Bacterial and viral coinfection in idiopathic pulmonary fibrosis patients: the prevalence and possible role in disease progression

Abstract

Background Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial pneumonia of unknown aetiology with a mean survival rate of less than 3 years. No previous studies have been performed on the role of co-infection (viral and bacterial infection) in the pathogenesis and progression of IPF. In this study, we investigated the role of viral/bacterial infection and coinfection and their possible association with pathogenesis and progression of IPF. Methods We investigated the prevalence and impact of bacterial and viral coinfection in IPF patients (n = 67) in the context of pulmonary function (FVC, FEV1 and DLCO), disease status and mortality risk. Using principal component analysis (PCA), we also investigated the relationship between distribution of bacterial and viral co-infection in the IPF cohort. Results Of the 67 samples, 17.9% samples were positive for viral infection, 10.4% samples were positive for bacterial infection and 59.7% samples were positive coinfection. We demonstrated that IPF patients who were co-infected had a significantly increased risk of mortality compared (p = 0.031) with IPF patients who were non-infected [Hazard ratio: 8.12; 95% CI 1.3–26.9]. Conclusion In this study, we report for the first time that IPF patients who were coinfected with bacterial and viral infection have significantly decreased FVC and DLCO (% predicted). Besides, the results demonstrated the increased AE-IPF, increased incidence of death and risk of mortality in infected/coinfected patients compared to non-infected IPF patients.

Hydroxychloroquine on the Pulmonary Vascular Diseases in Interstitial Lung Disease: Immunologic Effects, and Virus Interplay

“…For this cohort study, patients with two or more outpatient visits or one hospitalization for ILD (ICD-9-CM code: 135, 237.7, 272.2, 277.3, 277.8, 500–505, 506.4, 508.1, 508.8, 515–516, 446.21, 446.4, 495, 517.2, 517.8, 518.3, 555, 710, 714.81, 720, 759.5) in the period of 2000 to 2012 were entered into the study. The new virus infection included ICD-9CM: 0.42, 0.53, 070.20, 070.22, 070.30, 070.32, 070.41, 070.44, 070.51, 070.54, 0.75, 078.5, 079.0–079.5, 079.81–079.83, 079.88–079.89, 480, 486–488 [ 7 , 8 , 9 , 18 ]. Patients aged ≥18 years who had a new ILD, or new virus infection were selected for the ILD cohort.…”

“…The primary outcomes were newly diagnosed PVD (ICD-9-CM code 415–417) within 1 year of the new viral infection [ 8 , 18 ]. These virus infections and atherosclerosis may play a critical role in PVD in the ILD cohort.…”

Platelet Activating Factor Receptor and Intercellular Adhesion Molecule–1 Expression Increases in the Small Airway Epithelium and Parenchyma of Patients with Idiopathic Pulmonary Fibrosis: Implications for Microbial Pathogenesis

“…Studies over the years have discovered that IPF patients suffer from respiratoryassociated infections that contribute to worsened disease pathogenesis [15][16][17]. It has been reported that IPF patients have a higher bacterial load in bronchoalveolar lavage (BAL) fluid than healthy or chronic obstructive pulmonary disease (COPD) cohorts [15,16]. The most common bacterial genus in IPF is Streptococcus, Hemophilus, Pseudomonas, Neisseria, and Veillonella [15,16].…”

“…It has been reported that IPF patients have a higher bacterial load in bronchoalveolar lavage (BAL) fluid than healthy or chronic obstructive pulmonary disease (COPD) cohorts [15,16]. The most common bacterial genus in IPF is Streptococcus, Hemophilus, Pseudomonas, Neisseria, and Veillonella [15,16]. Moreover, research has also found that some viruses, namely the human rhinovirus (HRV) and influenza virus, are involved in affecting patients [15,18].…”

“…The most common bacterial genus in IPF is Streptococcus, Hemophilus, Pseudomonas, Neisseria, and Veillonella [15,16]. Moreover, research has also found that some viruses, namely the human rhinovirus (HRV) and influenza virus, are involved in affecting patients [15,18]. A synergy between bacteria and virus has been documented, detailing that it causes superinfections that exacerbate IPF progression, reducing lung function and lowering the survival rate compared to uninfected patients [15].…”