Chronic suppurative otitis media (CSOM): Clinical features and diagnosis

Authors:
Jessica Levi, MD
Robert C O'Reilly, MD
Section Editor:
Glenn C Isaacson, MD, FAAP
Deputy Editor:
Carrie Armsby, MD, MPH

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Mar 2017. | This topic last updated: Nov 02, 2016.

INTRODUCTION Chronic suppurative otitis media (CSOM) is one of the most common
childhood infectious diseases worldwide and is a common cause of hearing impairment in
resource-limited settings, although it is less frequently seen in resource-rich settings [1]. It is
characterized by chronic drainage from the middle ear associated with tympanic membrane
(TM) perforation (picture 1) [2,3]. CSOM is often preceded by an episode of acute otitis media
(AOM).

The epidemiology, pathogenesis, clinical features, diagnosis, and management of CSOM are
reviewed here. The prevention, treatment, and complications of CSOM are discussed in detail
separately. CSOM in the setting of tympanostomy tubes is also reviewed separately.
(See "Chronic suppurative otitis media (CSOM): Treatment, complications, and
prevention" and "Tympanostomy tube otorrhea in children: Causes, prevention, and
management".)

AOM, otitis media with effusion, and cholesteatoma in children, and acute and chronic otitis
media in adults are reviewed separately:

(See "Acute otitis media in children: Epidemiology, microbiology, clinical manifestations,

and complications".)
(See "Otitis media with effusion (serous otitis media) in children: Clinical features and
diagnosis".)
(See "Acute otitis media in adults (suppurative and serous)".)
(See "Chronic otitis media, cholesteatoma, and mastoiditis in adults".)

TERMINOLOGY It is important to distinguish CSOM from other chronic conditions affecting

the middle ear:

Chronic suppurative otitis media (CSOM) CSOM is chronic inflammation of the

middle ear associated with tympanic membrane (TM) perforation and chronic discharge
(otorrhea) [1]. The definition of "chronic" in the entity of CSOM varies somewhat. The World
 Health Organization defines CSOM as otorrhea lasting at least two weeks [1,4]; however,
"chronic" is more commonly defined as symptoms persisting for >6 weeks. (See 'Ear
discharge' below.)
Tympanostomy tube otorrhea (TTO) TTO is defined as active drainage through an
existing tympanostomy tube and is primarily caused by bacterial infection. TTO can have
early onset (within two weeks of tube placement) or late onset (>2 weeks after tube
placement). TTO is reviewed in greater detail separately. (See "Tympanostomy tube
otorrhea in children: Causes, prevention, and management".)
Chronic otitis media with effusion (OME) OME (also called serous otitis media) is
defined as middle-ear effusion without acute signs of infection. Like CSOM, OME often
occurs after acute otitis media (AOM) and is associated with conductive hearing loss;
however, in OME the TM is not perforated and therefore otorrhea does not typically occur.
OME is reviewed in greater detail separately. (See "Otitis media with effusion (serous otitis
media) in children: Clinical features and diagnosis" and "Otitis media with effusion (serous
otitis media) in children: Management".)

EPIDEMIOLOGY

Prevalence It is estimated that there are 31 million new cases of CSOM per year worldwide,
with nearly one-quarter occurring in children <5 years old [5]. CSOM is uncommon in resource-
rich settings, with a prevalence of <1 percent in the United States [3]. It occurs more frequently
in resource-limited settings, with prevalences ranging from 6 to 46 percent depending on the
geographic area and population studied [6-8]. One study of CSOM in a resource-limited setting
found that the prevalence declined from 9 percent in the early 1990s to 5 percent in the early
2010s [9].

One theory regarding the higher prevalence in resource-limited settings is that the cost of
treatment is prohibitive [10]. Lack of public awareness about CSOM and delays in seeking care
are also likely important contributors [11-13].

CSOM typically occurs in children under the age of two years [7,14,15]; however, high rates
have also been reported in older children and adults [6,9]. In a prospective study that followed
young children in Greenland (a region with a high rate of CSOM), the mean age of onset of
CSOM was 11 months [8]. In another prospective study carried out in Ethiopia, the mean age at
presentation was 5.9 years; however, otorrhea had started before the age of two years in nearly
70 percent of patients [7].

Studies have varied regarding the relative frequencies among males and females [12,15-17].
Some studies have reported that males are more likely to develop the cholesteatomatous form
of CSOM and are more likely to have persistent disease [18,19].

The reported frequency of bilateral disease ranges from 27 to 55 percent [7,11].

Risk factors The risk of CSOM is increased among children with one or more of the
following:

A history of multiple episodes of acute otitis media (AOM) [20,21]

Early otitis media (ie, occurring in the first few months of life) [22]
Chronic secretory otitis media [23]

Additional risk factors for CSOM represent a combination of common risk factors for AOM as
well as factors associated with low socioeconomic status and inadequate health care [24].
These include:

Living in crowded conditions [20,21]

Living in a large family [8,20,21]
Daycare attendance [8,20,21]
Low parental education level [19,20]
Poor nutrition and lower levels of zinc, selenium, calcium, and vitamin A [7,15,25,26]
Passive smoke exposure [8]
History of tympanostomy tubes [20]
Frequent upper respiratory tract infections [8,15,20] and nasopharyngitis [7]
Infectious and chronic diseases, such as measles, human immunodeficiency virus
infection, tuberculosis, diabetes, and cancer [7,15,27]
Other comorbid conditions, such as cleft lip/palate, Down syndrome, cri du chat
syndrome, choanal atresia, and other craniofacial anomalies [12,20]
Unhygienic practices, such as bathing in contaminated ponds and rivers, unsterile ear
piercing, and cleaning ears with cotton buds [11,12]

A genetic predilection is also suspected to play a role. This is suggested by the increased risk of
CSOM seen in the Inuit of Alaska, Canada, and Greenland; Australian Aborigines; and certain
Native Americans (particularly the Apache and Navajo) [8,24].

A family history of otitis media also increases the risk of CSOM [21]. Maternal history of otorrhea
and CSOM are risk factors for development of CSOM in children [8,19].

PATHOGENESIS

Anatomic classification of CSOM CSOM can be classified according to the degree of

involvement of the structures of the middle ear (figure 1) [28]:

Tubotympanic type In tubotympanic CSOM, the disease is confined to the pars tensa
with central perforation. The risk of bone erosion and other serious complications (eg,
intracranial infection) is low.
 Atticoantral type In atticoantral CSOM, the disease involves the pars flaccida or
posterosuperior marginal quadrant. Cholesteatoma is commonly present and intra- and
extracranial complications may occur.

Tympanostomy tube otorrhea (TTO) is sometimes included as a third classification. TTO is

reviewed separately. (See "Tympanostomy tube otorrhea in children: Causes, prevention, and
management".)

Progression from AOM to CSOM CSOM is likely a multifactorial disease resulting from
interactions between bacterial, environmental, and host factors. CSOM generally results from
acute otitis media (AOM) that is not diagnosed promptly or is inadequately treated. Infrequently
it can result from chronic otitis media with effusion (OME). CSOM can occur in a patient with a
previously intact tympanic membrane (TM) or a TM with a pre-existing perforation or
tympanostomy tube. There are also reports of CSOM following traumatic perforations [29].
(See "Acute otitis media in children: Epidemiology, microbiology, clinical manifestations, and
complications", section on 'Complications and sequelae' and "Tympanostomy tube otorrhea in
children: Causes, prevention, and management".)

Eustachian tube dysfunction (ETD) coupled with a nasopharyngeal reservoir of pathogens may
play a role in the progression from AOM to CSOM [1,3,30]. In one study, ETD was observed
twice as frequently in ears affected by CSOM compared with ears of control subjects [31].
However, another study found no difference in the paratubal structures themselves in patients
with CSOM compared with healthy controls [32]. In another series, there was no correlation
between cultures from the external auditory canal (EAC) or middle ear and nasopharyngeal
cultures, indicating the nasopharynx may not serve as a reservoir for the bacteria causing
CSOM [33].

An alternative theory is that the nasopharyngeal bacteria may contribute to the initial AOM
preceding CSOM, but bacteria from the EAC enter the middle ear through the perforated TM as
the infection becomes chronic, leading to a secondary infection and chronic drainage [24].

Contaminated water may also play a role in the pathogenesis of CSOM. Swimming or bathing in
unclean water can lead to middle-ear contamination with bacteria in the setting of TM
perforation [3,24]. However, swimming in chlorinated swimming pools does not appear to
increase the risk of chronic ear drainage [34].

Biofilms have also been implicated in the pathogenesis of CSOM. The role of biofilms in patients
with cholesteatoma is better defined, but there is some evidence that biofilms also play a role in
CSOM [35-41]. Biofilms may account for some of the difficulty in treating CSOM, since they are
difficult to eradicate.

Other factors that may lead to the progression from AOM to CSOM include overproduction of
mucin, decreased ciliary motion in the middle ear, and upregulation of proinflammatory
cytokines [42,43]. (See 'Role of immune system' below.)
Role of immune system Environmental allergies and abnormalities in humoral immunity and
inflammatory cytokines are suspected to play a role in CSOM:

Environmental allergies Environmental allergies may be more common in patients with

CSOM. Positive allergy testing to perennial aeroallergens was seen in 16 of 20 (80
percent) patients with CSOM compared with 8 of 17 (47 percent) patients with AOM and 5
of 15 (33 percent) controls without otitis media [44]. Immunoglobulin E (IgE) was elevated
in the serum and middle-ear secretions of these patients, with an increased ratio of middle
ear to serum levels in patients with CSOM compared with those with AOM.
Among an adult population with CSOM, allergic rhinitis was more common among the
patients with CSOM compared with controls (62.5 versus 37.5 percent, p = 0.02). The
prevalence of allergic rhinitis (diagnosed by positive skin prick test) was also significantly
higher among affected patients than controls (24.6 and 13.8 percent, respectively) [45].
Humoral immunity Immunoglobulin levels were below normal in 3 of 69 (4.3 percent) of
patients with CSOM in one series, suggesting a defect in humoral immunity in a small
subset of patients [46].
Inflammatory cytokines Interferon-gamma (IFN-gamma) has been shown to have
immunoregulatory properties in OME, and it may play a similar role in CSOM. Middle-ear
secretions were collected and examined in 358 children with CSOM [47]. The children were
then treated and followed for nine months. IFN-gamma concentrations were significantly
lower in the 61 percent of children in whom CSOM resolved compared with the 39 percent
of children who had persistent drainage (mean IFN-gamma concentration 27.2 versus
73.1 pg/mL, respectively). Levels of IFN-gamma also inversely correlated with
concentrations of immunoglobulin G (IgG), IgE, and immunoglobulin A (IgA) in the fluid.
Another study found that proinflammatory cytokines were upregulated in patients with
CSOM, which may indicate that differences in host response plays a role in why some
children do not recover well from an episode of AOM and go on to develop CSOM [48].

MICROBIOLOGY Studies regarding the relative frequencies of different pathogens vary

somewhat depending on the geographic area and population studied. Commonly isolated
bacteria include Staphylococcus aureus (methicillin-resistant [MRSA] and methicillin-sensitive
[MSSA]), Pseudomonas, Proteus, coagulase-negative staphylococci, Enterococcus, and
anaerobes (including with Peptostreptococcus, Fusobacterium, Prevotella, and Porphyromonas)
[15,49-55]. Polymicrobial growth is common [54].

In patients with bilateral CSOM, the bacteria can be different in each ear [56]. Bacteria isolated
from swabs of middle ear discharge may differ from samples obtained more invasively. In a
study of 244 patients with CSOM who underwent tympanomastoidectomy, bacterial growth in
intraoperative mastoid granulation tissue cultures differed from preoperative middle ear
discharge culture in 22 percent of cases [50].
Fungi are also identified in cultures from patients with CSOM, with Aspergillus being the most
common [54,57]. The presence of fungi may be due to treatment with antibiotic drops and may
not represent the original infectious organisms. Occasionally, tuberculosis is seen.

Bacteriology in patients with CSOM and cholesteatoma may be different. In one series of 119
children with CSOM, those with cholesteatoma were 30 times more likely to have mixed
infections compared with patients with noncholesteatomatous CSOM [58]. Among 368 patients
(adults and children) with CSOM, those with cholesteatoma were more likely to have S.
aureus than Pseudomonas, while patients without cholesteatoma had the reverse [59].

In a 13-year study (culminating in 2013) involving mostly adult patients, there was little change
in the bacteriology of CSOM; however, resistance patterns did change somewhat with increased
resistance to quinolones and aminoglycosides among Pseudomonas isolates [17].

CLINICAL PRESENTATION

Ear discharge CSOM is characterized by chronic purulent middle ear discharge. The
definition of "chronic" in the entity of CSOM varies somewhat; the most common suggested
cutoff for duration of suppuration is six weeks (range, two weeks to three months) [3].

The otorrhea may be persistent or intermittent. In one study, 73 percent of patients had
intermittent drainage, while the remaining 27 percent had continuous otorrhea [7]. Many patients
have had ear drainage for >1 year (range 0 to 20 years) before seeking medical advice [12,16].

Patients do not typically complain of ear pain. Any report of fever, dizziness, or pain should alert
the clinician to consider complications of CSOM. (See "Chronic suppurative otitis media
(CSOM): Treatment, complications, and prevention", section on 'Complications'.).

Hearing loss Hearing loss (threshold of hearing >25 decibels [dB]) occurs in approximately
50 to 60 percent of patients with CSOM [11,27,60]; however, estimates of the prevalence may
vary substantially depending on the definition used [61].

Hearing loss is moderate to severe in up to two-thirds of affected patients [7,18,60,62,63]. In

one series of 115 patients with CSOM, the average hearing threshold was 40 dB [60].
Conductive hearing loss is more common than sensorineural hearing loss (SNHL), but both may
occur [1,60,64-68].

Longer duration of otorrhea is associated with greater degree of hearing loss [65]. Lower
socioeconomic status is associated with a greater risk of CSOM and, therefore, greater risk of
hearing loss, but age of onset and number of episodes do not appear to be risk factors [64]. The
site of the perforation corresponded to degree of hearing loss, with posterior perforations having
a greater dB level hearing loss, probably as a result of loss of protection of the round window
membrane from impinging sound pressure waves [65]. Hearing loss may occur in the
contralateral ear despite lack of evidence of bilateral disease [63].
The hearing loss in CSOM usually results from middle-ear pathology and the inner ear is
typically not affected; however, mixed hearing loss (conductive and sensorineural) can occur
[66,69-71]. SNHL is thought to result from chemical inflammatory mediators produced from the
chronic infection passing through the round window, causing the loss of hair cells in the cochlea
[42]. Ototoxicity of ototopical drops may also play a role [72].

Cholesteatoma Cholesteatoma (picture 2) should be considered when CSOM does not

resolve with maximal medical treatment. It occurs in 1 to 18 percent of all patients with CSOM
[6,11,18,73]. Cholesteatoma, in conjunction with CSOM, should be distinguished from isolated
cholesteatoma, which can have a similar presentation, but is a distinct entity. (See 'Differential
diagnosis' below and "Cholesteatoma in children".)

Physical exam findings Physical examination in patients with CSOM typically reveals
tympanic membrane (TM) perforation and purulent middle ear drainage. Most commonly, a
large central TM perforation is present (picture 1 and picture 3); perforation of the
posterosuperior quadrant is the less common [11,65]. Discharge can range from purulent to fetid
to cheese-like, and can fill the ear canal. There is typically minimal to no edema of the external
auditory canal. There may be granulation tissue, but it should be distinguished from retraction-
pocket cholesteatoma in which the granulation tissue occupies the pars flaccida of the TM.
Middle-ear mucosa, when it is seen, can be polypoid or edematous and can appear pale, red, or
may be normal.

DIAGNOSIS The diagnosis of CSOM is based upon consistent clinical findings (eg, hearing
loss, chronic ear discharge). Cultures are not required to make the initial diagnosis and are
generally reserved for unresponsive disease. They should be obtained through the tympanic
membrane perforation, since cultures taken from the external auditory canal may be unreliable
or misleading [74]. However, patients usually fail medical treatment for reasons other than
microorganism resistance. Thus, alternative or additional diagnoses should be considered and a
computed tomography scan of the temporal bones obtained to evaluate for cholesteatoma or
other processes when a patient is unresponsive to appropriate medical treatment. (See 'Clinical
presentation' above and 'Differential diagnosis' below.)

DIFFERENTIAL DIAGNOSIS The most common and important condition in the differential
diagnosis for CSOM is cholesteatoma, particularly the acquired form, which can also present
with hearing loss and/or chronic otorrhea. Congenital cholesteatoma, which is far less common
than acquired cholesteatoma, may also present with middle ear effusion or chronic otorrhea. It
can be difficult to distinguish the two entities, since cholesteatoma can also occur in conjunction
with CSOM. Keratin debris seen on exam, as opposed to just purulence, and prolonged duration
of suppuration both are suggestive of cholesteatoma. Symptoms such as dizziness or facial
nerve weakness should also make one consider cholesteatoma. A careful physical exam along
with computed tomography (CT) scanning of the temporal bones, which may reveal bone
erosion or destruction, should identify cholesteatoma in most cases.
(See 'Cholesteatoma' above and "Cholesteatoma in children".)
The differential diagnosis also includes acute and chronic otitis media. A perforated tympanic
membrane (TM) distinguishes CSOM from both acute and otitis media with effusion, in which
the ear drum is intact. Acute otitis media (AOM) can lead to TM perforation in some cases and
may progress to CSOM. The duration of symptoms is the main differentiating factor between
these two conditions. (See 'Clinical presentation' above and "Acute otitis media in children:
Epidemiology, microbiology, clinical manifestations, and complications", section on 'Clinical
manifestations' and "Acute otitis media in children: Epidemiology, microbiology, clinical
manifestations, and complications", section on 'TM perforation' and "Otitis media with effusion
(serous otitis media) in children: Clinical features and diagnosis", section on 'Clinical features'.)

CSOM can also occur in the presence of tympanostomy tubes, which is discussed in greater
detail separately. (See "Tympanostomy tube otorrhea in children: Causes, prevention, and
management".)

Other conditions that may present with otorrhea include (see "Evaluation of otorrhea (ear
discharge) in children" and "Hearing impairment in children: Etiology"):

Foreign body, particularly in young children with chronic drainage. (See "Evaluation of
otorrhea (ear discharge) in children", section on 'Foreign body'.)
Petrous apicitis (petrositis, infection of the petrous bone and air cells), which generally
presents with retro-orbital pain, cranial nerve six palsy, and ear drainage. (See "Acute
mastoiditis in children: Clinical features and diagnosis", section on
'Pathogenesis' and "Acute mastoiditis in children: Clinical features and diagnosis", section
on 'Complications'.)
Tuberculosis of the temporal bone, particularly in underdeveloped areas or among at-risk
populations (eg, nursing home or prison contacts, poor health care), can present as
painless otorrhea. Testing for tuberculosis can help differentiate this from other infectious
causes of CSOM. (See "Tuberculosis disease in children" and "Skeletal tuberculosis".).=
Langerhans cell histiocytosis (see "Clinical manifestations, pathologic features, and
diagnosis of Langerhans cell histiocytosis" and "Evaluation of otorrhea (ear discharge) in
children", section on 'Granulation tissue'). A CT scan will help differentiate this entity from
CSOM.
Malignancy (rare in pediatric populations) (see "Evaluation of otorrhea (ear discharge) in
children", section on 'Neoplasm'). These patients usually present with pain. A CT scan will
help differentiate this as well.

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 and otitis media with effusion in children".)

SUMMARY

Chronic suppurative otitis media (CSOM) is one of the most common childhood infectious
diseases worldwide and is the most common cause of hearing impairment in resource-
 limited settings, although it is less frequently seen in resource-rich settings.
(See 'Introduction' above and 'Epidemiology' above.)
CSOM generally results from an acute otitis media (AOM) that is not diagnosed promptly
or is inadequately treated. The AOM then progresses to tympanic membrane (TM)
perforation and subsequent contamination from the external auditory canal
(EAC) and/or nasopharyngeal reservoir. (See 'Pathogenesis' above.)
Commonly isolated bacteria in CSOM include Staphylococcus aureus (methicillin-
resistant [MRSA] and methicillin-sensitive [MSSA]), Pseudomonas, Proteus, coagulase-
negative staphylococci, Enterococcus, and anaerobes (including
with Peptostreptococcus, Fusobacterium, Prevotella, and Porphyromonas). Polymicrobial
growth is common. (See 'Microbiology' above.)
CSOM is characterized by purulent middle ear discharge that is chronic (typically >6
weeks) and hearing loss associated with a TM perforation. The otorrhea can be recurrent
or persistent. CSOM is usually painless. (See 'Clinical presentation' above.)
Physical examination in patients with CSOM typically reveals a large central TM
perforation and purulent middle ear drainage (picture 1 and picture 3). There is usually
minimal to no edema of the EAC. (See 'Physical exam findings' above.)
The diagnosis of CSOM is based upon consistent clinical findings (eg, hearing loss,
chronic otorrhea). Cultures are not required to make the initial diagnosis and are generally
reserved for unresponsive disease. (See 'Diagnosis' above.)
The most common and important condition in the differential diagnosis for CSOM is
cholesteatoma, which can also present with hearing loss and/or chronic otorrhea. It can be
difficult to distinguish the two entities, since cholesteatoma can also occur in conjunction
with CSOM. (See 'Differential diagnosis' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES

1. Verhoeff M, van der Veen EL, Rovers MM, et al. Chronic suppurative otitis media: a
review. Int J Pediatr Otorhinolaryngol 2006; 70:1.

2. WHO. Child and adolescent health and development. Prevention of blindness and
deafness. Chronic suppurative otitis media. Burden of illness and management options.
Geneva, Switzerland: WHO; 2004.
http://www.who.int/pbd/deafness/activities/hearing_care/otitis_media.pdf (Accessed on
September 17, 2012).

3. Bluestone CD. Epidemiology and pathogenesis of chronic suppurative otitis media:

implications for prevention and treatment. Int J Pediatr Otorhinolaryngol 1998; 42:207.

4. Smith AW. WHO activities for prevention of deafness and hearing impairment in children.
Scand Audiol Suppl 2001; :93.

5. Monasta L, Ronfani L, Marchetti F, et al. Burden of disease caused by otitis media:

systematic review and global estimates. PLoS One 2012; 7:e36226.
6. Rupa V, Jacob A, Joseph A. Chronic suppurative otitis media: prevalence and practices
among rural South Indian children. Int J Pediatr Otorhinolaryngol 1999; 48:217.

7. Melaku A, Lulseged S. Chronic suppurative otitis media in a children's hospital in Addis

Ababa, Ethiopia. Ethiop Med J 1999; 37:237.

8. Koch A, Home P, Pipper C, et al. Chronic suppurative otitis media in a birth cohort of
children in Greenland: population-based study of incidence and risk factors. Pediatr Infect Dis J
2011; 30:25.

9. Orji FT, Ukaegbe O, Alex-Okoro J, et al. The changing epidemiological and

complications profile of chronic suppurative otitis media in a developing country after two
decades. Eur Arch Otorhinolaryngol 2016; 273:2461.

10. Adoga A, Nimkur T, Silas O. Chronic suppurative otitis media: Socio-economic

implications in a tertiary hospital in Northern Nigeria. Pan Afr Med J 2010; 4:3.

11. Kamal N, Joarder AH, Chowdhury AA, Khan AW. Prevalence of chronic suppurative otitis
media among the children living in two selected slums of Dhaka City. Bangladesh Med Res
Counc Bull 2004; 30:95.

12. Neogi R, Dan A, Maity K, et al. Clinico-epidemiological profile of chronic suppurative

otitis media patients attending a tertiary care hospital. J Indian Med Assoc 2011; 109:324.

13. Elsayed Yousef Y, Abo El-Magd EA, El-Asheer OM, Kotb S. Impact of Educational
Program on the Management of Chronic Suppurative Otitis Media among Children. Int J
Otolaryngol 2015; 2015:624317.

14. Lasisi AO, Olaniyan FA, Muibi SA, et al. Clinical and demographic risk factors associated
with chronic suppurative otitis media. Int J Pediatr Otorhinolaryngol 2007; 71:1549.

15. Eason RJ, Harding E, Nicholson R, et al. Chronic suppurative otitis media in the
Solomon Islands: a prospective, microbiological, audiometric and therapeutic survey. N Z Med J
1986; 99:812.

16. Yagi HI. Chronic suppurative otitis media in Sudanese patients. East Afr Med J 1990;
67:4.

17. Kim SH, Kim MG, Kim SS, et al. Change in Detection Rate of Methicillin-Resistant
Staphylococcus aureus and Pseudomonas aeruginosa and Their Antibiotic Sensitivities in
Patients with Chronic Suppurative Otitis Media. J Int Adv Otol 2015; 11:151.

18. Matanda RN, Muyunga KC, Sabue MJ, et al. Chronic suppurative otitis media and
related complications at the University Clinic of Kinshasa. B-ENT 2005; 1:57.

19. Jensen RG, Home P, Andersson M, Koch A. Long-term follow-up of chronic suppurative
otitis media in a high-risk children cohort. Int J Pediatr Otorhinolaryngol 2011; 75:948.
20. van der Veen EL, Schilder AG, van Heerbeek N, et al. Predictors of chronic suppurative
otitis media in children. Arch Otolaryngol Head Neck Surg 2006; 132:1115.

21. Fliss DM, Shoham I, Leiberman A, Dagan R. Chronic suppurative otitis media without
cholesteatoma in children in southern Israel: incidence and risk factors. Pediatr Infect Dis J
1991; 10:895.

22. Lasisi AO, Olayemi O, Irabor AE. Early onset otitis media: risk factors and effects on the
outcome of chronic suppurative otitis media. Eur Arch Otorhinolaryngol 2008; 265:765.

23. Schutte PK, Beales DL, Dalton R. Secretory otitis media--a retrospective general
practice survey. J Laryngol Otol 1981; 95:17.

24. Bluestone CD, Klein JO. Consultation with the specialist: Chronic suppurative otitis
media. Pediatr Rev 1999; 20:277.

25. Elemraid MA, Mackenzie IJ, Fraser WD, et al. A case-control study of nutritional factors
associated with chronic suppurative otitis media in Yemeni children. Eur J Clin Nutr 2011;
65:895.

26. Lasisi AO. The role of retinol in the etiology and outcome of suppurative otitis media. Eur
Arch Otorhinolaryngol 2009; 266:647.

27. Taipale A, Pelkonen T, Taipale M, et al. Chronic suppurative otitis media in children of
Luanda, Angola. Acta Paediatr 2011; 100:e84.

28. Daniel SJ. Topical treatment of chronic suppurative otitis media. Curr Infect Dis Rep
2012; 14:121.

29. Gilyoma JM, Chalya PL. Ear, nose and throat injuries at Bugando Medical Centre in
northwestern Tanzania: a five-year prospective review of 456 cases. BMC Ear Nose Throat
Disord 2013; 13:4.

30. Mills R, Uttley A, McIntyre M. Relationship between acute suppurative otitis media and
chronic secretory otitis media: role of antibiotics. J R Soc Med 1984; 77:754.

31. Ycetrk AV, Unl HH, Okumu M, et al. The evaluation of eustachian tube function in
patients with chronic otitis media. Clin Otolaryngol Allied Sci 1997; 22:449.

32. Terzi S, Beyazal eliker F, zgr A, et al. The evaluation of eustachian tube paratubal
structures using magnetic resonance imaging in patients with chronic suppurative otitis media.
Acta Otolaryngol 2016; 136:673.

33. Jonsson L, Schwan A, Thomander L, Fabian P. Aerobic and anaerobic bacteria in

chronic suppurative otitis media. A quantitative study. Acta Otolaryngol 1986; 102:410.

34. Stephen AT, Leach AJ, Morris PS. Impact of swimming on chronic suppurative otitis
media in Aboriginal children: a randomised controlled trial. Med J Aust 2013; 199:51.
35. Saunders J, Murray M, Alleman A. Biofilms in chronic suppurative otitis media and
cholesteatoma: scanning electron microscopy findings. Am J Otolaryngol 2011; 32:32.

36. Lampikoski H, Aarnisalo AA, Jero J, Kinnari TJ. Mastoid biofilm in chronic otitis media.
Otol Neurotol 2012; 33:785.

37. Khosravi Y, Ling LC, Loke MF, et al. Determination of the biofilm formation capacity of
bacterial pathogens associated with otorhinolaryngologic diseases in the Malaysian population.
Eur Arch Otorhinolaryngol 2014; 271:1227.

38. Lee MR, Pawlowski KS, Luong A, et al. Biofilm presence in humans with chronic
suppurative otitis media. Otolaryngol Head Neck Surg 2009; 141:567.

39. Gu X, Keyoumu Y, Long L, Zhang H. Detection of bacterial biofilms in different types of

chronic otitis media. Eur Arch Otorhinolaryngol 2014; 271:2877.

40. Kaya E, Dag I, Incesulu A, et al. Investigation of the presence of biofilms in chronic
suppurative otitis media, nonsuppurative otitis media, and chronic otitis media with
cholesteatoma by scanning electron microscopy. ScientificWorldJournal 2013; 2013:638715.

41. Home P, Bjarnsholt T, Wessman M, et al. Morphological evidence of biofilm formation in

Greenlanders with chronic suppurative otitis media. Eur Arch Otorhinolaryngol 2009; 266:1533.

42. Mittal R, Lisi CV, Gerring R, et al. Current concepts in the pathogenesis and treatment of
chronic suppurative otitis media. J Med Microbiol 2015; 64:1103.

43. Agius AM, Wake M, Pahor AL, Smallman LA. Nasal and middle ear ciliary beat
frequency in chronic suppurative otitis media. Clin Otolaryngol Allied Sci 1995; 20:470.

44. Lasisi AO, Arinola OG, Olayemi O. Role of elevated immunoglobulin E levels in
suppurative otitis media. Ann Trop Paediatr 2008; 28:123.

45. Nemati S, Jafari Shakib R, Shakiba M, et al. Allergic Rhinitis in Adults with Chronic
Suppurative Otitis Media. Iran J Otorhinolaryngol 2015; 27:261.

46. Arguedas A, Loaiza C, Herrera JF, Mohs E. Antimicrobial therapy for children with
chronic suppurative otitis media without cholesteatoma. Pediatr Infect Dis J 1994; 13:878.

47. Lasisi AO, Olayemi O, Arinola OG, Omilabu SA. Interferon-gamma in suppurative otitis
media: significance of otorrhoea type and disease outcome. J Laryngol Otol 2009; 123:1103.

48. Si Y, Zhang ZG, Chen SJ, et al. Attenuated TLRs in middle ear mucosa contributes to
susceptibility of chronic suppurative otitis media. Hum Immunol 2014; 75:771.

49. Kenna MA, Bluestone CD. Microbiology of chronic suppurative otitis media in children.
Pediatr Infect Dis 1986; 5:223.
50. Ahn JH, Kim MN, Suk YA, Moon BJ. Preoperative, intraoperative, and postoperative
results of bacterial culture from patients with chronic suppurative otitis media. Otol Neurotol
2012; 33:54.

51. Choi HG, Park KH, Park SN, et al. The appropriate medical management of methicillin-
resistant Staphylococcus aureus in chronic suppurative otitis media. Acta Otolaryngol 2010;
130:42.

52. Park MK, Jung MH, Kang HJ, et al. The changes of MRSA infections in chronic
suppurative otitis media. Otolaryngol Head Neck Surg 2008; 139:395.

53. Brook I. The role of anaerobic bacteria in chronic suppurative otitis media in children:
implications for medical therapy. Anaerobe 2008; 14:297.

54. Vishwanath S, Mukhopadhyay C, Prakash R, et al. Chronic suppurative otitis media:

optimizing initial antibiotic therapy in a tertiary care setup. Indian J Otolaryngol Head Neck Surg
2012; 64:285.

55. Aduda DS, Macharia IM, Mugwe P, et al. Bacteriology of chronic suppurative otitis media
(CSOM) in children in Garissa district, Kenya: a point prevalence study. Int J Pediatr
Otorhinolaryngol 2013; 77:1107.

56. Orji FT, Dike BO. Observations on the current bacteriological profile of chronic
suppurative otitis media in South eastern Nigeria. Ann Med Health Sci Res 2015; 5:124.

57. Ibekwe AO, al Shareef Z, Benayam A. Anaerobes and fungi in chronic suppurative otitis
media. Ann Otol Rhinol Laryngol 1997; 106:649.

58. Papastavros T, Giamarellou H, Varlejides S. Role of aerobic and anaerobic

microorganisms in chronic suppurative otitis media. Laryngoscope 1986; 96:438.

59. Vartiainen E, Vartiainen J. Effect of aerobic bacteriology on the clinical presentation and
treatment results of chronic suppurative otitis media. J Laryngol Otol 1996; 110:315.

60. de Azevedo AF, Pinto DC, de Souza NJ, et al. Sensorineural hearing loss in chronic
suppurative otitis media with and without cholesteatoma. Braz J Otorhinolaryngol 2007; 73:671.

61. Jensen RG, Koch A, Home P. The risk of hearing loss in a population with a high
prevalence of chronic suppurative otitis media. Int J Pediatr Otorhinolaryngol 2013; 77:1530.

62. Olatoke F, Ologe FE, Nwawolo CC, Saka MJ. The prevalence of hearing loss among
schoolchildren with chronic suppurative otitis media in Nigeria, and its effect on academic
performance. Ear Nose Throat J 2008; 87:E19.

63. Couzos S, Lea T, Mueller R, et al. Effectiveness of ototopical antibiotics for chronic
suppurative otitis media in Aboriginal children: a community-based, multicentre, double-blind
randomised controlled trial. Med J Aust 2003; 179:185.
64. Lasisi AO, Sulaiman OA, Afolabi OA. Socio-economic status and hearing loss in chronic
suppurative otitis media in Nigeria. Ann Trop Paediatr 2007; 27:291.

65. Maharjan M, Kafle P, Bista M, et al. Observation of hearing loss in patients with chronic
suppurative otitis media tubotympanic type. Kathmandu Univ Med J (KUMJ) 2009; 7:397.

66. Walby AP, Barrera A, Schuknecht HF. Cochlear pathology in chronic suppurative otitis
media. Ann Otol Rhinol Laryngol Suppl 1983; 103 Suppl:1.

67. Papastavros T, Varlejides S. Reversible and permanent bone conduction threshold shift
in cases of chronic suppurative otitis media. Am J Otol 1986; 7:338.

68. Kaplan DM, Fliss DM, Kraus M, et al. Audiometric findings in children with chronic
suppurative otitis media without cholesteatoma. Int J Pediatr Otorhinolaryngol 1996; 35:89.

69. Lannigan FJ, O'Higgins P, Mcphie P. The cellular mechanism of ossicular erosion in
chronic suppurative otitis media. J Laryngol Otol 1993; 107:12.

70. Udaipurwala IH, Iqbal K, Saqulain G, Jalisi M. Pathological profile in chronic suppurative
otitis media--the regional experience. J Pak Med Assoc 1994; 44:235.

71. Isaacson G, Temple University School of Medicine, 2013, personal communication.

72. Haynes DS, Rutka J, Hawke M, Roland PS. Ototoxicity of ototopical drops--an update.
Otolaryngol Clin North Am 2007; 40:669.

73. Thornton D, Martin TP, Amin P, et al. Chronic suppurative otitis media in Nepal: ethnicity
does not determine whether disease is associated with cholesteatoma or not. J Laryngol Otol
2011; 125:22.

74. Brook I, Gober AE. Reliability of the microbiology of spontaneously draining acute otitis
media in children. Pediatr Infect Dis J 2000; 19:571.