The Microbiology of Acute Exacerbations in Chronic Rhinosinusitis - A Systematic Review

Abstract

BackgroundAcute exacerbations (AE) in chronic rhinosinusitis (CRS) are a common and important clinical issue. However, relatively little is known regarding the underlying microbiology that drives exacerbations or how it relates to the microbiome of CRS. The purpose of this study is to examine the literature to characterize the microbiome associated with acute exacerbations in a chronic rhinosinusitis setting. Understanding this disease process may facilitate targeted antibiotic therapy, reduced antibiotic resistance, and offer more effective disease control and treatment efficacy.ObjectiveTo characterize the microbiome associated with acute exacerbations of chronic rhinosinusitis (AECRS).MethodsWe conducted a systematic review of the literature on Medline, Embase, and Web of Science databases from January 1990-June 2021 to identify studies related to AE in CRS. Exclusion criteria include non-English, non-human studies, and case reports. Studies without culture or PCR data were also excluded.ResultsFourteen studies were identified which provided detailed data regarding sinus microbiome in AECRS patients. In these patients, a total of 1252 individual isolates were identified. While common acute pathogens were identified in high frequencies in the sinonasal cultures (Staphylococcus pneumonia, Haemophilus influenza), the predominant bacteria were Staphylococcus aureus (including methicillin-sensitive Staphylococcus aureus) and Pseudomonas aeruginosa. Patient characteristics that may represent higher risk phenotypes were not consistently collected in the studies. Discussion of antimicrobial sensitivities and/or resistance were included in 7/14 studies.ConclusionsThis systematic review identifies the predominant microbiology species that may contribute to AECRS. Further studies are needed to understand the pathogenic role of bacteria and viruses in AECRS and to identify associated comorbidities and patient phenotypes that may predispose to AE. The optimal treatment regimen for AECRS remains unclear.

A Novel Model of Staphylococcus aureus-Induced Lymphoplasmacytic Rhinosinusitis in Rats

“…Various studies have linked S. aureus to the CRS pathophysiology, in particular the more severe disease phenotypes [ 6 , 7 ]. S. aureus is the most frequently cultured bacteria in patients with CRS exacerbation [ 8 ] and influences inflammation by disrupting epithelial barrier function, impairing mucociliary clearance and inducing innate and adaptive immune responses, which may result in polyp formation [ 6 ]. Clinically, rhinosinusitis can be classified according to the duration of symptoms, including acute, subacute, or chronic [ 9 , 10 ].…”

Staphylococcus aureus Biofilm-Secreted Factors Cause Mucosal Damage, Mast Cell Infiltration, and Goblet Cell Hyperplasia in a Rat Rhinosinusitis Model

“…Numerous studies have identified Staphylococcus aureus as a potential driver of disease in CRS [ 8 ]. Indeed, S. aureus is often cultured from the sinuses of CRS patients during the exacerbation of the disease [ 9 ]. Furthermore, S. aureus induces the secretion of various cytokines such as thymic stromal lymphopoietin (TSLP), IL-33 and IL-22 in nasal mucosa [ 10 , 11 ].…”

Staphylococcus aureusbiofilm secreted factors cause mucosal damage, mast cell infiltration and goblet cell hyperplasia in a rat rhinosinusitis model

“…Numerous studies have associated Staphylococcus aureus as a potential driver of disease in CRS (Vickery, Ramakrishnan, & Suh, 2019). Indeed, S. aureus is often cultured from the sinuses of CRS patients during the exacerbation of the disease (Okifo, Ray, & Gudis, 2022). Furthermore, S. aureus induces secretion of various cytokines such as thymic stromal lymphopoietin (TSLP), IL-33 and IL-22 in nasal mucosa (Lan et al, 2018;Mulcahy, Leech, Renauld, Mills, & McLoughlin, 2016).…”