Seroepidemiology of Chlamydia pneumoniae TWAR Infection in Seattle Families, 1966-1979

Aldous, M. B.; Grayston, J. T.; Wang, San-Pin; Foy, Hjordis M.

doi:10.1093/infdis/166.3.646

Cited by 161 publications

(102 citation statements)

References 9 publications

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“…We entirely agree that it is unlikely that a 22% cumulative incidence rate over 3 months was caused by acute exogenous infections because, as D.L. Hahn states, the annual nonepidemic C. pneumoniae acute infection rate in the adult population is reported to be ,2% [8]. To our knowledge, our study was not conducted during a community epidemic of C. pneumoniae infection [1].…”

Section: From the Authorssupporting

confidence: 50%

From the authors

Biscione¹

2005

Eur Respir J

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Section: From the Authorssupporting

confidence: 50%

From the authors

Biscione¹

2005

Eur Respir J

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“…11 Antibody prevalence studies suggest that Ͼ50% of adults have been exposed to it. 12 C pneumoniae, an obligate intracellular parasite, is known to readily infect mononuclear phagocytes. 8 Macrophages, which derive from monocytes, are characteristically localized within atherosclerotic plaques.…”

Section: See P 1538mentioning

confidence: 99%

Randomized Secondary Prevention Trial of Azithromycin in Patients With Coronary Artery Disease and Serological Evidence for Chlamydia pneumoniae Infection

et al. 1999

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Background-Chlamydia pneumoniae commonly causes respiratory infection, is vasotropic, causes atherosclerosis in animal models, and has been found in human atheromas. Whether it plays a causal role in clinical coronary artery disease (CAD) and is amenable to antibiotic therapy is uncertain. Methods and Results-CAD patients (nϭ302) who had a seropositive reaction to C pneumoniae (IgG titers Ն1:16) were randomized to receive placebo or azithromycin, 500 mg/d for 3 days, then 500 mg/wk for 3 months. Circulating markers of inflammation (C-reactive protein [CRP], interleukin [IL]-1, IL-6, and tumor necrosis factor [TNF]-␣), C pneumoniae antibody titers, and cardiovascular events were assessed at 3 and 6 months. Treatment groups were balanced, with age averaging 64 (SDϭ10) years; 89% of the patients were male. Azithromycin reduced a global rank sum score of the 4 inflammatory markers at 6 (but not 3) months (Pϭ0.011) as well as the mean global rank sum change score: 531 (SDϭ201) for active drug and 587 (SDϭ190) for placebo (Pϭ0.027). Specifically, change-score ranks were significantly lower for CRP (Pϭ0.011) and IL-6 (Pϭ0.043). Antibody titers were unchanged, and number of clinical cardiovascular events at 6 months did not differ by therapy (9 for active drug, 7 for placebo). Azithromycin decreased infections requiring antibiotics (1 versus 12 at 3 months, Pϭ0.002) but caused more mild, primarily gastrointestinal, adverse effects (36 versus 17, Pϭ0.003). Conclusions-In CAD patients positive for C pneumoniae antibodies, global tests of 4 markers of inflammation improved at 6 months with azithromycin. However, unlike another smaller study, no differences in antibody titers and clinical events were observed. Longer-term and larger studies of antichlamydial therapy are indicated. (Circulation. 1999;99:1540-1547.)

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“…Seroepidemiological studies performed worldwide have demonstrated that 40%-86% of asymptomatic adults have antibodies to C. pneumoniae [6][7][8][9]. In Jordan, a single study demonstrated 61.1% seroprevalence of C. pneumoniae-specific IgG antibodies among apparently healthy male adults [10].…”

Section: Introductionmentioning

confidence: 99%

Role of Chlamydia pneumoniae in community-acquired pneumonia in hospitalized Jordanian adults

Al-Aydie

Obeidat

Al-Younes

2016

J Infect Dev Ctries

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Introduction: This study investigated the role of Chlamydia pneumoniae in the etiology of community-acquired pneumonia (CAP) in Jordanian adults. Methodology: Eighty hospitalized CAP patients and 110 healthy adults were enrolled. Overall prevalences of C. pneumoniae IgG antibodies in sera and the rate of acute infection were estimated, using the microimmunofluorescence method (MIF), at titers of 1:16 and 1:512, respectively. Moreover, a nested polymerase chain reaction (PCR) was used to detect C. pneumoniae DNA in nasopharyngeal and blood Buffy coat samples. Results: Overall chlamydial IgG prevalence was higher in CAP cases than controls (70% versus 61.8%). Similarly, higher rate of acute infection was found in patients than in controls (16.3% versus 5.5%). By focusing on subjects testing positive at 1:16, acute infection was detectable in 23.2% of CAP cases, compared with 8.8% of seropositive controls. Chlamydial DNA was confirmed in 8.2% and 8.8% of nasopharyngeal specimens from controls and patients, respectively. Moreover, 10.9% and 7.5% of Buffy coats from controls and cases, respectively, were PCR-positive. When performances of both assays for detection of the pathogen were assessed, the sensitivities of MIF and PCR were low and comparable. However, MIF demonstrated higher specificity, positive predictive value, and negative predictive value than PCR. Conclusions: MIF-based data indicate that C. pneumoniae could be a potential causal agent of CAP in Jordan. This study may serve as a basis to elucidate the exact role C. pneumoniae and other co-infecting pathogens in the etiology of respiratory tract disease.

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Seroepidemiology of Chlamydia pneumoniae TWAR Infection in Seattle Families, 1966-1979

Cited by 161 publications

References 9 publications

From the authors

From the authors

Randomized Secondary Prevention Trial of Azithromycin in Patients With Coronary Artery Disease and Serological Evidence for Chlamydia pneumoniae Infection

Role of Chlamydia pneumoniae in community-acquired pneumonia in hospitalized Jordanian adults

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