Chapter 1

Tuberculosis (TB) remains a major health concern in developed countries. In children,

approximately 85% of reported cases are limited to the lung; the remaining 15% involve only
extra-pulmonary or both pulmonary and extra-pulmonary sites

1 2

. Among the extra-

pulmonary presentations, tuberculous otitis media (TOM) with otorrhoea is extremely rare,
accounting for 0.05-0.9% of chronic infections of the middle ear 3.
The pathogenesis of TOM is controversial. The Mycobacterium can reach the middle
ear via a haematogenous route, via mucus aspiration through the Eustachian tube or by direct
implantation through the external auditory canal and tympanic membrane perforation 4..
Diagnosis of TOM may be difficult and delayed, mainly because of a low index of suspicion,
its low prevalence and non-specific clinical signs mimicking chronic otomastoiditis (COM),
such as painless otorrhoea refractory to standard antibiotics, tympanic membrane perforation
and unilateral conductive hearing loss

1 5 6.

As in all COM cases, imaging is mandatory in

order to study the extension of the disease and any possible complications, even if it is of
little benefit in differential diagnosis, since radiological findings are not specific and signs of
aggressiveness are common to other middle ear infections. Thus, identification of
Mycobacterium tuberculosis remains the gold standard of diagnosis and therefore a necessary
step in the presence of a high clinical suspicion. In fact, prompt diagnosis as well as early
treatment are very important to avoid severe complications such as facial paralysis 1,
sensorineural hearing loss 1 and abscess of the parotid 7 or brain 8.
In this case report we present a 16-year 7-month old boy who have chronic otitis
media, who was found to have TB otitis media,chronic mastoiditis duplex, undergoing middle
ear surgery at the Audiology and Otology Unit of the Institutions ENT Department and
abscess evacuation on cerebellum by neurosurgery Kariadi Hospital Semarang.

Chapter 2
CASE PRESENTATION
The case reported 16-year 7-month old boy was referred to an emergency unit from Panti
Wilasa hospital to Kariadi Hospital cause of loss of consciousness.
His first documented diagnosis of bilateral otitis media had been made 6 years earlier, when
he was 10 years old. The symptoms in right ear and that of left ear was since 1 years earlier.
Patient had purulent otorrhea, painless, diminished hearing loss. No history of fever, facial
asymmetry, giddiness. The patient denied any history of chronic cough or hemoptysis with
expectoration, anorexia or weight loss, headache or any complaints related to vision. Htaken
treatment in the form of topical ear drops and some medication with no relief of symptom,
though the exact details of the treatment taken was not available. He paid subsequent visits
to the pediatrician over the next 6 years for otitis media that persisted despite multiple
courses of various antibiotics. Because of the chronic nature of the infection he was referred
to the ear, nose, and throat department and get antibiotics. When treated with oral and/or
aural antibiotic drops the drainage would clear transiently during treatment but would
typically reappear within 1 weeks of discontinuing medication.
Since 1 months ago the boy always felt headache and pain behind ear. He underwent CT of
paranasalis sinus. The result was mastoiditis dupleks. He did a frequent outpatient to ENT
specialist.
Since 1 week ago,the boy complained a sudden headache,intermitenly, with no medication.If
the headache became more severe, he fainted for about 30 minutes and then regained his
conciousness.While the headache begin, he had no nausea or vomitus. No

cough, no

influenza, no fever. The pain became worsen in retroauricula. No seizure. Defecation dan
urination was normal. At the time when he had loss his conciousness, his parents carried him
to Sultan Agung Hospital then he was underwen CT cranial and referred to ENT specialist.
The MSCT examination result was normal, then he was discharged from hospital. He was
given a medication that consist of 2 drugs (unknown) and eardrops.
3 days after discharged, the boy did not complaint any of pain. The following day, he felt pain
that became more severe. Then he had loss his conciousness. His parents took him to Panti
Wilasa hospital and hospitalized for 1 weeks then he was discharged.

Since 1 day before admitted, the boy was complained a headache with no nausea and vomit
that happened only once. The boy became unconciousness again then his parents took him to
Panti Wilasa hospital and referred to dr.Kariadi Hospital

Figure 1. Patient Profile

In Emergency department of Kariadi hospital, the boy still unconciousness,Glassglow Coma
Scale (GCS) E3M5V4, vital signs within normal limits. Status localist right ear and left there
was mukopurulen othorrea, and subtotal tympanic membrane perforation. Nose and throat
within normal limits, no lumps on the neck. The patient was consulted by opthalmologist and
there was an increament of intracranial pressure. There were no seizure, no hemipharese, no
facial asymetry. The microbiologist unit did a swab in ear discharge of right and sinistra
auricula and stained for Ziehl-Nielsen. The microscopic revealed a positive acid fast bacill
and then the boy was medicated by antituberculosis drug therapy of INH, rifampicin,
pyrazinamide and ethambutol was commenced and also steroid, despite reservations about
starting treatment on the basis of a swab result alone. The culture from ear swab revealed
Staphylococcus haemoliticus. Examination of the head with contrast MSCT Scan May 4th,
2015 there were lesions rounded shapes, limit portion partly irregular edges firmly on the
right cerebellum 1,78x1,88x2,31 cm size with surrounding edema urgent IV to the left
ventricle, cerebellar abscess tends picture. (Figure 3). It found signs of increased intracranial
pressure and mastoiditis otomastoiditis right and left. (Figure 2). Thoracic X-rays of the heart
and lungs within normal limits (Figure 4). Laboratory tests obtained leukocytosis (14,700 /
uL). The patient was also being consulted to neurosurgery departement and ENT departement
then he was programmed for craniotomy surgery of abcess evacuation and mastoidectomy.
The boy was hospitalized in High Care Unit

Figure 3. MSCT Scan of Mastoid non kontras revealed duplex mastoiditis

Gambar 6. Rontgen thorak

Figure 2. MSCT Scan of the head with contrast

revealed cerebellar abscess

Figure 3. X-Ray Thorax revealed

normal

Second day in HCU, the boy was undergone a craniotomy surgery of abcess
evacuation and radical mastoidectomy. Capsul of abscess sent to pathology anatomi

departement. From Craniotomy obtained pus as much as 5 ml. There was a defect in the wall
mastoidectomy postero inferior mastoid where duramater was exposed to the surrounding
granulation tissue. (Figure 5).

Figure 5. Mastoidectomy shown a defect on mastoid cortex

The third day in HCU, the boy regained his conciousness after surgery. Evaluation from
optalmologist revealed no papil edema as a sign of increament of intracranial pressure.
The Fourth day in HCU, the boy was moved into pediatrics ward on isolation room
He is a second child from 2 children, her sibblings are normal. There was no child in his
family history who has disease like him and no chronic cough. His immunization history did
not complete.
Her father is a labor with average income is Rp 1.500.000,-/month and her mother is a
housewife. The child stay in house with his father, mother and his elder brother. Health cost
was covered by JKN PBI class III. Social economic revealed was low economic society.
From physical examination on pediatrics ward, a 17-year 7-month old boy, with weight was
50 kg and height was 172,5 cm. General conditions were compos mentis, spontaneous
breathing, and no retraction. Blood pressure was 110/80 mmHg. Heart rate was 89
beats/minute and regular with good pulse. Respiratory rate was 21 times/minutes. Body
temperature was 37,60C. There were dry gauzess covered post craniotomy, with minimal
production was minimal. There was not discharge on left ear. On right ear, there was a
gauzess covered, there was not discharge. Nasal flare was negative, no nasal discharge,
mouth was normal. Chest: symmetrical, lungs breath sound were vesicular, regular, normal
and no wheezing. The first and second heart sound were normal, no noisy, and no gallop.

Abdomen was flat, no enlargement of liver and spleen. The bowel sound was normal. All
extremities were not cyanotic, capilary refill <2. Physiology reflex was positve normal and
there were no pathology reflex. There was no klonus at inferior extremity. The muscle tone
was normal. Antropometry examination was HAZ: -0,25 SD; BMI: -1,98 SD. Nutritional
status was good nutrition, with normal weiht and normal stature.
Cranial nerve examination were: olfactorius nerve (N I) is difficult to assess; optikus nerve
(N II) was normal with positive light reflex; occulomotor nerve (N III), troklearis nerve (N
IV) and abdusen nerve (N VI) were normal, the eyeball was free to move. Trigeminal nerve
(N V) was normal, with positive corneal reflex. Fascialis nerve (N VII) was normal with
symetrical nasolabial folds. Vestibulocochlear nerve (N VIII) was difficult to access.
Glassofaringeal nerve ( N IX) and vagus nerve (N X)were difficult to access, swallowing was
good. Accessorius nerve (N XI) was difficult to assess. Hipoglossus nerve (N XII) was
normal, and there was no tongue deviation.
Laboratory examination was obtained high blood leucocyte 15,6 x 10 3 / uL. It was fit with the
last blood examination at Panti Wilasa Hospital which had 12,6 x 103/uL and 20,9 x 103/uL
repeatedly at 2016 April 7th and 20,9 x 103/uL at 2016 April 11th. Leucocyte differential
count was still normal. Peripheral blood smear picture was obtained light anisoistosis and
light poikilocytosis. There was high leucocyte estimation with neutrophilia and atypical
lymphocyte. Thrombocyte estimation was risen and there was also found big thrombocyte.
Glucose level was still normal and also the electrolyte. Results of a human
immunodeficiency
virus (HIV) antibody test were negative.
Initial

diagnosis

for

this

patient

were

post

craniotomi

ec

cerebellar

abscess,

meningoenchepalitis TB, mastoiditis duplex, tuberculous otitis media. He get manitol and
dexametason treatment until three days and tappering off and fixed dose combination for TB
treatment 3 tab/24 hours, ceftriaxone 1g/12 hours, gentamicyn 200 mg/24 hours,
metronidazole 400 mg/12 hours.
On the second treatment in pediatrics ward, he was getting better. He obtained stained of
sputum. The result was Klebsiela spp (ESBL) on the 8 th of treatment and he got amicasin as
the sensitivity of the sputum culture. Gentamicin was stopped. The others antibiotic
continued until 4-6 weeks.

The patient underwent lumbar puncture on day care 12 th, and obtained 0.44% decrease in
CSF glucose, MN 2, PMN 0, protein 71. Microscopic was not found either AFB, gramnegative bacteria and gram-positive bacteria. CSF culture results was sterile.
Children also underwent ear toliet 3 times a week, and examination Gene Xpert for ear
granulation tissue and TB culture examination and inspection PA granulation tissue. The
result was not found MTB.
Children also performed spirometry with the results PEV1 / FVC 110.1%; PEV1 77.8%;
FEV1 70%. It was revealed mild restrictive.
Children were treated for 20 days, His conditions when discharge were well, no complaints,
postoperative wound dry, no headache, no parese n. Facial, no hemiparese. He programmed
to control routine at ENT departement and will do a hearing test and control to Repirology
departement. Drugs given at home were cefixime 200 mg / 12 hours; metronidazole 400 mg /
8 hours; 3 adult FDC tablets / 24 hours, ear drops tarivid 10 GTT / 12 hours.(figure 6)

Figure 6. The wound post operation craniotomy and radical mastoidectomy on

retroauricula was dry and good healing proscess

Chapter 3

Tuberculosis remains the leading cause of death secondary to infectious diseases

worldwide in persons older than 5 years. 1 Tuberculosis of middle ear is a comparatively rare
entity usually seen in association with or secondary to pulmonary tuberculosis. Tuberculosis
is one the major infectious disease with predominant involvement of lung and lymph nodes
but tuberculosis of the middle ear is uncommon.2 It is one of the most common infectious
diseases of developing countries including Indonesia. 3 TB can also be transmitted
congenitally and is associated with a high incidence of ear involvement. However, congenital
TB is extremely rare and hardly ever presents with isolated ear involvement. It is difficult to
assess its true incidence as the large reported series have been selected from hospitalized
subgroups with established tuberculosis.4,5,6 Early diagnosis and prompt treatment may
prevent ear damage and the central nervous system complication.4,5,6
History
The involvement of the temporal bone by tuberculosis was first described by Jean
Louis Petit in 18 th century.7 The clinical signs of the disease were first outlined by Wilde in
1853.8 In1882, Koch demonstrated Tuberculous bacillus and Esche isolated bacillus in the
secretion of middle ear in 1883.9,10
Incidence
It is difficult to assess its true incidence as the large reported series have been selected
from hospitalized sub-groups with established tuberculosis.4,5,6 Primary tuberculosis of the ear
has rarely been reported, and the disease is usually secondary to infection in lungs, larynx,
pharynx and nose.4,11 In the west, the annual incidence of tuberculous otitis media has
decreased during the past 60 years from 5.5 cases per 100,000 population before 1953 to 2.3
cases after 1953.9,13,14 This decrease has been attributed to the declining incidence of
tuberculosis itself. However, in areas where tuberculosis is endemic, data have shown that
there has been a steady increase in its incidence. 15 In preantibiotc era, 2-8% of all the cases of
chronic suppurative otitis media were tuberculosis in nature and infants less than 1 year of
age comprised 50% of these.16 There are only very few cases of tuberculous otitis media
reported in the literature. Mills study mentioned that the incidence of tuberculous otitis media
has fallen dramatically since the beginning of this century.17 At that time 3-5% of cases of
otitis media were due to tubercle bacillus, whereas today the condition is rare. 17 Turner and

Eraser study reported in 1915 that 2.8% of all cases of suppurative otitis media were due to
tuberculosis.17
Kirsch et al study revealed 9.5% of children with tuberculous otitis media were less
than 5 years of age.16 The incidence of tuberculosis of middle ear is very low, tuberculosis
accounts for only 0.04% of all cases of chronic suppurative otitis media. 12 When it does
occur, it is associated with substantial morbidity, and a delay in initiating therapy can lead to
serious complications. In view of the extremely low incidence (<1%) of ear disease, it often
precludes the diagnosis, especially in the absence of concomitant tuberculous focus
elsewhere.19
Etiopathogenesis
Tuberculous otitis media (TOM) is caused by Mycobacterium tuberculosis, of which
bovis and hominis are generally affecting the ears. Sometimes rare species of mycobacterial
infections can cause atypical in special situations especially in immunodeficiencies.
Mycobacterium bovis is less frequently seen than Mycobacterium hominis. TOM is usually
due to ingestion of infected cow's milk. The route of spread of tuberculosis to middle ear has
been argued for many years; the most logical route of entry of organisms being via pharyngotympanic tube.20 ADAMS in a study of tuberculosis patients undergoing thoracoplasty
showed abnormal pharyngo- tympanic tube patency in all patients who developed otitis
media.5 Tuberculosis involving tympanic membrane is usually secondary to pulmonary
tuberculosis, spreading through the Eustachian tube, most often by the forceful expulsion of
haemoptysis and infected blood into the tympanum. The condition usually begins as an
apparent serous otitis media. Infection can also reach the middle ear via external auditory
canal or by haematogenous spread. Proctor and windsay study found the strong evidence of
tubercle bacilli reached the ear by haematogenous route. 21 The latter results in the direct
involvement of the mastoid bone producing necrosis and it progress to involve middle ear.21
Congenital form
Rarely there can be a congenital tuberculous otitis media. The fetus or the newly born
are susceptible to various forms of contamination; directly through the placental circulation;
by aspiration of infected amniotic fluid or in the act of birth, by contact with infected genital
mucosa. It can also occur with congenital form of transmission of infection from mother to
fetus.21

Clinical Presentation
The clinical signs and symptoms of tuberculous otitis media were first documented in
1853.22 Since then, many so called characteristic clinical feature have been described in the
literature.23 Generally tuberculosis of middle ear is unilateral. Tuberculosis of middle ear is
characterized by painless otorrhoea which fails to respond to the usual antimicrobial
treatment, in a patient with evidence of tubercle infection elsewhere followed by multiple
tympanic membrane perforations, abundant granulation tissue, and bone necrosis,
preauricular lymphadenopathy.23,24 There may be multiple perforations in the early stages, but
they coalesce into a total tympanic membrane perforation accompanied by a pale granulation
tissue.4,14,22
MYERSON'S experience demonstrated that a discharge from the middle ear
appearing without pain in a tuberculous individual should be considered Tuberculous.25 In
early stages of tuberculous otitis media, the drum looks dull and some dilated vessels can be
observed.26 The tympanic membrane then becomes thickened and landmarks are obliterated. 26
The exudate in the middle ear may be thick and is sometimes confused with the infected
keratin debris of a cholesteatoma. Periauricular fistulas, lymphadenopathy, and facial palsy
are infrequent findings. Late complications include facial paralysis, labyrinthitis,
postauricular fistulae,subperiosteal abscess, petrous apicitis, and intracranial extension of
infection. Facial nerve palsy has been reported in cases of tuberculosis otitis media even if the
anti tuberculosis therapy has been started. Associated facial nerve paralysis is seen in
approximately 16% of adult cases and 35% of pediatric cases.15,27 Tuberculous otitis media is
more likely to cause infection of the labyrinth than the usual purulent forms of otitis. 29
However, due to gradual spread of the disease, symptoms caused by involvement of the
labyrinth are uncommon, even though the function is destroyed.26
In this Case, the patient had othorrea since he was 10 years old. It was initially on
unilateral otitis on right otitis media, and then bilateral He had painless otorrhoea which fails
to respond to the usual antimicrobial treatment, hearing loss and followed by multiple
tympanic membrane perforations. There was no preauricular lymphadenopathy. Long term
evaluation, the painless purulent otorhea still ongoing, the patient had severe headache and
also loss of consciousness, there was no facial nerve palsy, no tinnitus, no dizziness. This
patient had mastoiditis duplex and cerebellar abscess caused by TOM and Chronic Supurative
Otitis Media (CSOM) by other microbia.
Differential diagnosis

The differential diagnosis of tuberculous otitis media includes fungal infections,

Wegener's granulomatosis, midline granuloma, sarcoidosis, syphilis, necrotizing otitis
externa, atypical mycobacterial infections, lymphoma, histiocytosis X and cholesteatoma. 30
These diagnoses can be ruled out clinically by the presence of pain and the type and
consistency of the discharge. In diagnosing tuberculous otitis media, it is important to
consider it as a differential diagnosis of chronic suppurative ottis media. The diagnosis of
tuberculous otitis media is often missed in the early stages or is made only after surgical
treatment for otitis media.12,13,31,32
Investigation
Pure Tone Audiogram
The main audiolologic feature of TOM is the deafness out of proportion with the
apparent degree of development of diease seen in the otoscopy. Generally it is moderate to
severe hearing loss. It can be conductive, senserioneural or mixed hearing loss. However,
McAdam and Rubio reported a case of slow development of hearing loss, suggesting
therefore that the hearing can be variable.33
In this case, the patient did not audiogram yet. He will perform this test 3 months after
mastoidectomy.
Radiology
Radiological studies such as simple x-ray mastoid or computersed tompgraphy (CT)
scan revealed no specific characteristics, but together with clinical and other complementary
tests,can strengthen the suspected diagnosis.
It also helps to find out the degree of involvement of structures and enable for better planning
when surgery is needed. Several authors argue that the detection of an x-ray of the mastoid
shows well pneumatization and sometimes filled by soft tissue, in patients with clinical of
chronic otitis media, suggests the possibility of etiology of tuberculosis.7,10,34. It is essential to
remember that a normal chest x-ray does not rule out the possibility of tubercular infection of
ear. Radiologic findings are often nonspecific. Bony erosion is uncommon 35, but
demineralization of the bone has been reported. A well-pneumatized mastoid with chronic
otitis media is suggestive of tuberculous otitis media but not diagnostic, as these cases can
also have sclerotic and destructive mastoid lesions. Recent studies have shown that CT is the
best modality available for the diagnosis of tuberculous mastoiditis; CT provides more

information than do standard plain films and it is more accurate and useful than polycycloidal
tomography and magnetic resonance imaging.36
In this case, patient underwent CT scan of paranasalis sinus revealed mastoiditis duplex with
errosion on hearing bone, and also undergone CT scan of head revealed cerebellar abscess.
He had a normal chest x-ray. But it was not excluded matoiditis and cerebellar abscess may
be caused by MTB.
Skin Test
This is a routine screening test for tuberculosis. In this test purified protein derivative (PPD)
is used. It is positive in tuberculosis. But a negative test does not exclude the possibility of
the presence of tuberculosis.35
In this case , the patient had negative test for PPD test.
Bacteriological and histological studies
The diagnosis of tuberculosis otitis media is based on demonstration of acid fast
bacilli within granuloma in biopsy materials, with or without the culture of mycobacterium
tuberculosis from the biopsy, aural discharge or aspirate of the middle ear. Demonstration of
acid fast bacilli in the ear discharge is difficult due to superadded infection. 2 Unfortunately,
culture of the discharge has a low yield. Therefore, the clinician must maintain a high index
of suspicion, perform multiple cultures and look diligently for evidence of tuberculous
infection of other organs.30 The positivity of Acid Fast Bacilli in ear discharge varies from 5
to 35% and on repeated examinations it improves to 50%. 37 However, confirming the
diagnosis can be difficult because the high rate of secondary bacterial infection of the
tuberculous middle ear (79%) can prevent the identification of Mycobacterium tuberculosis
on either staining or culture.9,38 Antiobiotic sensitivity to various anti tubercular drugs is
gaining importance in recent years because of increase bacterial resistance. Diagnosis is made
from direct smear examination and culture of discharge, histopathological examination from
middle ear. Histology of tissues reveals granulations with epitheloid cells and multinucleated
giant cells (Langhans giant cells), areas of central necrosis, lymphocytic infiltration,
ulceration and signs of bone resorption. Histopathological examination of the involved
middle ear and mastoid mucosa will show three types of changes: military, granulomatous
and caseous.4 The military type is associated with superficial infection, the granulomatous
type with superficial bony involvement the caseous type with massive necrosis and
sequestration.4

In this case, the patient had a positive of acid fast bacilli in the ear discharge and also fond
the other gram positive bacterial. It seems suspicous of superadded infection. The culture of
his discharge revealed Staphylococcus hemolyticus. Histopathology of granulation discharge
showned infection non specific, there was no either granulations with epitheloid cells and
multinucleated giant cells (Langhans giant cells), areas of central necrosis, and lymphocytic
infiltration. The culture of granulation and gene expert revealed negatif for MTB and
mycobacterium other than TB. The capsule abscess also not found tuberculosis. Culture of
LCS, there was sterile.
Staining for AFB in TB otitis generally has less than 60% sensitivity. Unfortunately,
the yield from mycobacterial cultures from extrapulmonary sites, including aural specimens,
is just as low in some studies. The use of antibiotic containing otic drops in many patients
before the diagnosis of TB otitis, especially preparations containing neomycin or
fluoroquinalones, may contribute to the failure to detect TB in aural cultures. Most cases of
suppurative otitis are treated empirically. Among those that do get cultured before or between
courses of antibiotics, superinfections cause a high percentage of cultures to grow bacterial
agents such as Streptococcus spp., Staphylococcus spp., Proteus. spp., and other bacteria
associated with otitis media that further delay the correct diagnosis.39
Other Test
If facilities are available, polymerase chain reaction (PCR) of the ear discharge can be done.
Other investigations such as erythrocyte sedimentation rate, along with serological status to
know the immune status of the patient are done.39
In this case, the patient did not obtain PCR. There were no facility in Kariadi Hospital.
Treatment
Medical Treatment
Antituberculous therapy is the treatment of choice for tuberculous otitis media. The
first cures for TOM through antibiotics were reported by Grief and Gould in 1948. The first
therapy of success for TOM used only streptomycin, but the current standard chemotherapy
using combination of drugs. It should be managed with antitubercular therapy (category-1). It
includes 4 drug regimen in first two months (Isoniazid, Rifampicin, Pyrizinamide and
Ethambutol) followed by 2 drug regimen in later 4 months (Isoniazid and Rifampicin). These
regimens are given as per criteria of Indonesia. Currently, the resistance to antitubercular
drugs is a major problem and one of the main factors of difficulty in combating the disease.

In this case, patient are given 3 tablet adult fixed dose combination (FDC) RHZE per day
for first 2 months and steroid (methylprednisolon 2 mg/kg/day) for 2 weeks and tappering off
for 4 weeks and followed by 2 drug regimen 3 tablet adult FDC (RH) for 10 months later.
These regimen are given caused by suspicious of meningitis TB in this patient. Although LCS
culture was sterile but the glucose level of LCS decerease 40%.
Surgical Treatment
Myerson advised a radical mastoidectomy if any of the following complications
develop: facial paralysis, subperiosteal abscess, labyrinthitis, mastoid tenderness and
headache.25 Surgery may be required in some cases to remove sequestra and improve
drainage.3 When surgery is combined with adequate chemotherapy, there is a good chance of
healing with a dry ear with a good prognosis.17
Recently, the role of surgery has been revised. In the past, it was done to provide
drainage, to control spread to central nervous system and to relieve facial paralysis. The
advent of specific chemotherapy has challenged all this, and today surgery should be reserved
for decompression of the facial nerve and for removal of necrotic material which might
provide a nidus for the organism to remain out of reach of anti tuberculous therapy.
Sometimes, demonstration of sequestra in temporal bone during surgery will give a clue to
diagnosis.
Complication of Otitis Media and Mastoiditis
Middle ear infections and mastoiditis are rare manifestations of extrapulmonary
tuberculosis in the United States and therefore many physicians do not include these
manifestations of TB in their differential diagnoses.2 Skolnik and colleagues2 estimated that
tuberculous otitis media was found in less than 0.3% of patients with tuberculosis, and that
less than 0.1% of all otitis media and mastoiditis infections were caused by tuberculosis.3
Acute and chronic otitis media can cause intratemporal and intracranial
complications. Intracranial complications include meningitis, brain abscess, epidural abscess,
subdural empyema, and lateral sinus thrombosis. These conditions are potentially dangerous
or even fatal. With the development of new antibiotics and improvements of inpatients care,
the incidence of intracranial complications has been remarkably reduced nowadays compared
with the pre-antibiotic era. However, mortality of these complications is still high and
improper use of antibiotics can change or conceal the characteristics of the disease which can
make diagnosis difficult. Otogenic brain abscess is the second most common intracranial

complication of acute otitis media (0.5 percent).1) In the past, the mortality rate of otogenic
brain abscess was 14 to 35 percent, but has now decreased to 3 percent.2) The selection of
antibiotics and appropriate surgical intervention are mighty important in the treatment of
otogenic brain abscess. However, the extent of surgical procedures and optimal timing for
these intervention are still matter of debate.40
Otogenic brain abscess may be extradural (most common), subdural, intracranial or
intracerebellar. Temporal lobe abscesses are more common than cerebellar abscesses.
Subdural abscess are uncommon and have a tendency to extend to nearby areas. The
inflammatory process most frequently spreads into the endocranium directly through
destruction of the bony walls of the middle ear or through thrombophlebitis or preformed
pathways Although, the current neurosurgical options are to drain the abscess repeatedly
through burr holes or to excise it completely with the capsule through a temporal or suboccipital route depending on its location, followed by a mastoidectomy by the ENT surgeon
to eradicate the primary source of infection.41
Cerebellar signs & symptoms were present in 75% of cases of cerebellar abscess.The
most common abnormality in physical examination was a decrease in the level of
consciousness (20 cases, 61%). Similarly, Deric also reported headache (92%), fever (91%)
and vomiting (68%) as the most common symptoms, while photophobia and vertigo were less
common (38% and 30% respectively)42. So, for all practical purposes, all theses symptoms
should suggest intracranial pathology if not proved otherwise and proper clinical examination
can help us guide in diagnosing otogenic brain abscess and its location41

Figure 7. Some of clinical manifestation of cerebellar

Basically, there are five situations involved in the development of abscesses in the CNS:
1. suppurative focus adjacent to the CNS (otitis, mastoiditis, sinusitis); 2. hematogenous
spread of infectious focus; 3. opening the dura mater: surgical or traumatic; 4.

immunosuppression; 5. unknown source.Contiguous foci of infection of the CNS, such as

otitis, mastoiditis, sinusitis and dental focus are the main cause.Usually lead to single abscess,
surface, adjacent to the focus, and has a good prognosis with clinical treatment as is the case
presented here. Classically, otitis and mastoiditis lead to the appearance of temporal abscess
or cerebellar or time-cerebellar combined42.
M. tuberculosis is a rare cause of brain abscess; however, this organism should be
considered in patients with disseminated tuberculosis or in individuals from areas
where tuberculosis is endemic. The present study noticed four (5.4%) TBA cases in five-year
study on brain abscesses. In all these four cases, there was an evidence of pus within the brain
and bacteriological proof of AFB in the pus by microscopy as well as by culture. In 1978,
Whitner reported a case of TBA and reviewed 57 similar cases in the world literature. He
found that only 16 of the 57 cases could be considered as verified TBAs in terms of the
following three criteria: 1. Macroscopic evidence from surgical or autopsy material of true
abscess formation within the brain substance, characterized by cavity formation with central
pus; 2. Sufficient histological description to assure that the inflammatory reaction in the
abscess wall was composed predominantly of vascular granulation tissue containing acute
and chronic inflammatory cells particularly polymorphonuclear leukocytes; and 3. Proof of
tuberculosis origin by either a positive culture of the pus for M. tuberculosis or demonstration
of acid-fast organisms in the pus or abscess wall. After Whitner reviewed the world literature,
isolated cases of TBAs have been reported. In most of these cases, proof
of tuberculosis origin was by either a positive culture of the pus for M. tuberculosis or
demonstration of acid-fast organisms in the pus, except in the study by Kaushik et al., the
diagnosis was confirmed by Polymerase chain reaction (PCR) for M. Tuberculosis MPB64.
Thus, newer techniques like PCR may provide useful tool for diagnosis of tuberculosis from
paucibacillary specimens like pus in which conventional methods may show low sensitivity.
Even in the present study, a new technique, In vitro HMRS, was evaluated for the diagnosis
of TBA. The case of concomitant tuberculous and pyogenic brain abscess showed spectra
similar to pyogenic brain abscess. However, succinate (marker for anaerobes) peak was
absent suggesting that the pus specimen may have facultative anaerobes. As there are no
major peaks in TBA except that of lactate-lipid, the total spectra were masked by the
pyogenic abscess spectra. However, the Gram stain, ZN stain, and gold standard conventional
culture gave the complete etiological diagnosis.42
Whitener's review of 16 cases also revealed the following common features in TBA: 1.
Frequent occurrence of TBA in the third and fourth decade of life; 2. A 35% incidence of
multiple brain abscesses; 3. Predominant supratentorial location of the abscess in the frontal
lobe; 4. Evidence of extra CNS tuberculosisin 85% cases; and 5. Occurrence of TBA despite
antituberculous treatment and presentation with rapidly progressive neurological deficit.42
Contrary to Whitener's observations, one of our patients was a 15-year-old girl.
clearly shows that TBA can occur at any age. Of four cases in the present study, one (25%) of

the patients presented with multiple brain abscesses involving temporal, parietal, and
occipital lobe. Remaining three cases had a solitary abscess involving frontal, temporal, and
parietal lobe. Multiple TBA is rare, with only a few reports appearing in the literature. Figure
8 also shows that TBA can occur in any part of brain involving the ventricles.42

Figure 8. Details of tuberculous brain abscess patients from the available literature
In the present study, the coexistence of pulmonary tuberculosis was seen in two
patients. CNS tuberculosisoccurs secondary to hematogenous spread of M. tuberculosis from
pulmonary Koch's. Among the laboratory diagnostic modalities used, ZN stain and culture
were found to detect the presence of AFB in all the four cases. There were three of the pus
specimens grew M. tuberculosis as sole isolate. The fourth case was of concomitant
tuberculous and pyogenic brain abscess. A second concomitant pathogen with TBA is rare.
There are very few reports of concomitant tuberculous and pyogenic brain abscess that
appeared in the literature, namely dual infection due to Streptococci, Toxoplasma,
andEchinococcus.42
TBAs are an unusual clinical presentation of central nervous system tuberculosis
occurring extremely infrequently in developed countries, and almost always in
immunocompromised patients. TBA is an uncommon clinical entity, even in countries
where tuberculosis is endemic. It occurs in only 4 to 8% of patients with CNS TB who do not
have HIV infection but in 20% of patients who do have HIV infection. We encountered one
such case which yielded a pure growth of M. tuberculosis. Fischl et al described a case of
TBA and toxoplasma encephalitis in a Haitian woman with AIDS. Farrar et al. reported TBA
in a 43-year-old man with a history of intravenous drug use. Vidal et al (2003) reported a case
of TBA in a patient with AIDS. They also reviewed the literature from 1981 to 2002 and
found eight cases of TBAs in HIV infected patients. Kaushik et al also reported TBA in a 26year-old male who was HIV seropositive. Of these four patients, from the present study,
patient no. 1 died who also had an altered level of consciousness at the time of admission. He
also gave history of fall but no history of extra CNS tuberculosis. Rest three patients were put
on anti-Koch's treatment and being followed up regularly.42

Brain abscess is one of the life threatening complications of chronic otitis media in
particular cholesteatoma. All the patients in this study presented with headache and
vomitting. The presence of these symptoms in association with cholesteatoma is very
suggestive of intracranial complications. Otogenic brain abscess affects usually children more
than adults. Sennoroglu et al, Nesic et al found high incidence of brain abscess in children
and young patients. Males are 4-8 time more affected than female as shown by Kempf et al,
Nesic et al, Kurien et al. In the present study fifty percent of patients were younger than 15
year and the mean age was 25 years with male to female ratio of 5:1.43
The diagnosis of Brain Abscess was established by CT scanning. CT scanning with
and without contrast is the best diagnostic tool and best monitor of treatment in Brain
Abscess . Its use had reduced the morbidity/mortality rate markedly. It is not only a guide to
the location and size of the abscess, but also locates the defects in the tegment and trautmans
triangle. Brain Abscess are located at the same side as the diseased ear1 . Temporal lobe
(cerebral) and cerebellum are the two common location for otogenic brain abscess. Deric et al
found 28 cerebral and one cerebellar abscess, whereby Sennoroglu et al found 54% cerebral
and 44% cerebellar abscess.43
The most common cause of brain abscess is direct extension of infection through a
bony defect, in the tegment antri (in case of cerebral abscess) or in trautmans triangle (in
case of cerebellar abscess). Proteous and anaerobe species were the most common organism
cultured from the ears and from the abscesses. Sennoroglu et al, Chen et al, and Qureshi et al
showed in their studies that proteous, streptococci and anaerobe species were the most
common organism in Brain Abscess. 43
Tuberculoma formation is the most frequent manifestation of parenchymal central
nervous system (CNS) tuberculosis. The tissue reaction to AFB depends on the host
immunity, the inoculum size of the bacteria, the specific tissue infected and whether the
patient received chemotherapy. The pathogenesis of tuberculous brain abscess is similar to
other forms of CNS tuberculosis. Tuberculous brain abscess characterized by a focal
collection of pus containing AFB and surrounded by a dense capsule of vascular granulation
tissue containing acute and chronic inflammatory cells; and presence of tubercular bacilli in
the pus. Clinically patients with cerebellar tubercular abscess present with fever, headache,
alteration of consciousness, seizure, cerebellar signs and or with hydrocephalus. Both CT and
magnetic resonance imaging (MRI) can detect intracranial abscesses; however, these studies
cannot easily differentiate between tuberculous and pyogenic abscesses. Findings on CT
scans are assumed to be characteristic of tuberculous abscesses if there is a thick-walled
lesion with surrounding edema, and pyogenic, if abscess walls is relatively thin. Recently,
MRI has been used for better tissue characterization in CNS tuberculosis. The gold standard
of diagnosis remains on demonstration of innumerable tubercle bacilli in aspirated pus.

However, the absence of tubercle bacilli does not necessarily imply the absence of a
tuberculous brain abscess.44
.

PROGNOSIS
In the past, many people died of tuberculous otitis media, before the advent of
streptomycin. Now with combined antituberculous therapy, the results improved. However,
generally there is no hearing improvement.26 The repair of hearing loss can be achieved after
cessation of otorrhoea by tympanoplasty. The recoveries of sensironeural hearing loss not
usually occur with the healing process. Facial paralysis will improve partially or completely.
The speed and extent of recovery were directly related to the time interval between the
installation of facial paralysis and the start of treatment.39
Children usually respond well to antituberculous treatment. Otorrhea usually resolves
within the first 2 months of the institution of pharmacotherapy. Tympanoplasty may be
performed to improve hearing in cases of conductive hearing loss, but should be delayed until
after medical therapy has begun to take effect, as surgical wounds may not heal well if
surgery is performed while there is still active infection.39

CONCLUSION
Tuberculous otitis media is a rare disease, if left untreated, can damage middle ear and
other surrounding structures. It should be considered in differential diagnosis of chronic
middle ear discharge that does not respond to usual therapy. Delay in diagnosis can lead to
complication. A high level of clinical suspicion is needed for early diagnosis and
antitubercular therapy should be started as soon as possible to prevent the possible
complication.46
Tubercular brain abscess are uncommon and tubercular cerebellar abscess are rarely
reported. Most of these cases occur in immunocompromised patients. Extrapulmonary
tuberculosis is observed in approximately 20% of all tuberculosis (TB) cases and its
incidence has increased in the recent years. Central nervous system (CNS) tuberculosis, the
most dangerous form of tuberculosis, accounts for approximately 5% of extrapulmonary
tuberculosis. In the differential diagnosis of intra-cranial tuberculosis (ICTS), images on the
radiological findings should be differentiated from other causes of space.45

In the central nervous system, tuberculosis is usually a meningeal infection or a

tuberculoma; rarely is it an abscess, and even more rarely is it a cerebellar abscess. Diagnosis
is frequently quite delayed in central nervous system involvement. Usually patients with
intracranial tuberculosis are immunocompromised. Among immunocompetent patients,
children and the elderly are most commonly affected..Tuberculous abscesses are more often
supratentorial and are believed to result from localized extension of infection from the
sinuses, mastoids,or bone. The primary focus of infection in this case remains in doubt.46

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