|
| ||
|
|
||
C. Pneumoniae (c + pneumoniae)
Terms modified by C. Pneumoniae Selected AbstractsChlamydia pneumoniae infections prevent the programmed cell death on THP-1 cell lineFEMS MICROBIOLOGY LETTERS, Issue 1 2002C.Romano Carratelli Abstract Chlamydia pneumoniae is an obligate intracellular bacterium which frequently causes airway infection in humans and has been implicated in chronic inflammatory disease and atherosclerosis. Here we show that infection with C. pneumoniae protects THP-1 cells against the apoptosis which spontaneously occurs in macrophages in the absence of an activation signal. Analysis by flow cytometry at different post-infection times revealed that 50±7% of THP-1 cells were apoptotic at 48 h after onset of the experiments, whereas C. pneumoniae -infected cultures (multiplicity of infection, MOI = 30) displayed only 18±4% of cells in apoptosis. At MOI = 20 and MOI = 10 the cells susceptible to apoptosis at 48 h were 28±5% and 35±6% respectively. Moreover, the results show that heat-inactivated bacteria do not give significant protection against apoptosis, even at higher MOI (MOI = 30), while UV-treated Chlamydia did provide a degree of protection against apoptosis. These data suggest that the anti-apoptotic effect of C. pneumoniae requires a heat-labile component released during infection, and that the effect is not lipopolysaccharide-dependent. [source] Simultaneous use of direct and indirect diagnostic techniques in atypical respiratory infections from Chlamydophila pneumoniae and Mycoplasma pneumoniaeJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 4 2009S. Pignanelli Abstract In 2008, 50 samples (BAL), coming from hospital patients, with acute respiratory symptoms have been investigated using two real-time PCR methods: one assay for the single detection of Chlamydophila pneumoniae and Mycoplasma pneumoniae DNA and one commercially available real-time duplex PCR assay for the detection of C. pneumoniae and M. pneumoniae DNA. Both techniques used here showed compliant results, with 100% concordance for detection of C. pneumoniae and 98% for detection of M. pneumoniae. The positive results obtained agreed with the clinical suspicion of such infections in some cases and with the presence of IgM specific for C. pneumoniae and M. pneumoniae in all cases of acute infection. J. Clin. Lab. Anal. 23:206,209, 2009. © 2009 Wiley-Liss, Inc. [source] Detection of Chlamydia pneumoniae by polymerase chain reaction,enzyme immunoassay in intestinal mucosal biopsies from patients with inflammatory bowel disease and controlsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 9 2002Wangxue Chen Abstract Background and Aim : It has been suggested that Chlamydia is an organism that may have the potential to cause inflammatory bowel disease (IBD) in susceptible individuals. Chlamydia pneumoniae has emerged as an important human pathogen in the last decade. The objective of the present study was to investigate the frequency of the presence of C. pneumoniae DNA in intestinal biopsies from patients with IBD and from non-IBD controls. Methods : The DNA was extracted from 222 colonoscopic biopsies, which were obtained from 11 patients with Crohn's disease (CD), 18 patients with ulcerative colitis (UC) and from 37 non-IBD control patients. The presence of the C. pneumoniae omp1 gene and C. trachomatis 16S rRNA gene was determined using a rapid and sensitive polymerase chain reaction-enzyme immunoassay (PCR-EIA). Results : The C. pneumoniae -specific DNA was detected in 32 (14.4%) of 222 endoscopic biopsies. Among them, C. pneumoniae DNA were found in nine of 42 (21.4%) biopsies from patients with CD, nine of 59 (15.3%) biopsies from patients with UC, and 14 out of 122 (11.4%) biopsies from non-IBD control patients, respectively. Moreover, the percentage of patients with at least one biopsy positive for C. pneumoniae was higher, although not statistically significant, in CD (36.4%) and UC patients (38.9%) compared to non-IBD controls (16.2%). In contrast, C. trachomatis DNA was detected in only two of 222 (0.9%) biopsy samples. Conclusion : The C. pneumoniae DNA was detected in the intestine of both patients with IBD and in non-IBD control patients, probably reflecting the high prevalence of this organism in the environment. The moderate yield of positive biopsies in our IBD patients and the fact that the detection rate of C. pneumoniae DNA was similar in endoscopic biopsies from IBD patients and non-IBD controls does not support a direct role for this organism in the pathogenesis of IBD. © 2002 Blackwell Publishing Asia Pty Ltd [source] Chlamydia pneumoniae and luminal narrowing after coronary angioplastyJOURNAL OF INTERNAL MEDICINE, Issue 1 2001K. J. Mattila Mattila KJ, Juvonen JT, Kotamäki MK, Saikku PA (Helsinki University Hospital, Helsinki; Kainuu Central Hospital, Kajaani, and National Public Health Institute, Oulu, Finland). Chlamydia pneumoniae and luminal narrowing after coronary angioplasty. J Intern Med 2001; 250: 67,71. Objectives.,Numerous studies have linked Chlamydia pneumoniae with atherosclerotic vessel disease and a trend for an association of the bacteria with restenosis after percutaneous transluminae coronary angioplasty (PTCA) has also been observed. The aim of this study was to assess the role of Chlamydia pneumoniae in the luminal narrowing taking place after PTCA. Design.,A noninterventional 6-month follow-up study. Setting.,A university hospital. Subjects.,A total of 122 patients with angiographically proven coronary heart disease (CHD) referred for PTCA. Interventions.,None. Main outcome measures.,The degree of luminal narrowing in the coronary arteries following coronary angioplasty. Results.,The levels of C. pneumoniae antibodies (IgG, IgA and IgM classes) and immune complexes were not associated with luminal narrowing after PTCA in multivariate analyses whilst smoking, plasma endothelin levels and diabetes were. The serologic parameters did not change during the follow up either. Conclusions.,These results do not support a role for C. pneumoniae in luminal narrowing following PTCA. [source] Chlamydia pneumoniae infection promotes the transmigration of monocytes through human brain endothelial cellsJOURNAL OF NEUROSCIENCE RESEARCH, Issue 5 2003A. MacIntyre Abstract We have investigated the effects of Chlamydia pneumoniae on human brain endothelial cells (HBMECs) and human monocytes as a mechanism for breaching the blood-brain barrier (BBB) in Alzheimer's disease (AD). HBMECs and peripheral blood monocytes may be key components in controlling the entry of C. pneumoniae into the human brain. Our results indicate that C. pneumoniae infects blood vessels and monocytes in AD brain tissues compared with normal brain tissue. C. pneumoniae infection stimulates transendothelial entry of monocytes through HBMECs. This entry is facilitated by the up-regulation of VCAM-1 and ICAM-1 on HBMECs and a corresponding increase of LFA-1, VLA-4, and MAC-1 on monocytes. C. pneumoniae infection in HBMECs and THP-1 monocytes up-regulates monocyte transmigration threefold in an in vitro brain endothelial monolayer. In this way, C. pneumoniae infection in these cell types may contribute to increased monocyte migration and promote inflammation within the CNS resulting from infection at the level of the vasculature. Thus, infection at the level of the vasculature may be a key initiating factor in the pathogenesis of neurodegenerative diseases such as sporadic AD. © 2002 Wiley-Liss, Inc. [source] Role of Chlamydia pneumoniae -infected macrophages in atherosclerosis developments of the carotid arteryNEUROPATHOLOGY, Issue 1 2003Satoshi Kuroda Chlamydia pneumoniae (C. pneumoniae) infection has been recently accepted as an important cause of atherosclerosis. However, the precise mechanisms remain unclear. The present study was aimed to clarify the distribution link among C. pneumoniae, chlamydial HSP 60, and activated macrophages. Atheromatous carotid plaques were obtained from 40 consecutive carotid endarterectomies (CEA). The specimens were prepared for HE and elastica,van Gieson staining. Parallel sections were stained immunocytochemically with monoclonal antibodies for a C. pneumoniae -specific antigen, chlamydial HSP 60, activated macrophages, and smooth muscle cells. Immunoreactivity for the C. pneumoniae -specific antigen was observed within the endothelial cells, activated macrophages, and smooth muscle cells in 36 of 40 specimens (90%). Chlamydial HSP 60 was found in all specimens positive for the C. pneumoniae -specific antigen, and mainly co-localized with the C. pneumoniae -specific antigen within the activated macrophages. The present results suggest that C. pneumoniae is a key microbial organ that causes atheroma developments in the carotid artery. Chlamydia pneumoniae -infected macrophages may come into the arterial intima and mediate inflammatory and autoimmune processes through the production of chlamydial HSP 60, leading to atherosclerosis. [source] Periodontology/Oral Medicine: Periodontal infections and cardiovascular disease,how strong is the association?ORAL DISEASES, Issue 6 2000GC Armitage In the past decade there has been renewed interest in the old hypothesis that infections increase the risk of developing cardiovascular disease and stroke. There is now a convincing body of evidence that atherosclerosis has a major inflammatory component and is much more than the simple vascular accumulation of lipids. Infectious agents that have been linked to an increased risk of coronary heart disease (CHD) include Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, and herpesviruses. The concept has emerged that each of these agents is an independent risk factor for CHD and that common chronic infections are important. In addition, periodontal infections have also been implicated as one of several factors contributing to the development of CHD. Evidence supporting a causative role of chronic infections in CHD is largely circumstantial. However, the evidence is sufficiently strong to warrant further examination of the possible link between chronic infections and CHD. In this review the lines of evidence for a causative role of C. pneumoniae in the development of CHD are summarized and contrasted with the lines of evidence suggesting a periodontal infection - CHD association. If common or widespread chronic infections are truly important risk factors for CHD, it is unlikely that a single infection will be shown to be causative. It is likely that the entire microbial burden of the patient from several simultaneous chronic infections is more important (eg, H. pylori -caused gastric ulcers +C. pneumoniae -caused bronchitis + periodontitis). Increased cooperation between cardiologists and periodontists will be required to determine if, and what, combinations of common chronic infections are important in the pathogenesis of CHD and stroke. [source] Viruses and atypical bacteria associated with asthma exacerbations in hospitalized children,PEDIATRIC PULMONOLOGY, Issue 6 2010Alberto F. Maffey MD Abstract Objectives and Working Hypothesis To evaluate the prevalence of respiratory viruses Mycoplasma pneumoniae and Chlamydophila pneumoniae and gain insight into their seasonal circulation pattern in children with acute asthma exacerbations in a temperate southern hemisphere region. Study Design Patients hospitalized between 3 months and 16 years of age were included in a 1-year prospective, observational, cross-sectional study. Respiratory secretions were collected and the presence of different viruses and atypical bacteria analyzed by immunofluorescence and polymerase chain reaction. Results Two hundred nine patients (118 females) aged (mean,±,SD) 4.4,±,4 years were included. A potential causative agent was detected in 78% of the patients. The most frequently detected viruses were respiratory syncytial virus (HRSV) (n,=,85; 40%) and rhinovirus (HRV) (n,=,52; 24.5%); M. pneumoniae and C. pneumoniae were detected in 4.5% and 2% of the cases, respectively. Patients with HRSV (vs. HRV) were hospitalized for a longer time (6.7 vs. 5.2 days, P,=,0.012), required more days of oxygen supply (5.1 vs. 3.4, P,=,0.005), had a longer duration of the exacerbation before hospitalization (3.6 vs. 1.9 days, P,=,0.001) and were younger (3.7 vs. 5.1 years, P,=,0.012). Three peaks of admissions were observed. A first peak (early autumn) caused by HRV, a second peak (winter) caused mainly by HRSV and a third one (spring), caused by HRSV, an increase in HMPV together with a second outbreak of HRV. Conclusions Children with an acute asthma exacerbation presented a high prevalence of respiratory viruses. Most hospitalizations corresponded to seasonal increases in prevalence of HRV and HRSV. Pediatr Pulmonol. 2010; 45:619,625. © 2010 Wiley-Liss, Inc. [source] Viral and atypical bacterial infections in the outpatient pediatric cystic fibrosis clinic,PEDIATRIC PULMONOLOGY, Issue 12 2006Hanne Vebert Olesen MD Abstract Background Respiratory viral and atypical bacterial infections are associated with pulmonary exacerbations and hospitalisations in cystic fibrosis patients. We wanted to study the impact of such infections on children attending the outpatient clinic. Methods Seventy-five children were followed for 12 months at regular clinic visits. Routine sputum/laryngeal aspirations were tested with PCR for 7 respiratory viruses. Antibodies against C. pneumoniae, M. pneumoniae and B. pertussis were measured every 3,4 months. FEV-1, FEF25,75 and specific airway resistance, "viral" symptoms and bacterial culture were recorded. Results Ninety-seven viral and 21 atypical bacterial infections were found. FEV-1 was significantly reduced during viral infection (,12.5%, p=0.048), with the exception of rhinovirus infection. A small change in FEV-1 (,3%) was seen during atypical bacterial infection (p=0.039). Viral and atypical bacterial infections caused no change in type and frequency of bacterial culture. Positive predictive value of "viral symptoms" was low (0.64%). Eight patients received "unnecessary" antibiotics because of viral symptoms. Conclusions Some viral infections and atypical bacterial infections affect FEV-1 acutely. Viral infections did not precipitate bacterial infection or change of colonisation. Clinical symptoms failed to diagnose viral infection accurately. Routine surveillance for virus or atypical bacteria seems not to be justified in this patient category. Pediatr Pulmonol. 2006; 41:1197,1204. © 2006 Wiley-Liss, Inc. [source] Role of ,atypical pathogens' among adult hospitalized patients with community-acquired pneumoniaRESPIROLOGY, Issue 8 2009Grace LUI ABSTRACT Background and objective: Agents such as Mycoplasma pneumoniae, Chlamydophila pneumoniae and Legionella pneumophila are recognized as important causes of community-acquired pneumonia (CAP) worldwide. This study examined the role of these ,atypical pathogens' (AP) among adult hospitalized patients with CAP. Methods: A prospective, observational study of consecutive adult CAP (clinico-radiological diagnosis) patients hospitalized during 2004,2005 was conducted. Causal organisms were determined using cultures, antigen testing and paired serology. Clinical/laboratory/radiological variables and outcomes were compared between different aetiologies, and a clinical prediction rule for AP was constructed. Results: There were 1193 patients studied (mean age 70.8 ± 18.0 years, men 59.3%). Causal organisms were identified in 468 (39.2%) patients: ,bacterial' (48.7%), ,viral' (26.9%), ,AP' (28.6%). The AP infections comprised Mycoplasma or Chlamydophila pneumoniae (97.8%) and co-infection with bacteria/virus (30.6%). The majority of AP infections involved elderly patients (63.4%) with comorbidities (41.8%), and more than one-third of patients were classified as ,intermediate' or ,high' risk CAP on presentation (pneumonia severity index IV,V (35.1%); CURB-65 2,5 (42.5%)). Patients with AP infections had disease severities and outcomes similar to patients with CAP due to other organisms (oxygen therapy 29.1% vs 29.8%; non-invasive ventilation 3.7% vs 3.3%; admission to the intensive care unit 4.5% vs 2.7%; length of hospitalization 6 day vs 7 day; 30-day mortality: 2.2% vs 6.0%; overall P > 0.05). Age <65 years, female gender, fever ,38.0°C, respiratory rate <25/min, pulse rate <100/min, serum sodium >130 mmol/L, leucocyte count <11 × 109/L and Hb < 11 g/dL were features associated with AP infection, but the derived prediction rule failed to reliably discriminate CAP caused by AP from bacterial CAP (area under the curve 0.75). Conclusions: M. pneumoniae and C. pneumoniae as single/co-pathogens are important causes of severe pneumonia among older adults. No reliable clinical indicators exist, so empirical antibiotic coverage for hospitalized CAP patients may need to be considered. [source] Chlamydia pneumoniae and newly diagnosed asthma: a case-control study in 1 to 6-year-old childrenRESPIROLOGY, Issue 2 2004Matti KORPPI Objective: The aim of the study was to evaluate the association between antibodies to Chlamydia pneumoniae and the onset of asthma in children. Methodology: In 1996,2000, 122 children aged 1,6 years, who were treated for new asthma as inpatients or outpatients in our hospital, were recruited. For each patient, two controls, matched by age, sex and municipality, were randomly selected from the same population. In 2000, 104 serum samples were available from patients (85%) and 120 from controls (49%) for microimmunofluorescence (MIF) assay for C. pneumoniae and C. trachomatis antibodies, and for enzyme immunoassay (EIA) for C. pneumoniae antibodies. Results: In EIA, the median IgG concentrations were 20 EIU (EIA units) in the patients, and 16 EIU in the controls. IgG was positive (> 30 EIU) in 37 (36%) patients and in 36 (31%) controls. IgA was positive (> 12 EIU) in four (4%) patients and in eight (7%) controls. In MIF, four (4%) patients and seven (6%) controls were IgG positive, and seven were also IgA positive. IgM antibodies were detected in four children by EIA, and in none by MIF. Conclusion: IgG antibodies to C. pneumoniae, though common in 1 to 6-year-old children as detected by EIA, did not differ between newly diagnosed asthma patients and controls in this case-control study. [source] Quantification of Chlamydia pneumoniae in cultured human macrophages and HL cells: comparison of real-time PCR, immunofluorescence and ELISA methodsAPMIS, Issue 1 2010KARI POIKONEN Poikonen K, Lajunen T, Silvennoinen-Kassinen S, Leinonen M, Saikku P. Quantification of Chlamydia pneumoniae in cultured human macrophages and HL cells: comparison of real-time PCR, immunofluorescence and ELISA methods. APMIS 2010; 118: 45,8. Chlamydia pneumoniae is an intracellular gram-negative bacterium, which replicates only in eukaryotic cells. Quantification of C. pneumoniae in cell culture is needed when studying e.g. the effect of drugs or host cell factors on infectivity and replication. Conventionally, this has been performed by immunofluorescence staining and microscopic counting of chlamydial inclusions. However, this method is usable only if the cell numbers do not fluctuate in cell culture vials and the inclusions are uniform. In macrophages, inclusions are often aberrant, their sizes vary, and multiple inclusions are also seen. Therefore, methods are needed to quantify exact amounts of C. pneumoniae in cells. Here, we describe a new method based on the real-time PCR quantification of chlamydial genomes adjusted to the number of human genomes in cultures. In human epithelial (HL) cell cultures, the C. pneumoniae inclusion numbers and the ratio of C. pneumonia genomes/human genome (Cpn/Hum) correlated significantly (r = 0.978, p < 0.001); thus with HL cells, both methods are usable. However, in macrophage cultures, the correlation was weaker (r = 0.133, p = 0.036) and we recommend PCR quantification for exact measurements. [source] Prevalence of Chlamydophila pneumoniae is higher in aorta and coronary artery than in carotid artery of coronary artery disease patientsAPMIS, Issue 12 2009HEM C. JHA Coronary artery disease (CAD) is a public health problem accounting for an estimated one-third of deaths overall. A potential link between infectious agents and atherosclerosis has been suggested. Data obtained from several seroepidemiological studies have suggested that infection with Chlamydiophila pneumoniae, Helicobacter pylori, cytomegalovirus and herpes simplex virus-1 can initiate or maintain the atherosclerotic process. However, there is no single study in which multiple infectious agents have been detected together in different vascular locations in the same population. This would help in determining if there is any leading pathogen in atheromatous plaques of CAD patients. Hence, we screened for C. pneumoniae, H. pylori, CMV and HSV-1 in different vascular locations of CAD patients using quantitative real-time (RT) PCR. We performed multiplex RT-PCR for detecting pathogens, viz. C. pneumoniae, H. pylori, CMV and HSV-1 in different vascular locations of CAD patients. Percent positivity scores for C. pneumoniae, H. pylori, CMV and HSV-1 in different vascular locations were as follows: aorta (64.7, 35.3, 11.7 and 11.7 respectively); carotid (27.2, 27.2, 9 and 0 respectively); coronary artery (58.3, 33.3, 16.6 and 8.3 respectively). Combined positivity for C. pneumoniae (C. pneumoniae IgA and RT-PCR for C. pneumoniae) was the highest compared with all other groups. Aorta and coronary artery were more susceptible to these pathogens as compared with carotid artery. Moreover, CAD patients' characteristics were associated with C. pneumoniae positivity (C. pneumoniae IgA and RT-PCR), suggesting thereby that C. pneumoniae may have caused chronic persistent infection in CAD. [source] Indications of infection with Chlamydia pneumoniae are associated with expansion of abdominal aortic aneurysmBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 4 2000R. A. P. Scott Background: This was a study of the possible association between the progression of abdominal aortic aneurysm (AAA) and indicators of infection with Chlamydia pneumoniae. Methods: Blood samples were taken from patients with AAA (3 cm diameter or greater detected by an aneurysm screening programme) who had been followed prospectively for up to 11·5 (mean 4·1) years. A sex- and age-matched control group was also recruited. Immunoglobulin (Ig) G and IgA antibodies against C. pneumoniae were measured by a microimmunofixation test. Analysis of variance, multiple linear regression and logistic regression were used for statistical analysis. Ninety men and ten women with a small AAA and 20 age-matched male controls were investigated. Outcome measures studied were AAA expansion, and IgA and IgG titres of antibodies against C. pneumoniae. Results: Forty-four (95 per cent confidence interval (c.i.) 31,55) per cent of the men with an AAA had IgA greater than 64 or IgA above 28 compared with 10 per cent of the women with an AAA (odds ratio (OR) 7·2 (95 per cent c.i. 1·0,160·8)) and 25 per cent of the controls (OR 2·24 (95 per cent c.i. 0·67,7·93)). IgA greater than 128 was significantly associated with greater expansion (5·3 versus 2·6 mm per year), even after adjustment for initial AAA size and age. A significant dose,response reaction was found between IgA titre and mean annual expansion (R = 0·45 (95 per cent c.i. 0·24,0·62)). The significant positive correlation remained after adjusting for initial AAA size and age. Finally, IgG greater than 128 was present significantly more often in patients with expansion above 1 cm annually (OR 12·6 (95 per cent c.i. 1·4,293)). Conclusion: A high proportion of men with AAA have signs of infection by C. pneumoniae. The progression of AAAs correlated with the presence of indicators of C. pneumonia infection, and a dose,response reaction between IgA titre and expansion was observed. © 2000 British Journal of Surgery Society Ltd [source] Elevated levels of anti- Chlamydia pneumoniae IgA and IgG antibodies in young adults with ischemic strokeACTA NEUROLOGICA SCANDINAVICA, Issue 3 2007B. Piechowski-Jó, wiak Introduction,,, Data on the role of Chlamydia pneumoniae in patients with ischemic stroke are inconsistent. We investigated the presence of anti- C. pneumoniae antibodies in young adults with ischemic stroke. Methods,,, 94 patients (<55 years) with ischemic stroke and 103 controls were enrolled. Indices of anti- C. pneumoniae IgA and IgG were assessed with an ELISA. We determined OR and 95% CI for the IgA and IgG seropositivity in stroke cases. Results,,, Mean IgA and IgG indices were higher in stroke patients vs controls (IgA: 1.40 vs 0.56; P < 0.001; IgG: 0.85 vs. 0.78; P < 0.003). The IgA seropositivity was associated with stroke risk (11.92; 5.94,23.92; P < 0.001) as well as IgG seropositivity was (2.31; 1.15,4.61; P < 0.016). Seropositivity assessed with combined IgA and IgG indices was associated with increased stroke risk (OR 9.35; 95% CI 4.78,18.29; P < 0.0001). After controlling for age and sex, the IgA seropositivity yielded a significantly adjusted OR for stroke (8.95; 4.44,18.07; P < 0.002), while IgG seropositivity did not (0.85; 0.53,1.63). Conclusions,,, We find an increased risk of stroke in young patients seropositive to C. pneumoniae in the IgA antibody class. Further studies to explore this finding are warranted. [source] Chlamydia pneumoniae and atherosclerosisCELLULAR MICROBIOLOGY, Issue 2 2004Robert J. Belland Summary Exposure to Chlamydia pneumoniae is extremely common, and respiratory infections occur repeatedly among most people. Strong associations exist between C. pneumoniae infection and atherosclerosis as demonstrated by: (i) sero-epidemiological studies showing that patients with cardiovascular disease have higher titres of anti- C. pneumoniae antibodies compared with control patients; (ii) detection of the organism within atherosclerotic lesions, but not in adjacent normal tissue by immunohistochemistry, polymerase chain reaction and electron microscopy and by culturing the organism from lesions; and (iii) showing that C. pneumoniae can either initiate lesion development or cause exacerbation of lesions in rabbit and mouse animal models respectively. The association of this organism with atherosclerosis has also provided sufficient impetus to conduct a variety of human secondary prevention antibiotic treatment trials. The results of these studies have been mixed and, thus far, no clear long-lasting benefit has emerged from these types of investigations. Studies of C. pneumoniae pathogenesis have shown that the organism can infect many cell types associated with both respiratory and cardiovascular sites, including lung epithelium and resident alveolar macrophages, circulating monocytes, arterial smooth muscle cells and vascular endothelium. Infected cells have been shown to exhibit characteristics associated with the development of cardiovascular disease (e.g. secretion of proinflammatory cytokines and procoagulants by infected endothelial cells and foam cell formation by infected macrophages). More detailed analysis of C. pneumoniae pathogenesis has been aided by the availability of genomic sequence information. Genomic and proteomic analyses of C. pneumoniae infections in relevant cell types will help to define the pathogenic potential of the organism in both respiratory and cardiovascular disease. [source] Microbiological etiology in clinically diagnosed community-acquired pneumonia in primary care in Örebro, SwedenCLINICAL MICROBIOLOGY AND INFECTION, Issue 7 2003F. Lagerström Objective, To study the etiology of clinically diagnosed community-acquired pneumonia (CAP) in antibiotically naive patients attending a primary care center and treated at their homes. Methods, A three-year prospective study was carried out, and 177 patients presenting with clinical signs of CAP were included. All patients had chest X-rays after inclusion, and 82 (46%) showed infiltrates. Nasopharyngeal swab culture was performed on all patients, and 51% produced a representative sputum sample. Paired sera were obtained from 176 patients. Results, Among the 82 patients with radiographically proven CAP, Streptococcus pneumoniae was detected in 26 patients (32%), Haemophilus influenzae in 23 (28%), Mycoplasma pneumoniae in 15 (18%), and Chlamydia pneumoniae in four (5%). Serologic evidence of a viral infection was found in 13 patients (16%). Among the 95 patients without infiltrates, S. pneumoniae was found in 21 (22%), H. influenzae in 14 (15%), M. pneumoniae in two (2%), and C. pneumoniae in five (5%). Viral infection was detected in 19 (20%) of these 95 patients. Conclusion, In primary care in Sweden, the initial antibiotic treatment in any patient with pneumonia should be effective against S. pneumonia and H. influenzae. In addition, M. pneumoniae should be targeted during recurrent epidemics. C. pneumoniae, and especially Legionella, seem to be uncommon in primary care. [source] Chlamydia pneumoniae, but not Bartonella quintana, is associated with coronary heart disease: results of a French case,control studyCLINICAL MICROBIOLOGY AND INFECTION, Issue 4 2003S. Badiaga Serologic cross-reactivity has been demonstrated between Bartonella quintana and Chlamydia pneumoniae. Therefore, the association between antibodies to C. pneumoniae and coronary heart disease (CHD) as described in the literature may be due to antibodies cross-reacting with B. quintana. To investigate this hypothesis, we evaluated, in a case,control study, the prevalence of C. pneumoniae and B. quintana antibodies among 296 cases with angiographically significant artery lesions and 170 controls without angiographically demonstrable coronary artery disease. The prevalence of C. pneumoniae antibodies was higher among cases than among controls: 69% versus 49% (P < 0.001; OR 1.39; 95% CI (1.55; 3.52)). Multiple logistic regression demonstrated that C. pneumoniae seropositivity is an independent risk factor for CHD (adjusted OR 2.31; 95% CI (1.49; 3.60)). No statistically significant association was demonstrated between B. quintana seropositivity and CHD. Antibodies to both C. pneumoniae and B. quintana were found in nine subjects (seven cases and two controls), suggesting co-infection rather than cross-reactivity. [source] | |||||||||||||