Seventeen Years of Ear Infection Data Reveal Alarming Rise in Antibiotic Resistance

Chronic suppurative otitis media, a persistent and often disabling infection of the middle ear, has quietly become a testing ground for one of medicine’s most consequential questions: how quickly can bacterial pathogens adapt to the drugs we throw at them, and what does that adaptation mean for the way doctors treat ordinary patients? A new retrospective study spanning seventeen years of clinical practice at a tertiary referral center in Turkey offers one of the longest continuous pictures yet of the microbial landscape inside chronically discharging ears, and its findings are a sobering reminder that treatment guidelines written for yesterday’s bacteria may already be obsolete.

The research, published in BMC Infectious Diseases by a team led by Mehmet Aslan of Inonu University Faculty of Medicine in Malatya, together with colleagues including Yusif Hajiyev of the University of Texas Medical Branch in Galveston, analyzed 595 ear cultures taken from patients with chronic suppurative otitis media between 2009 and 2025. Of those samples, 427 yielded identifiable pathogens, providing a rich dataset that the investigators stratified in two ways: by age, comparing pediatric patients aged sixteen or younger with adults, and by the presence or absence of cholesteatoma, an abnormal skin growth that can invade the middle ear and remodel its local environment.

The headline organisms were unsurprising to anyone who follows ear infections. Pseudomonas aeruginosa, a notoriously hardy Gram-negative bacterium that thrives in moist, inflamed cavities, accounted for 29.5 percent of isolates, making it the single most common pathogen in the cohort. Staphylococcus aureus, the versatile Gram-positive coccus responsible for a vast range of human infections, came second at 21.3 percent. But the third-place finisher deserves attention: fungal pathogens, primarily species of Aspergillus, made up 11.2 percent of the positive cultures, a substantial share that underscores how often chronically inflamed ears become colonized by opportunistic molds rather than bacteria alone.

Age mattered more than the researchers might have expected. Adults produced a positive culture in 84.3 percent of sampled cases, compared with just 69.3 percent among pediatric patients, a statistically significant difference with a p-value of 0.002. The reasons are not fully resolved by the study, but the gap suggests that the microbial ecology of a child’s chronically draining ear differs in meaningful ways from an adult’s, whether because of differing immune responses, prior antibiotic exposure, or the natural history of the disease itself. For clinicians, it is a caution against assuming that culture results and treatment responses in children will mirror those seen in grown-ups.

The most striking stratification, however, involved cholesteatoma. This keratinizing squamous epithelial growth, which behaves in some ways like a slowly expanding tumor of skin trapped inside the middle ear, turned out to act as what the authors describe as a distinct pathological modulator of the microbial flora. Aspergillus species were significantly more prevalent in ears without cholesteatoma, appearing in 13.5 percent of non-cholesteatoma cultures but only 2.2 percent of cholesteatoma cases, a difference the researchers confirmed with Fisher’s exact test at p = 0.001. Conversely, Escherichia coli, an enteric bacterium not classically associated with ear disease, was significantly overrepresented in cholesteatoma cases, at 10.8 percent versus 4.5 percent in non-cholesteatoma ears, with p = 0.041.

That E. coli association is biologically intriguing. Cholesteatoma creates a protected, keratin-rich niche where ordinary defenses are disrupted, and the presence of a gut-associated organism hints at altered colonization dynamics, possibly involving local anatomical changes, Eustachian tube dysfunction, or biofilm communities that differ fundamentally from those in straightforward chronic otitis. Whatever the mechanism, the practical implication is clear: the presence of cholesteatoma should change a clinician’s mental model of which pathogens are likely, and therefore which empirical therapy is rational, before any culture result comes back from the laboratory.

The temporal analysis is where the study delivers its most alarming message. The investigators divided the seventeen-year window into three periods and tracked resistance of Pseudomonas aeruginosa to imipenem, a carbapenem antibiotic often held in reserve as a last reliable option for serious Gram-negative infections. In the 2009 to 2014 period, the point estimate for imipenem resistance was 5.9 percent. Between 2015 and 2019, it fell to zero percent in the sampled isolates. Then, in the 2020 to 2025 period, it jumped to 33.3 percent. Comparing the first and last periods yields a statistically significant difference, with p = 0.021, although the authors are careful to note that the wide confidence intervals in the earlier years, when sample sizes were smaller, demand cautious interpretation of the exact trajectory.

Even more troubling is the picture with ciprofloxacin, the fluoroquinolone that forms the backbone of topical therapy for chronic suppurative otitis media worldwide. Resistance was alarmingly high across the board: 69.6 percent of Pseudomonas aeruginosa isolates, 78 out of 112 tested, were resistant, and the same held for E. coli, where 18 of 26 isolates, or 69.2 percent, resisted the drug. Because fluoroquinolone ear drops are the standard first-line empirical treatment for discharging ears in much of the world, a resistance rate approaching seventy percent in the dominant pathogen effectively undermines monotherapy as a reliable strategy. The authors conclude, based on systemic breakpoint testing, that standard empirical topical fluoroquinolones may be unreliable as sole treatment in their setting.

It is worth pausing on what breakpoint testing means, because it anchors the study’s clinical argument. When a laboratory tests an isolate, it measures the minimum inhibitory concentration, or MIC, the lowest drug concentration that stops bacterial growth. That number is then compared against clinical breakpoints, thresholds established by regulatory and microbiological bodies that translate laboratory values into predictions of therapeutic success at achievable drug exposures. When the authors say that breakpoint data suggest fluoroquinolone monotherapy may fail, they are not making a speculative laboratory observation; they are reporting that the measured MICs of circulating strains exceed the concentrations at which the drugs are expected to work in patients. That distinction matters, and it is what elevates the finding from an academic curiosity to a treatment-guideline problem.

The study has the limitations inherent to its design. It is retrospective, drawing on patient files at a single tertiary referral center, which means the cohort may overrepresent complicated or treatment-refractory cases and may not reflect community-level disease. Culture-based microbiology misses organisms that are difficult to grow, and the fungal fraction in particular may be underestimated or shaped by sampling practices. The imipenem resistance trend, while statistically significant at its endpoints, rests on period-level comparisons whose early-period confidence intervals are wide enough that the authors themselves urge restraint in over-reading the year-by-year swing. Ethics approval was obtained from the Inonu University Ethics Committee, informed consent was waived given the retrospective design, and the work was supported by the university’s individual research project unit under open access publication support, project number TSA-2026-5033.

Yet even with those caveats, the seventeen-year arc tells a coherent and uncomfortable story. The core etiology of chronic suppurative otitis media has not changed: Pseudomonas aeruginosa and Staphylococcus aureus remain the primary culprits, just as they were when the first cultures were drawn in 2009. What has changed is the pharmacological terrain. Resistance to carbapenems, drugs that were once dependable, has emerged in a substantial fraction of recent isolates, and fluoroquinolone resistance has reached levels that call routine monotherapy into question. Meanwhile, cholesteatoma has been shown to reshape the microbial community in ways that are statistically robust and clinically actionable, shifting the expected balance between fungi and enteric bacteria depending on whether the growth is present.

The authors’ prescription is dynamic rather than static: therapeutic protocols, they argue, must be continuously adapted to regional temporal trends and to individual cholesteatoma status, rather than relying on fixed empirical regimens. In practice, that means clinicians treating chronically discharging ears should obtain cultures early, interrogate local antibiograms rather than assuming national or international norms, and consider combination or culture-directed therapy where fluoroquinolone resistance is prevalent. It also means that surveillance studies of this kind, unglamorous as they are, function as early-warning systems. A thirty-fold rise in carbapenem resistance point estimates within a single decade, even with statistical caveats, is the kind of signal that health systems ignore at their peril, whether the battlefield is the middle ear or the intensive care unit.

Subject of Research: Long-term microbial shifts and antibiotic resistance in chronic suppurative otitis media and the modulating role of cholesteatoma

Article Title: A 17-year longitudinal analysis of microbial shifts and resistance profiles in chronic suppurative otitis media: the modulating role of cholesteatoma

Article References: A 17-year longitudinal analysis of microbial shifts and resistance profiles in chronic suppurative otitis media: the modulating role of cholesteatoma. (n.d.). https://doi.org/10.1186/s12879-026-14592-w

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14592-w

Keywords: chronic suppurative otitis media, cholesteatoma, Pseudomonas aeruginosa, Staphylococcus aureus, antimicrobial resistance, ciprofloxacin resistance, imipenem resistance, Aspergillus, Escherichia coli, ear infections, fluoroquinolones, longitudinal study