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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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StatPearls [Internet].

Otitis media with effusion.

Frederick T. Searight ; Rahulkumar Singh ; Diana C. Peterson .

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Last Update: May 20, 2023 .

  • Continuing Education Activity

Otitis media with effusion (OME) is a condition in which there is fluid in the middle ear but no signs of acute infection. As fluid builds up in the middle ear and Eustachian tube, it places pressure on the tympanic membrane. The pressure prevents the tympanic membrane from vibrating properly, decreases sound conduction, and therefore results in decreased hearing. This activity reviews the pathophysiology and presentation of otitis media with effusion and highlights the role of the interprofessional team in its management.

  • Describe the risk factors for otitis media with effusion.
  • Explain the presentation of a patient with otitis media with effusion.
  • Summarize the treatment options for otitis media with effusion.
  • Review the importance of improving care coordination among interprofessional team members to improve outcomes for patients affected with otitis media with effusion.
  • Introduction

Otitis media with effusion (OME) is a condition in which there is fluid in the middle ear but no signs of acute infection. As fluid builds up in the middle ear and Eustachian tube, it places pressure on the tympanic membrane. The pressure prevents the tympanic membrane from vibrating properly, decreases sound conduction, and therefore results in a decrease in patient hearing. Chronic OME is defined as OME that persists for 3 or more months on examination or tympanometry, although some clinicians recommend reserving the term ‘chronic otitis media’ for patients in which the tympanic membrane has perforated. [1]

Risk factors for OME include passive smoking, bottle feeding, daycare nursery, and atopy.  [2]  Both children and adults can develop OME. However, the etiology of these populations is different. The Eustachian tube is positioned more horizontally in younger children. As the child develops into an adult, the tube elongates and angles caudally. Therefore, OME is more common in children, and the position of the head at this age can influence the development of OME.  [3]  Children with development anomalies including the palate, palate muscles, decreased muscle tone for palate muscles, or bone development variations are at increased risk of development of OME, e.g., cleft palate, Down Syndrome.  [4]  Beyond these anatomical variations, patients with Downs syndrome can have mucociliary function disorders that increase the risk of developing OME.  [2] [5]

  • Epidemiology

OME is one of the most frequent infectious diseases in children and is the most common cause of acquired hearing loss in childhood.  [6]  The disease commonly affects children between the ages of 1 and 6.  There is a higher prevalence at the age of 2, which drops after the age of 5. OME is more prevalent during the winter months, corresponding to higher patient rates of upper respiratory infections. 

  • Pathophysiology

After an acute otitis media in children, fluid builds up in the middle ear, inhibiting vibration of the tympanic membrane and subsequent transmission of sound into the inner ear. With this deficit, children may have a decreased ability to communicate in noisy environments. The child may show signs of inattention or decreased academic performance.

In patients with large adenoids, the adenoids can obstruct the Eustachian tube resulting in a poorly ventilated middle ear. This type of blockage may result in OME. Because the adenoids are a lymphatic structure, it is possible that they can transmit bacteria into the Eustachian tube and allow the growth of biofilms. Such bacterial growth can cause inflammation that would also facilitate blockage and fluid build-up within the middle ear.

  • Histopathology

The first line of defense in the middle ear is thought to be the mucociliary defense system in the Eustachian tube. Immunoglobulins produced by the mucosa contribute to this defense system. Due to the significant elevation of these immunoglobulins in effusions, these defense systems may be overactive in OME.  [7]

  • Toxicokinetics

Otitis may also be caused by inflammation driven by viruses or allergies. While allergy is a significant risk factor for otitis media, clinical practice guidelines (2004) concluded that there was little evidence to support specific management strategies for allergy-induced OME. However, it is logical to conclude that aggressive treatment of allergic rhinitis may assist patients that develop OME in conjunction with allergies. [8]

  • History and Physical

Hearing loss, although not always present, is the most common complaint in OME patients. Patients or parents of patients may complain of communication difficulties, withdrawal, and lack of attention. During an exam, a clinician may notice impaired speech and language development. Otalgia and earache can be intermittent in these patients. In many instances, they will have the symptom of aural fullness or a sensation that the ear is popping. In adults, OME is more often unilateral. Adult patients may report tinnitus and the sensation of a foreign body in the external auditory canal. In either children or adults, OME commonly occurs concurrently with upper respiratory infections. Therefore, it is good to ask patients about prior or recurrent ear infections, nasal obstruction, and upper respiratory tract infections.

During a physical examination, signs of OME include opacification of the tympanic membrane and loss of the light reflex. There may also be a retraction of the tympanic membrane with decreased mobility. If gross retraction of the tympanic membrane is observed, intervention may be required to prevent the formation of a retraction pocket, such as modified cartilage augmentation tympanoplasty. [9] [1]

Age appropriate audiometry and tympanometry should be tested in patients with otitis media with effusion. A ‘flat’ tympanogram will support a diagnosis of otitis media with effusion.  [10] Hearing can be tested in infants with the use of auditory brainstem responses (ABR). This exam tests the electrical activity of the brainstem to acoustic stimuli. The test detects both the frequency range and sound intensity levels in which the patient’s brain responds. Patients do not need to be able to speak and do not even need to be awake to perform the test. Therefore, it is ideal for children from birth to 5 years of age.  [11]

With older children and adults, although ABR testing can still be performed, it is more common to do a classic audiology exam. This exam consists of playing sounds to the patient’s left and right ears at different tones and intensities. Patients are requested to raise either the right or left hand when they hear a sound in the right or left ears, respectively. Results will identify the frequency range and normal hearing levels of the patient.

Individuals with normal hearing can detect lower frequencies at a lower decibel (i.e., intensity) than higher frequencies, meaning that a normal individual needs a sound to be louder to perceive high frequencies than lower frequencies. During an audiology exam, the range of frequencies that an individual can perceive is plotted on an audiograph. The decibel (dB) range of individuals with OME is decreased in the audiograph. 

Hearing loss levels (reduction in hearing thresholds from normal levels):

  • Slight impairment: 26-40 dB
  • Moderate impairment: 41-60 dB
  • Severe impairment: 61-80 dB
  • Severe hearing loss: 71-90 dB
  • Profound impairment, including deafness: 81 dB or higher. [12]
  • Treatment / Management

Otitis media with effusion generally resolves spontaneously with watchful waiting. However, if it is persistent, myringotomy with tympanostomy tube insertion is considered an effective treatment. [13]  In this treatment, a ventilation tube allows for air entry into the middle ear, preventing the re-accumulation of fluid. After this procedure, many patients do not need additional therapy due to the growth and development of the Eustachian tube angle, which will allow for drainage. The most common complication is the development of persistent otorrhea. Otorrhea is seen in nearly 1 in 6 (16%) of children within 4 weeks of surgery, and in 26% of children during the entire period, the tube is in place.

Adenoidectomy is currently utilized in cases of OME that involve enlarged adenoids and is an important addition to management in patients with OME.  [14]

Childhood hearing loss can affect language development. [15]  Therefore hearing aids may be considered a non-invasive option to treat OME. [16]

Clinician decisions for the correct interventional treatment of OME for a specific patient include a variety of factors.

  • Comorbidities of the patient
  • The severity of hearing loss
  • OME presence unilaterally or bilaterally
  • Effusion duration
  • Age of patient

Social factors

  • Cost to patient
  • Patient’s likelihood of adherence to treatment
  • Familial assistance with treatment

A patient-focused approach should be adopted when assessing hearing disability. How the child is coping socially and at school is more important than the results of audiometry investigations. [17] [18] [19]  Although most OME patients will warrant a conservative management approach as opposed to more invasive interventions, all physical and social factors should be examined to provide a patient-centered treatment plan that optimizes outcomes for the patient. [20] [21] [22]

  • Differential Diagnosis

OME needs to be distinguished from acute otitis media  [23] , and in adults, OME can be caused by a nasopharyngeal carcinoma infiltrating the Eustachian tube.  [24]

  • Surgical Oncology

Although patients with OME may show no signs or symptoms except for the loss of hearing associated with OME, 5.7% of patients develop the OME due to an obstruction caused by a nasopharyngeal carcinoma. Examination of the nasopharynx, as well as the external acoustic meatus, is suggested with OME patients. If abnormalities are observed within the nasopharynx, a biopsy of the postnasal space is suggested.  [25]

  • Radiation Oncology

In patients with nasopharyngeal carcinoma, OME can be induced by radiation treatments. This type of OME may persist over several months.  [26]  More research is needed to determine the risks of developing OME post-radiotherapy and how irradiation dosages may influence this complication.  [27]

  • Pertinent Studies and Ongoing Trials

Several different therapies have been tried to find effective treatment options for OME. The use of oral steroids in children has shown some benefits. However, it is unknown whether these benefits are clinically significant. [28]  Otic drops have also been utilized to maintain tympanostomy tube patency. These trials showed no statistical differences in the occlusion rate between patients that received the drug therapy and control (no drug) conditions. [29]

  • Treatment Planning

OME is most commonly caused by either viral or allergy-related factors, not bacterial infection. Therefore, the use of antibiotics is not recommended. Also, corticoids for the treatment of allergies have not been significantly proven to impact the outcomes of OME in patients. For these reasons, antibiotics and corticoids are not recommended to treat OME. The best practice for OME patients is watchful waiting for three months as a first-line measure. In cases where OME persists, a specialist referral may be made to assess for surgical treatment options. [30]

  • Toxicity and Adverse Effect Management

Ototopical drops can be ototoxic if they enter the middle ear and reach the inner ear. [31]  However, ototopical drops are not routinely used to treat OME.

  • Medical Oncology

Radiotherapy after nasopharyngeal carcinoma can produce various complications. The most common complication is xerostomia (i.e., dry mouth caused by a lack of saliva). In some cases, a persistent OME may develop, facilitating the need for additional therapy or surgical intervention. [31]

Most cases of OME resolve on their own. In persistent cases, the condition impedes a patient's ability to hear. Therefore, communication and socialization can be affected. In young children, hearing deficits can cause learning problems or delayed language development. The impact of OME on these factors has not been fully studied. [32]  Unusual complications of OME include dizziness, behavioral disorders, and clumsiness. [33]

  • Complications

Long-term changes of the middle ear and tympanic membrane may occur with persistent OME, resulting in permanent hearing loss. Ventilation tubes are used to try and prevent these long-term complications. However, even in treated patients, complications such as tympanosclerosis may occur.   [34]

  • Postoperative and Rehabilitation Care

Alongside medical and surgical treatment of OME, Eustachian tube rehabilitation may also be useful in management. Rehabilitation of the Eustachian tube can include muscle strengthening exercises for the tensor veli palatini and levator veli palatini muscles via auto-insufflation, breathing exercises, and education for the improvement of nasal hygiene. [35]

  • Consultations

Contact with a wide range of medical professionals, including audiologists and otolaryngologists, is important in OME to ensure holistic care for these patients.

  • Deterrence and Patient Education

To avoid the potential of ventilation tube complications, many doctors and parents prefer non-invasive therapies, e.g., hearing aid usage. Reassurance and explanation of the ‘watchful waiting’ approach is an important part of management for patients who do not have speech, language, or developmental problems and for those in whom audiometry shows normal hearing. If ‘watchful waiting” is utilized, the patient should be watched closely for changes in symptoms or signs of increased pressure on the tympanic membrane, as rupture would induce a poor prognosis for future hearing in these patients.

Parents of children with recurrent OME should be informed and educated about the anatomy of the middle ear. Clinicians should identify the family activities of the child in relation to the head position (e.g., breastfeeding, sleeping patterns). Manipulation of the head position during these activities may allow for optimal drainage and assist the child in the prevention of subsequent episodes of OME in the future. 

  • Enhancing Healthcare Team Outcomes

Management goals of OME include: eliminating middle ear fluid, improving hearing, and preventing future episodes. In all cases, communication between health care providers, nurse practitioners, patients, and patients' families will assist clinicians to identify optimal treatment plans for patients with OME. 

Children in whom ‘watchful waiting’ is the adopted strategy should be reassessed every 3-6 months until there is a resolution of the effusion or intervention is required. Also, families should be informed about signs and symptoms indicative of progressed pathology. In these instances, subsequent conversations about alterations to the treatment plan may be needed. The outcome for most children is good.

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Acute Otitis Media on Otoscopy. This otoscopic image shows tympanic membrane erythema and bulging, consistent with acute otitis media. Contributed by Wikimedia Commons, B. Welleschik (CC by 2.0) https://creativecommons.org/licenses/by/2.0/

Acute Otitis Media Pathophysiology. This illustration shows the common etiologies and pathophysiology of acute otitis media. Purchased from Shutterstock

Disclosure: Frederick Searight declares no relevant financial relationships with ineligible companies.

Disclosure: Rahulkumar Singh declares no relevant financial relationships with ineligible companies.

Disclosure: Diana Peterson declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

  • Cite this Page Searight FT, Singh R, Peterson DC. Otitis Media With Effusion. [Updated 2023 May 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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  • Clinical Practice Guideline: Tympanostomy Tubes in Children (Update). [Otolaryngol Head Neck Surg. 2022] Clinical Practice Guideline: Tympanostomy Tubes in Children (Update). Rosenfeld RM, Tunkel DE, Schwartz SR, Anne S, Bishop CE, Chelius DC, Hackell J, Hunter LL, Keppel KL, Kim AH, et al. Otolaryngol Head Neck Surg. 2022 Feb; 166(1_suppl):S1-S55.
  • Clinical Practice Guideline: Otitis Media with Effusion (Update). [Otolaryngol Head Neck Surg. 2016] Clinical Practice Guideline: Otitis Media with Effusion (Update). Rosenfeld RM, Shin JJ, Schwartz SR, Coggins R, Gagnon L, Hackell JM, Hoelting D, Hunter LL, Kummer AW, Payne SC, et al. Otolaryngol Head Neck Surg. 2016 Feb; 154(1 Suppl):S1-S41.
  • Clinical practice guideline: Tympanostomy tubes in children. [Otolaryngol Head Neck Surg. 2013] Clinical practice guideline: Tympanostomy tubes in children. Rosenfeld RM, Schwartz SR, Pynnonen MA, Tunkel DE, Hussey HM, Fichera JS, Grimes AM, Hackell JM, Harrison MF, Haskell H, et al. Otolaryngol Head Neck Surg. 2013 Jul; 149(1 Suppl):S1-35.
  • Review Grommets (ventilation tubes) for hearing loss associated with otitis media with effusion in children. [Cochrane Database Syst Rev. 2005] Review Grommets (ventilation tubes) for hearing loss associated with otitis media with effusion in children. Lous J, Burton MJ, Felding JU, Ovesen T, Rovers MM, Williamson I. Cochrane Database Syst Rev. 2005 Jan 25; (1):CD001801. Epub 2005 Jan 25.
  • Review Otitis media with effusion. [Pediatrics. 2004] Review Otitis media with effusion. American Academy of Family Physicians, American Academy of Otolaryngology-Head and Neck Surgery, American Academy of Pediatrics Subcommittee on Otitis Media With Effusion. Pediatrics. 2004 May; 113(5):1412-29.

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Infectious Diseases: A Case Study Approach

2:  Acute Otitis Media

Aimee Dassner; Jennifer E. Girotto

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Chief Complaint

“Increased irritability and right ear pain.”

History of Present Illness

JL is a 22-month-old female who presents to her primary care provider (PCP) with a 2-day history of rhinorrhea and a 1-day history of increased irritability, fever (to 101.5°F per Mom), and right-ear tugging. Mom denies that JL has had any nausea, vomiting, or diarrhea.

Past Medical History

Full-term birth via spontaneous vaginal delivery. Hospitalized at 9 months of age for respiratory syncytial virus–associated bronchiolitis. Two episodes of acute otitis media (AOM), with last episode about 6 months earlier.

Surgical History

Social history.

Lives with mother, father, and her 5-year-old brother who attends kindergarten. JL attends daycare 2 d/wk, and stays at home with maternal grandmother 3 d/wk.

No known drug allergies

Immunizations

Home medications.

Vitamin D drops 600 IU/d

Physical Examination

Vital signs (while crying).

Temp 100.7°F, P 140 bpm, RR 35, BP 100/57 mm Hg, Ht 81 cm, Wt 23.7 kg

Fussy, but consolable by Mom; well-appearing

Normocephalic, atraumatic, moist mucous membranes, normal conjunctiva, clear rhinorrhea, moderate bulging and erythema of right tympanic membrane with middle-ear effusion

Good air movement throughout, clear breath sounds bilaterally

Cardiovascular

Normal rate and rhythm, no murmur, rub or gallop

Soft, non-distended, non-tender, active bowel sounds

Genitourinary

Normal female genitalia, no dysuria or hematuria

Alert and appropriate for age

Extremities

1. Which of the following clinical criteria is not part of the diagnostic evaluation or staging of acute otitis media (AOM) for this patient?

A. Rhinorrhea

D. Contour of the tympanic membrane

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Risk factors for persistent otitis media with effusion in children: a case-control study.

Author information, affiliations, orcids linked to this article.

  • Kim SH | 0000-0002-1694-9435
  • Song CI | 0000-0002-2705-4100
  • Kim YJ | 0000-0002-2832-036X
  • Choi JH | 0000-0003-3284-9407
  • Lee JY | 0000-0003-4172-2766

Yeungnam University Journal of Medicine , 30 Jun 2018 , 35(1): 70-75 https://doi.org/10.12701/yujm.2018.35.1.70   PMID: 31620573  PMCID: PMC6784671

Abstract 

Free full text , risk factors for persistent otitis media with effusion in children: a case-control study, ju yeon lee.

1 Department of Pediatrics, Jeju National University Hospital, Jeju, Korea

Se-Hyung Kim

2 Department of Otorhinolaryngology, Jeju National University School of Medicine, Jeju, Korea

Chan Il Song

Young ree kim.

3 Department of Laboratory Medicine, Jeju National University School of Medicine, Jeju, Korea

Yoon-Joo Kim

4 Department of Pediatrics, Jeju National University School of Medicine, Jeju, Korea

Jae Hong Choi

Otitis media with effusion (OME) is defined as middle ear effusion without acute signs of infection. OME usually resolves spontaneously; however, persistent OME may require the insertion of a ventilation tube. This study investigated risk factors for persistent OME in children who undergo ventilation tube insertion.

Children who were admitted to undergo ventilation tube insertion at Jeju National University Hospital between August 2015 and July 2016 were enrolled as the case group. Healthy children without persistent OME from August 2016 to July 2017 were enrolled as the control group. Baseline characteristics and predisposing factor data were collected using an interview questionnaire. Middle ear fluids were collected from the case group.

A total of 31 patients underwent ventilation tube insertion. The mean age of the case group was 4.53 years, with a male-to-female ratio of 21:10. Twenty-nine (93.5%) children attended a daycare center, and 21 (67.7%) had experience with bottle feeding. Fifteen (48.4%) children in the case group and 3 (9.7%) in the control group first attended a daycare center at <1 year of age (odds ratio=9.96; 95% confidence interval=2.44-39.70; p =0.001). No bacteria were found in middle ear fluid collected from the 31 operated children. Nasopharyngeal bacterial colonization was found in 13 (41.9%) and 17 (54.8%) children in the case and control groups, respectively.

Earlier attendance at a daycare center was the only predisposing factor for ventilation tube insertion in our study. The aseptic nature of middle ear fluids found in children with OME highlights the efficacy of antimicrobial use.

  • INTRODUCTION

Otitis media with effusion (OME) is characterized by a nonpurulent effusion from the middle ear without symptoms such as otalgia or fever. OME is believed to follow an episode of acute otitis media or abnormal Eustachian tube function. Individuals with OME usually exhibit no specific symptoms; the disease is self-limited within approximately 3 months without specific treatment [ 1 ]; however, it does recur in 30-40% of cases [ 2 ].

Some birth cohorts have reported that >90% children experience at least one episode of OME before 4 years of age [ 2 , 3 ]. OME is the most common cause of acquired hearing impairment in children; permanent hearing loss related to otitis media has a prevalence of 2-35 per 10,000. Although symptoms are not severe, the highest incidence of OME occurs during a highly important period of language skill development. Thereafter, periodic hearing tests are essential to preserving hearing ability in OME patients [ 4 ].

The ultimate treatment goal for OME is to mitigate hearing loss. American guidelines recommend that physicians manage children with OME who are not at risk with watchful waiting for 3 months from the date of effusion onset without antimicrobial treatment [ 4 , 5 ]. However, the guidelines also recommend that clinicians offer ventilation tube insertion to children with documented hearing difficulties, structural abnormalities of the tympanic membrane or middle ear, increased risk for speech and/or language difficulties, and/or reduced quality of life in cases of OME lasting ≥3 months [ 5 ].

Predisposing factors for persistent OME that require ventilation tube insertion include: attendance at a day care center, familial history of otitis media, low socio-economic status, tobacco smoke exposure and adenoid hypertrophy [ 6 , 7 ]. Allergic tendency or biofilm formation of nasal colonizing bacteria is suspected to contribute to the pathogenesis of persistent OME [ 8 - 10 ]. Recurrent otitis media is known to be another risk factor for persistent OME. Although the pathogenesis of recurrent otitis media is multifactorial, the invasion of nasopharyngeal colonizing bacteria is believed to be related [ 11 , 12 ]. The most frequent pathogens colonizing the nasopharynx include Streptococcus pneumoniae, Haemophilus influenzae , and Moraxella catarrhalis .

In Korea, the clinical guidelines for pediatric otitis media has been updated [ 13 ]. This domestic guideline recommends the appropriate use of antimicrobials, an indication for ventilation tube insertion, and the importance of hearing tests during treatment for OME, which were not different from other guidelines [ 4 , 13 ]. However, long-term antimicrobial use (>3 months) for the treatment of OME was usually found in the clinical field.

A previous domestic study investigating OME reported risk factors for children undergoing recurrent ventilation tube insertion or ventilation tube insertion for children with craniofacial abnormalities [ 14 ]. We investigated the risk factors for persistent OME in children according to need for middle ear ventilation. Our aim was to determine the relationship between the colonization of bacteria in the nasopharynx and middle ear effusion.

  • MATERIALS AND METHODS

1. Study subjects and design

The present investigation was a prospective case-control study. Children <12 years of age, who were admitted for ventilation tube insertion at Jeju National University Hospital (JNUH) between August 2015 and July 2016, were enrolled as the case group. All participants were enrolled when they were definitively diagnosed with OME by two otolaryngologists. The children were scheduled to undergo middle ear ventilation for persistent OME 3 months after diagnosis, despite previous antimicrobial use. Patients with immunodeficiency disorders or craniofacial abnormalities, such as cleft palate and/or cleft lip, were excluded. However, patients who previously underwent ventilation tube insertion were included.

A group of age- and sex-matched subjects representing the controls was chosen from a group of healthy children without persistent OME, who visited the JNUH between August 2016 and July 2017. Apart from no history of persistent OME, subjects with recurrent acute otitis media were excluded. The present study was approved by the Institutional Review Board of Jeju National University Hospital (IRB No. 2015-05-006). Informed written consent was obtained from all participants before enrollment.

2. Data and specimen collection

Baseline characteristics and predisposing factors for the case and control groups were collected using a questionnaire interview. Investigated factors included: age, sex, familial member, pattern of daycare center attendance, recent history of antimicrobial use, history of breastfeedin, exposure to tobacco smoke in the house and vaccination history. Daycare center attendance was defined as attendance at a daycare center for at least 6 months, or younger subjects who attended a daycare center when enrolled in the study. Breastfeeding was defined in children who were breastfed for at least 2 months, and was distinguished from bottle feeding. History of pneumococcal conjugate and H. influenzae type b vaccination was also examined.

3. Statistical analysis

Statistical analysis was performed using R software version 3.4.3 (R Foundation for Statistical Computing, Vienna, Austria). The relationship between the investigated risk factors and middle ear ventilation tube insertion was analyzed using the chi-square test. Multivariate logistic regression analysis was performed, and the data are expressed as odds ratio (OR) and 95% confidence interval (CI). All tests were two tailed, and p <0.05 was considered to be statistically significant.

A total of 31 patients (21 male, 10 female) underwent ventilation tube insertion. The mean age of the case group was 4.53 years (median age, 4.20 years [range, 0.95-12.00 years]); the mean age of the control group was 4.06 years (median age, 3.88 years [range, 0.74-12.22 years]). In the case group, 26 patients underwent bilateral ventilation tube insertion, and 11 underwent unilateral insertion. There were no complications after the operation. Before the operation, hearing tests, such as tympanometry or pure tone audiometry, were performed in 20 (64.5%) patients. All of them had hearing loss; more specifically, 18 (90%) had 20-40 dB hearing loss, and 2 had <20 dB hearing loss. We determined ventilation tube insertion after counselling in 11 patients who did not undergo a hearing test because the parents complained of middle ear effusion >3 months.

In the case group, 29 (93.5%) children attended a daycare center, which was more than in the control group (n=23); this difference was not statistically significant (OR=5.04; 95% CI=0.98-26.09; p =0.084) ( Table 1 ). However, the number of subjects <1 year of age who attended a daycare center was 15 (48.4%) in the case group, which was significantly more than the number of children in the control group (n=3 [48.4%]); this difference was statistically significant (OR=9.96; 95% CI=2.44-39.70; p =0.001) ( Fig. 1 ). There were more breastfed children in the control group (n=22) than in the case group (n=19) ( p =0.592), and more bottle-fed children in the case group (n=21) than in the control group (n=18) ( p =0.599). However, these feeding habits had no statistically significant influence on ventilation tube insertion for OME ( Table 1 ). Exposure to household tobacco smoke appeared to have no significant effect on persistent OME. Regardless of whether subjects had siblings, there were no differences in the prevalence of persistent OME. In the case group, there were no siblings who underwent ventilation tube insertion.

otitis media with effusion case study

Odds ratio of patient characteristics who underwent ventilation tube insertion. DCC, daycare center; Hib, Haemophilus influenzae type b; PCV, pneumococcal conjugate vaccine.

General characteristics of otitis media in the case and control groups

OR, odds ratio; CI, confidence interval; Hib, Haemophilus influenzae type b; PCV, pneumococcal conjugate vaccine.

Eighteen (58.1%) children in the case group and 16 (51.6%) in the control group were taking antibiotics for persistent OME. Contrary to expectations, no bacteria were isolated from middle ear effusions collected from those who underwent ventilation tube insertion. The positive nasopharyngeal carriage rate was 41.9%(13/31) in the case group: S. pneumoniae (n=6); H. influenzae (n=2); and M. catarrhalis (n=6). In the control group, the nasopharyngeal carriage rate was 54.8%(17/31): S. pneumoniae (n=6); H. influenzae (n=7); and M. catarrhalis (n=5) ( Table 2 ).

Microbiological status of otitis media in the case and control groups

Values are presented as number (%).

This investigation was a prospective study aimed at determining risk factors for ventilation tube insertion for persistent OME that did not spontaneously improve in children. Another goal of this study was to identify the relationship between nasopharyngeal colonizing bacteria and persistent middle ear effusion. Two otolaryngologists with experience in ventilation tube insertion in the middle ear were involved in this study. Indications for ventilation tube insertion were significant hearing loss due to persistent middle ear effusion, and persistent OME >3 months, which was refractory to spontaneous improvement despite of the use of antibiotics.

OME may occur after an upper respiratory tract infection due to poor Eustachian tube function or as a result of recurrent acute otitis media. A major risk factor for developing OME is age because of its direct correlation with the angulation of the Eustachian tube. Other factors reported to increase the risk for developing OME include daycare center attendance, exposure to tobacco smoke, low socio-economic status, shorter duration of breastfeeding, adenoid hypertrophy, and recurrent otitis media [ 6 , 7 , 15 , 16 ].

In our study, children <1 year of age, who attended a daycare center, was the only statistically significant risk factor ( Fig 1 ). Usually, younger children had more respiratory tract infections than adults because of their immature immune system. In addition, daycare center attendance enhances close contact with other children in confined spaces. In the present study, however, daycare attendance regardless of age had no clinically significant association with persistent OME. We speculate that the difference is the diluted result because of high attendance rates at daycare centers in both the case and control groups (52/62 [83.9%]). We did not use data for recurrent otitis media as a risk factor for persistent OME. The recall ability of the patients’ parents regarding the number of episodes or treatment of otitis media was uncertain. Attendance at a daycare center, however, was easy to recall, and this factor was believed to be related to recurrent otitis media. We used this particular questionnaire for our investigation based on previous studies [ 17 , 18 ].

Exposure to household tobacco smoke and breastfeeding were not significant factors for persistent OME. We had no method to quantitatively evaluate the level of smoke exposure or breastfeeding. There was no relationship between bottle feeding and persistent OME. We speculate that this can be explained by the fact that most of our participants combined breast and bottle feeding.

Experts have recommended the use of pneumatic otoscopy or tympanometry to assess OME with hearing loss [ 4 ]. Furthermore, the first-line treatment choice to manage persistent OME in individuals not at risk is watchful waiting for 3 months from the date of effusion onset. This recommendation was applied to children with hearing loss <20 dB. Ventilation tube insertion is the definitive treatment for removing middle ear effusions and an effective method to prevent conductive hearing loss caused by middle ear effusion. Operative methods, such as ventilation tube insertion, are especially recommended when structural damage to the tympanic membrane, tympanosclerosis, cholesteatoma, symptoms of otalgia or vertigo, and hearing loss >40 dB, are found [ 4 , 19 ].

Previous studies have reported that bacterial prevalence in middle ear effusions is 20-50%, although the population was diagnosed as acute otitis media or OME [ 20 - 23 ]. We assumed that some bacteria could be expected to be found in middle ear effusions, and the pathogen could have a relationship with nasopharyngeal colonizing bacteria. However, no bacteria were isolated from any of the 31 middle ear effusion samples collected. This may be explained by the indication for ventilation tube insertion that was applied to the study population, which was different from other studies. Regardless of antimicrobial use in the recent 2 months, the sterile nature of middle ear effusions support no need for antibiotics to treat persistent OME. The American clinical guidelines also made strong recommendations against using systemic antibiotics for treatment OME in children [ 4 ].

Recently, molecular genetic techniques, such as polymerase chain reaction (PCR), have replaced conventional culture methods. Using these recently developed techniques, detection rates of causative pathogens have increased. This methodology has been applied to middle ear fluid specimens [ 24 , 25 ]. However, we could not perform a PCR assay due to a storage problem. In addition, considering the over-detection of inactive bacteria in PCR assays, we focused on living bacteria isolated using conventional culture methods.

The contribution of nasopharyngeal colonizing bacteria to otitis media has been established, and the bacterial pathogens had been studied [ 26 , 27 ]. In our study, there was no difference in antimicrobial use during a recent 2-month period between the case and control groups. However, nasopharyngeal colonization rates in the control group (54.8%) were greater than those in the case group (41.9%). This result suggests that other factors, in addition to nasopharyngeal colonizing bacteria, contribute to persistent OME. We cannot draw definitive conclusions because some patients in the control group visited our hospital complaining of respiratory symptoms.

This study had some limitations, the first of which were the relatively small sample size and its single-center design. Other predisposing factors, such as adenoid hypertrophy and allergic disorders, could not be investigated. If patients who spontaneously improved after the diagnosis of OME were investigated, risk factors for ventilation tube insertion could be more defined. Despite these limitations, this study should prompt clinicians to prospectively investigate risk factors for ventilation tube insertion in patients with OME disease only. Additionally, during the study period, we applied strict indications for ventilation tube insertion while considering the guidelines. We were able to confirm the principle of test hearing loss watching for spontaneous improvement. The sterile middle ear fluid found in children with OME children support the efficacy of antimicrobial use. Earlier attendance at a daycare center was the only statistically significant risk factor and, therefore, should prompt careful consideration before a decision is made to send a child to a daycare center. Future studies investigating OME should further examine the relationship between ventilation tube insertion and antimicrobial use. Furthermore, we believe that molecular-based methods investigating middle ear effusion and nasopharyngeal aspirates are promising research areas to pursue.

  • Acknowledgments

This work was supported by a research grant from Jeju National University Hospital in 2015.

No potential conflict of interest relevant to this article was reported.

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Research Article

Nasal microbial composition and chronic otitis media with effusion: A case-control study

Contributed equally to this work with: Rebecca E. Walker, Carlos A. Camargo Jr., Edwin A. Mitchell

Roles Conceptualization, Data curation, Formal analysis, Funding acquisition, Investigation, Methodology, Project administration, Resources, Software, Validation, Visualization, Writing – original draft, Writing – review & editing

* E-mail: [email protected]

Affiliation Department of Paediatrics: Child and Youth Health, The University of Auckland, Auckland, New Zealand

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Roles Conceptualization, Data curation, Investigation, Methodology, Resources, Software, Writing – review & editing

¶ ‡ These authors also contributed equally to this work.

Affiliation Centre for Longitudinal Research–He Ara ki Mua, Department of Population Health, The University of Auckland, Auckland, New Zealand

Roles Conceptualization, Formal analysis, Methodology, Supervision, Writing – review & editing

Affiliation Department of Emergency Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States of America

Roles Conceptualization, Formal analysis, Methodology, Resources, Supervision, Writing – review & editing

Affiliation Division of Otolaryngology-Head and Neck Surgery, Counties-Manukau District Health Board, Manukau SuperClinic, Manukau City, Auckland, New Zealand

Roles Conceptualization, Methodology, Supervision, Writing – review & editing

Roles Conceptualization, Formal analysis, Methodology, Supervision, Validation, Writing – review & editing

Roles Conceptualization, Formal analysis, Funding acquisition, Methodology, Resources, Supervision, Writing – review & editing

  • Rebecca E. Walker, 
  • Caroline G. Walker, 
  • Carlos A. Camargo Jr., 
  • Jim Bartley, 
  • David Flint, 
  • John M. D. Thompson, 
  • Edwin A. Mitchell

PLOS

  • Published: February 22, 2019
  • https://doi.org/10.1371/journal.pone.0212473
  • Reader Comments

Table 1

Chronic otitis media with effusion (COME) in children can cause prolonged hearing loss, which is associated with an increased risk of learning delays and behavioural problems. Dispersal of bacterial pathogens from the nasal passages to the middle ear is implicated in COME. We sought to determine whether there is an association between nasal microbial composition and COME in children.

A case-control study of children aged 3 and 4 years was conducted. Cases undergoing placement of tympanostomy tubes for COME were compared to healthy controls. Nasal swabs were collected and a questionnaire was administered. The V1-3 region of the 16S rRNA gene was amplified, and sequenced on the Illumina MiSeq.

73 children with COME had a lower Shannon diversity index than 105 healthy controls (1.62 [.80] versus 1.88 [.84], respectively; P = .046). The nasal microbiota of cases and controls differed in composition using Bray-Curtis dissimilarity (p = 0.002). Children with COME had a higher abundance of otopathogens and lower abundance of commensals including alpha haemolytic Streptococci and Lactococcus . Cluster analysis revealed 4 distinct nasal microbial profiles. Profiles that were Corynebacterium -dominated (aOR 4.18 [95%CI, 1.68–10.39], Streptococcus -dominated (aOR 3.12 [95%CI, 1.08–9.06], or Moraxella -dominated (aOR 4.70 [95%CI, 1.73–12.80] were associated with COME, compared to a more mixed microbial profile when controlling for age, ethnicity, and recent antibiotics use.

Conclusions

Children with COME have a less diverse nasal microbial composition with a higher abundance of pathogens, compared to healthy children who have a more mixed bacterial profile with a higher abundance of commensals. Further research is required to determine how nasal microbiota may relate to the pathogenesis or maintenance of COME, and whether modification of the nasal microbiota can prevent or treat children at risk of COME.

Citation: Walker RE, Walker CG, Camargo CA Jr, Bartley J, Flint D, Thompson JMD, et al. (2019) Nasal microbial composition and chronic otitis media with effusion: A case-control study. PLoS ONE 14(2): e0212473. https://doi.org/10.1371/journal.pone.0212473

Editor: Brenda A. Wilson, University of Illinois at Urbana-Champaign, UNITED STATES

Received: August 29, 2018; Accepted: February 4, 2019; Published: February 22, 2019

Copyright: © 2019 Walker et al. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Data Availability: The dataset is available in the SRA repository https://www.ncbi.nlm.nih.gov/bioproject/PRJNA414455/ .

Funding: This work was supported by: REW -The Oticon Foundation (Grant no. 3701863) http://www.oticon.org.nz/ ; REW -CRC Starship Foundation (Grant No. 18071300) https://www.starship.org.nz/ ; REW -Brian Johns Fellowship Trust (Grant no. 4711); EAM -Deafness Research Foundation (Grant no. 2013/08) https://www.nfd.org.nz/ . The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

Introduction

Chronic otitis media with effusion (COME) is diagnosed when fluid gathers behind the tympanic membrane for three months or longer [ 1 ]. The hearing loss associated with COME may impact language acquisition, and increase the risk of learning delays and behavioural problems [ 2 ].

COME has historically been regarded as a sterile inflammatory condition, as pathogens were seldom cultured from effusion in the middle ear (ME). However, with the advent of culture-independent methods, otopathogens have been found in COME as often as in the closely-related condition acute otitis media (AOM) [ 3 , 4 ]. This discrepancy in findings may be explained by bacteria that are less likely to be detected by culture because they are residing in a biofilm state [ 5 ]. The key otopathogens are non-typeable Haemophilus influenzae , Streptococcus pneumoniae , Moraxella catarrhalis , and to a lesser extent Staphylococcus aureus [ 3 ].

While pathogenic bacterial biofilms residing in the ME may be involved in the maintenance of chronic effusion [ 6 ], it is unknown whether the nasal microbiota are also involved. The composition of both commensals and potential pathogens in the nasal microbiota may affect the risk of pathogens spreading to the ME. Commensal bacteria provide resistance against pathogen overgrowth by competing for nutrients and epithelial cell binding sites, producing antimicrobials, disrupting bacterial biofilms, and inducing the host’s immune system [ 7 , 8 ].

Low bacterial diversity in a niche is often a marker of disease [ 9 ] and is associated with AOM [ 10 ]. Higher abundances of Haemophilus , Moraxella , and Neisseria in the nose have also been found to be associated with AOM [ 11 ]. Conversely, lower abundances of Staphylococcus , Corynebacterium , Propionibacterium , Streptococcus (usually not S . pneumoniae ) and Lactococcus have been found in children with AOM [ 10 , 11 ].

There are no published data on associations between nasal microbiota compositions and COME using cluster analysis. Nasal microbiota compositions characterized by Moraxella , Streptococcus , or Haemophilus have been reported to be associated with upper respiratory infection (URI) [ 12 ] asthma [ 13 ], AOM [ 12 ], pneumonia, or bronchiolitis [ 14 , 15 ]. Protective compositions may also be emerging, with those dominated by Staphylococcus , Sphingobium , Corynebacterium , or Dolosigranulum associated with reduced risk of AOM [ 12 ] and asthma [ 16 ].

We investigated whether nasal microbial composition is associated with COME. Commensal bacteria in the nasal passages may protect against otopathogen overgrowth, or ongoing otopathogen overgrowth in the nasal passages may maintain persistence of effusion in the ME. We hypothesized that COME would be associated with a less diverse nasal microbiome; higher relative abundance of the otopathogens H . influenzae , S . pneumoniae , and M . catarrhalis ; and lower relative abundance of the commensals S . epidermidis , Corynebacterium , Propionibacterium , Dolosigranulum , Lactococcus , Lactobacillus , and the alpha haemolytic Streptococci (AHS) spp.

Study design and setting

As previously reported, a case-control study of children aged 3 and 4 years was conducted in Auckland, New Zealand, to compare children with COME to healthy children [ 17 ]. Briefly, recruitment and data collection were conducted between May 2012 and November 2013. Cases were referred for tympanostomy tube placement (TTP), and had a recent medical history of COME and/or signs of COME confirmed by an otorhinolaryngologist during surgery. Controls were selected at random from children enrolled in primary care practices that had referred children for TTP in the previous year. Controls had no medical history of TTP, no episodes of otitis media with effusion (OME) lasting longer than one month in the past year, and never had OME lasting longer than three months. Cases and controls were excluded if they had craniofacial abnormalities or immunodeficiency.

The parent or legal guardian was informed about the study and provided written consent. The study was approved by the Northern X Regional Ethics Committee (reference NTX/11/EXP/027)

Specimen collection

A sterile paediatric FLOQ swab (Copan, California, USA) moistened with sterile saline was inserted into subjects’ anterior nares. The swab was rotated in each nostril three times and placed into a 2ml tube of sterile STGG medium (skim milk, oxoid tryptone soya broth, glucose, and glycerol). Samples were stored at -80°C.

DNA extraction, PCR, library preparation, sequencing, and bioinformatics

DNA was extracted from nasal samples and negative controls using the Qiagen Allprep kit (Qiagen, California, USA). We had 3 negative controls consisting of STGG broth and a swab exposed to the air, STGG broth only, and reagents only. The 16S ribosomal gene was PCR amplified using primers 27F and 534R to target the V1-3 region. Sequencing libraries were generated using the Nextera XT Index kit (Illumina Inc., San Diego. CA, USA) and amplicons sequenced on the Illumina MiSeq. USEARCH 64 (version 7) analysis pipeline was used. For operational taxonomic unit (OTU) assignment the UPARSE algorithm [ 18 ] was followed using a de novo picking approach with OTUs assignment clustered at 97% sequence similarity. Full details of the sample preparation, sequencing and nasal microbiota analysis are provided in Appendix A in S1 File .

Statistical analysis was carried out in R version 3.3.3 ( www.r-project.org/ ) using the Phyloseq [ 19 ], vegan [ 20 ], DESeq2 [ 21 ], and cluster packages [ 22 ].

Downstream analysis

OTUs were filtered to remove contaminants (see Appendix A in S1 File ). OTUs with a total read number less than .005% of total reads and samples containing less than 1000 reads were removed. Additional species-level identification was achieved by aligning representative sequences using the Basic Local Alignment Search Tool (BLAST). Due to the limitations of classification using the 16S rRNA gene, these species identifications are not definitive.

Subject characteristics

Statistical analysis was conducted using JMP 13, SAS Institute Inc., Cary, NC, 1989–2016. Categorical variables were analyzed using a chi-squared test and continuous variables were analyzed using a Student t-test. A P < .05 was considered statistically significant.

Diversity analysis

Alpha diversity was calculated with absolute numbers using the Shannon diversity index in the R vegan package. Beta diversity was assessed with the Bray-Curtis dissimilarity measure. Permutation multivariate analysis of variance (PERMANOVA) using distance matrices was used to assess differences and significance was tested using ADONIS.

Differential abundance

DESeq2 package from R was used for differential abundance analysis with Benjamini-Hochberg adjustment to control for multiple testing. We adjusted for age, ethnicity and antibiotic usage in the past month. A two-tailed P < .05 was considered statistically significant.

OTU presence

For OTUs that were differentially abundant, presence of any reads was compared between cases and controls in JMP 13 using a Chi-square test with Benjamini-Hochberg adjustment, and a two-tailed P < .05 test for statistical significance.

Cluster profiling

OTUs were collapsed at the genus level. To assess nasal microbiota profiles, we partitioned using a medoid clustering approach (PAM) and the Bray-Curtis dissimilarity metric. Number of clusters was selected using the gap statistic [ 23 ]. Using JMP 13, cluster was entered into a multivariable logistic regression model along with age, ethnicity, and antibiotics in the last month, which were identified as potential confounding variables. A two-tailed P < .05 test was considered statistically significant.

Study population

Of 190 subjects who provided nasal samples, 12 were excluded due to having fewer than 1000 reads in total. The subjects whose samples were included did not differ from those whose samples were excluded, in terms of the subject characteristics listed in S1 Table .

As shown in Table 1 , the mean age of the cases was younger than controls, there were more children of Asian ethnicity in the control group than in the case group, and the cases were younger than the controls when they were first given antibiotics. There was no difference between cases and controls for sex, season seen, method of delivery, being fully vaccinated, antibiotic exposure in the last month, attendance at daycare, or having older siblings.

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https://doi.org/10.1371/journal.pone.0212473.t001

Microbiota analysis

A total of 3,606,750 sequences were assembled from pair-end reads across all samples. After filtering and chimera removal, 3,428,213 sequences were assembled into 300 OTUs. The median number of sequences per sample was 21,255 in cases (range 1,011–80,297) and 9,562 in controls (range 1,100–82,013).

OTU9 was classified in Greengenes as Alloiococcus , however the representative sequence matched Dolosigranulum pigrum in BLAST. This is a known misclassification in the Greengenes database. The representative sequence for OTU1 matched Corynebacterium pseudodiptheriticum using BLAST. OTU1 made up 97% of all reads of genus Corynebacterium .

Core microbiome

The core nasal microbiome, defined as those OTUs present in over 80% of all samples, consisted of 16 taxa including Corynebacterium , Moraxella , Streptococcus , unknown Bacilli ( Staphylococcus ), Alloiococcus/Dolosigranulum pigrum , and Neisseria ; see S2 Table .

Shannon diversity index was lower in children with COME than in healthy controls (mean = 1.62 [.80] versus mean = 1.88 [.84] respectively; P = .046); see Fig 1 . Shannon diversity index was also measured using only subjects with the most frequently observed ethnicity (European) due to the strong inverse correlation between COME and Asian ethnicity. In this sensitivity analysis Shannon diversity was also lower in children with COME than in the healthy controls; see Appendix B in S1 File . We also found a significant difference in the microbial composition of children with COME and healthy controls (Bray-Curtis dissimilarity, unadjusted R2 = 0.02, P < .002); see S1 Fig .

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Diversity calculated using absolute abundance. Controls have higher alpha diversity than cases ( P < .046).

https://doi.org/10.1371/journal.pone.0212473.g001

OTUs that were more common in children with COME were OTU3 ( Streptococcus) , OTU4 ( Moraxella) , and OTU6 ( H . influenzae) ( Fig 2 ). Examining their representative sequences on BLAST, OTU3 matched S . pneumoniae ( but also S . mitis at 99%), and OTU4 matched M . catarrhalis ( but also M . caprae at 99%).

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Calculated using R package DESeq2. Log2 fold change from 105 healthy controls to 73 children with chronic otitis media with effusion, controlling for age, ethnicity and recent antibiotic usage.

https://doi.org/10.1371/journal.pone.0212473.g002

All three OTUs that had greater abundance in the cases were also found to be present in a majority of the control samples (see S3 Table ). OTU6 ( H . influenzae) was found in 68% of the cases and 52% of the controls, OTU3 ( Streptococcus ) was found in 99% of the cases and 100% of the controls and OTU4 ( Moraxella ) was found in 92% of the cases and 85% of the controls. No significant differences were observed between detection of these OTUs in cases compared to controls.

Taxa more common in the healthy controls were three Streptococcus OTUs of uncertain species, Streptococcus infantis , Propionibacterium acnes , Lactococcus sp., Neisseria sp., Lautropa sp., Capnocytophaga sp., and two Oxalobacteraceae OTUs.

Cluster profiles

Nasal microbiota clustered into 4 distinct profiles consisting of a Corynebacterium -dominated cluster (40% of case subjects were in this cluster, and 27% of control subjects), S treptococcus -dominated cluster (cases: 19%, controls: 15%), Moraxella -dominated cluster (cases: 27%, controls: 19%), and a mixed profile cluster (cases: 14%, controls: 39%); see Fig 3 . Cluster was not associated with age, ethnicity, or antibiotics in the last month in univariable analyses. In an unadjusted analysis, Corynebacterium -dominated (OR 4.25 [95%CI, 1.84–10.47]), Streptococcus -dominated (OR 3.59 [95%CI, 1.34–9.98]), and Moraxella -dominated (OR 4.10 [95%CI, 1.64–10.72]) profiles were associated with COME, compared to the more mixed microbial profile. When controlling for potential confounders (age, ethnicity, and antibiotics in the last month), the Corynebacterium -dominated (aOR 4.18 [95%CI, 1.68–10.39], Streptococcus -dominated (aOR 3.12 [95%CI, 1.08–9.06]), and Moraxella -dominated (aOR 4.70 [95%CI, 1.73–12.80]) profiles remained associated with COME compared to the mixed profile.

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Profiles were partitioned using a medoid clustering approach (PAM) and the Bray-Curtis dissimilarity metric, based on absolute abundance. Four cluster profiles are indicated: Corynebacterium -dominated profile with prominent Moraxella and Streptococcus (1), Streptococcus -dominated profile (2), mixed profile (3), and Moraxella -dominated profile (4). A heatmap of the 25 most abundant genera is displayed adjacent.

https://doi.org/10.1371/journal.pone.0212473.g003

Our findings that the nasal microbiota of children with COME had lower diversity, higher relative abundance of otopathogens, and a lower relative abundance of commensal bacteria–compared with healthy controls–indicates that the nasal microbiota may be important in initiating or maintaining COME.

Nasal and nasopharyngeal diversity have not previously been examined in OME or COME. Two studies have found low diversity to be associated with AOM [ 10 , 24 ], two have found no association [ 11 , 12 ], and one found that children with AOM had higher diversity [ 25 ]. The association observed between COME and low nasal diversity may reflect well-balanced microbiota exhibiting a higher resilience to infection, however the causal direction of such relationships has not been fully established [ 9 ]. It could equally signify that a bacterial infection that led to COME has also caused an overgrowth of pathogenic bacteria in the nose, which would result in lower alpha diversity by reducing the evenness of bacterial abundance.

A high load of pathogenic bacteria in the nasal passages may increase the risk of movement of those bacteria up the ET to the ME. S . pneumoniae , non-typeable H . influenzae and M . catarrhalis are the three main bacterial pathogens that have been identified in relation to COME [ 26 ], and are commonly detected in the ME effusion of children with COME [ 3 ]. Specific strains of these otopathogens are shared between the nasopharynx and the ME in individuals [ 27 ]. In some animal models, injection of bacteria into the nose results in ME carriage of those bacteria. [ 28 ] Polymicrobial infection further increases the risk of spread to the ME, as shown by nasal challenges using co-infection with multiple bacteria or respiratory viruses [ 29 , 30 ].

We found that children with COME had higher nasal levels of H . influenzae , a Streptococcus OTU matching S . pneumoniae (and S . mitis ), and a Moraxella OTU resembling M . catarrhalis (and M . caprae ). Haemophilus has been found to be differentially abundant in children with recurrent AOM [ 25 ]. This correlation may reflect overgrowth of these pathogens initiating or maintaining COME by spreading to the ME. Although these three OTUs had higher differential abundance in the cases than the controls, they were all present in more than half of the controls. These OTUs may therefore be endogenous pathobionts, common microorganisms of children’s noses that may be disrupted and become infectious due to stimuli such URI [ 9 ]. URI often precedes OM, and can disrupt the airway microbiota. Viruses may promote adherence and virulence of otopathogens [ 31 ] by disrupting the airway epithelial barrier [ 32 ], decreasing mucociliary clearance [ 33 ], inducing the host to supply nutrients to pathogenic bacteria [ 34 ], and provoking biofilms to release virulent dispersed bacteria [ 35 ].

We also found that certain commensal bacteria were more common in controls. These included several AHS spp., a Lactococcus sp., and Propionibacterium acnes . AHS have been reported to help prevent otopathogen infection and OM [ 36 ]. Nasal Lactococcus also has higher relative abundance in healthy children than in children with AOM [ 11 ]. Propionibacteria appear to be protective against S . pneumoniae colonization, URI, and OM, and nasal levels are inversely associated with levels of S . pneumoniae and S . aureus [ 11 , 37 , 38 ].

We report the first cluster analysis of nasal bacterial profile in any OM-related condition. Our observation that a mixed nasal profile was inversely associated with COME compared with profiles dominated by Corynebacterium , S treptococcus , or Moraxella has not previously been reported in relation to OM. This finding may indicate that a more mixed profile is protective against infection. Adult profiles tend to be more mixed, more stable, and more resistant to infection that those of children [ 39 ].

The association between COME and a profile dominated by Corynebacterium was unexpected, as this genus has previously been inversely associated with otitis media [ 25 ]. Nearly all reads of Corynebacterium belonged to an OTU classified in BLAST as Corynebacterium pseudodiptheriticum . This species is an opportunistic pathogen [ 40 , 41 ]. However, it was not differentially abundant in our cases. The association may therefore be due to a higher abundance of S treptococcus and Moraxella in the Corynebacterium -dominated cluster than in the mixed cluster, rather than a direct association with Corynebacterium pseudodiptheriticum itself.

Randomized controlled trials of probiotics have demonstrated that bacterial interference can be successful in reducing nasal colonization with otopathogens to treat URIs and OM in children [ 42 ], although not all trials show a protective effect for every condition [ 43 ]. Such studies support the plausibility of certain microbial compositions, such as the mixed bacterial profile that we observed, helping to protect against disease.

The study has potential limitations. Cases and controls differed by ethnicity, however similar results were found in a sensitivity analysis that examined all major findings in the largest single ethnicity, and when including ethnicity in a multivariable analysis. Limitations of 16S rRNA gene sequencing are that it is unable to distinguish between live and dead microbial DNA, and is poorly suited to distinguishing between many bacteria below the genus level, including genera that include both respiratory pathogens and commensals. We did identify the key otopathogen H . influenzae using 16S rRNA sequencing, however future research using whole genome sequencing would enable more precise differentiation between pathogen and commensal species and strains. We did not include analysis of the virome which may have provided additional clarification. Finally, this case-control study could not investigate the causal direction of the association between COME and nasal bacterial composition, therefore we recommend future longitudinal studies.

The spread of pathogenic bacteria from the nasal passages to the ME may be involved in the pathogenesis of COME. Children with COME had a different nasal microbial profile to healthy controls, with lower diversity, higher abundance of pathogens, and lower abundance of commensals. Pathogens were equally likely to be present in the noses of healthy controls as in children with COME, and may therefore be endogenous pathobionts. Higher abundance of these pathobionts may increase the risk of COME, or help to maintain effusion once established. More research is required to determine the order of events leading to COME. If a more diverse and mixed nasal bacterial composition dominated by commensals proves to be protective against the spread of bacteria to the ME, this may present new opportunities to prevent or treat COME by influencing the microbiota of the nasal passages.

Supporting information

Appendix A. Detailed Methods and Appendix B. Detailed Results.

https://doi.org/10.1371/journal.pone.0212473.s001

S1 Table. Comparison of characteristics of participants whose nasal samples were included in the analysis with those that had unusable samples, with Benjamini-Hochberg adjustment.

https://doi.org/10.1371/journal.pone.0212473.s002

S2 Table. The core microbiome of 73 children with chronic otitis media with effusion and 105 healthy controls.

https://doi.org/10.1371/journal.pone.0212473.s003

S3 Table. Presence of differentially abundant operational taxonomic units in 73 samples with chronic otitis media with effusion and 105 healthy controls, with Benjamini-Hochberg adjustment.

https://doi.org/10.1371/journal.pone.0212473.s004

S1 Fig. Non-metric multidimensional scaling (NMDS) ordination plot of Bray–Curtis community dissimilarities of OTUs for children with chronic otitis media with effusion and healthy controls, with variance stabilizing transformation to correct for difference in sequencing depth.

https://doi.org/10.1371/journal.pone.0212473.s005

Acknowledgments

We would like to thank Ann Paddy, DHSc, who administered the questionnaires and performed part of the physical examinations for the children involved in the study. Dr. Rinki Murphy reviewed the manuscript and provided statistical advice. We would like to acknowledge the staff at Waitakere and North Shore Hospital, Bede Saldanha and Denise Burdett for going above and beyond reception support, and especially ear nurse specialist Barbara Middleton. Finally, a thank you to the families and their general practitioners whose help and support made the study possible.

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INTRODUCTION  —  Acute otitis media (AOM) is primarily an infection of childhood and is the most common pediatric infection for which antibiotics are prescribed in the United States [ 1,2 ]. The vast majority of the medical literature focuses on the diagnosis, management, and complications of pediatric AOM, and much of our information of AOM in adults is extrapolated from studies in children.

This topic will address the etiology, diagnosis, and treatment of AOM in adults. Issues related to AOM and other common middle ear pathology in children are discussed separately. (See "Acute otitis media in children: Clinical manifestations and diagnosis" and "Acute otitis media in children: Epidemiology, microbiology, and complications" and "Acute otitis media in children: Treatment" and "Otitis media with effusion (serous otitis media) in children: Clinical features and diagnosis" and "Otitis media with effusion (serous otitis media) in children: Management" .)

Evaluation and management of chronic otitis media (COM) in adults are also discussed separately. (See "Chronic otitis media and cholesteatoma in adults" .)

DEFINITION  —  Acute otitis media (AOM) is an acute, suppurative infectious process marked by the presence of infected middle ear fluid and inflammation of the mucosa lining the middle ear space ( picture 1 ). The infection is most frequently precipitated by impaired function of the Eustachian tube, resulting in the retention and suppuration of retained secretions ( figure 1 ). AOM may also be associated with purulent otorrhea if there is a ruptured tympanic membrane. AOM usually responds promptly to antimicrobial therapy.

EPIDEMIOLOGY OF ACUTE OTITIS MEDIA  —  Acute otitis media (AOM) occurs much more commonly in children than in adults. The overall incidence of AOM has decreased over the last several decades.

Most cases of AOM occur in young children ages 6 to 24 months, with the incidence of AOM declining significantly after age 5 [ 1,3 ]. A 2005 global disease burden modeling-based study estimated the annual incidence of AOM as follows: children under age 5 years, 45 to 60 percent; children aged 5 to 14 years, 19 to 22 percent; children and adults aged 15 to 24 years, 3.1 to 3.5 percent; and adults aged 25 to 85 years, 1.5 to 2.3 percent [ 4 ]. The incidence of AOM among adults in resource-rich countries is likely less than 1 percent based upon data from this study. In a 2014 to 2018 study of adult outpatient visits to United States veterans administration medical centers, the incidence of AOM and otitis media with effusion (OME) was 2.7 and 1.4 per 1000 person-years, respectively [ 5 ]. In a 2015 to 2018 Netherlands study including patients age ≥15, there was an overall incidence of AOM of 5.3 per 1000 person-years; the incidence declined with age (age 15 to 39, 7.1 per 1000 person-years; age ≥64 years, 2.7 per 1000 person-years) [ 6 ].

The incidence of AOM in children in the United States has fallen over the past two decades. In the United States, both outpatient visits and antibiotic prescriptions for AOM in children under age 5 declined by one-third between 1995 and 2006 [ 7 ]. In addition, there was a downward trend in visits for AOM in children under age 7 from 2001 to 2011, and an especially rapid decline in visits for children under age 2 during 2010 to 2011 [ 8 ].

The introduction of routine pneumococcal vaccination in infants may be a contributor to this decline in incidence. The 7-valent pneumococcal vaccine (PCV7) was introduced in the United States in 2000 and replaced by the 13-valent pneumococcal ( PCV13 ) vaccine in 2010.

The declining incidence in AOM has also been seen other countries, potentially due to the introduction of the pneumococcal vaccine. As an example, in Sweden, following the introduction of general pneumococcal vaccination for infants in 2009, the incidence of AOM declined by 42 percent in children under age 5 and by 21 percent in children ages 5 to 17 [ 9 ]. (See "Pneumococcal vaccination in children" .)

MICROBIOLOGY  —  The majority of data on the microbiology of acute otitis media (AOM) has been documented by cultures of middle ear fluid obtained by needle aspiration (myringotomy) in children, but the microbiology of AOM in adults is similar to that seen in the pediatric population.

In children, the most common bacterial pathogens are Streptococcus pneumoniae and nontypeable Haemophilus influenzae , with Moraxella catarrhalis the third most common bacterial etiology [ 3,10 ]. Globally, S. pneumoniae and H. influenzae combined caused 50 to 60 percent of pediatric AOM cases, while M. catarrhalis was responsible for 3 to 14 percent [ 11 ]. Group A streptococcus and Staphylococcus aureus are less frequent causes of AOM in general pediatric populations, although S. aureus may be a significant pathogen in adults based upon limited studies. Additionally, Group A streptococcus may be an important pathogen in patients with severe AOM requiring hospitalization [ 12,13 ]. Representative studies include:

● A 1991 study of the myringotomy samples of 34 adults with AOM reported the major pathogens to be nontypeable H. influenzae (26 percent), S. pneumoniae (21 percent), M. catarrhalis (3 percent), Group A streptococcus (3 percent), and S. aureus (3 percent) [ 14 ].

● A South Korean study analyzing middle ear fluid from a mixed adult and pediatric population with AOM and spontaneous tympanic membrane perforation revealed the major pathogens to be S. aureus (21 percent, including methicillin-resistant S. aureus [MRSA] in 4 percent), S. pneumoniae (16 percent), Pseudomonas species (8 percent), H. influenzae (5 percent), and Klebsiella (5 percent) [ 12 ]. Coagulase-negative staphylococci were isolated in 24 percent of cultures, however, suggesting possible contamination by ear canal flora.

● In 60 adults with severe AOM requiring hospitalization, almost 50 percent were culture-negative, while culture-positive cases demonstrated Group A streptococcus (15 percent), S. pneumoniae (10 percent), Pseudomonas (8 percent), and S. aureus (5 percent) [ 13 ]. The source of culture (fluid from perforated tympanic membrane versus myringotomy) in this study was not reported.

● Most common causative organisms:

• Streptococcus pneumoniae – S. pneumoniae is one of the most important bacterial causes of AOM. There are no studies of which pneumococcal serotypes are most likely to cause AOM in adults, but in children there has been a detectable shift in causative serotypes since the introduction of the 7-valent and 13-valent pneumococcal vaccines (PCV7 and PCV13 ). (See "Acute otitis media in children: Epidemiology, microbiology, and complications", section on 'Effect of infant immunization' .)

In adults, the Centers for Disease Control and Prevention (CDC) recommends immunization with PCV13 and the 23-valent pneumococcal polysaccharide vaccine (PPSV23) depending on age and/or coexisting medical conditions. Although there are no data evaluating the prevention of AOM by pneumococcal vaccines in adults as there are in children, these vaccines are likely to have some protective effect. Recommendations on vaccine administration in adults are discussed elsewhere. (See "Pneumococcal vaccination in adults" .)

• Haemophilus influenzae – AOM due to H. influenzae in patients of all ages is due to nontypeable strains in the majority of patients [ 14 ]. (See "Epidemiology, clinical manifestations, diagnosis, and treatment of Haemophilus influenzae ", section on 'Nontypeable H. influenzae' .)

• Moraxella catarrhalis – M. catarrhalis is responsible for 3 to 14 percent of AOM in children and is the third most common otopathogen [ 11 ]. High-quality data in adults are more limited, but in one study M. catarrhalis caused 3 percent of adult AOM cases [ 14 ].

• Staphylococcus aureus – AOM due to S. aureus , including methicillin-resistant strains, is uncommon in children. It is possibly more common as a cause of AOM in adults, but the actual incidence is unknown. S. aureus is known to occur in patients with chronic suppurative otitis media (CSOM) and may be associated with persistent otorrhea following insertion of tympanostomy tubes [ 15 ]. (See "Chronic otitis media and cholesteatoma in adults", section on 'Microbiology of chronic suppurative otitis media' .)

• Group A streptococcus – Before antibiotics, Group A streptococcus was a leading cause of AOM and resulted in significant severe middle ear disease, causing frequent perforation of the tympanic membrane and mastoiditis [ 16,17 ]. Group A streptococcus is now an uncommon cause of AOM, although the reason for this is not known [ 18 ]. However, when it occurs, cases of Group A streptococcal AOM in adults may be particularly fulminant and was found to be the most common cause of severe AOM requiring hospitalization in one study [ 13 ].

● Viral pathogens:

• A viral upper respiratory infection is a common predisposing factor for AOM in children, and viruses may coinfect the middle ear along with bacteria [ 19 ]. This is likely true in adults as well, although studies in the adult population are lacking. In children, studies using reverse transcription polymerase chain reaction (RT-PCR) have detected viruses in 11 to 71 percent of the middle ears with AOM; rhinovirus and respiratory syncytial virus were most commonly identified, although parainfluenza, coronavirus, and adenovirus were also occasionally detected [ 20 ]. Since the onset of the coronavirus disease 2019 (COVID-19) pandemic, several studies in adults have reported cases of AOM in patients with COVID-19; in some cases, the causative virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was detected in the middle ear fluid [ 21-23 ].

● Less common or rare causative organisms:

• Mycoplasma pneumoniae – Some patients with lower respiratory tract infection due to M. pneumoniae have concurrent AOM, although the etiologic role of M. pneumoniae in the AOM is uncertain. Studies of M. pneumoniae in adult AOM are lacking. In a Finnish study of children (ages two months to two years) with AOM, 4 percent of middle ear fluid samples tested positive for M. pneumonia, but most (69 percent) of these M. pneumoniae -positive samples also tested positive for a typical AOM pathogen ( M. catarrhalis, S. pneumoniae, H. influenzae ) [ 24 ].

• Rare causes include diphtheritic otitis, tuberculous otitis, and otogenous tetanus, and otitis media due to Chlamydia trachomatis .

PATIENT FACTORS CONTRIBUTING TO THE DEVELOPMENT OF ACUTE OTITIS MEDIA  —  Eustachian tube dysfunction, entities causing Eustachian tube compression or outlet obstruction, or an abnormality of host immunologic response can be a predisposing factor in the development of acute otitis media (AOM).

Eustachian tube dysfunction  —  Eustachian tube dysfunction is the most important factor in the pathogenesis of middle ear infections in both childhood and adulthood ( figure 1 ). Eustachian tube dysfunction induces a relative negative pressure in the middle ear space, with the lack of aeration and accumulation of fluid providing an environment conducive to the development of AOM or otitis media with effusion. Anatomic changes in adolescence, with descent of the soft palate muscle sling relative to the Eustachian tube orifice, improves Eustachian tube patency. This anatomic change contributes to the decline in incidence of AOM with age. However, poor tubal function can persist into adulthood, and AOM can still occur at any age due to Eustachian tube dysfunction. (See "Eustachian tube dysfunction" .)

Eustachian tube obstruction  —  Anything causing external compression of the Eustachian tube, or obstruction of the Eustachian tube or of its outlet, can also predispose to AOM, particularly unilateral AOM. Examples include malignancy (ie, lymphoma, nasopharyngeal carcinoma) and post-radiation fibrosis. (See 'Recurrent acute otitis media' below and "Eustachian tube dysfunction", section on 'Obstructive dysfunction' .)

Immune dysfunction  —  The respiratory mucosal membrane that lines the Eustachian tube, middle ear space, and mastoid air cells presents an immunologic defensive barrier, and any abnormality of this barrier may increase the risk of infection.

In response to any infection, there is an increase in production of mucus (which contains the potent antibacterial enzyme lysozyme) by the respiratory epithelium [ 25 ]. Along with increased mucus production, there is dilatation of mucosal blood vessels, which brings white blood cells and antibodies to the area, all of which contribute to the mucopurulent defensive barrier.

In addition, respiratory epithelium contains motile cilia, which promote the mobilization of secretions. Ineffective mucociliary clearance due to ciliary dyskinesia may impair the normal function of this important host immunologic defense [ 26,27 ]. (See "Primary ciliary dyskinesia (immotile-cilia syndrome)", section on 'Otitis' .)

The incidence of AOM and related complications is increased in children with congenital or acquired immunologic deficiencies, a risk that persists into adulthood [ 25 ]. All major classes of immunoglobulins have been identified in middle ear effusions of patients with AOM, and the presence of type-specific antibodies in these effusions is associated with an earlier resolution of infection. (See "Clinical manifestations, epidemiology, and diagnosis of common variable immunodeficiency in adults", section on 'Sinopulmonary infections' .)

The risks of AOM and its complications are also increased in patients who have a concomitant malignancy, use immunosuppressive drugs, or have a history of previous radiation of the nasopharyngeal region [ 28 ].

PRESENTATION AND DIAGNOSIS  —  It is essential to make an accurate diagnosis of acute otitis media (AOM) to avoid overtreatment with inappropriate antibiotic therapy. Evaluation of the patient's clinical presentation and a careful otoscopic examination are important in making the correct diagnosis.

Clinical manifestations  —  In adults, an upper respiratory tract infection or exacerbation of seasonal allergic rhinitis often precedes the onset of AOM. In adults, AOM is typically unilateral and is associated with otalgia (ear pain) and decreased or muffled hearing. The pain may be mild, moderate, or severe. If the tympanic membrane has ruptured, the patient may report a sudden relief of pain, possibly accompanied by purulent otorrhea.

Dysequilibrium may be present but is described infrequently. Conductive hearing loss, which may occur due to the presence of middle ear fluid, is usually transient.

Other symptoms, such as high fever, severe pain behind the ear, or facial paralysis, suggest unusual complications. (See 'Other possible complications of acute otitis media' below.)

Diagnosis with otoscopy  —  In adults with suspected AOM, the diagnosis is confirmed by the presence of typical features on otoscopic examination ( figure 2 ).

Key features include:

● Bulging tympanic membrane ( picture 1 )

● Reduced mobility of the tympanic membrane when pneumatic pressure is applied (if pneumatoscopy is available)

Other features, which may or may not be present in adults with AOM include:

● Partial or complete opacification of the tympanic membrane

● Erythema of tympanic membrane

Examination with a handheld otoscope is essential for an accurate diagnosis of AOM. The addition of pneumatoscopy allows evaluation of tympanic membrane motion and is therefore also recommended for diagnosis. Otomicroscopy, generally available only in otorhinology specialty practices, permits even greater visualization of the tympanic membrane.

Examination typically demonstrates tympanic membrane bulging, opacification, erythema ( picture 1 ), and poor mobility when pneumatic pressure is applied using a pneumatic otoscope ( movie 1 and picture 2 ). A normal tympanic membrane is translucent ( picture 3 ). By contrast, when there is fluid in the middle ear, the tympanic membrane appears cloudy, yellowish, or opaque. When there is an air-fluid level present, the tympanic membrane appears translucent above and opaque below the line of demarcation ( picture 4 ). If there is an associated tympanic membrane rupture, there may be a visible perforation and possibly purulent material in the ear canal.

Some patients with suspected AOM may have a significant amount of cerumen partially or completely obstructing the ear canal, preventing adequate evaluation of the tympanic membrane. For these patients, we advise cautious removal of the obstructing material with either gentle curettage or aspiration under direct visualization. When AOM is a concern, removal of cerumen via irrigation should always be avoided because of risk of tympanic membrane rupture. If the obstructing cerumen cannot safely be relieved via curettage or aspiration, referral to otorhinology is appropriate.

The predictive value and accuracy of abnormal otoscope findings has been studied in children but has not been reported for adults with AOM [ 29-31 ]. In a pediatric population, the triad of a bulging tympanic membrane, impaired mobility, and redness or cloudiness of the tympanic membrane predicted the diagnosis of AOM, confirmed with myringotomy, in 83 to 99 percent of cases ( table 1 ) [ 31 ]. In another study, a bulging tympanic membrane was more predictive of AOM than a red tympanic membrane [ 29 ].

DIFFERENTIAL DIAGNOSIS  —  The differential diagnosis of acute otitis media (AOM) includes otitis media with effusion (OME) ( figure 2 ), chronic otitis media (COM), external otitis (otitis externa), herpes zoster infection, and other deep space head and neck infections.

Otitis media with effusion  —  An entity that is commonly clinically misidentified as AOM in adults is OME ( figure 2 ). OME is defined by the presence of middle ear fluid without acute signs of bacterial infection or illness. OME can result from recent viral infection, barotrauma, or allergy and may precede or follow an episode of AOM. Eustachian tube dysfunction is often a predisposing factor. Rarely, OME is caused by obstruction of the Eustachian tube orifice in the nasopharynx by a mass such as nasopharyngeal carcinoma or other cancer, or as a result of radiation treatment for nasopharyngeal malignancy. Thus, any case of recurrent, unilateral otitis media with effusion warrants nasopharyngoscopy and possibly computed tomography (CT) to rule out obstructive pathology. (See "Eustachian tube dysfunction" and "Eustachian tube dysfunction", section on 'Obstructive dysfunction' .)

OME is often characterized by a temporary conductive hearing loss and a sense of aural fullness. If the effusion becomes chronic, it may be a precursor to tympanic membrane retraction and perforation.

Otoscopic findings of OME include visible fluid (often yellowish, but sometimes clear) behind an intact tympanic membrane. For patients with longstanding Eustachian tube dysfunction, the tympanic membrane may also be retracted. A normal tympanic membrane is shown in a photograph ( picture 3 ) compared with a retracted tympanic membrane ( picture 5 ). Viscous bubbles may also be seen behind the tympanic membrane, particularly during pneumatic otoscopy. Pneumatic otoscopy reveals reduced mobility of the ear drum when there is fluid in the middle ear. The tympanic membrane may even appear mildly erythematous in OME.

In patients with symptoms of ear fullness associated with hearing loss in whom direct examination of the tympanic membrane is difficult or limited, referral for audiometry and tympanometry is appropriate. In patients with symptoms due to OME, audiometry will reveal a mild to moderate conductive hearing loss, and tympanometry will be abnormal ( figure 3 ). If sensorineural hearing loss is identified on audiometry, patients should be referred to otolaryngology.

In the majority of cases, OME resolves without treatment within 12 weeks. In a small percentage of cases, the effusion persists and requires additional intervention, such as pressure equalization tubes.

● For patients who are minimally or mildly symptomatic (with intermittent aural fullness, no or minimal discomfort, and no or minimal conductive hearing loss), no treatment other than reassurance is necessary.

● For patients who are more symptomatic (with persistent aural fullness, minimal to moderate discomfort, and conductive hearing loss), simple maneuvers such as intermittent autoinsufflation may be helpful in relieving symptoms until the effusion resolves. This can be done by pinching the nose while gently exhaling through the nose, forcing air back through the Eustachian tube and thus repressurizing the ear.

● For adult patients with moderately symptomatic OME due to acute seasonal allergic rhinitis, short-term treatment with antihistamines, systemic decongestants, and/or nasal corticosteroids can be used. High-quality data regarding the efficacy of these treatments in adults are lacking, but we find short-term (≤12 weeks) use of one or a combination of these agents to be helpful for these patients in our clinical practice. (See "Pharmacotherapy of allergic rhinitis" .)

● For adult patients with moderately symptomatic OME due to an upper respiratory tract infection, we use either short-term treatment (6 to 10 weeks, or less if symptoms resolve) with nasal saline , systemic decongestants, nasal corticosteroids, or a combination of these therapies. With more severe symptoms, or in the case of unavoidable air travel, we also may treat with topical vasoconstrictor decongestants such as oxymetazoline (duration of treatment never to exceed 48 hours). However, air travel with the presence of an effusion is not recommended due to potential barotrauma to the ear. (See "The common cold in adults: Treatment and prevention", section on 'Moderate to severe symptoms' and "Pharmacotherapy of allergic rhinitis" and "An overview of rhinitis", section on 'Nasal decongestant sprays' .)

● If the effusion does not resolve within 12 weeks, or if there is persistent pain, troublesome hearing loss, or concern over barotrauma (ie, unavoidable airplane travel before resolution of the effusion), the patient should be referred for possible myringotomy with tube placement.

● For patients with recurrent, unilateral OME, fiberoptic nasopharyngoscopy should be performed to rule out nasopharyngeal pathology, such as nasopharyngeal carcinoma, especially in high-risk groups. (See "Epidemiology, etiology, and diagnosis of nasopharyngeal carcinoma", section on 'Geographic and ethnic distribution' .)

● If sensorineural hearing loss is demonstrated, particularly in the presence of normal tympanometry, immediate referral to an otolaryngologist is warranted for possible therapy with glucocorticoids and to rule out a retrocochlear lesion. (See "Evaluation of hearing loss in adults" .)

A systematic review of small studies of autoinsufflation in children did not demonstrate a significant difference in tympanometry results between intervention and control patients [ 32 ]. Similar studies are not available in adults, but the maneuver is without adverse effects and may be helpful to some patients in relieving symptoms while the effusion resolves on its own.

OME develops primarily from a mechanical/obstructive phenomenon. There is no evidence that decongestants and antihistamines are beneficial in the treatment of OME in children [ 33 ]. However, in adults, nasopharyngeal swelling from an upper respiratory tract infection or seasonal allergic rhinitis can induce transient Eustachian tube dysfunction, and decongestants might relieve symptoms by alleviating nasal congestion. As a result, most patients are treated with decongestants, antihistamines, or nasal corticosteroids despite a lack of high-quality data demonstrating a clear benefit in OME. (See "The common cold in adults: Diagnosis and clinical features", section on 'Acute otitis media' and "Pharmacotherapy of allergic rhinitis" .)

There are no available randomized trials of myringotomy for the treatment of OME in adults, but case series have shown myringotomy for OME to be effective, with infrequent adverse effects [ 34 ]. Myringotomy with tube placement is contraindicated in patients with irreversible Eustachian tube dysfunction secondary to etiologies such as cancer or radiation therapy involving the Eustachian tube. Placement of a tympanostomy tube in these patients may potentially result in chronic otorrhea, and hearing loss from a chronic effusion must be weighed against the potential development of a chronically draining ear [ 35 ]. There is increasing evidence that Eustachian tube balloon dilation ("tuboplasty") can help patients with refractory Eustachian tube dysfunction, although experience with this procedure is relatively limited and data on long-term outcomes for such procedures are lacking [ 36 ]. (See "Eustachian tube dysfunction", section on 'Surgical management if symptoms persist despite medical therapy' .)

There are limited data regarding the yield of nasopharyngoscopy in the routine workup of isolated otitis media with effusion, but individuals from China, Southeast Asia, and Northern Africa are at increased risk for nasopharyngeal carcinoma, and such patients should be considered for referral to otorhinology for further evaluation [ 37 ]. (See "Epidemiology, etiology, and diagnosis of nasopharyngeal carcinoma", section on 'Geographic and ethnic distribution' .)

Chronic otitis media  —  COM is diagnosed when there is a subacute or chronic tympanic membrane perforation which occurs in the setting of a chronic ear infection or recurrent infections.

● Benign COM is characterized by a tympanic membrane perforation without accompanying drainage.

● In COM with effusion (or chronic serous otitis media) there is continuous, typically straw colored, serous drainage through the perforated tympanic membrane.

● Chronic suppurative otitis media (CSOM) is defined by chronic purulent drainage through the perforated tympanic membrane.

Some otologists alternatively classify COM based on the presence of either a chronic tympanic membrane perforation ("COM mucosal disease") or cholesteatoma ("COM benign squamous disease"). The term "active" is also used if there is otorrhea and "inactive" if it remains dry. (See "Chronic otitis media and cholesteatoma in adults" .)

Bullous myringitis  —  Bullous myringitis is an infectious condition in which blisters (bullae) or vesicles develop on the tympanic membrane [ 38,39 ] ( picture 6 ). The disorder may mimic AOM with a thickened and erythematous tympanic membrane, but the pathologic process is limited to the tympanic membrane and does not affect the contents of the middle ear. Compared with AOM, bullous myringitis may be particularly painful.

The etiology is unknown, but it is believed to be viral. In studies published over 50 years ago, experimental infection of adult volunteers with M. pneumoniae resulted in hemorrhagic bullous myringitis [ 40 ]. However, subsequent studies of bullous myringitis have not identified M. pneumoniae as a causative agent.

External otitis (Otitis externa)  —  External otitis is characterized by a painful, inflamed, erythematous ear canal, occasionally involving a small portion of the auricle. The ear canal may be partially occluded by inflammatory debris. However, there is no middle ear effusion present in external otitis. The tympanic membrane in the majority of cases appears normal, without bulging or retraction, although there might be some minimal erythema present. (See "External otitis: Pathogenesis, clinical features, and diagnosis" and "External otitis in adults: Treatment" .)

Herpes zoster  —  The diagnosis of herpes zoster is established with development of the classic dermatomal vesicular rash. However, prodromal pain may precede the rash by several days or, less commonly, a week or more. Herpes zoster may occur in the absence of any visible lesions (zoster sine herpete), making the diagnosis more difficult.

The Ramsay Hunt syndrome (herpes zoster oticus) is characterized by the triad of ipsilateral facial paralysis, ear pain, and vesicles involving the auditory canal and auricle, and can also cause vertigo. (See "Epidemiology, clinical manifestations, and diagnosis of herpes zoster", section on 'Rash' and "Epidemiology, clinical manifestations, and diagnosis of herpes zoster", section on 'Ramsay Hunt syndrome (herpes zoster oticus)' .)

Deep space head and neck infections  —  Some deep space head and neck infections may cause referred pain to the ear and are discussed separately. (See "Deep neck space infections in adults" .)

TREATMENT OF ACUTE OTITIS MEDIA  —  Antibiotics are the mainstay of treatment of uncomplicated acute otitis media (AOM) in adults, and initial antibiotic choice is determined by knowledge of the most common causative pathogens. (See 'Microbiology' above.)

In children with AOM, at least one-quarter of cases are attributable to a viral respiratory pathogen, and some episodes of AOM resolve without antibacterial agents. In the United States, the American Academy of Pediatrics and the American Academy of Family Physicians present initial observation as an option for certain children with mild symptoms [ 41 ]. (See "Acute otitis media in children: Treatment", section on 'Antibiotic therapy versus observation' .)

In adults with AOM, however, data about the incidence of viral etiologies or the safety of withholding antimicrobial drugs are limited. Since AOM is unusual in adults, and complications may be significant, it seems prudent to treat all adults patients with antibiotic therapy. (See 'Other possible complications of acute otitis media' below.)

While awaiting response to antibiotic therapy, it is important to address the relief of pain, which can be significant. Most patients can be treated effectively with an analgesic such as a nonsteroidal antiinflammatory medication or acetaminophen .

Choice of initial antibiotic  —  Our choice for first-line therapy is amoxicillin-clavulanate .

● In most adults, the dose is amoxicillin 875 mg with clavulanate 125 mg orally twice daily.

● However, in patients at high risk for severe infections or infections with resistant S. pneumoniae (eg, those who live in regions with ≥10 percent penicillin-non-susceptible S. pneumonia e, are older than 65 years, are immunocompromised, have been recently hospitalized, or have used antibiotics in the past month), we use a higher dose of the amoxicillin component:

• Amoxicillin 1000 mg with clavulanate 62.5 mg, extended-release, orally twice daily (for lower-weight patients and/or those with milder infections)

• Amoxicillin 2000 mg with clavulanate 125 mg, extended-release, orally twice daily (for higher-weight patients and/or those with more severe infections)

If patients cannot use amoxicillin-clavulanate , we typically use a cephalosporin, as discussed elsewhere (see 'Penicillin allergy' below). However, if amoxicillin-clavulanate or one of the cephalosporins are unavailable or cost prohibitive, then amoxicillin may be used as alternative first-line therapy.

● In most adults, the dose of amoxicillin is 500 mg orally three times daily or 875 mg orally twice daily.

● In patients at high risk for severe infections or infections with resistant S. pneumoniae (eg, those who live in regions with ≥10 percent penicillin-non-susceptible S. pneumonia e, are older than 65 years, are immunocompromised, have been recently hospitalized, or have used antibiotics in the past month), we advise the use of high-dose amoxicillin :

• Amoxicillin 1000 mg orally three times daily

The rationale for our preference for amoxicillin-clavulanate is its spectrum of activity, which will cover the most common otopathogens. The preferred antibacterial drug for the patient with AOM must be active against S. pneumoniae , nontypeable H. influenzae , and M. catarrhalis [ 42-45 ]. Although data are not available for adults with AOM, one-third to one-half of H. influenzae isolates from middle ear fluid of children with AOM in the United States produce beta-lactamase, and nearly all isolates of M. catarrhalis produce beta-lactamase. S. aureus may also be an important pathogen in adults based upon limited studies. Clinicians should be aware that even high-dose amoxicillin is ineffective in treating AOM due to beta-lactamase-producing H. influenzae or M. catarrhalis (which are increasing in prevalence) and AOM due to S. aureus. (See 'Microbiology' above and "Acute otitis media in children: Epidemiology, microbiology, and complications" .)

Beta-lactamase inhibitors are ineffective against penicillin-non-susceptible S. pneumoniae because the mechanism of resistance is different and the addition of clavulanate does not extend the coverage for these organisms; however, this resistance usually can be overcome by the increased dose of amoxicillin described above. High doses of amoxicillin are effective against most penicillin-non-susceptible S. pneumoniae isolates in AOM since these typically display only intermediate, not full resistance to penicillin.

There are no society guideline recommendations regarding antibiotic choice in the treatment of AOM in adults, although there are recommendations for adolescents. Additionally, there are society recommendations for antibiotic choice in the treatment of acute bacterial sinusitis in adults, an infection with similar microbiology to AOM [ 46 ]. (See "Acute otitis media in children: Treatment" and "Uncomplicated acute sinusitis and rhinosinusitis in adults: Treatment", section on 'Antibiotics' .)

Penicillin allergy  —  Acceptable alternatives to amoxicillin-clavulanate therapy in patients with an allergy to penicillin depend upon the type and severity of the previous reaction ( algorithm 1 ). Severe reactions are characterized by urticaria, anaphylaxis, angioedema, or Stevens-Johnson syndrome. (See "Allergy evaluation for immediate penicillin allergy: Skin test-based diagnostic strategies and cross-reactivity with other beta-lactam antibiotics", section on 'Patients reporting a past reaction to amoxicillin or ampicillin' and "Penicillin allergy: Immediate reactions" .)

● In patients without severe reactions, and who do not have a known allergy to a cephalosporin, we use one of the following as alternative first-line therapy:

• Cefdinir , 300 mg orally twice daily or 600 mg once daily.

• Cefpodoxime , 200 mg orally twice daily.

• Cefuroxime , 500 mg orally twice daily.

• Ceftriaxone , 1 to 2 g intravenously (IV) or 1 g intramuscularly (IM) once daily for three days. Although a single dose may be sufficient in pediatric patients, clinical trials in pediatric patients demonstrated a three-day course to be more effective [ 47 ].

● For patients with a known severe allergy to beta-lactam antibiotics or who have a known allergy to cephalosporins, we use doxycycline or a macrolide. For these patients, antibiotic choices include:

• Doxycycline , 100 mg orally every 12 hours

• Azithromycin , 500 mg orally on day 1, then 250 mg orally days 2 through 5

• Clarithromycin , 500 mg orally every 12 hours

Among S. pneumoniae isolates, there is a high rate of resistance to macrolides ( azithromycin and clarithromycin ). We do not use trimethoprim-sulfamethoxazole because of a high rate of resistance among both H. influenzae and S. pneumoniae and because it is not effective against Group A streptococcus. Similarly, we do not use clindamycin because it has no activity against H. influenzae .

Duration of therapy  —  High-quality data regarding optimal duration of therapy are lacking, but we treat patients with mild to moderate infections for five to seven days, and those with more severe infections (significant hearing loss, severe pain, and/or marked tympanic membrane erythema) with a 10-day course of antibiotics. Patients with severe AOM and systemic symptoms may require more intensive initial treatment, including middle ear fluid cultures, blood cultures, and initial treatment with intravenous antibiotics.

Lack of initial response  —  With appropriate antimicrobial therapy, most patients with AOM are significantly improved within 48 to 72 hours. If there is no improvement, the patient should be re-examined. The patient may have developed a new focus of infection or have received inadequate therapy. We manage failures of first-line therapy in adults similarly to failures of initial therapy in pediatric AOM:

● If the patient received an antibiotic other than amoxicillin-clavulanate as the initial regimen and is able to tolerate penicillins, we treat with high-dose extended-release amoxicillin-clavulanate (2000 mg amoxicillin with 125 mg clavulanate, extended-release) orally twice daily for 10 days.

● If the patient failed initial treatment with amoxicillin-clavulanate , one of the following options are used:

• Cefdinir 300 mg orally twice daily or 600 mg once daily for 10 days.

• Cefpodoxime 200 mg orally twice daily for 10 days.

• Cefuroxime 500 mg orally twice daily for 10 days.

• Ceftriaxone 1 to 2 g IV once daily for three or more days (the duration of treatment depends upon the clinical response; patients should be examined after three days to determine the need for additional therapy).

• Levofloxacin 500 mg orally once daily for 5 to 10 days (the duration of treatment depends upon the clinical severity and response to therapy). Use of a fluoroquinolone should be considered only if no other options are available.

• Moxifloxacin 400 mg orally once daily for 5 to 10 days (the duration of treatment depends upon the clinical severity and response to therapy). Use of a fluoroquinolone should be considered only if no other options are available.

The oral cephalosporins are less potent against penicillin-non-susceptible S. pneumonia than amoxicillin-clavulanate . Ceftriaxone is typically effective and will treat most penicillin-non-susceptible S. pneumoniae strains. Only the fluoroquinolones with activity against respiratory pathogens ( levofloxacin or moxifloxacin ) should be considered for use in the treatment of uncomplicated AOM. Like all fluoroquinolones, however, they have a boxed warning from the US Food and Drug Administration (FDA) due to potential serious side effects, and they should be used only as a last resort when there are no other available options for therapy.

In patients with severe infections, or who are at high risk for infection with resistant organisms or severe infection, and who fail to respond to second-line therapy, middle ear fluid (obtained via tympanocentesis) sent for culture may help guide subsequent antibiotic choices.

Management of acute tympanic membrane rupture in acute otitis media  —  The majority of acute tympanic membrane perforations that occur as a result of AOM will heal spontaneously. When it occurs, the perforation allows drainage of infected fluid, relieving middle ear pressure and permitting the extensively vascularized tympanic membrane to heal more quickly. There are no data in pediatric or adult patients as to whether adding a topical antibiotic in patients with AOM and a ruptured tympanic membrane has benefit over treating with oral antibiotics alone.

In patients with AOM and acute tympanic membrane rupture, some UpToDate authors treat with topical antibiotic ear drops in addition to oral antibiotics, while other authors treat with oral antibiotic alone.

If a topical antibiotic is used, we choose one without any known ototoxicity (eg, we avoid aminoglycoside containing preparations), and we treat for 7 to 10 days ( table 2 ).

Additionally, until there is documented healing of the tympanic membrane perforation, the patient should use appropriate water precautions:

● No swimming or diving

● Avoid getting water in the affected ear when bathing or showering (ie, use a cotton ball coated with petroleum jelly in the ear to create a barrier)

In some cases, especially in recurrent or severe episodes of AOM, perforations may become chronic. (See 'Chronic tympanic membrane perforation' below.)

WHEN TO REFER

Recurrent acute otitis media  —  Patients with recurrent unilateral acute otitis media (AOM; ie, more than two episodes over a six-month time period) should undergo investigation for Eustachian tube or nasopharyngeal pathology. Fiberoptic nasopharyngoscopy and/or contrast magnetic resonance imaging (MRI) of the skull base and nasopharynx should be performed to rule out the possibility of a malignant process obstructing the Eustachian tube orifice. (See "Eustachian tube dysfunction", section on 'Obstructive dysfunction' .)

Persistent hearing loss following acute otitis media  —  Transient subjective hearing loss can occur in the affected ear during an episode of AOM due to the presence of fluid in the middle ear. However, subjective hearing loss that persists for more than one to two weeks following resolution of the infection and effusion is abnormal and should be followed up with an audiogram and otolaryngologic consultation.

Chronic tympanic membrane perforation  —  Tympanic membrane rupture may occur in AOM but will heal spontaneously in most cases. However, in recurrent or severe episodes of AOM, perforations may become chronic. Patients with perforations that persist for twelve weeks or longer (with or without associated suppurative drainage) should be referred to an otolaryngologist for further management. (See "Chronic otitis media and cholesteatoma in adults" .)

OTHER POSSIBLE COMPLICATIONS OF ACUTE OTITIS MEDIA  —  Other complications following an episode of acute otitis media (AOM) in adults are rare but can occur due to a variety of factors, such as impaired immune status, abnormal anatomy, inadequate antibiotic treatment, or a particularly virulent pathogen. Complications may result from seeding of vascular channels and extension along preformed pathways including the oval window, round window, internal auditory canal, or endolymphatic duct.

Mastoiditis and other infectious complications in adults develop in less than 0.5 percent of cases of AOM [ 48,49 ]. Among combined adult and pediatric United States emergency department visits for complications of AOM between 2009 and 2011, the most common diagnoses were acute mastoiditis (0.16 percent), labyrinthitis (0.06 percent), and facial paresis (0.03 percent) [ 50 ]. In another study including only adults, acute mastoiditis also accounted for the majority of the complications [ 49 ].

Mastoiditis  —  The mastoid bone (the portion of the petrous temporal bone that lies superior to the middle ear cavity) ( figure 1 ) contains air cells and is connected by the mastoid antrum to the middle ear. Most cases of AOM are associated with some degree of subclinical mastoiditis (inflammation or infection), although the incidence of clinically significant mastoiditis has been low since the introduction of antibiotics. Prior to antibiotics, acute coalescent mastoiditis complicated approximately 20 percent of cases of AOM, but, following the introduction of antibiotics, the incidence fell to 0.4 percent by 1959 and to 0.24 percent by 1993 [ 51,52 ]. In a United Kingdom study, from 1982 through 2012, the overall incidence of mastoiditis was 5.6 per 10,000 AOM episodes, with a higher rate in adults >20 years compared with patients ≤20 years (11.4 versus 3.7 per 10,000 AOM episodes, respectively) [ 53 ].

Mastoiditis is more common in children than adults; when it occurs in older adults, it may be particularly severe [ 54,55 ].

A spectrum of disease is associated with mastoiditis. Mastoid effusion is seen on computed tomography (CT) in all patients with AOM, but in the vast majority of cases it is not clinically significant. Clinically significant suppurative mastoiditis may present with fever, posterior ear pain and/or local erythema over the mastoid bone, edema of the pinna, or a posteriorly and downwardly displaced auricle.

In coalescent mastoiditis, the infection occupies the mastoid air spaces, causing destruction of the bony septae that separates the air spaces, and CT demonstrates characteristic loss of the trabecular bone [ 56 ].

When pus enters the mastoid air cells under pressure, it may lead to the dissolution of surrounding bone, and the infection may then spread to regional structures. Complicated mastoiditis (when infection spreads beyond the mastoid bone) can lead to dangerous complications due to proximity of the mastoid to the posterior cranial fossa, lateral sinuses, facial nerve canal, semicircular canals, and the petrous tip of the temporal bone.

If symptoms are present suggesting complicated mastoiditis (including swelling over the mastoid, facial paralysis, vertigo, sensorineural hearing loss, or other evidence that the infection has spread locally beyond the mastoid), surgical consultation should be obtained and CT performed. If there is a concern for the development of an intracranial complication (ie, septic lateral sinus thrombosis, intracranial abscess), then magnetic resonance imaging (MRI) should also be done.

Any patient with acute suppurative mastoiditis should be admitted to the hospital and started on intravenous (IV) antibiotics, and surgical consultation should be obtained. When suppurative mastoiditis occurs as a complication of AOM, antibiotics with activity against S. pneumoniae and H. influenzae should be given. When it presents as a complication of chronic otitis media (COM), coverage should include S. aureus (including methicillin-resistant S. aureus [MRSA]), Pseudomonas , and enteric Gram-negative rods. (See "Chronic otitis media and cholesteatoma in adults", section on 'Mastoiditis' .)

If patients with suppurative or coalescent mastoiditis do not respond to conservative therapy with IV antibiotics, surgical intervention is warranted, including mastoidectomy for debridement of infected and necrotic bone. (See "Chronic otitis media and cholesteatoma in adults", section on 'Surgical treatment' .)

Labyrinthitis  —  Labyrinthitis may occur infrequently as a result of both acute and chronic ear infections, and it presents as nausea, vomiting, vertigo, tinnitus, and hearing loss.

Serous labyrinthitis is a pre-suppurative condition in which the labyrinth undergoes inflammatory changes in association with acute suppurative otitis media. It is not associated with permanent auditory or vestibular dysfunction, and treatment is predominantly medical (treatment of the AOM and symptomatic treatment of the vertigo, nausea, etc), unless persistent granulation tissue or cholesteatoma are present. (See "Treatment of vertigo", section on 'Symptomatic treatment' and "Chronic otitis media and cholesteatoma in adults", section on 'Cholesteatoma removal' .)

Rarely, purulent (suppurative) labyrinthitis can develop, caused by direct extension of the AOM infection into the inner ear. This presents with more intense vertigo, tinnitus, hearing loss, vomiting, nausea, and also a clinical presentation of a more acutely ill patient.

Facial paralysis  —  Facial paralysis can occur as a rare complication of AOM through two different mechanisms.

There can be direct spread of the infection from the middle ear (via microdehiscences in the bony canal of the facial nerve, the Fallopian canal) to the nerve itself; as the inflamed nerve swells within this confined channel, a compression injury results in facial paralysis.

In the setting of an infection (more commonly seen in COM with cholesteatoma than in AOM), erosion of the bone overlying the facial nerve can directly compress the facial nerve; this typically occurs in the tympanic or vertical mastoid segment of the nerve. In AOM, however, facial nerve paresis can occur in the absence of any evidence of bony dehiscence in the facial canal. In a retrospective study of 24 adults with AOM complicated by facial nerve palsy, 54 percent had no evidence of bony dehiscence on high-resolution temporal bone CT [ 57 ].

Hearing loss  —  Hearing loss can occur as a result of both acute and chronic ear infections, although it is more commonly seen in cases of COM. The hearing loss is usually conductive in nature due to either ossicular erosion or tympanic membrane perforation.

Sensorineural hearing loss may rarely occur, particularly in the setting of a new infection in an adult without a prior history of ear infections. In COM, the round window membrane is much thicker, and thus inflammatory material (which may be ototoxic) is much less likely to enter the inner ear. (See "Etiology of hearing loss in adults" .)

Petrositis (petrous apicitis)  —  The petrous apex of the temporal bone also contains air cells and is susceptible to infection, but typically only in the setting of mastoiditis. Due to closely related neural and vascular structures, inflammation and infection of the petrous apex can result in neural compromise. The inflammation may extend into Dorello's canal (containing the sixth cranial nerve and inferior petrosal sinus) and the Gasserian ganglion (sensory ganglion of the trigeminal nerve), causing the triad of symptoms known as Gradenigo syndrome: lateral rectus palsy, retro-orbital pain, and otorrhea. The classic triad is not always present, but the presence of both otorrhea and retro-orbital eye pain should raise the suspicion for petrositis.

The acute form typically develops rapidly in a normally pneumatized petrous apex air cell system. Diagnosis is supported by temporal bone CT, demonstrating opacification of the mastoid air cells system and petrous apex, bony erosion within the petrous apex, and enhancement of the cavernous sinus. High-resolution MRI with gadolinium demonstrates a low-intensity signal on T1-weighted images, high-intensity signal on T2-weighted images, with ring enhancement. MRI findings are important in distinguishing petrositis from other lesions of the petrous apex.

The most common organism responsible for petrositis is Pseudomonas aeruginosa , although S. aureus , S. pneumoniae , and anaerobes also have been reported [ 58 ]. In a review of 44 cases of petrositis treated over 40 years at a single institution, most cases occurred in adults and were related to otitis media.

Treatment consists of appropriate intravenous antibiotic therapy to cover the most likely responsible organisms. Consultation with an infectious disease specialist should be obtained early. Surgical exploration is usually reserved for those who do not respond quickly to antibiotic therapy, or who develop complications from the infection [ 59 ]. For patients treated medically and for those requiring surgery, prolonged antibiotics (eg, six weeks) are indicated.

Otitic meningitis  —  Otitic meningitis is the most common intracranial complication of chronic otitis and mastoiditis, although meningitis may also occur in association with AOM as well. All forms of otitic meningitis typically present with the classic signs of meningitis, including fever, neck stiffness, photophobia, and mental status changes, although some of these symptoms and signs may be absent initially [ 60 ]. The meningitis is usually generalized, and lumbar puncture with cerebrospinal fluid (CSF) studies demonstrate typical CSF findings of bacterial meningitis, and bacteria may even be seen on Gram stain of the spun CSF. (See "Clinical features and diagnosis of acute bacterial meningitis in adults" .)

The most common pathogens are S. pneumoniae , although other pathogens, including H. influenzae, Group A streptococcus, and Neisseriae meningitidis may also be causative in some cases. In one study of 12 adults treated for otitic meningitis due to AOM, all seven cases with positive cerebrospinal fluid cultures were caused by S. pneumoniae [ 61 ]. In another study including both adults and children, the major pathogen was also identified as S. pneumoniae [ 61,62 ]. Successful treatment of otitic meningitis requires appropriate treatment, including IV antibiotics, and may additionally require surgical drainage of the mastoid. (See "Initial therapy and prognosis of community-acquired bacterial meningitis in adults" .)

Epidural, subdural, and brain abscess  —  Epidural, subdural, and brain abscesses are all rare complications of AOM in adults.

Epidural abscesses occur most commonly secondary to erosion of the posterior fossa plate. Less commonly, erosion of the tegmen mastoideum can lead to a middle fossa epidural abscess. Epidural abscesses resulting from acute or chronic ear infections present most commonly as headache that is occasionally relieved by profuse otorrhea. Treatment requires surgical drainage after identification of the abscess on MRI or CT imaging, in addition to intravenous antibiotics. (See "Intracranial epidural abscess" .)

The presentation of a subdural abscess may closely mirror that of an epidural abscess, although neurologic signs are more likely to accompany abscesses that occur in the subdural space (between the dura and arachnoid meningeal layers). The mechanism underlying the development of a subdural abscess is thought to be bone erosion followed by septic thrombophlebitis. Treatment is the same as for epidural abscess. (See "Intracranial epidural abscess" .)

Brain abscesses that occur in association with an acute or chronic ear infection will typically involve the temporal lobe or cerebellum. Successful treatment requires drainage of the brain abscess, followed by surgical eradication of the mastoid infection and a prolonged course of IV antibiotic therapy. (See "Pathogenesis, clinical manifestations, and diagnosis of brain abscess" and "Treatment and prognosis of bacterial brain abscess" .)

Otitic hydrocephalus  —  Otitic hydrocephalus is a rare syndrome of increased intracranial pressure and suppurative otitis media, which occurs in the absence of a brain abscess or meningitis [ 63 ]. The pathogenesis seems to involve abnormal cerebrospinal fluid metabolism secondary to inflamed meninges, and the typical case occurs following prolonged otitis media. The most common presenting symptom is headache on the side of the involved ear. Papilledema is noted on examination, and there is evidence of hydrocephalus on imaging (CT or MRI). Appropriate management includes treatment of the ear disease and conventional measures of lowering intracranial pressure. (See "Evaluation and management of elevated intracranial pressure in adults" .)

Septic lateral sinus thrombosis  —  Septic lateral sinus thrombosis (or sigmoid thrombophlebitis) may occur as a result of AOM in the setting of concomitant acute mastoiditis. The lateral, or sigmoid, sinus runs through the posterior portion of the mastoid cortex, where it eventually forms the jugular bulb and internal jugular vein.

Septic lateral sinus thrombosis often presents subacutely, with an earache that persists for several weeks before the onset of the headache. Signs of increased intracranial pressure, lower cranial neuropathies, and Griesinger's sign (postauricular edema due to emissary vein thrombophlebitis) are variable and signify progression of the condition. Sigmoid thrombophlebitis may extend to the jugular vein, with resultant internal jugular vein thrombosis.

Treatment requires IV antibiotics and, if necessary, drainage of the perisinus abscess via a transmastoid approach with exposure of the sigmoid sinus. Anticoagulation may be indicated. (See "Septic cavernous sinus thrombosis", section on 'Treatment' and "Septic lateral sinus thrombosis", section on 'Treatment' .)

SOCIETY GUIDELINE LINKS  —  Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute otitis media, otitis media with effusion, and external otitis" .)

SUMMARY AND RECOMMENDATIONS

● Definition and overview – Acute otitis media (AOM) is an acute, suppurative infectious process marked by the presence of infected middle ear fluid and inflammation of the mucosa lining the middle ear space ( picture 1 ). The infection is most frequently precipitated by impaired function of the Eustachian tube, resulting in the retention and suppuration of retained secretions ( figure 1 ). AOM may also be associated with purulent otorrhea if there is a ruptured tympanic membrane. AOM usually responds promptly to antimicrobial therapy. (See 'Definition' above.)

● Microbiology – Common bacteria causing AOM in both children and adults are Streptococcus pneumoniae and Haemophilus influenzae . Group A Streptococcus, Staphylococcus aureus , and Moraxella catarrhalis are less frequent causes. (See 'Microbiology' above.)

● Pathogenesis of AOM in adults – Eustachian tube dysfunction, commonly related to seasonal allergic rhinitis or upper respiratory tract infection, is the most important factor in the pathogenesis of middle ear infections in adults. (See 'Patient factors contributing to the development of acute otitis media' above.)

● Clinical presentation and diagnosis – AOM is typically associated with the development of unilateral otalgia and decreased hearing. Otoscopy is required for accurate diagnosis; the addition of pneumatic otoscopy, if available, is helpful in providing additional diagnostic information ( movie 1 and picture 2 ). The tympanic membrane in AOM is bulging, opacified, immobile, and often erythematous ( picture 1 ). On physical examination (or audiometry if available), a conductive hearing loss may be demonstrated. (See 'Presentation and diagnosis' above and 'Diagnosis with otoscopy' above.)

● Otitis media with effusion: Presentation and diagnosis – An entity that is commonly mistaken for AOM is otitis media with effusion (OME) ( figure 2 ). OME is often characterized by hearing loss and a sense aural fullness. Otoscopy reveals the presence of middle ear fluid ( picture 4 ) without a bulging tympanic membrane or evidence of active infection. In OME, the tympanic membrane is intact and may or may not be retracted ( picture 5 ), depending on the chronicity of the effusion. (See 'Otitis media with effusion' above.)

● Otitis media with effusion: Management – In OME, the majority of effusions will resolve over the course of 12 weeks, and most patients can be observed over this time period. In patients with substantial symptoms, we offer treatment with antihistamines (for OME due to allergic rhinitis), oral decongestants, and/or nasal corticosteroids. Myringotomy with tympanostomy tubes may be considered for persistent symptomatic effusions at 12 weeks and earlier for selected patients with need for immediate pressure equalization (eg, air travel that cannot be deferred). Patients with recurrent, unilateral OME should be referred for full nasopharyngeal evaluation to rule out obstructive pathology. (See 'Otitis media with effusion' above.)

● Antibiotics for adults with AOM: Initial therapy – We suggest that adults with AOM be managed with antibiotic treatment rather than "watchful waiting" ( Grade 2B ). The preferred antibacterial drug for the patient with AOM must be active against S. pneumoniae , nontypeable H. influenzae , and M. catarrhalis. We suggest amoxicillin-clavulanate rather than amoxicillin ( Grade 2C ). Amoxicillin-clavulanate is active against the increasingly prevalent otopathogens that produce a beta-lactamase, whereas amoxicillin is not. Resistance to penicillins in S. pneumoniae is by a different mechanism than beta-lactamase production, and AOM due to resista nt S. pneumoniae can usually be treated by high-dose amoxicillin, including formulations of amoxicillin-clavulanate that contain high-dose amoxicillin.

Second- or third-generation cephalosporins are alternative agents in patients with mild penicillin allergy or who are known to tolerate cephalosporins. Alternatives in patients who are highly penicillin-allergic and/or allergic to cephalosporins include doxycycline . (See 'Treatment of acute otitis media' above.)

● Antibiotics for patients who do not respond to initial therapy – Patients who do not respond symptomatically within 48 to 72 hours should be re-examined. Treatment regimens for patients who did not respond to the initial antibiotic course include high-dose amoxicillin-clavulanate (if this was not used initially), a second- or third-generation cephalosporin, if one was not initially used, or a second-line agent as described above. (See 'Lack of initial response' above.)

● Management of ruptured tympanic membrane in AOM – The tympanic membrane may rupture as a result of the infection in some patients with AOM. In patients with AOM and acute tympanic membrane rupture, some UpToDate authors treat with topical antibiotic ear drops in addition to oral antibiotics, while other authors treat with oral antibiotics alone. If one does choose to treat, agents containing ototoxic medications (eg, aminoglycosides) should be avoided ( table 2 ). Water precautions should be used until there is documented healing of the tympanic membrane. (See 'Management of acute tympanic membrane rupture in acute otitis media' above.)

● Indications for referral – Patients with recurrent AOM (>2 episodes in a six-month period), persistent hearing loss following AOM, and chronic tympanic membrane perforation following AOM (>12 weeks) should be referred for otorhinology consultation. (See 'When to refer' above.)

ACKNOWLEDGMENT  —  The editorial staff at UpToDate acknowledge Jerome Klein, MD, who contributed to an earlier version of this topic review.

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Determinants of chronic otitis media with effusion in preschool children: a case-control study

Affiliations.

  • 1 Department of Paediatrics: Child and Youth Health, The University of Auckland, Private Bag 92019, Auckland, 1142, New Zealand. [email protected].
  • 2 Division of Otolaryngology-Head and Neck Surgery, Counties-Manukau District Health Board, Manukau SuperClinic™, PO Box 98743, Manukau City, Auckland, 2241, New Zealand.
  • 3 Department of Paediatrics: Child and Youth Health, The University of Auckland, Private Bag 92019, Auckland, 1142, New Zealand.
  • PMID: 28056905
  • PMCID: PMC5217332
  • DOI: 10.1186/s12887-016-0767-7

Background: Chronic otitis media with effusion (COME) is a prevalent upper airway infection resulting in hearing loss. The aim of this research was to determine risk factors for COME in preschool children.

Methods: A case-control design was conducted in Auckland, New Zealand from May 2011 until November 2013. The cases were children aged 3 and 4 years referred for tympanostomy tube placement due to a diagnosis of COME (n = 178). The controls were a random sample of healthy children aged 3 and 4 years from primary care practices (n = 209). The children's guardians completed an interviewer-administered questionnaire that covered topics including socio-demographic information, pregnancy and birth, infant feeding practices, home environment, and respiratory health. In addition, skin prick tests for atopy were performed. Odds ratios (OR) estimating the risk of COME independently associated with the exposures were calculated using a logistic regression model.

Results: Children with COME frequently had nasal obstruction (OR: 4.38 [95% CI: 2.37-8.28]), always snored (OR: 3.64 [95% CI: 1.51-9.15]) or often snored (OR: 2.45 [95% CI: 1.04-5.96]), spent more hours per week in daycare (OR per hour/week: 1.03 [95% CI: 1.00-1.05]), had frequent colds (OR: 2.67 [95% CI: 1.59-4.53]), had siblings who had undergone tympanostomy tube placement (OR: 2.68 [95% CI: 1.22-6.02]), underwent long labour (OR: 2.59 [95% CI: 1.03-6.79]), and had early introduction of cow's milk (OR: 1.76 [95% CI: 1.05-2.97]). Asian ethnicity (OR: 0.20 [95% CI: 0.07-0.53]) and having older siblings (OR: 0.54 [95% CI: 0.31-0.93]) were inversely associated with COME.

Conclusion: COME in preschool children was associated with pathogen exposure, respiratory infection, and nasal obstruction. Strategies to prevent pathogen transmission warrant investigation. The novel findings of long labour and early cow's milk introduction require replication in future studies.

Keywords: Biofilms; Cow’s milk; Long labour; Nasal obstruction; Otitis media with effusion; Risk factors; Snoring; Upper respiratory tract infections.

Publication types

  • Research Support, Non-U.S. Gov't
  • Case-Control Studies
  • Child, Preschool
  • Logistic Models
  • New Zealand / epidemiology
  • Otitis Media with Effusion / ethnology
  • Otitis Media with Effusion / etiology*
  • Retrospective Studies
  • Risk Factors

COMMENTS

  1. Otitis Media With Effusion

    Otitis media with effusion (OME) is a condition in which there is fluid in the middle ear but no signs of acute infection. ... Prevalence of and risk factors for otitis media with effusion in primary school children: case control study in Erzurum, Turkey. Turk J Pediatr. 2015 May-Jun; 57 (3):230-5. [PubMed: 26701940] 6. Coleman A, Cervin A ...

  2. Clinical Practice Guideline: Otitis Media with Effusion (Update)

    Nonconsecutive studies, case-control studies, or studies with poor, nonindependent, or inconsistently applied reference standards: Cohort study, control arm of a randomized trial, case series, or case-control studies; poor quality prognostic cohort study ... Otitis media with effusion: Also called ear fluid, otitis media with effusion can ...

  3. PDF Otitis Media: Diagnosis and Treatment

    Otitis media with effusion is defined as middle ear effusion in ... expert opinion, or case series. For information about the SORT evidence ... A large prospective study

  4. Otitis Media With Effusion

    Pathophysiology. Otitis media with effusion (OME) can occur during the resolution of acute otitis media (AOM) once the acute inflammation has resolved. Among children who have had an episode of acute otitis media, as many as 45% have persistent effusion after 1 month, but this number decreases to 10% after 3 months.

  5. Acute Otitis Media

    Acute Otitis Media. In: Cho JC. Cho J.C.(Ed ... "Acute Otitis Media." Infectious Diseases: A Case Study Approach Cho JC. Cho J.C.(Ed.), Ed. Jonathan C. Cho. McGraw-Hill ... clear rhinorrhea, moderate bulging and erythema of right tympanic membrane with middle-ear effusion + + + Pulmonary + + Good air movement throughout, clear breath sounds ...

  6. Otitis Media With Effusion Clinical Presentation

    Determinants of chronic otitis media with effusion in preschool children: a case-control study. BMC Pediatr. 2017 Jan 6. 17 (1):4. [QxMD MEDLINE Link]. . Williamson I, Vennik J, Harnden A, et al. Effect of nasal balloon autoinflation in children with otitis media with effusion in primary care: an open randomized controlled trial.

  7. Proposed Quality Indicators for Aspects of Pediatric Acute Otitis Media

    Acute otitis media (AOM) is a common pediatric condition characterized by middle ear effusion (MEE) and acute signs and symptoms of inflammation. 1 It can manifest by a viral and/or bacterial infection that presents as otalgia, otorrhea, and/or nonspecific symptoms such as fever, irritability, tugging of the ear, or poor feeding in younger children. 2 AOM is generally self-limiting, but its ...

  8. Risk factors for persistent otitis media with effusion in children: a

    Otitis media with effusion (OME) is defined as middle ear effusion without acute signs of infection. OME usually resolves spontaneously; however, persistent OME may require the insertion of a ventilation tube. This study investigated risk factors for persistent OME in children who undergo ventilation tube insertion.

  9. Impact of Otitis Media With Effusion in Early Age on Auditory

    Objective: Early-onset otitis media with effusion (OME) can affect the development of the auditory nervous system and thus lead to auditory processing abnormalities. This study aims to review the effect of childhood OME on auditory processing abilities in children. Methods: A systematic review of the literature, restricted to the English language from 1990 to 2022 was conducted using search ...

  10. Clinical Practice Guideline: Otitis Media with Effusion (Update)

    Otitis media with effusion (OME) The presence of fluid in the middle ear without signs or symptoms of acute ear infection. Chronic OME OME persisting for 3 mo from the date of onset (if known) or from the date of diagnosis (if onset is unknown). Acute otitis media (AOM) The rapid onset of signs and symptoms of inflammation of the middle ear.

  11. Nasal microbial composition and chronic otitis media with effusion: A

    Objectives Chronic otitis media with effusion (COME) in children can cause prolonged hearing loss, which is associated with an increased risk of learning delays and behavioural problems. Dispersal of bacterial pathogens from the nasal passages to the middle ear is implicated in COME. We sought to determine whether there is an association between nasal microbial composition and COME in children ...

  12. Risk factors for otitis media with effusion in Chinese schoolchildren

    Otitis media with effusion (OME), which refers to the accumulation of fluid in the middle ear cavity without any signs of acute infection [4] ... This was a nested case-control study drawn from a large-scale school-screening in Hong Kong with targeted subjects of age 6-7 in the first year of primary school.

  13. Acute otitis media in adults

    INTRODUCTION — Acute otitis media (AOM) is primarily an infection of childhood and is the most common pediatric infection for which antibiotics are prescribed in the United States [].The vast majority of the medical literature focuses on the diagnosis, management, and complications of pediatric AOM, and much of our information of AOM in adults is extrapolated from studies in children.

  14. PDF Management of Otitis Media with Effusion in Children

    Hearing impairment is the commonest presentation (90%) of OME at home or in school. The hearing impairment is of conductive type. Common associated presentations are otalgia (60%), upper respiratory tract infection/URTI (40%), AOM (30%) and tonsillitis (18%).25, level III.

  15. Masked speech recognition by 6-13-year-olds with early-childhood otitis

    1. Introduction. Otitis media (OM) is one of the most common early-childhood diseases and causes transient, frequently recurrent, and intermittent conductive hearing loss (CHL), especially in the lower frequencies (e.g. Moore, Hartley, and Hogan Citation 2003).Most OM episodes happen during the first three years of life, with the first episode occurring 6-18 months after birth (e.g. Haggard ...

  16. Incidence of Seromucous Otitis in Schools in Southern Algeria

    The natural evolution of SMO does not always lead to spontaneous regression, and many cases require early management and strict monitoring to prevent complications, so it is necessary to introduce screening as part of school hygiene in order to reduce the incidence of chronic otitis in adults. Introduction: Seromucous otitis (SMO) is a very common pathology, affecting almost 50% of children.

  17. Role of follow-up gallium scintigraphy in the evaluation of malignant

    It is important to differentiate it from otitis media with antineutrophilic cytoplasmic antibody (ANCA)-associated vasculitis, eosinophilic otitis media, tumors, and tuberculosis. Disease outcomes are statistically poor; therefore, early differential diagnosis and intervention are important. ... Study approval statement This case study followed ...

  18. Determinants of chronic otitis media with effusion in preschool

    Background: Chronic otitis media with effusion (COME) is a prevalent upper airway infection resulting in hearing loss. The aim of this research was to determine risk factors for COME in preschool children. Methods: A case-control design was conducted in Auckland, New Zealand from May 2011 until November 2013. The cases were children aged 3 and 4 years referred for tympanostomy tube placement ...