Viral and Bacterial Infections With IPF Greatly Raise Risk of Death

Vanda Pinto, PhD avatar

by Vanda Pinto, PhD |

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Joint infection with a virus and bacteria in people with idiopathic pulmonary fibrosis (IPF) significantly raises their risk of dying — by more than eight times — relative to patients with no such infections, a study reported.

Viral plus bacterial infections were linked to acute exacerbations and disease progression in these people.

The study, “Bacterial and viral coinfection in idiopathic pulmonary fibrosis patients: the prevalence and possible role in disease progression,” was published in the journal BMC Pulmonary Medicine.

Several factors, including smoking and infections, are known to trigger the development of IPF, characterized by scarring, or fibrosis, in the lungs. However, the specific mechanisms that cause IPF or lead to its progression are not fully known.

Recent studies report an elevated mortality risk in IPF patients with a greater bacterial load in their bronchoalveolar lavage (BAL) fluid, collected after washing the lungs with a saline solution during a bronchoscopy. This procedure allows clinicians to examine a patient’s airways with the help of a lighted flexible tube.

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Research has also “demonstrated a role for a number of viruses in [IPF] initiation and progression,” the study noted.

How a simultaneous viral and bacterial infection affects IPF patients, however, has never been evaluated.

An international team of scientists with the Kermanshah University of Medical Sciences in Iran, Trinity College Dublin in Ireland, and the Karolinska Institute in Sweden investigated the prevalence of viral and bacterial infections in IPF patients, as well as the incidence of such co-infections.

Samples of nasopharyngeal lavage — the fluid collected after rinsing the nasal passages and throat — and BAL were obtained from 67 IPF patients between June 2017 and September 2018.

Researchers screened for bacteria known to cause respiratory infections, such as Pseudomonas aeruginosa, Streptococcus pneumoniae, Staphlococcus aureus, Klebseilla pneumoniae, and Haemophilus influenza. The presence of viruses that cause lung infections — namely influenza, parainfluenza, adenovirus, rhinovirus, coronavirus, and respiratory syncytial virus (RSV) — was also assessed.

Participants had a mean age of 62.8 and most, 38 or 56.7%, were men. Most of these patients, 55 or 82.1%, were classified  as having acute exacerbations, or sudden episodes of symptom worsening, while the remaining 12 (17.9%) were stable.

Forty of the 67 samples were positive for both viral and bacterial infection, with rhinovirus (39.7%) and H. influenza (46%) detected at the highest rates.

“A significantly greater percentage of coinfected IPF patients (55%) were found to be in the [acute exacerbation] phase of disease compared with non-infected patients (0%). This suggests that virus and bacterial coinfection led to an increase in the severity of the disease,” the researchers wrote.

All these patients were diagnosed with chronic pneumonia in recent years, and were classified as having moderately severe disease at the time of study enrollment. Among acute exacerbation patients, 16.3% had symptoms suggestive of viral infection, such as fever, muscle aches, and pain.

Several lung function parameters were analyzed, including the carbon monoxide diffusing capacity (DLCO), forced vital capacity (FVC), and forced expiratory volume in 1s (FEV1). DLCO measures the lungs’ ability to transfer oxygen to the bloodstream, while FVC determines the total amount of air a person is able to exhale after taking a deep breath. FEV1 indicates the volume of air that can be forcibly exhaled in one second.

IPF patients with co-infections were seen to have lower FVC and DLCO values, meaning poorer lung function, compared with non-infected patients. No difference in FEV1 values was evident between the two groups.

Researchers, who followed these people for five years, also reported a significantly greater number of co-infected IPF patients dying (37.5%) during those years than non-infected patients (0%). Survival time from diagnosis also significantly differed between these groups, with non-infected patients living a median of 42.5 months and co-infected patients a median of 32.9 months.

Using statistical analysis, the researchers determined that IPF patients who had co-infections had a slightly more than eight times greater risk of death that non-infected patients.

A significant decline in FVC values — reflecting declining lung function — was seen in IPF patients with bacterial infections, viral infections, and co-infection over the study’s years compared with non-infected patients. This decline was also significantly greater in co-infected patients than in those with bacterial or viral infections only.

“These results suggest that the status of co-infection in IPF patients may be a good prognostic factor for accelerated disease progression,” the researchers wrote. They also “suggest that the use of antiviral and/or antibacterial therapies may be useful in treating disease progression in co-infected IPF patients.”

They concluded that this work “demonstrated that the coinfection is significantly associated with an enhanced risk of death by [acute exacerbation] in IPF” and supports “bacterial and viral co-infection as novel prognostic marker” in disease treatment.

Researchers highlighted that further analyses are needed to confirm these findings.