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.