Discussion
In this case series, we report otitis media as a new manifestation of COVID-19. Otitis media or inflammation of the middle ear is a general term that is further categorized to acute otitis media (AOM), otitis media with effusion (OME), and chronic suppurative otitis media (CSOM)(3).
Our case series includes 8 patients presenting over a two-months period during the COVID-19 pandemic. Six out of the eight patients had otalgia, with seven patients having hearing loss. Effusion in the middle ear was evident on otoscopic examination in six patients. Three patients had typical signs of AOM, with one patient having AOM with tympanic membrane perforation. Two patients had smell dysfunction. COVID-19 was confirmed by typical changes on CT chest and positive PCR assay on naso- or oropharyngeal swabs. Interestingly, in one patient, PCR assay was positive on middle ear effusion and negative on oropharyngeal swab.
We suggest that concomitant occurrence of otitis media in these patients could be a manifestation or complication of COVID-19. AOM and OME follow a seasonal pattern, with the incidence being the highest during the fall and winter and lowest during spring and summer in parallel to the incidence of upper respiratory infections(3). Our patients presented with otitis media in the second and third months of spring when of a low incidence of otitis media is expected. In addition, AOM and OME are most common in the young children(3), while all patients in this case series were adults without any pathology in the nasopharynx.
Viruses, including respiratory syncytial virus, rhinovirus, adenovirus, coronavirus, bocavirus, influenza virus, parainfluenza virus, enterovirus and human metapneumovirus, are known causes of upper respiratory infections and can induce AOM(3). Viruses can be the sole infective cause of AOM or play a role as co-infection with bacteria and, rarely, with other viruses(4). Viral infections can disrupt immune function and reduce the normal mucociliary clearance of mucosal cells by changing the properties of the nasopharyngeal mucus and the Eustachian tube leading to negative middle ear pressure(3). Negative middle ear pressure in turn predisposes the middle ear to effusion formation or secondary bacterial or viral infection(4).
Angiotensin-converting enzyme-2 (ACE2) receptor is the cellular entry route for SARS-CoV-2. High levels of ACE2 receptors are expressed in the nasal respiratory epithelium goblet, basal and ciliated cells(5). Because of the enriched populations of the ciliated cells, glands and goblet cells in the inferior part of the Eustachian tube(6), we suggest that this portion of the tube can be a route for SARSCoV-2 infection of the middle ear.