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Noninvasive Sampling of Mucosal Lining Fluid for the Quantification of In Vivo Upper Airway Immune-mediator Levels
Published on: August 7, 2017
Microbiological profile of adenoid hypertrophy correlates to clinical diagnosis in children
Anita Szalmás1, Zoltán Papp, Péter Csomor
1Department of Medical Microbiology, Medical and Health Science Center, University of Debrecen, Nagyerdei Krt. 98, Debrecen 4032, Hungary.
Insights
Bacterial biofilms in adenoids are linked to recurring acute otitis media (RAOM) in children. Persistent human bocavirus (HBoV) in adenoids is associated with otitis media with effusion (OME).
Area of Science:
- Pediatric Otolaryngology
- Infectious Diseases
- Immunology
Background:
- Adenoid hypertrophy is common in children and linked to recurring acute otitis media (RAOM), otitis media with effusion (OME), and obstructive sleep apnea syndrome (OSAS).
- Clinical presentations of these conditions overlap but may stem from distinct immunologic and infectious profiles.
- Histopathologic findings in adenoid specimens can vary based on these underlying factors.
Purpose of the Study:
- To investigate the distinct immunologic and infectious profiles associated with different clinical manifestations of adenoid hypertrophy.
- To correlate histopathologic findings in adenoid tissue with specific clinical outcomes such as RAOM, OME, and OSAS.
- To identify potential microbial culprits, including bacterial biofilms and respiratory viruses, contributing to these pediatric conditions.
Main Methods:
- Adenoidectomy specimens from 59 children with adenoid hypertrophy were analyzed.
- Specimens underwent hematoxylin-eosin (H.E.) and Gram staining for histopathology and bacterial detection.
- Real-time PCR was employed to detect specific respiratory viruses in the adenoid tissues.
Main Results:
- Patients were categorized into RAOM (n=25), OME (n=19), and OSAS (n=15) groups.
- Bacterial biofilms were found in 21 cases, significantly associated with RAOM (n=20, P < 0.001).
- OME cases showed no bacterial biofilms, normal mucosa, and a strong correlation with human bocavirus (HBoV) detection (P < 0.001).
Conclusions:
- Bacterial biofilms in adenoids may cause respiratory epithelium damage and recurring acute infections leading to RAOM.
- Persistent respiratory viruses, particularly HBoV, in OME cases might induce lymphoid hyperplasia, causing ventilation issues and impaired middle ear immunity.
- Understanding these distinct microbial and viral associations is crucial for targeted management of adenoid hypertrophy-related pediatric conditions.
Objective:
Adenoid hypertrophy is a common condition in childhood, which may be associated with recurring acute otitis media (RAOM), otitis media with effusion (OME), and obstructive sleep apnea syndrome (OSAS). These different clinical characteristics have some clinical overlap; however, they might be explained by distinct immunologic and infectious profiles and result in various histopathologic findings of adenoid specimens.
Methods:
A total of 59 children with adenoid hypertrophy undergoing adenoidectomy were studied. Three series of identical adenoid specimens were processed to hematoxylin-eosin (H.E.) and Gram staining and to respiratory virus specific real-time PCR, respectively.
Results:
According to the clinical characteristics, patients were recruited into three groups: RAOM (n = 25), OME (n = 19), and OSAS (n = 15). Bacterial biofilms were detected in 21 cases, while at least one of the studied respiratory viruses was detected in 52 specimens. RAOM cases were significantly associated with biofilm existence (n = 20, P < 0.001). In contrast, OME group was characterized by the absence of bacterial biofilm and by normal mucosa. Showing a statistically significant correlation, all OME cases were positive for human bocavirus (HBoV, P < 0.001).
Conclusions:
Bacterial biofilms might contribute to the damage of respiratory epithelium and recurring acute infections resulting in RAOM. In OME cases persisting respiratory viruses, mainly HBoV, can cause subsequent lymphoid hyperplasia leading to ventilation disorders and impaired immunoreactivity of the middle ear cleft.
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