Chlamydia pneumoniae

The aim of this study was to determine the etiology of community-acquired pneumonia (CAP) and the impact of age, comorbidity, and severity on microbial etiologies of such pneumonia. Overall, 395 consecutive patients with CAP were studied prospectively during a 15-mo period. Regular microbial investigation included examination of sputum, blood culture, and serology. Sampling of pleural fluid, transthoracic puncture, tracheobronchial aspiration, and protected specimen brush (PSB) sampling were performed in selected patients. The microbial etiology was determined in 182 of 395 (46%) cases, and 227 pathogens were detected. The five most frequent pathogens were Streptococcus pneumoniae (65 patients [29%]), Haemophilus influenzae (25 patients [11%]), Influenza virus A and B (23 patients [10%]), Legionella sp. (17 patients [8%]), and Chlamydia pneumoniae (15 patients [7%]). Gram-negative enteric bacilli (GNEB) accounted for 13 cases (6%) and Pseudomonas aeruginosa for 12 cases of pneumonia...

Thirty serum samples of patients suffering from rheumatoid arthritis after screening of rheumatoid factor, C-reactive protein and ESR were collected and including in present study to detect the IgG antibody against Chlamydia pneumoniae by ELISA test. The results showed only 2(6%) patients had seropositive of C. pneumoniae, this lead to suggest that C. pneumoniae may be one of the etiological or trigger factor in patients of rheumatoid arthritis.

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.

This is the first study to analyze atheromatous plaques for the presence of bacterial DNA from ten species, including periodontal species and Chlamydia pneumoniae. We examined 129 samples of DNA extracted from atheromas from 29 individuals for the presence of bacterial 16S rDNA sequences from ten different species: Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans (A.a.), Tannerella forsythensis, Eikenella corrodens, Prevotella intermedia, Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus mutans, Treponema denticola and C. pneumoniae. All determinations were made using real-time quantitative polymerase chain reaction (PCR) methods employing SYBR®Green. Species from the Bacteroides family were found in about 17% of the young but ∼80% in elderly patients. Almost half of the samples contained DNA from A. a. and C. pneumoniae, although the proportion of the latter was minimal. S. aureus and S. epidermidis were found with the lowest frequency, 5 and 10%, respectively. S. mutans was found in ∼20% of the samples. The proportions of each bacterial species were calculated relative to the total amount of prokaryotic DNA. The data support our previous findings of an association between periodontal organisms and vascular inflammation. We conclude that DNA from oral infectious agents is commonly found in atheromas from young but especially from elderly subjects, and that the contribution of C. pneumoniae to the inflammation may be minimal.

Latency, chronicity and recurrent nature are the features of Chlamydia pneumoniae biology which play a central role in the course and outcome of C. pneumoniae–host interaction. Since redox status is directly an indicator of inflammatory response via molecular signaling mechanisms, we decided to study the regulatory role of macrophage cellular redox balance on the molecular indices of C. pneumoniae chronicity. We examined GSH–GSSG status, the activities of antioxidant enzymes (SOD, GPx and γ-GCS), along with their protein and gene expression, the MOMP and cHSP-60 protein and gene expression, and the consequence of redox balance on the establishment of productive infection in macrophages. Results showed that C. pneumoniae caused changes in GSH–GSSG levels, antioxidant enzymes activity, mRNA gene and protein expression in macrophages. The relevance of this to the state and status of C. pneumoniae in macrophages was assessed by inhibitor induced attenuation of antioxidant enzymes and there was evidence that, while SOD attenuation did not significantly affect MOMP and cHSP-60 gene and protein expression, γ-GCS attenuation increased cHSP-60 gene and protein expression. The increase in molecular evidence of chronic forms of C. pneumoniae (cHSP-60) was consistent with decrease in normal forms of C. pneumoniae. These findings reflect the importance of redox balance modulation on the outcome of C. pneumoniae infection in macrophages, a significant process in the pathogenesis of chlamydial diseases.

This work aims at the genotyping characterization for Chlamydia pneumoniae in patients with cardiovascular diseases in Karbala Province-Iraq.Blood samples were collected from each subject. Bacterial DNA was extracted from patient fresh blood. Samples were subjected for molecular detection of C. pneumoniae by using convential polymerase chain reaction (PCR) depending on 16SrRNA. Also, virulence genes for C.pneumoniae including outer membrane protein (omp1) and heat shock protein (hsp) were detected byPCR technique. Five samples (7.75%) revealed positive results for C. pneumoniae by PCR technique in blood samples of patients group, whereas all control samples were negative. Regarding virulence genes, four samples (80%) out of five samples expressed positive for omp1, whereas only two samples (40%) expressed positive result for hsp.

Microbial-based therapy of cancer is one of the earliest non-surgical anticancer therapies. The main limitation of such therapies is the toxicity of the therapeutic dose. This article discusses a novel approach that exploits cancer multidrug resistance (MDR) to provide a safer microbial-based therapy. As multidrug resistant cells can only contain limited amounts of a variety of susceptible drugs including certain antibiotics, we can take advantage of MDR to create a micro-environment (antibiotic free) that favors growth of intracellular bacteria within cancer cells. Thus, this approach targets cancer cells and spares normal cells (shielded by antibiotic): providing a more selective thus safer anticancer treatment. This article also explores the potentials of Chlamydia pneumoniae as an anti-cancer agent in this MDR-selective microbial-based therapy: its unique life cycle and the immune response to its infection suggest that it could be used directly, in the proposed approach, without any pre-requirements. Copyright © 2013 Elsevier Ltd. All rights reserved.

Male circumcision has been shown to reduce the risk of acquiring and transmitting a number of venereal infections. However, little is known about the association between male circumcision and the risk of Chlamydia trachomatis infection in the female partner. The authors pooled data on 305 adult couples enrolled as controls in one of five case-control studies of invasive cervical cancer

The recognition of atherosclerosis as an inflammatory disease in its genesis, progression, and ultimate clinical manifestations, has created an intriguing area of vascular research. The century-old &#x27;infectious&#x27; hypothesis of atherosclerosis has been rekindled and has implicated a number of microorganisms that may contribute to the inflammatory stimuli. Cumulative evi- dence from seroepidemiological, pathological, in vitro, and clinical antibiotic studies have linked the common respiratory pathogen, Chlamydia pneumoniae ,w ith atherosclerosis. Seroepidemio- logical observations provide circumstantial evidence, but they are weakened by prospective data. Pathological studies have demonstrated the preferential existence of C pneumoniae in athero- sclerotic plaque tissues, while animal model experiments have shown the induction of athero- genesis by C pneumoniae. Finally, immunological processes, whereby C pneumoniae could participate in key atherogenetic and atherothrombotic e...

We have previously shown that infection with the C. pneumoniae AR39 strain once monthly for 9 consecutive months significantly exacerbated atherosclerosis in mice with LDL receptor deficiency (LDLR–/–) in the presence of a high cholesterol diet. To further optimize the LDLR–/– mouse model for studying the mechanisms of C. pneumoniae atherogenesis, we have tested a different infection protocol with intranasal inoculation twice monthly for 6 consecutive months in the present study. We found that C. pneumoniae infection for 6 months was sufficient to produce a 130%, significantly greater exacerbation of aortic atherosclerosis in LDLR–/– mice in the presence of a high cholesterol diet. Mice receiving a high cholesterol diet alone displayed a lesion area index of 18.2 ± 6.1 (S.D.) while mice treated with both the high cholesterol diet and C. pneumoniae infection had a lesion area index of 41.8 ± 15.2 (S.D.). However, the chlamydial infection did not significantly alter the mouse serum total cholesterol or the LDL levels induced by the high cholesterol diet. This study not only confirms our previous findings that C. pneumoniae infection can exacerbate aortic atherosclerosis lesion in the LDLR–/– mice, but also further optimizes the LDLR–/– mouse model for future mechanism studies.

Recently, infections have been implicated in the pathogenesis of Alzheimer's disease. Apart from the direct effects of pathogens, it can be hypothesized that inflammatory mechanisms, such as the production of pro-inflammatory mediators by resident glia, may result in neurotoxicity. Here, we examined the inflammatory responses in murine microglial cell (MMC) and murine astrocyte cell (MAC) lines following infection with Chlamydia pneumoniae (Cpn), a pathogen that has recently been associated with Alzheimer's disease. Furthermore, we determined whether these inflammatory responses are sufficient to cause neuronal cell death in vitro. MMCs and MACs were infected with Cpn. Subsequently, various chemo- and cytokines were determined in the culture supernatant fluid of infected/control cells at different time points post-infection. Significantly higher levels of monocyte chemoattractant protein 1, interleukin (IL)-6, tumour necrosis factor (TNF)-α and IL-1β were found in supernatant fluids of infected MMCs compared with controls. In contrast, in the supernatant fluid of infected MACs, only monocyte chemoattractant protein 1 and IL-6 displayed significantly higher levels compared with controls. Moreover, neurotoxicity was examined up to 72 h after transferring the conditioned supernatant fluid to a neuronal cell layer. No neuronal cell death was observed when supernatant fluids from infected/mock-treated MACs were transferred. However, when neurones were exposed to conditioned supernatant fluid from infected MMCs, a significant increase in cell death was observed compared with mock. Furthermore, adding neutralizing antibodies against IL-6 and TNF-α to that conditioned supernatant fluid prevented neuronal cell death by ∼50%. In conclusion, these data suggest that Cpn infection results in a pro-inflammatory milieu, particularly by activating MMCs, that ultimately results in neurodegeneration with prominent roles for both IL-6 and TNF-α.