CASE REPORT

A 17TH YEARS OLD BOY WITH TUBERCULOUS OTITIS MEDIA, MASTOIDITIS

DUPLEX AND CEBERERRAL ABSCESS

PRESENTED BY:
Islammiyah Dewi Yunianti

SUPERVISOR:
Dr. Dwi Wastoro Dadiyanto, SpA (K)

DEPARTMENT OF CHILD HEALTH

MEDICAL FACULTY OF DIPONEGORO UNIVERSITY/
DR. KARIADI HOSPITAL SEMARANG
2016

CONTENTS

CONTENT

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CHAPTER I INTRODUCTION

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CHAPTER II CASE REPORT

...............................................

CHAPTER III DISCUSSION

...............................................

RESUME

...............................................

PROBLEM SCHEME

...............................................

REFERRENCES

...............................................

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.
a

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.
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.
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
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.

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. 9,16,20,21,26
Unfortunately, the yield from mycobacterial cultures from extrapulmonary sites, including
aural specimens, is just as low in some studies .9,16,21,30 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.
7,9,14,18,21

A Case of Tuberculous Otitis

Media
Tanya Halvorsen, MD1
Heather Townsend, MD2
William Stauffer, MD, MSPH, DTM & H3
Kiran Belani, MD4
Deepak Kamat, MD, PhD5Clin Pediatr. 2006;45:83-87

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.
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 colleagues [2] 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.2)
Korean J Audiol 2014;18(2):76-79

A Case of Otogenic Brain Abscess Causing Lossof

Consciousness
Min Kyu Kwak, Jae Ho Chung, Seung Hwan Lee, and Chul Won Park

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 location

Figure 7. Some of clinical manifestation of cerebellar

IOSR Journal of Dental and Medical Sciences (IOSR-JDMS)
e-ISSN: 2279-0853, p-ISSN: 2279-0861.Volume 15, Issue 5 Ver. V (May. 2016), PP 36-47
www.iosrjournals.org
DOI: 10.9790/0853-1505053647 www.iosrjournals.org 36 | Page

Monitoring the Evolution of Otogenic Brain Abscess--Changing

Trends in Management
Dr Abhinandan Bhattacharjee1, Dr Rudra Prakash Singh2, Dr Jerina Nazrin3
1(Assistant

Professor, Department Of ENT, Silchar Medical College, Assam, India)

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
treatment1-4 as is the case presented here. Classically, otitis and mastoiditis lead to the
appearance of temporal abscess or cerebellar or time-cerebellar combined

1. 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.[2] 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[1] 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
oftuberculosis 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[1]
reviewed the world literature, isolated cases of TBAs have been reported.[617] 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.,[15] the diagnosis was confirmed by Polymerase chain
reaction (PCR) for M. tuberculosisMPB64. 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 1HMRS, was evaluated for the diagnosis of TBA.
Absence of multiplet of amino acids-lipids at 0.9 ppm seems to be a hallmark of
TBAs. Similar findings have been reported in the literature.[18,19] An attempt was
made to compare these spectra with the pus specimen, which showed pure growth of
anaerobe (pyogenic brain abscess). Pus specimens which showed the presence of
anaerobes on culture revealed the presence of multiplet at 0.9 ppm, along with lactatelipid at 1.3 ppm, acetate at 1.92 ppm, and succinate at 2.4 ppm [Figure
[Figure1a1a and andb].b]. 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.
2. Whitener's[1] 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.
3. Contrary to Whitener's[1] observations, one of our patients was a 15-year-old
girl. Table 2 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.[17,20] Table 2 also shows that TBA can occur in
any part of brain involving the ventricles.[10]

4.
5. Table 2
6. Details of tuberculous brain abscess patients from the available literature
7. 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.[15]
8. Among the laboratory diagnostic modalities used, ZN stain and culture were found to
detect the presence of AFB in all the four cases. Table 1 shows that 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.[21] There are very few reports of concomitant tuberculous and pyogenic brain
abscess that appeared in the literature, namely dual infection due to Streptococci,
[12] Toxoplasma,[21] andEchinococcus.[22]
9. 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.[23] It occurs in only 4 to 8% of patients with CNS TB
who do not have HIV infection[1] but in 20% of patients who do have HIV infection.
[24,25] We encountered one such case which yielded a pure growth of M.
tuberculosis. Fischl et al[21] 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[13] (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.[15] also reported TBA in
a 26-year-old male who was HIV seropositive.
10. 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.

Cerebellar Abscess: A Rare

Presentation of Tuberculous
Meningitis.

Source: Journal of Pioneering Medical Sciences . Apr-Jun2016, Vol. 6 Issue 2, p125-125. 1p.

Author(s): Samina, J.; Muhammad, K.; Sonia, Q.; Ali, Faisal S.; Farah, N. Q.

Abstract:Tuberculous Meningitis is common in tuberculosis (TB) endemic regions. It is one

the most devastating slow growing infectious disease varying from asymptomatic to a debilitating
condition among children worldwide. Here we present the case of a young girl with fever, vomiting
and headache. Radio-imaging revealed posterior cranial fossa mass in right cerebellum with
moderate hydrocephalus. She underwent craniotomy and mass excision. Her histopathology
showed chronic granulomatous inflammation. Her mycobacterial gene expert was positive. She
showed gradual recovery postoperatively on antituberculous therapy.

Brain abscess is one of the life threatening complications of chronic otitis

media in particular cholesteatoma4,5. All the patients in this study
presented with headache and vomitting1-3. The presence of these
symptoms in association with cholesteatoma is very suggestive of
intracranial complications6 . Otogenic brain abscess affects usually
children more than adults1,2. Sennoroglu et al, Nesic et al found high
incidence of brain abscess in children and young patients1,7. Males are 48 time more affected than female as shown by Kempf et al, Nesic et al,
Kurien et al4,7,8. 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
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 Abscess2 . 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 4 triangle2-4. 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 abscess1,
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)1,9. 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 Abscess1,5,10. Successful
management of otogenic brain abscess should include local drainage of
the abscess, administration of systemic antibiotic and cleansing of primary
focus of infection. Medical treatment should start first empirically and later
to be modified according to the results of C/S. In addition, steroid, anti
edema and anti epileptic drugs should be used1,4. The surgical treatment
of brain abscess is very controversial. In general neurosurgeons prefer to
drain the abscess through a burr hole and some time through a
craniotomy with abscess excision. Once the patients condition stabilized,
the source of infection has to be eradicated through a radical
mastoidectomy4,11,12. Unfortunately, this approach is causing trauma to
healthy brain tissue and spreading the infection to healthy brain areas7 .
On the contrary, ENT surgeon drain their abscess through the radical
mastoid cavity following the route of infection using aspiration technique.
By doing so they are combining two procedures in one; draining and
cleansing1,11. Four cases in this study were drained by neurosurgeon
through a burr hole and/or craniotomy. The other two were drained
transmastoid by ENT surgeons. Post-operative follow up is very important
and CT is the method of choice2 . In our department immediate radical
mastoidectomy and drainage of the abscess through the dura is the
standard procedure to treat otogenic brain abscess. Through this
technique we had no mortality and very mild morbidity rate1,3,11. This
approach shortened the hospital stay and is cost effective. C
Bahrain Medical Bulletin, Vol. 27, No. 1, March 2005 Otogenic Brain
Abscess Management Abdul Aziz Ashoor, Fachartzt FHNO*

Tuberculoma formation is the most frequent manifestation of parenchymal central nervous

system (CNS) tuberculosis.[5,6] 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.[5,6] The pathogenesis of tuberculous brain abscess is similar to other forms of
CNS tuberculosis.[2-4] 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.[6]
Clinically patients with cerebellar tubercular abscess present with fever, headache, alteration
of consciousness, seizure,[6] cerebellar signs[7] and or with hydrocephalus.[4] Both CT and

magnetic resonance imaging (MRI) can detect intracranial abscesses; however, these studies
cannot easily differentiate between tuberculous and pyogenic abscesses.[8] 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.[9] Recently,
MRI has been used for better tissue characterization in CNS tuberculosis.[10] The gold
standard of diagnosis remains on demonstration of innumerable tubercle bacilli in aspirated
pus.[11] However, the absence of tubercle bacilli does not necessarily imply the absence of a
tuberculous brain abscess.[4,12] The mainstay of management of tubercular abscess is total
surgical excision as it will confirm the diagnosis, will minimize the morbidity and shorten the
hospital stay.[4,12] It is to be followed by adequate doses of anti-tubercular chemotherapy.
[4,11,12]
Agrawal A, Shanthi V, Ramakrishna BA.
Tubercular cerebellar abscess in a child. J Mahatma Gandhi Inst
Med Sci 2015;20:77-8.

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.
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.4,7,10,25

A Case of Tuberculous Otitis

Media
Tanya Halvorsen, MD1
Heather Townsend, MD2
William Stauffer, MD, MSPH, DTM & H3
Kiran Belani, MD4
Deepak Kamat, MD, PhD5Clin Pediatr. 2006;45:83-87

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.
The Internet Journal of Otorhinolaryngology
Volume 9 Number 1
1 of 6
Tuberculous Otitis Media: A Review of Literature
P Adhikari
Citation
P Adhikari. Tuberculous Otitis Media: A Review of Literature. The Internet Journal of
Otorhinolaryngology. 2008 Volume 9
Number 1.

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.[1-3] 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
ndings should be differentiated from other causes of space
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.
We encountered a young, healthy woman with cerebellar abscess whose initial complaint was a chronic
headache. Chronic headache is considered the seventh most common complaint recorded for ambulatory
care encounters in the United States.3 Her case underscores that common symptoms can have uncommon
causes. In this era of resurgent tuberculosis, we must remain alert for the uncommon, subtle manifestations

of this disease, as inclusion of tuberculosis in the differential diagnosis of common complaints requires a
high index of suspicion. Fortunately, timely initiation of therapy can lead to reduced morbidity and
mortality.

A 36-year-old woman was admitted to the family

medicine inpatient service with a 6-week history
of persistent left-sided headaches. Onset of headaches
occurred 4 days after extraction of a carious
right second molar, and the pain was initially localized
to the right frontal region. She described
the headache as the worst in her life and characterized
the headache as squeezing, throbbing,
sharp, and hammerlike: She denied anyassociation
of facial swelling or abscess formation with
her toothache. After the molar extraction, penicillin
was prescribed, but she stopped taking it after
four doses because of the onset of the rightsided
headache. She denied any associated nausea,
vomiting, visual blurring, or fever and any history
of headaches or migraines. She further stated that
the headaches were not relieved by either regularstrength
acetaminophen or acetaminophen in
combination with hydrocodone
Before her admission she had made four trips
to two emergency departments. Her headaches
had been diagnosed and managed as sinusitis on
the first visit, as cluster headache on the second
visit, and as temporomandibular joint syndrome
on the third visit. On her fourth visit, she was referred
to an oral surgeon, who diagnosed muscle
spasms and injected her jaw. After the injection
her right-sided headache was reduced to a feeling
of pressure, but she had an onset of a similar, leftsided
headache. Findings during a review of systems
were noncontributory and in particular were
negative for chronic cough, weight loss, night
sweats, fever, or other constitutional symptoms.
Her medical history was notable for hypothyroidism
diagnosed 3 years earlier. Her medications
included depo-medroxyprogesterone (for
contraception), flurbiprofen, hydrocodone, naproxen,
and L-thyroxine. She worked as a hair
dresser and lived with her 2 children and fiance.
She denied using alcohol, tobacco, or illicit drugs,
and her family history was unremarkable. A careful
history obtained later revealed possible exposure
to tuberculosis. She stated that 3 months before
admission, one of her co-workers had been
diagnosed with tuberculosis (based on a positive
tuberculin skin test and chest radiograph) and was

undergoing treatment with a three-drug antituberculosis

drug regimen. She further stated that
she (and all her other co-workers) had received
tuberculin skin testing and had tested negative
A 22-month-old boy was referred
to an emergency unit
specialist for evaluation of persistent/
recurrent suppurative otitis
media. His first documented diagnosis
of bilateral otitis media had
been made 16 months earlier,
shortly after starting day care. He
paid eight subsequent visits to the
pediatrician over the next 5
months 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 for bilateral
tympanostomy tube placement.
When treated with oral and/or
aural antibiotic drops the
drainage would clear transiently
during treatment but would typically
reappear within 4 days of discontinuing
medication. Despite
treatment, his middle ear infection
persisted with chronic drainage
and the patient had an adenoidectomy
and five additional surgeries
for tympanostomy tube replacement
in the 11 months following
the initial procedure.

Usually patients with intracranial tuberculosis are

immunocompromised. Among immunocompetent
patients, children and the elderly are most
commonly affected. Our patient did not fit into either
category. Intracranial tuberculosis is usually
insidious, with symptoms taking days to weeks to
evolve, as in the case with our patient. Early symptoms
are generally nonspecific and include malaise,
low-grade fever, irritability, and intermittent
headaches. Specific neurologic symptoms occurring
later include stiff neck, altered cognition, and
cranial nerve palsies. Cranial nerve palsies, although
found in fewer than one fourth of patients,
are considered the most specific manifestation of
intracranial tuberculosis. Our patient had deficits
in cranial nerves III, V, VII, and VIII in addition
to the constellation of nonspecific symptoms.
Cerebrospinal fluid examination is also usually
nonspecific, with the common abnormalities exemplified

in our patient: elevated protein count,

elevated white blood cell count (predominantly a
lymphocytosis), and decreased glucose levels.
Tuberculous abscesses are more often supratentoria1 5
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. The patient had both an
extraction of a carious tooth and had sinusitis. The
brain stem is rarely the site of a focal tuberculous
lesion; when it occurs, it is more often a brain
stem tuberculoma, and only rarely is a true abscess
described. The abscess in our patient was in the
area of the right brain stem involving the pons,
midbrain, cerebral peduncle, and middle cerebellar peduncle, a rare location for the development
of a tubercular abscess.
The definitive diagnosis of a tubercular brain
abscess is established when tubercle bacilli are
identified. In 1978 Whitener5 proposed the following
criteria for establishing a diagnosis of tubercular
brain abscess:
1. Macroscopic evidence of pus formation within
brain parenchyma. (Our patient had two distinct
abscess cavities, from one of which 3 mL
to 4 mL of pus were aspirated.)
2. Histologic confirmation that the abscess wall
was composed of vascular granulation tissue
containing acute and chronic inflammatory
cells. (Macroscopic examination of our patient's
abscess wall showed multiple soft, hemorrhagic
and friable tissue fragments; microscopically
there were acute, but no chronic,
inflammatory cells.)
3. Bacteriologic proof of the tuberculous origin.
Bacteriologic proof of tuberculous origin is
usually difficult, implying a positive finding of
acid-fast bacilli on staining and M tuberculosis on
culture. The absence of these findings, as in this
case, however, does not necessarily imply the absence
of a tuberculous brain abscess. Dastur and
Desai6 recorded a history of tuberculosis infection
in only 47 percent of 107 cases, and ArsenF
recorded the same in only 52 percent of 101 cases
of tuberculous brain abscesses, confirmed retrospectively,
on the basis of response to antituberculosis
drug therapy.
When tested, our patient was anergic to both
the tuberculin skin test and the control panel. Tuberculin
skin tests, however, although well established
as a means of screening for persons infected
with M tuberculosis, now give more than the usual
false-negative responses because of the increased

occurrence of cutaneous anergy secondary to acquired

immunodeficiency syndrome and its associated
suppressed immunologic response. Gram
stain of the abscess revealed numerous polymorphonuclear
leukocytes with no organisms, and
staining was negative fot acid-fast bacilli. Notably,
the patient had begun antimicrobial and antituberculosis
therapy prior to culturing. In addition,
Gram stain and culture of cerebrospinal fluid for
acid-fast bacilli were negative. Direct examination
of cerebrospinal fluid for acid-fast bacilli is disappointing,
however, with a reported 10 to 40 percent
detection rate, which can increase to 87 per

462 }ABFP Nov.-Dec.1998 Vol. 11 No.6

Historically, brain abscesses were usually caused by contiguous

infection following sinusitis or middle-ear infection
and carried a poor prognosis [1,2], but as a result of
improved neuro-imaging, surgery and antibiotic treatment,
brain abscesses are now relatively rare, and mortality
has improved.
Several aspects of management remain controversial,
including the need for surgery and optimal surgical
approaches, type and length of antibiotic treatment, and
need for monitoring during treatment. No randomized
controlled prospective trials are available.

Pyogenic brain abscess, a 15 year

survey
Jannik Helweg-Larsen1*, Arnar Astradsson2, Humeira Richhall2, Jesper
Erdal3, Alex Laursen4 and Jannick Brennum2
Helweg-Larsen et al. BMC Infectious Diseases 2012, 12:332

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.

Kerangkanya case report:

Omsk tb + OMSK bakteri mastoidditis

dupleks komplikasi ke intrakranial

abses serebelum

Penyusunan dapus nya

Yg dbold wrna nya sama tu sitasi nya, yg
tidak ada berarti mnyesuaikan sm dapus
dibawah ini angkanya:
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