Tuberculosis (TB) can attack almost every organ in the human body and threatens millions of lives worldwide. Approximately one-third of total human population is infected by Mycobacterium tuberculosis.1 India is the country with the highest burden of TB, with the World Health Organization statistics for 2013 giving an estimated incidence figure of 2.1 million cases of TB for India out of a global incidence of 9 million.2 Tuberculosis can be pulmonary or extrapulmonary. Extrapulmonary contributes 12 to 15% of all cases of which middle ear TB constitutes less than 1%. The incidence of tuberculous otitis media (TOM) is 1.9 to 42.8 per million. Mycobacterium tuberculosis is the most common agent causing TB worldwide.1


A 32-year-old female presented with a 2-year history of right-sided otorrhea and hearing loss. The discharge was insidious in onset, scanty, mucopurulent, nonfoul smelling, and occasionally stained with blood. Hearing loss was insidious in onset and gradually progressive. Otoscopy revealed edema of the external auditory canal with polypoidal tissue seen arising from the posterosuperior quadrant of tympanic membrane. Audiometry showed mixed hearing loss of 50, 55, and 60 dB with air-bone gap of 30, 35, and 40 dB at frequencies of 0.5, 1, and 2 kHz respectively. The patient was treated with topical and systemic antibiotics with no relief for which the patient was investigated and was diagnosed as diabetic. She was put on oral hypoglycemic agents, but there was no relief in discharge despite adequate blood sugar control. The discharge was sent for culture and sensitivity, which was reported sterile. As there was no relief in symptoms of the patient, modified radical mastoidectomy was performed. Intraoperatively, the middle ear was found to be filled with exuberant and pale granulation tissue, which was removed and sent for histopathological examination. The long process of incus was necrosed. Histopathological examination showed giant cells and macrophages with necrotic and calcified tissue (Fig. 1).

On the 10th postoperative day, external auditory canal was found to be filled with discharge along with gaping of the postauricular incision, which led to suspicion of the patient suffering from TOM. The patient was then investigated to rule out tuberculous etiology. Chest X-ray, Mantoux test, and sputum for acid-fast bacilli were done, which came out to be inconclusive. The patient was then put on category I antituberculous therapy (ATT). After 4 weeks of ATT, her ear was dry and the postauricular wound healed.

Fig. 1

Histopathological section showing giant cells (red arrow) and necrosis (green arrow) (hematoxylin and eosin, 40×)



In developing countries, TB is very common. It is caused by M. tuberculosis, Mycoplasma hominis, and Mycobacterium bovis. Mycoplasma hominis and M. bovis species usually affect the ear.3 Tuberculosis of middle ear is rare and usually occurs due to infected cow's milk.4 In patients with known or suspected TB along with chronic middle ear infection, TOM should be suspected; however, lack of evidence of TB elsewhere does not exclude TOM possibility.5 Diabetes mellitus is a risk factor for active TB regardless of study design, the incidence of TB in the community, or the place of study.6 The risk of TB attributed to diabetes is 25%.7

Wallmer8 described classical features of TOM which includes painless otorrhea, pale granulation tissue, hearing loss (conductive, sensorineural, and mixed), ipsilateral facial nerve paralysis, multiple tympanic membrane perforation, and bony necrosis. Nowadays, chronic ear discharge, resistant to conventional antibio­tic therapy, is the most frequent finding.1 Jean Louis Petit first described TB of the temporal bone in the 18th century.9 Due to concurrent presence of other bacteria, bacteriological tests are often negative.1 Local antibiotic treatment causes further masking of growth of M. tuberculosis. Ziehl–Neelsen staining is characterized by low sensitivity.10 Culture is more sensitive, but it is usually difficult to culture acid-fast bacilli in extrapulmonary TB. Histopathology is a more reliable diagnostic test.1 Middle ear mucosal biopsy shows Langerhans giant cells, epithelioid cells along with caseous necrosis.11 Tuberculous otitis media may be caused by three routes (hematogenous, Eustachian tube, and direct implantation). Radiological examination is nonspecific. Differential diagnosis may include chronic suppurative otitis media, Wegener's granulomatosis, histiocytosis X, sarcoidosis, and osteomyelitis.1 Medical management is the treatment of choice while surgical intervention is usually controversial. Surgery should be considered in cases where there is no definite clinical diagnosis, in patients presenting with complications, and for taking biopsy. Cho et al10 have reported better results in patients who have undergone surgery followed by ATT as compared with nonoperated patients with TOM.1


Tuberculous otitis media should be suspected in patients with a continuously discharging ear, not responding to antibiotics. The suspicion should be raised in patients with a co- immunosuppressant condition, such as diabetes, as they are more prone to develop TB. Antituberculous therapy is the main line of treatment, with surgery being reserved for complications mainly.

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