Acute otitis media (AOM) is diagnosed based on visualization of a full or bulging tympanic membrane with middle ear effusion. The distribution of bacteria causing AOM in North America under the influence of pneumococcal conjugate vaccination and antibiotic selection pressure has resulted in a predominance of β-lactamase–producing Haemophilus influenzae followed by penicillin-resistant Streptococcus pneumoniae. Although guidelines continue to endorse amoxicillin as the preferred treatment, amoxicillin/clavulanate in high dosage would be the preferred treatment based on the otopathogen mix currently. Antibiotic prophylaxis has fallen into disfavor as a preventative strategy for AOM recurrences.
Key points
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The diagnosis of acute otitis media (AOM) requires visualization of a tympanic membrane that is full or bulging, with middle ear effusion present.
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Recent antibiotic pressure and vaccination with the pneumococcal conjugate vaccine have resulted in the emergence of β-lactamase–producing Haemophilus influenzae and Moraxella catarrhalis as the leading organisms causing AOM, followed by Streptococcus pneumoniae.
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Current American Academy of Pediatrics guidelines endorse amoxicillin as the preferred treatment of AOM, but the recent increase in amoxicillin-resistant H influenzae and M catarrhalis would suggest high-dose amoxicillin-clavulanate as a preferred treatment.
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Cefdinir, cefuroxime, and cefpodoxime proxetil are the preferred oral cephalosporins for the treatment of AOM. Among these, cefdinir is the most palatable.
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Recent evidence suggests cellular and humoral immunodeficiency against AOM-causing organisms in children with recurrent AOM.
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Antibiotic prophylaxis is no longer recommended as a preventative strategy for AOM recurrences.
Epidemiology
AOM is an infectious disease that primarily affects young children. Onset of AOM in the first 6 months is not common because infants in this age group are still protected from infection by maternal antibodies acquired transplacentally. If a child experiences AOM in the first 6 months of life, then frequent AOM likely will occur throughout the first few years of life. Most AOM occurs between 6 and 24 months of age; the peak incidence is between 9 and 15 months of age. AOM occurs with modest frequency between 2 and 3 years of age but its appearance quickly diminishes between 3 and 5 years of age. AOM can occur at any age, including adolescence and adulthood, but it is not a common infectious disease in those years of life. The frequency of AOM and OME events in children is shown in Fig. 1 .
Origin
The bacteria that cause AOM vary from country to country because of vaccination and antibiotic prescribing habits. In North America virtually all vaccinations against pneumococcus in children are with the 13-valent pneumococcal conjugate vaccine (PCV13). Most children are treated with antibiotics, predominantly amoxicillin in a standard dose (40 mg/kg/d divided twice daily) or a high dose (80 mg/kg/d divided twice daily) for 10 days. As a consequence of PCV and amoxicillin use, the etiology of AOM continues to change over time.
Health care providers must be cautious when they read reports of the etiology of AOM if the study was conducted outside of North America. The availability and extent of use of 7-valent pneumococcal conjugate vaccine (PCV7) varies and the introduction of PCV13 varies. The use of antibiotics at all (observation option), and the primary choice, dose, and routine duration of antibiotics all influence the bacterial etiology and the extent of antibiotic resistance.
The most recent data on the distribution of bacteria causing AOM in North America are shown in Table 1 (J Casey and ME Pichichero, unpublished data). The mix of organisms and the resistance to amoxicillin among the otopathogens as shown in Table 1 , and the in vitro activity of antibiotic choices available ( Fig. 2 ) suggest that a β-lactamase–stable aminopenicillin (amoxicillin/clavulanate) in high dosage would be the preferred treatment (discussed later).
| % of Total Pathogen | |
|---|---|
| Streptococcus pneumoniae | 12 |
| Amoxicillin-resistant | 20 |
| Haemophilus influenzae | 56 |
| Amoxicillin-resistant | 50 |
| Moraxella catarrhalis | 22 |
| Amoxicillin-resistant | 100 |
a Based on results from Legacy Pediatrics, Rochester, NY, 2011–2012 respiratory season.
Much confusion surrounds the role of upper respiratory infection (URI) viruses as a cause of AOM and OME. Although no doubt exists that viral URI plays a key role in the pathogenesis of AOM and OME, the role is more facilitation of bacterial AOM than a primary origin for these viruses (see section on Immunology). Respiratory syncytial virus, influenzae, parainfluenzae, rhinovirus, metapneumovirus, and others can be detected in the nasopharyngeal secretions of children with an URI, followed by AOM or OME. The nasopharyngeal secretions can reflux from the nasopharyngeal region via the eustachian tube into the middle ear space. Therefore, detection of the virus in middle ear fluid (MEF) using tympanocentesis does not inform on whether the virus causes AOM. With modern polymerase chain reaction (PCR) techniques, the DNA or RNA of viruses can be detected in the nasopharyngeal region and MEF of many children with AOM and OME. The presence of a respiratory virus without a bacterial otopathogen simultaneously detected is uncommon, probably occurring in around 2% to 10% of cases. Even with that low detection rate, studies have not systematically used PCR molecular methods for both viral and bacterial detection in the same nasopharyngeal and MEF samples.
OME can persist after an AOM for some time. Approximately half of the children who experience AOM will have OME 1 month after initial diagnosis, one-third will have OME 2 months after AOM, and 10% will have OME 3 months after AOM ( Fig. 3 ). Years ago, health care providers would ask for a follow-up visit 2 weeks after diagnosis of AOM to determine that the infection had resolved. When they observed the tympanic membrane and found OME, they presumed a treatment failure had occurred and would prescribe more and stronger antibiotics. That practice is no longer followed, largely because of the discovery that OME persists so long after AOM and can easily be confused with persistent AOM.
OME can become chronic (>3 months in duration). When this occurs, ample evidence suggests that the common otopathogens form biofilms. Biofilms comprise microbes in a colony, which reduces their process of dividing, slows their metabolism, and allows them to communicate with each other to share survival mechanisms through a process called quorum sensing . Biofilm colonies exist in a matrix of DNA, and cover themselves with a shield of biomaterial that prevents the penetration of antibiotics and antibodies. Most clinicians are familiar with biofilms as bacteria that grow on implanted catheters. Biofilms of the Pseudomonas sp form in patients with cystic fibrosis. Biofilm colonies occasionally shed a few organisms from the colony, and the microbes change their biology and are termed planktonic . When biofilms form in chronic OME they consist of the major otopathogens as single-species colonies or as polymicrobial colonies consisting of 2 or even 3 species of otopathogen. Because the biofilms do not elicit an immune response, little clinical evidence shows that they exist because minimal inflammation is seen in the middle ear when the biofilms is present.
Pathogenesis
Approximately 90% to 95% of AOM and OME cases are preceded by a viral URI. Upper airway allergy may cause eustachian tube dysfunction and lead to OME, and much less frequently to AOM. OME precedes and follows AOM. This concept is fairly new. Most health care providers were taught that OME follows AOM, but not that OME also precedes AOM.
Viral URI sets the stage for AOM and OME through increasing mucus production, slowing the beat of cilia in the nasopharyngeal region, creating nasopharyngeal inflammation, and downregulating the innate and adaptive immune response (see section on Immunology). Next, the eustachian tube closes because of inflammation occurring as part of the viral URI process. Negative pressure builds in the middle ear space, resulting in a retracted tympanic membrane. The distortion of the tympanic membrane caused by retraction can easily be confused with bulging. The middle ear also produces mucus to keep the surface of the middle ear cells moist. With the eustachian tube closed, the mucus builds up and causes fluid to be visible behind the tympanic membrane; this is OME. However, when OME develops, the middle ear is still sterile and the absence of a virus or bacteria results in the tympanic membrane remaining generally translucent. The secretions in the nasopharyngeal region are then literally sucked into the middle ear space when the eustachian tube temporarily relaxes for a part of a second. Once the secretions and accompanying virus and bacteria that were in the nasopharyngeal region gain entry to the middle ear space, the environment is free of immune control factors, and the bacteria begin to divide. In response to the local bacteria invasion the innate immune response is activated, resulting in the influx of neutrophils. The neutrophils release mediators of inflammation, and the health care provider observes that pathogenic process when glimpsing the tympanic membrane that has become thickened with edema, perhaps red, but most importantly observes bulging from the pressure of an inflammatory response (see sections on Clinical Manifestations and Diagnosis).
Clinical manifestations
Because nearly all AOM and OME events occur in the context of a viral URI, the clinical manifestations of AOM and OME often include those of a viral URI ( Table 2 ). That is, children with AOM and OME often have rhinorrhea, nasal congestion, and elevated body temperature. When children have a cold they are cranky, feed poorly, and sleep poorly. URI causes increased mucus production in the nasopharyngeal region that drips into the stomach, sometimes causing the child to vomit. Altogether it is apparent that the clinical manifestations of a viral URI are indistinct from those of AOM or OME.
| Source and Symptoms | Sensitivity (%) | Specificity (%) |
|---|---|---|
| Ear pain | 54 | 82 |
| Ear rubbing | 42 | 87 |
| Fever | 40 | 48 |
| Cough | 47 | 45 |
| Rhinitis | 75 | 43 |
| Excessive crying | 55 | 69 |
| Poor appetite | 36 | 66 |
| Vomiting | 11 | 89 |
| Sore throat | 13 | 74 |
| Headache | 9 | 76 |
Two-thirds of children with AOM have fever, but that means one-third do not. OME is not associated with fever, but if the child has a concurrent viral URI, that may cause fever. Therefore, ample evidence now confirms that the diagnosis of AOM or OME cannot rely on clinical manifestations.
Health care providers often presume that a child pulling at the ears has an AOM. This is not correct. Even pulling the ear is not a clear clinical manifestation of AOM or OME. When the tympanic membrane becomes retracted, the change in its position causes sensory nerve receptors to fire off, and this is associated with discomfort or even pain and ear tugging. For confirmation of this evidence, the reader is encouraged to recall an airplane ride and a child crying suddenly when the cabin was given positive pressure as the plane ascended. Several small children on board may have begun to cry as their eardrums began to retract from the pressure.
Diagnosis
AOM is a visual diagnosis based on viewing the tympanic membrane. Stated another way, it is not possible to diagnose AOM accurately without visualizing the tympanic membrane. The examination is difficult and training in diagnosis often is limited and much outdated.
A glimpse of a small portion of the tympanic membrane is not sufficient to diagnose AOM. The clinician is advised to make an effort to clear all or nearly all of the ear canal cerumen to view all or nearly all of the tympanic membrane.
The key diagnostic feature of AOM is a bulging or full appearance of the tympanic membrane ( Fig. 4 ). The bulging is from pressure behind the tympanic membrane caused by inflammation in the middle ear space. AOM is not associated with a retracted tympanic membrane, and therefore a determination of retraction of the tympanic membrane is a viral-mediated phenomenon or associated with OME ( Fig. 5 ). A bulging tympanic membrane can be difficult to distinguish from one that is retracted. Use of pneumatic otoscopy is helpful in this setting because positive pressure on insufflation will result in movement backward by a bulging tympanic membrane, and negative pressure will result in movement forward by a retracted tympanic membrane.
Because of the inflammation in the middle ear space during AOM, typically the tympanic membrane becomes thickened and nontranslucent or completely opaque. A translucent tympanic membrane is unlikely to be associated with AOM ( Fig. 6 ). With a translucent or semitranslucent tympanic membrane and MEF visualized behind the tympanic membrane, the likely diagnosis is OME (see Fig. 5 ).
