Summary

Tuberculous otitis media is a rare disease. Due to thecondition’s rarity and its usually indolent course, the di-agnosis is often delayed. This can lead to irreversiblecomplications, such as permanent hearing loss or facialnerve paralysis. Tuberculosis of the middle ear cleft, asthis disease’s first presentation, is indeed very rare.Surgery may be carried out prior to diagnosis occasion-ally, i.e., middle ear exploration for chronic middle eardisease. We present four cases of tuberculous otitismedia which occurred as the first presentation of the dis-ease. The patients did not present with the classic symp-toms of middle ear tuberculosis. The diagnosis wasbased on the histology following middle ear explorationfor chronic middle ear disease. None of the patients pre-sented any other systemic involvement. We present a re-view of this disease’s clinical symptoms and the diag-nostic tests available.

Key words: Tuberculosis – Otitis media

Introduction

Tuberculosis, a communicable disease caused by My-cobacterium tuberculosis, is a relatively uncommon dis-ease in the western world. Following the introduction ofBCG immunization, the improvements in hygiene, bet-ter standards of living, and improved access to healthcare, together with the introduction of antituberculouschemotherapeutic agents, the incidence of tuberculosiswas declining steadily [10, 14, 16], until recently, as ithas begun increasing again [2, 4]. The recent resurgenceof the disease in western countries is attributable to theHIV epidemic, immigration from countries in which tu-berculosis is common, the transmission of tuberculosis

Original Paper

Tuberculous Otitis Media:A Difficult Diagnosis and Report of Four Cases

Victor Vital, Athanasia Printza, Thomas Zaraboukas

Aristotle University of Thessaloniki, Greece

Pathol. Res. Pract. 198: 31–35 (2002) 0344-0338/02/198/1-31 $15.00/0

PATHOLOGYRESEARCH AND PRACTICE© Urban & Fischer Verlaghttp://www.urbanfischer.de/journals/prp

in congregate settings, growing numbers of the home-less and changes in health care infrastructure [2, 4, 9,16, 18]. The incidence of tuberculosis in the UnitedStates dropped from 84,304 in 1953 to 22,201 in 1985[16]. From 1985 through 1992, however, the incidenceincreased by 20% [4]. In 1998 more than 350,000 newcases of the disease were reported in Europe, comparedwith 231,000 reported in 1991 [19]. The reported inci-dence of tuberculosis in Greece was 8.6 cases per100,000 people in 1994 and 11 and 9.3 cases respective-ly in 1998 and 1999 (reporting procedures changed ac-cording to the guidelines issued by the WHO and theEuro TB since 1998) [19].

The historically classic triad of presentation symp-toms in tuberculous otitis media is: painless otorrhoea,multiple small perforations of the tympanic membrane,and concomitant peripheral facial nerve paralysis. Thesetypical symptoms may often be absent [1, 5, 11, 12, 13,14, 18, 21]. The otologist today more commonly en-counters a patient with an ear with a chronic dischargeand a high index of suspicion is required to diagnose tuberculous otitis early and to begin treatment accord-ingly.

Mycobacterium tuberculosis can affect multiple sitesin the head and neck, i.e., the cervical lymph nodes, lar-ynx, pharynx, oral cavity, nasal cavity, salivary glands,cervical spine, middle ear, and the mastoid [1, 6, 7, 8, 9,16]. Before the recent increase in tuberculosis, it was es-timated that cervical lymphadenopathy, the most com-mon manifestation of the disease in the head and neck,affected 5%–10% of all patients with tuberculosis [4,16].

Address for correspondence: Victor Vital, 71, MitropoleosStr., 546 22 Thessaloniki, Greece.Tel.: +3031-277-698, or -285-515, Fax: +3031-224-504.E-mail: vvital@med.auth.gr

We review four cases of middle ear tuberculosis.Chronic otorrhoea was the first presentation of tubercu-losis in those four patients who were submitted to mid-

dle ear exploration for chronic middle ear disease. Westudied retrospectively the diagnostic difficulties ofmiddle ear tuberculosis.

32 · V. Vital et al.

1

2a 2b

3a 3b

4a 4b

Fig. 1. Granulomas and nonspecific inflammatory infiltra-tion – Case 1 (×40, Haematoxylin-Eosin stain).

Fig. 2. a: Granuloma – Case 2 (×100, Haematoxylin-Eosinstain). b: Granulomas and nonspecific inflammatory infil-tration – Case 2 (×25, Haematoxylin-Eosin stain).

Fig. 3. a: Granuloma with epitheloid cells and Langhansgiant Cells. Nonspecific inflammatory infiltration – Case 3(×40, Haematoxylin-Eosin stain). b: Granuloma – Case 3(×100, Haematoxylin-Eosin stain).

Fig. 4. a: Caseating granuloma – Case 4 (×40, Haema-toxylin-Eosin stain). b: Caseous necrosis with fibrosis –Case 4 (×40, Haematoxylin-Eosin stain).

Case Report

Case 1. A 46-year-old Caucasian woman presentedwith a three-year history of right-side, painless otor-rhoea refractory to medical treatment (including strepto-mycin ear drops administered by previous physicians).Examination of the ear showed multiple central perfora-tions of the tympanic membrane with pulsatile otor-rhoea. Pure tone audiometry (PTA) showed an ipsilater-al conductive hearing loss of 40 dB. An exploration ofthe ear in the form of atticotomy revealed abundantgranulations in the middle ear cleft. The ossicles wereintact. Biopsies were sent for histology and culture. Thepatient had a tympanoplasty with temporal fascia and T-tube insertion. The histological examination revealednumerous granulomas and non-specific inflammatoryinfiltration (Fig. 1). The culture confirmed the presenceof M. tuberculosis. The purified protein derivative(PPD) skin test was positive. A chest X-ray showed nopulmonary involvement and the sputum, urine andblood cultures were negative. There was no past or fam-ily history of tuberculosis. She was treated with antitu-berculous chemotherapy for six months and a course ofantibiotic-steroid ear drops for three weeks. Her recov-ery was complete, with no sign of relapse for ten years.The ventilation tube was removed one year postopera-tively. Her hearing returned to normal.

Case 2–4. The history and the presenting symptomsof our patients are summarised in Table 1 and the exami-nation findings in Table 2. Our patients presented only

chronic otorrhoea and hearing loss. They had sufferedfrom otorrhoea refractory to treatment for a period rang-ing from thirteen months to longer than three years, dur-ing which they had visited more than one physician. Onlyone of them had a positive family history that had goneundetected prior to diagnosis. As a result, suspicion fortuberculosis was only raised during surgery. The present-ed patients were submitted to middle ear exploration forchronic middle ear disease. The type of operation and thesurgical, histological and microbiological findings aresummarised in Table 3. Histology of granulation tissueobtained for biopsy revealed granulomas and nonspecificinflammatory infiltration (Fig. 1, Fig. 2), granulomaswith epitheloid cells and Langhans giant cells (Fig. 3),granulomas with caseous necrosis and fibrosis (Fig. 4).They all had positive PPD skin test results. Two tissuecultures grew M. tuberculosis. The chest X-rays wereclear and none had positive sputum, urine or blood cul-tures. Our patients underwent six months of drug therapyand three weeks of ear drops following granulation tissueremoval from the middle ear cleft. Their recovery wascomplete and no relapse occurred with a mean follow-upperiod of 6.25 years. The ventilation tube was removedone year postoperatively for the three patients and 2.5years postoperatively for one patient, resulting in a smallresidual dry perforation in that case. Hearing returned tonormal for the three patients. One patient who had suf-fered from chronic otorrhoea for more than three yearsand had had a previous tympanoplasty suffered a residualhearing loss of 50 dB (mixed type).

Tuberculous Otitis Media · 33

Table 1. History

Patient 1 Patient 2 Patient 3 Patient 4

Age 46 48 19 56Sex female female female maleInitial symptom painless painless painless painless

otorrhoea otorrhoea otorrhoea otorrhoeaSide right (R) left (L) right (R) left (L)Other symptoms hearing loss (R) hearing loss (L) hearing loss (R) hearing loss (L)Duration of symptom 3 years 18 months 13 months >3 years*Past history clear clear clear clearFamily history clear clear positive clear

* Tympanoplasty 3 years ago for chronic otitis media

Table 2. Examination findings

Patient 1 Patient 2 Patient 3 Patient 4

Otoscopy multiple central two central polypoidal gelatinous polypoidal gelatinousperforations, perforations, mass at the mass at thepulsatile otorrhoea pulsatile otorrhoea tympanic membrane tympanic membrane

PTA* 40 dB (R) 40 dB (L) 45 dB (R) 55 dB (L)conductive hearing loss conductive hearing loss condutive hearing loss mixed hearing loss

* PTA: Pure tone audiometry

Discussion

The clinical diagnosis of tuberculous otitis media is dif-ficult because few patients exhibit the typical features ofpainless otorrhoea, multiple small perforations of thetympanic membrane and concomitant peripheral facialnerve paralysis and bony necrosis [1, 5, 11, 12, 13, 14,18, 21]. The diagnosis of otomastoid tuberculosis is notoften suspected until surgery, when typical pale granula-tions and the cheesy necrotic tissue are revealed. In thecases we have reported, none of the patients presentedfacial paralysis or bony necrosis, and only two out offour patients had multiple perforations of the tympanicmembrane.

Otorrhoea is the most consistent finding [1, 7, 11, 13,14, 15, 21]. It may be painless or associated with ear-ache [7, 12, 13, 15]. Painless, profuse otorrhoea oc-curred in all our patients. Multiple small perforations arerarely noticed. It is believed that they quickly coalesceinto a total tympanic membrane perforation. More often,a single perforation is found [1, 13, 14, 15, 21]. Two pa-tients in our study had a total perforation and two pa-tients had multiple perforations. Seventh nerve peripher-al palsy is reported in about 20% of patients [4, 13, 14,21] and is believed to occur more frequently in children.When facial palsy is associated with chronic otorrhoeawith no evidence of cholesteatoma, middle ear tubercu-

losis should be suspected [1, 14, 15, 21]. In two of ourpatients the facial nerve was found partially exposedduring surgery without any clinical implications. Hear-ing loss is usually conductive due to fluid in the middleear, ossicular destruction, which occurs early, or densefibrous connective tissue. Mixed or sensorineural lossmay occur if the labyrinth becomes involved [1, 2, 13,14, 16, 21]. Three of our patients presented conductivehearing loss. One patient with a long history of otor-rhoea had a mixed-type hearing loss of 55 dB. The meanpreoperative hearing loss was 45 dB. Draining sinustracts may present in up to 20% of cases [4] and bonysequestra may form if the diagnosis is delayed [2, 3,16]. There is frequent enlargement of the preauricularand cervical lymph nodes [2, 16].

The middle ear mucosa appears granular or polypoid.Granulations are commented on by many authors asbeing a most significant feature [1, 12, 13, 14, 15, 16,21]. Two of our patients presented abundant granulationtissue occupying both the entire tympanic cavity and thetympanic membrane area, imitating a thickened tympan-ic membrane. About 50% of patients with otologic evi-dence of M. tuberculosis have radiographic pulmonarydisease [4, 16]. All the cases we present had isolatedmiddle ear tuberculosis with no evidence of disease inany other systems.

The first step in the diagnosis is a high index of suspi-cion for tuberculosis [9]. A positive past or family historyof tuberculosis, a history of contact with people sufferingfrom tuberculosis, the presence of concomitant pul-monary lesions (findings in chest X-rays) and persistentotorrhoea unresponsive to conventional treatment shouldraise the suspicion for tuberculosis [5, 13, 16]. Duringsurgery the presence of abundant pale granulation tissuein the middle ear and mastoid air cells – in the absence ofcholesteatoma in a patient with facial nerve paralysis andhearing loss – is highly suggestive of tuberculosis.

34 · V. Vital et al.

Table 3. Operation type, surgical, histological and microbiological findings

Patient 1 Patient 2 Patient 3 Patient 4

Operation middle ear exploration, middle ear exploration, mastoid exploration, mastoid exploration,atticotomy, atticotomy, tympanoplasty (fascia atticoantrostomytympanoplasty (fascia tympanoplasty (fascia graft), T-tube tympanoplasty type IIIgraft), T-tube graft), T-tube (cartilage-fascia), T-tube

Surgical findings granulations granulations granulations granulations

Facial nerve intact intact exposed exposed

Ossicles intact intact intact discontinuity

Histological granulomas, granulomas, granulomas caseating granulomas,findings inflammatory inflammatory epitheloid cells, caseous necrosis,

infiltration infiltration Langhans giant cells, fibrosisinflammatory infiltration

Tissue culture obtained obtained not obtained not obtainedM. tuberculosis M. tuberculosis

Table 4. Recovery. Follow-up

Patient 1 Patient 2 Patient 3 Patient 4

Recovery complete complete complete completeFollow-up 10 years 8 years 5 years 2 yearsPerforation none none small, dry noneHearing normal normal normal 50 dB

The diagnosis is based on a positive tuberculin skintest and, most importantly, on the demonstration of acid-fast bacilli (AFB) in exudate or tissue preparations [16].The presumptive diagnosis is often made on the histolo-gy of granulation tissue obtained for biopsy [9]. In a se-ries of 22 patients with middle ear tuberculosis reviewedby Windle-Taylor and Bailey, the diagnosis was estab-lished by the histological findings in 20 of the 22 patients[21]. The demonstration of AFB in ear discharge materi-al or tissue will offer a definitive diagnosis [16]. It israre, though, to recognize AFB with routine microscopyon clinical specimens other than sputa, due to the verylow numbers of mycobacteria [11]. Tissue biopsies ob-tained for histology should also be submitted for micro-biology (AFB staining and culture). Due to low numbersof mycobacteria, AFB may also remain undetected afterZiehl-Neelsen tissue sample staining, with success ratesranging from 27% to 60% (the higher number being theexception) [4, 11]. The definitive method for diagnosisis culture, which is even more important in the diagnosisof atypical mycobacterial infections in the immunocom-promised patient [11]. The culture of exudates is nega-tive in 70% of cases [16]. The chronic use of ear drops,especially those containing neomycin, is believed to af-fect the sensitivity of cultures [11]. It is often necessaryto do tissue cultures (reported success rate up to70–90%) [20]. Newer techniques based on polymerasechain reaction may speed up the diagnosis of mycobacte-rial species and the identification of mutations associa-tion with drug resistance when widely applied [4, 9, 16].

The treatment of middle ear tuberculosis consists pri-marily of administering oral antituberculous chemother-apy. Surgery is carried out to remove bony sequestra, totreat complications, or in the case of mastoid explo-ration [11, 13, 14, 16, 21]. All patient contacts should besought out and tested. There is a high risk for neonatalcontact and those vulnerable need special attention [16].Inadequate therapy – the result of poor patient compli-ance or improper dosing – frequently leads to drug resis-tance.

Tuberculous otitis media is a difficult diagnosis.Surgery may occasionally be carried out prior to diagno-sis in the form of exploration of the mastoid for facialnerve palsy or for chronic middle ear disease. A highindex of suspicion is required for an early diagnosis,thus avoiding irreversible complications and surgical in-tervention.

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Received: June 11, 2001Accepted in revised version: October 16, 2001

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