Chronic rhinosinusitis and antibiotics: the good, the bad, and the ugly.

Background: Despite the recognition that bacteria are universally present in the sinuses of patients with chronic rhinosinusitis (CRS) no compelling role for a primary infectious etiology of CRS has been elucidated. CRS is a constellation of inflammatory diseases that typically involve either noneosinophilic or eosinophilic processes, distinct conditions that must be treated individually. Methods: The bacteria that are present in the sinuses may be innocuous bystanders but alternatively may contribute to the presence and severity of the disease through their ability to influence immune responses, function as immune adjuvants, provide antigens or superantigens that contribute to adaptive immune activation, or in forming the basis for the frequent acute superinfections. However, those bacteria that do contribute to the persistence and severity of CRS primarily reside in biofilms, and, as such, are not capable of being eradicated with antibiotics at the doses at which they can be used, even when local irrigation is considered. Results: Biofilms create an inhospitable environment for antibiotic potency by down-regulating the metabolic activity of their “core” bacteria, decreasing the oxygen concentration, and altering the pH at the core of the biofilm. Conclusion: Ultimately, if topical antibiotics are considered, they should be primarily focused on treating acute exacerbations and choices of antibiotics should optimally be based on endoscopic culture. This should be done with the recognition that while under certain circumstances antibiotics can ameliorate the severity of CRS, even if bacterial eradication were possible, this would not eliminate the underlying primary pathogenic mechanism or the natural history of these conditions. (Am J Rhinol Allergy 27, 467–472, 2013; doi: 10.2500/ajra.2013.27.3960) C hronic rhinosinusitis (CRS) is a constellation of common and debilitating diseases affecting nearly 14.2% of the U.S. population.1 Historically, these diseases have been primarily categorized into two groups: CRS with nasal polyps (CRSwNPs) and CRS without NPs, reflecting the recognition that CRSwNPs is more prominently associated with eosinophilia. However, noneosinophilic pathogenic sinus disease is recognized to produce NPs and, similarly, not all patients with eosinophilic sinusitis have NPs (at least at the time they present). Insofar as noneosinophilic and the various eosinophilic presentations of CRS have distinct pathogenic mechanisms, for the purpose of this study, we will primarily focus on the pathology-based terms noneosinophilic and eosinophilic CRS with the recognition that the former comprises most of the CRS without NP and the latter most of the CRSwNP subjects.2,3 Eosinophilic sinusitis comprises at least two conditions, including aspirin-exacerbated respiratory disease (AERD) and, most commonly, chronic hyperplastic eosinophilic sinusitis (CHES). CHES is a disease of the upper respiratory tract that mirrors the disease of the lower airways that is often concomitantly expressed in these patients— asthma.4 It is a classically Th2-mediated condition with high levels of interleukin (IL)-4, IL-5, IL-13, and other cytokines and chemokines that together drive the influx of eosinophils into the tissues, cause allergic (IgE) sensitization, and drive goblet cell metaplasia.5–7 In addition to their