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CASE REPORT
Year : 2022 | Volume
: 28
| Issue : 3 | Page : 262-264
Klebsiella ozaenae subperiosteal mastoid abscess: A brief report and literature review
Meera Niranjan Khadilkar1, Deviprasad Dosemane1, Ethel Suman2, Farnaz Nasrin Islam1
1 Department of Otorhinolaryngology and Head and Neck Surgery, Kasturba Medical College, Mangalore, Manipal Academy of Higher Education, Manipal, India
2 Department of Microbiology, Kasturba Medical College, Mangalore, Manipal Academy of Higher Education, Manipal, India
Correspondence Address:
Dr. Meera Niranjan Khadilkar
Department of Otorhinolaryngology and Head and Neck Surgery, Kasturba Medical College, Mangalore, Manipal Academy of Higher Education, Manipal - 575 001
India
Source of Support: None, Conflict of Interest: None
CheckDOI: 10.4103/indianjotol.indianjotol_82_22
Subperiosteal abscess (SPA) is a known sequel of acute mastoiditis typically afflicting children and less often the elderly, caused by Streptococcus, Staphylococcus, and anaerobes. Atrophic rhinitis is a progressive disease with nasal mucosal and turbinate atrophy, thick dried crusts, and foul odor called ozaena, caused by Klebsiella ozaenae. We present an interesting case of SPA in the mastoid in a patient with atrophic rhinitis, astonishingly caused by a common pathogen, K. ozaenae, and a review of literature. The presence of coexistent atrophic rhinitis and mastoiditis should always compel otolaryngologists to consider K. ozaenae as the common etiology.
Keywords: Abscess, atrophic rhinitis, Klebsiella, mastoiditis
Subperiosteal abscess (SPA) is the most frequent complication of acute mastoiditis, with a rate of 7%–32%, the average rate being 58%.[1],[2] It is known to typically afflict children and less often adults, especially those older than sixty.[1],[3] SPA is also known to be the most common extracranial complication of chronic otitis media (COM) with mastoiditis, with a rate of 26%–38%.[4],[5] Etiology includes Streptococcus pneumoniae, followed by Group A streptococci, coagulase-negative staphylococci, Haemophilus influenzae, Turicella otitidis, and anaerobes.[3],[6],[7] The usage of antibiotics has diminished the occurrence of mastoiditis; however, antibiotic use with multidrug-resistant bacterial emergence has amplified the risk of masked mastoiditis.[8] Masked mastoiditis is an uncommon insidious, subclinical complication of acute or COM. The oligosymptomatic nature often poses a diagnostic challenge.[9]
Atrophic rhinitis is a progressive disease with nasal mucosal and turbinate atrophy and presence of thick dried crusts leading to foul odor or ozaena. The most common causative agent for primary atrophic rhinitis is Klebsiella ozaenae,[10] a subspecies of Klebsiella pneumoniae, known to typically affect the upper airway.[11] We present an interesting case of SPA in the mastoid in a patient with atrophic rhinitis, astonishingly caused by a common pathogen, K. ozaenae, and a review of relevant literature.
Case ReportA 65-year-old man, a known diabetic and hypertensive on regular treatment, came with a throbbing left earache for 2 days and a nonprogressive mildly painful swelling behind the ear for 2 years. He gave no history of otorrhea. He also complained of reduced hearing, more on the left. There was also lingering foul-smelling nasal discharge, often noticed by people around him; he was unable to perceive the foul smell. He had no other nasal symptoms. Examination revealed a posterosuperior wall bulge in the left external auditory canal; tympanic membrane appeared intact. A tender, fluctuant, inflamed swelling of 5 cm × 2 cm was noted postaurally pushing the pinna laterally. Bilateral nasal cavities were roomy; greenish crusts were noted. General random blood sugar at admission was 158 mg/dL.
Pure-tone audiometry exhibited hearing loss of more than 90 dB in the left ear, the air-bone gap being 30 dB. High-resolution computed tomography temporal bone demonstrated left otomastoiditis with a peripherally enhancing collection measuring 40 mm × 21 mm × 42 mm in the subperiosteal region, underlying osteolysis, and erosion of the mastoid cortex [Figure 1].
Figure 1: (a) High-resolution computed tomography of temporal bone coronal section showing peripherally enhancing subperiosteal collection (single black arrow). (b) Axial section with soft-tissue density in mastoid cortex (*) and erosion of mastoid (double black arrows) (c) Left nasal cavity with greenish crusting and mucopurulent dischargeThe patient was started on intravenous piperacillin-tazobactam 4.5 g twice daily and metronidazole infusion 500 mg thrice daily and saline nasal douching. He underwent left cortical mastoidectomy and myringotomy; around 15 ml of pus was drained. Interestingly, both the preoperative nasal swab and the surgical exudate from the abscess showed growth of K. ozaenae [Figure 2], sensitive to piperacillin and tazobactam, ciprofloxacin, ceftriaxone, carbapenems, amoxicillin-clavulanate, and cefepime in decreasing order of sensitivity.
Figure 2: Photograph showing (a) Large, mucoid, and pink colonies of Klebsiella ozaenae isolated on MacConkey agar. (b) Grayish-white mucoid colonies of Klebsiella ozaenae isolated on blood agar. (c) Hematoxylin and eosin stain showing Klebsiella ozaenae as Gram-negative rodsThe patient improved symptomatically and was dismissed on the 6th postoperative day on oral amoxicillin-clavulanate 625 mg thrice daily for a week with saline nasal douching. He was followed up every month for 3 months, thereafter telephonic follow-up was done for a year. The patient was symptomatically better; he also claimed to hear better, though audiometry was not repeated.
DiscussionMasked mastoiditis is a suppurative subclinical infection of mastoid air cells, involving both mucosa and bony structures. The pathogenesis is an incompletely healed acute otitis media and obstruction of the key area of mastoid by mucosal edema and granulation tissue. This may lead to an effusion-free middle ear cavity, with drainage occurring through the Eustachian tube More Details. The inflammatory process may last from weeks to months or even years, before becoming symptomatic due to complications, or healing.[12] Persistent inflammation in mastoid air cells causes deep-seated earache, postaural pain, decreased hearing, and recurring fever. Most of the patients show no changes or only thickening of the tympanic membrane.[9] SPA occurs as a consequence of an uninterrupted pathway between the middle ear and mastoid. Infection may spread through the tympanomastoid suture, or along vascular channels in the cribriform area. Typical presentation is in infants with complicated acute otitis media with acute mastoiditis; occurrence in older age groups must preclude underlying COM with cholesteatoma.[13]
Factors such as middle ear anatomy and pathology, mastoid microbiota, bacterial virulence, host immunity, and the use of antibiotics also play a vital role in pathogenesis.[12] Our patient was a known diabetic. Diabetics are more prone to respiratory, urinary, and subcutaneous tissue infections.[8] Badrawy et al. reported a higher incidence of masked mastoiditis in diabetics.[14] Infection may be a result of malnutrition and poor immune status due to aging.[8] Imaging of temporal bone shows soft-tissue density in the middle ear and mastoid with erosion or mastoid cortical bone defect and contrast-enhanced subperiosteal shadows,[15] similar to our findings.
The clinical diagnosis was not challenging in our patient; nevertheless, the finding of K. ozaenae in the mastoid was unexpected. K. ozaenae is a weakly pathogenic Gram-negative aerobe belonging to Enterobacteriaceae and contributes to the natural flora of the upper airways.[16] This bacterium is a variant of K. pneumoniae, and is deemed a distinct species due to its association with specific human disease. It has been linked with the causation of ozaena and upper respiratory infection and has been isolated in sputum, blood, and external auditory meatus, without ozaena features. It has also been implicated in infection of soft tissue and urinary tract, otitis media, meningitis, and abscesses in the brain, liver, lungs, spleen, gallbladder, pituitary gland, and eye.[11],[16],[17] Tadesse et al. studied the bacteriology of 152 pediatric patients with otitis media and noted 6 (3.9%) patients with K. ozaenae.[18] Berger et al. described a case of otitis media and externa with mastoiditis; culture of external auditory canal revealed K. pneumoniae and K. ozaenae.[19] Goldstein et al. reported a 52-year-old diabetic man with posttraumatic otitis media, mastoiditis, and bacteremia. Culture reports were suggestive of K. ozaenae growth in the mastoid and blood.[20] Siegel documented a case of an elderly diabetic woman with chronic sinusitis, who developed otitis and meningitis, and the causative pathogen was found to be K. ozaenae.[21] All these patients improved with medical therapy. Interestingly, none of the cases indicates the occurrence of SPA.
Our literature review revealed one report of atrophic rhinitis complicated by mastoid and extradural abscess described by Stoker in 1909.[22] Infection from the nasopharynx most probably reached the middle ear and mastoid through the eustachian tube, thence progressing to masked mastoiditis and SPA. This also explains why our patient was relatively doing well for 2 years; K. ozaenae seldom causes serious infections.[11]
Treatment options described for SPA include cortical mastoidectomy, incision and drainage of abscess with myringotomy, and postaural needle aspiration with good antibiotic cover.[1],[6],[7],[15],[23] On the contrary, ozaena is managed conservatively with nasal irrigation, humidification, and antibiotics such as cephalosporins and quinolones; surgical options such as Young's procedures are reserved for persistent crusting.[10] Our patient recovered well after cortical mastoidectomy and drainage of SPA with antibiotic therapy and nasal douching.
ConclusionSPA is a known sequel of mastoiditis. However, causation by K. ozaenae is atypical. The presence of coexistent atrophic rhinitis and mastoiditis should always compel otolaryngologists to consider K. ozaenae as the common etiology.
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The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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Conflicts of interest
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