expression of penicillin resistance in S. pneumoniae.     

Molecular analysis of the genetic variation among penicillin-susceptible and penicillin-resistant Streptococcus pneumoniae serotypes in Canada

Few studies have examined the genetic relatedness within and between serotypes of Streptococcus pneumoniae. Penicillin-susceptible S. pneumoniae (PSSP) isolates (n=170) and penicillin-resistant S. pneumoniae (PRSP) isolates (n=48) belonging to 13 different serotypes from across Canada were studied to further understand the molecular epidemiology of S. pneumoniae. PRSP of serotypes 6B, 14, and 19F appeared to be novel clones, differentiated by pulsed-field gel electrophoresis from the recognized international penicillin-resistant clones belonging to these serotypes. In addition, not all PRSP strains shared similar genetic backgrounds with PSSP strains of the same serotype, suggesting that in Canada, certain PRSP strains have emerged from new unique lineages of PRSP. Although there was significant heterogeneity among S. pneumoniae of different serotypes, certain serotypes (3, 7F, and 22F) appeared to be more clonally related despite having originated from different geographic regions.     

Penicillin-resistant viridans streptococci have obtained altered penicillin-binding protein genes from penicillin-resistant strains of Streptococcus pneumoniae

Penicillin-resistant strains of Streptococcus pneumoniae possess altered forms of penicillin-binding proteins (PBPs) with decreased affinity for penicillin. The PBP2B genes of these strains have a mosaic structure, consisting of regions that are very similar to those in penicillin-sensitive strains, alternating with regions that are highly diverged. Penicillin-resistant strains of viridans groups streptococci (e.g., S. sanguis and S. oralis) that produce altered PBPs have also been reported. The PBP2B genes of two penicillin-resistant clinical isolates of S. sanguis were identical in sequence to the mosaic class B PBP2B genes found in penicillin-resistant serotype 23 strains of S. pneumoniae. Emergence of penicillin resistance appears to have occurred by the horizontal transfer of an altered PBP2B gene from penicillin-resistant S. pneumoniae into S. sanguis. The PBP2B genes of three penicillin-resistant S. oralis strains were similar to the mosaic class B PBP2B gene of penicillin-resistant strains of S. pneumoniae but possessed an additional block of diverged sequence. Penicillin resistance in S. oralis has also probably arisen by horizontal transfer of this variant form of the class B mosaic PBP2B gene from a penicillin-resistant strain of S. pneumoniae.     

Studies on respiratory infections in primary care clinic (IV). Antibiotic sensitivity of bacteria isolated from patients with respiratory infections visiting 21 private clinics in the Tohoku District of Japan

We determined the MICs of ampicillin, methicillin, cefaclor, cefixime, cefteram, ofloxacin and ciprofloxacin against a total of 1,448 strains from 11 species: 464 strains of Staphylococcus aureus, 306 strains of Streptococcus pneumoniae, 114 strains of Streptococcus pyogenes, 37 strains of Branhamella catarrhalis, 329 strains of Haemophilus influenzae, 32 strains of Escherichia coli, 66 strains of Klebsiella pneumoniae, 26 strains of Enterobacter cloacae, 20 strains of Serratia marcescens, 12 strains of Pseudomonas aeruginosa and 42 strains of Acinetobacter calcoaceticus, isolated from the throat swab and the sputum of 2,539 patients with respiratory infections who visited 21 private clinics in Tohoku district of Japan during the period from January to April in 1989. Ciprofloxacin and ofloxacin were more active against S. aureus, B. catarrhalis, P. aeruginosa and A. calcoaceticus than other antibiotics. Ampicillin and cefteram were more active against S. pneumoniae and S. pyogenes than other antibiotics. New-quinolones and cephems of new-generation were active against H. influenzae, E. coli, K. pneumoniae, E. cloacae and S. marcescens. Of 30 strains of S. aureus which were resistant (MIC greater than or equal to 12.5 micrograms/ml) to ampicillin, only one strain was resistant (MIC greater than or equal to 12.5 micrograms/ml) to methicillin. Twenty strains (6.5%) of S. pneumoniae and 49 strains (14.9%) of H. influenzae were resistant (MIC greater than or equal to 1.56 micrograms/ml) to ampicillin. Of 101 strains of H. influenzae of which their beta-lactamase activity was determined by Nitrocephin-method, 27 (26.7%) were beta-lactamase-positive strains. The above results indicated that MRSA is only rarely found in primary care clinics but the incidence of ampicillin-resistant H. influenzae in primary care clinics is almost the same as that of the intensive care clinic, i.e. medical school-affiliated hospitals. Therefore caution should be exercised as regards antibiotic resistance of the causative organism even in primary care clinics.     

Pneumococcal and Haemophilus influenzae meningitis in a children's hospital in Ethiopia: serotypes and susceptibility patterns

Streptococcus pneumoniae and Haemophilus influenzae are responsible for most pyogenic meningitis cases in children in Ethiopia. Resistance of S. pneumoniae and H. influenzae to penicillin and chloramphenicol respectively has been reported globally. Resistance has been related to specific serotypes of S. pneumoniae or to beta-lactamase-producing H. influenzae strains. This study describes the serotypes/ serogroups and susceptibility pattern of the two organisms causing meningitis in Ethiopian children. There were 120 cases of meningitis caused by S. pneumoniae (46) and H. influenzae (74) over a period of 3 years (1993-95). Nineteen children died from pneumococcal and 28 from haemophilus meningitis. Penicillin-resistant pneumococcal meningitis (4/8 = 50%) caused a greater mortality rate than penicillin-susceptible pneumococcal meningitis (15/38 = 39%). Common serotypes accounting for 76% of S. pneumoniae were type 14, 19F, 20, 1, 18 and 5; and serotypes 14, 19F and 7 (accounting for 17% of strains) showed intermediate resistance to penicillin G. 97% of the H. influenzae isolates were type b, and in only two cases beta-lactamase-producing. 72% of isolates of the S. pneumoniae we identified belong to serotypes preventable by a 9-valent vaccine. Our study highlights the possibility of resistant pyogenic meningitis in children in Ethiopia due to emerging resistant strains of S. pneumoniae and H. influenzae isolates.     

Carriage of penicillin-susceptible and non-susceptible pneumococci in healthy young children in Göteborg, Sweden

OBJECTIVES: To study carriage of Streptococcus pneumoniae among healthy young children, determine the proportion of strains with decreased susceptibility to penicillin, and study possible risk factors for the carriage of penicillin-resistant strains. METHODS: Between February 1996 and February 1997, 620 healthy, 18-month-old children in Goteborg, Sweden were screened for carriage of S. pneumoniae with decreased susceptibility to penicillin. Nasopharyngeal samples were obtained from children visiting child health centres for routine health control. RESULTS: Streptococus pneumoniae was found in 322 samples and 18 strains (5.6%, CI95 3.4; 8.8) of all pneumococci showed decreased susceptibility to penicillin G with minimum inhibitory concentrations (MICs) ranging from 0.125 to 1.0 mg/l. The proportion of strains with decreased susceptibility was similar to that found in a laboratory-based material (6%), from the same geographical area and time period. A majority of the children with strains with decreased susceptibility to penicillin (n = 11) were not attending day-care centres. CONCLUSIONS: The prevalence of S. pneumoniae with reduced susceptibility to penicillin is still low in unselected healthy Swedish children.     

Investigation of Streptococcus pneumoniae and Haemophilus influenzae isolated from pediatric outpatients nationwide with a respiratory tract infection at the first consultation (2002-2003)--with special reference to the results of nasopharyngeal culture in pediatric patients with no previous history of antibacterial drug administration

We previously reported that penicillin-resistant Streptococcus pneumoniae (PRSP) and beta-lactamase-nonproducing ampicillin-resistant (BLNAR) were detected at a frequency of 27% and 35% in 468 strains of Streptococcus pneumoniae and 557 strains of Haemophilus influenzae isolated from pediatric patients diagnosed with respiratory infection in 20 pediatric outpatient facilities throughout Japan between November 2002 and June 2003. Here, we have added additional considerations regarding results of nasopharyngeal culture from 558 pediatric patients diagnosed with pneumonia, bronchitis, or otitis media and having no previous history of antibacterial drug administration. No significant difference was seen in the detection of S. pneumoniae or H. influenzae between nasal and oral specimens, or between patients with pneumonia, bronchitis, and otitis media. The detection of S. pneumoniae in pediatric patients 4 years old was significantly higher, however than that in pediatric patients 5 years old. The detection of H. influenzae in pediatric patients with a history of attending group childcare facilities was significantly higher than that in pediatric patients with no such history. No significant differences were seen among groups in the percentage of PSRP and BLNAR isolated among S. pneumoniae and H. influenzae strains. Nasopharyngeal culture of pediatric patients with respiratory infection yielded a higher frequency of S. pneumoniae in younger than older patients and a higher frequency of H. influenzae in pediatric patients with a history of attending group childcare facilities. The detection of resistant bacteria was considered related to other factors, such as the type of antibacterial drugs used, that are not discussed here.