Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature.

Tuberculous Otitis Media
Troy Callender, M.D.
November 12, 1992

Despite tremendous advances in the treatment and prevention of tuberculosis (TB) it remains one of the most common, lethal infectious diseases in the United States. Worldwide, TB is the single most important bacterial infection, with more than 7 million active cases. Fortunately the ear is rarely infected by mycobacterium tuberculosis; current incidence is estimated to be between 0.9% and 0.04%. The tubercle bacillus can spread to the middle ear by several routes. The most common route is hematogenous. Other routes of infection include regurgitation of the tubercle bacillus through the eustachian tube, through previously existing tympanic membrane perforations; and by direct extension from a nasopharyngeal site of infection. 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.

Classically, tuberculous otitis media is described as having an insidious onset with painless otorrhea, multiple tympanic membrane perforations, abundant pale granulation tissue in the middle ear, early severe hearing loss out of proportion to clinical findings, and bone necrosis. However, the current literature indicates most patients actually present with a single perforation. Indications of tuberculous otitis media include hearing loss out of proportion to clinical findings, failure to respond to the usual medical therapy, post-mastoidectomy recurrence of granulation tissue, slow wound healing, persistent otorrhea, and the formation of bony sequestra.

The evaluation of these patients should include a history of contact to active tuberculosis, placement of a PPD skin test with control, culture and stain of ear drainage for AFB, biopsy of granulation tissue for histology and culture, and evaluation of the immune system if indicated. All patients should be evaluated with a chest x-ray, urinalysis, sputum for AFB culture and smear, gastric aspirates in children, and lumbar puncture if CNS involvement is suspected or if the patient has miliary TB. On examination of the ear, the tympanic membrane will appear dull and thickened with dilated vessels on the surface early and will later develop perforations from liquification of caseous tubercles. There will also be abundant granulation tissue in the middle ear. Late complications include facial paralysis, labyrinthitis, postauricular fistulae, subperiosteal abscess, petrous apicitis, and intracranial extension of infection. Radiologic evaluation of the temporal bone cannot differentiate TB from non-specific infections. 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.

The differential diagnosis of tuberculous otitis media includes fungal infections, Wegener's granulomatosis, midline granuloma, sarcoidosis, syphilis, necrotizing otitis externa, atypical mycobacterial infections, and histiocytosis X.

The treatment of tuberculous otitis media is primarily medical and should include a 6- to 9-month course of Isoniazid, Rifampin, and Pyrazinamide. Indications for surgical intervention include the late complications of tuberculous otitis media; cases unresponsive to medical therapy; extensive disease with bone sequestra or necrotic bone; and reconstruction of the tympanic membrane and ossicular chain after the middle ear disease has been eradicated.

Case Presentation

A 10-month-old African American female, developed persistent otitis media at 4 months, which failed to respond to multiple courses of antibiotics. On referral to the Pediatric Otolaryngology Service, examination was remarkable for bilateral dull, thickened, erythematous tympanic membranes with poor mobility on insufflation. Myringotomy on June 22, 1992 revealed granulation tissue filling the middle ear cleft bilaterally. Post-operatively she was improved but had persistent scant otorrhea in spite of outpatient medical therapy. A CT scan of the temporal bones was obtained and showed opacification but no destructive lesions. The patient was returned to the OR on September 23, 1992. Middle ear tissue was obtained for routine AFB, fungal cultures, and histologic examination, and her ventilation tubes were replaced. She was admitted and a pediatric infectious disease consultation was obtained.

Additional historical data obtained at that time revealed the patient to have had close contact with a relative with active tuberculosis. Complete evaluation during this admission was remarkable for elevated total IgG and IgG1, + ELISA HIV with an indeterminate western blot, miliary CXR pattern consistent with TB, CSF analysis showing 62 WBC's, 2 RBC's, 82% monos, a glucose of 36 mg/dl and protein of 38 mg/dl consistent with tuberculous meningitis. A CT scan of the brain revealed tuberculomas in the posterior fossa and a PPD skin test was positive with 19 mm to 20 mm of induration. ABR was compatible with a mild conductive loss.

Treatment was instituted with isoniazid, rifampin, pyrazinamide, and kanamycin. She was also treated with oral prednisone. She had a dramatic otologic response with resolution of granulation tissue over 2 to 3 weeks. Except for occasional fever she was otherwise well. She was kept in the hospital for 4 weeks to insure compliant therapy and is being closely followed as an outpatient. Final cultures at eight weeks show no AFB growth.

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