1105
Otitis Media and Mastoiditis Due to Mycobacterium fortuitum: Case Report,
Review of Four Cases, and a Cautionary Note
Robert M. Plemmons, C. Kenneth McAllister,
Douglas A. Liening, and Maria C. Garces
From the Infectious Disease, Otolaryngology, and Area Laboratory
Services, Brooke Army Medical Center, Fort Sam Houston, Texas
Mycobacterium fortuitum is a rarely reported cause of otitis media and mastoiditis. We report
such a case recently seen at our institution and review the four previously published cases of this
disease entity. Amikacin is recommended in the current medical literature as empirical treatment
of disease due to M. fortuitum, but the isolate from our patient showed high-level resistance to
amikacin, which is rare in clinical isolates of this species; this resistance was probably related to
prior treatment with topical aminoglycosides. Our patient's infection responded to a 12-month
course of therapy with clarithromycin and trimethoprim-sulfamethoxazole.
Case Report
A l4-year-old girl with a history of persistent otitis media
in the right ear (for which multiple pressure equalization tubes
had been previously placed) underwent right-sided mastoidectomy at our institution. During the 4 months before surgery,
she had had purulent otorrhea from the right ear that was
unresponsive to multiple courses of therapy with systemic antibiotics and topical otic preparations, including topical aminoglycosides and steroids. At mastoidectomy, abundant granulation tissue was noted in the middle ear and mastoid air space.
Culture of a specimen of this tissue yielded pure growth of
M. fortuitum (identified by standard biochemical methods and
mycolic acid profile).
One week after the procedure, the patient's mastoidectomy
wound dehisced and began draining serous fluid. Cultures of
this wound drainage also yielded pure growth of M. fortuitum.
The patient remained afebrile, and there was no evidence of
systemic toxic effects. Results of laboratory studies were all
normal, including a WBC count of 7,800/mm3 (normal differential blood cell count) and an erythrocyte sedimentation rate
of 4 mm/h. Empirical treatment with intravenous amikacin and
cefoxitin was started, but susceptibility testing of the
M. fortuitum isolate (performed by the Nocardia/Mycobacteria
Received 7 September 1995; revised 22 February 1996.
This work was presented in part at the 33rd Annual Meeting of the Infectious
Diseases Society of America held in San Francisco on 16-18 September 1995.
Reprints or correspondence: Dr. Robert Plemmons, U.S. Army Medical
Corps, Infectious Disease Service, Department of Medicine, Brooke Army
Medical Center, Fort Sam Houston, Texas 78234.
Clinical Infectious Diseases 1996;22:1105-6
This article is in the public domain.
Research Laboratory, University of Texas Health Science Center, Tyler, TX) subsequently revealed resistance to both of
these drugs (MIC of amikacin, >64 tLg/mL; MIC of cefoxitin,
64 tLg/mL). Her antibiotic therapy was then changed to oral
clarithromycin (500 mg twice a day); the MIC of clarithromycin was 2 tLg/mL.
One month later, the mastoidectomy wound bed had filled in
with granulation tissue, but serous drainage was still occurring;
therefore, oral trimethoprim-sulfamethoxazole (320/1,600 mg
[two double-strength tablets] twice a day) was added to the
therapeutic regimen. The MIC of sulfamethoxazole was ~ I
tLg/mL. She also received hyperbaric oxygen therapy and underwent a very limited debridement of the wound edges, which
had developed a thickened, scarred appearance.
Cultures of tissue from the debridement (performed 6 weeks
after clarithromycin therapy was started) yielded M fortuitum.
Two months later, the wound was almost completely healed,
although a small amount of drainage persisted. Cultures of this
drainage failed to yield mycobacteria. The patient completed
a 12-month course of combination antibiotic therapy; her mastoidectomy wound completely healed, and the otitis media resolved.
Discussion
Although reports of otic infections due to atypical mycobacteria are becoming more common, cases of such infections due
to M. fortuitum remain quite rare; to our knowledge, only four
cases have been documented in the medical literature [2, 57]. Reports of three of these prior cases [2, 5, 6] documented
the use of pressure equalization tubes (a proposed risk factor
for otic infection due to mycobacteria [3 D, while the report of
the fourth case [7] did not specifically mention their use.
The earliest reported case of otic disease due to M fortuitum
occurred in a 63-year-old man with mastoiditis complicated by
a subperiosteal abscess at the mastoidectomy site [5]. Cultures
of abscess drainage yielded M. fortuitum that was "resistant
to all drugs tested" (no specific susceptibility data were reported). This patient was treated with a combination of isoniazid, rifampin, ethambutol, and ethionamide; no duration of
therapy or outcome was reported.
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Cases of otitis media and mastoiditis due to nontuberculous
mycobacteria, while apparently rare, have been reported with
increasing frequency in recent years [1-4]. We report a case
ofotitis media and mastoiditis due to Mycobacterium fortuitum,
a rapidly growing mycobacterial species, and review the four
other published cases of otic infections due to this organism.
1106
cm
Plemmons et al.
Long-term treatment regimens should be based on the results
of susceptibility testing (best performed by a reference laboratory). Single oral drugs have been used successfully as longterm treatment in this setting [1, 3].
Clinicians treating patients with infections due to rapidly
growing mycobacteria need to be aware that the response to
therapy is slower than that to therapy for the more familiar
pyogenic infections [10]. A recently published study detailing
the clinical courses of five patients with otic infections due to
M abscessus showed that these patients required treatment
with oral erythromycin for 3 months to 1 year before their
infections were eradicated [3].
The role of surgery in the treatment of wound infections due
to M fortuitum has not been studied in a systematic fashion.
Most authors who have addressed the subject on an anecdotal
basis have recommended initial debridement and removal of
foreign bodies (e.g., pressure equalization tubes) [3, 10].
Acknowledgment
The authors thank Dr. David P. Dooley for reviewing this manuscript and offering helpful suggestions.
References
1. Lowry PW, Jarvis WR, Oberle AD, et al. Mycobacterium chelonae causing
otitis media in an ear-nose-and-throat practice. N Engl J Med 1988;
319:978-82.
2. Moennan J, Dierick J, Mestdagh J, Boedts D, Van Cauwenberge P. Mastoiditis caused by atypical mycobacteria. Int J Pediatr Otorhinolaryngol
1993;28:69-76.
3. Franklin DJ, Starke JR, Brady MT, Brown BA, Wallace RJ Jr. Chronic
otitis media after tympanostomy tube placement caused by Mycobacterium abscessus: a new clinical entity? Am J Otol 1994; 15:313-20.
4. Nylen 0, Alestig K, Fasth A, et al. Infections of the ear with nontuberculous mycobacteria in three children. Pediatr Infect Dis J 1994; 13:
653-6.
5. Austin WK, Lockey MW. Mycobacteriumfortuitum mastoiditis. Arch Otolaryngol 1976; 102:558-60.
6. Neitch SM, Sydnor JB, Schleupner CJ. Mycobacterium fortuitum as a
cause of mastoiditis and wound infection. Arch Otolaryngol1982; 108:
11-4.
7. Dalovisio JR, Pankey GA, Wallace RJ, Jones DB. Clinical usefulness of
amikacin and doxycycline in the treatment of infection due to Mycobacterium fortuitum and Mycobacterium chelonei. Rev Infect Dis 1981; 3:
1068-74.
8. Sanders WE Jr, Hartwig EC, Schneider NJ, Cacciatore R, Valdez H.
Susceptibility of organisms in the Mycobacterium fortuitum complex
to antituberculous and other antimicrobial agents. Antimicrob Agents
Chemother 1977; 12:295-7.
9. McFarland EJ, Kuritzkes DR. Clinical features and treatment of infection
due to Mycobacterium fortuitum/chelonae complex. In: Remington JS,
Swartz MN, eds. Current clinical topics in infectious diseases. Boston:
Blackwell Scientific Publications, 1993: 188 - 202.
10. Wallace RJ Jr, Swenson 1M, Silcox VA, Bullen MG. Treatment ofnonpulmonary infections due to Mycobacterium fortuitum and Mycobacterium
chelonei on the basis of in vitro susceptibilities. J Infect Dis 1985; 152:
500-14.
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In the second case, a 45-year-old woman with a mastoidectomy wound infection due to M fortuitum was treated with
amikacin and erythromycin for 6 months [6]. The M fortuitum
isolate from her wound was susceptible to both amikacin and
erythromycin, and the wound was reportedly completely healed
after 4 months of treatment.
The third case occurred in an 8-year-old boy who was treated
with isoniazid monotherapy (again, no susceptibility data were
reported) [2]. The only follow-up information provided was
that the patient was "in good health" 10 months later. In the
fourth case no history beyond "chronic recurrent otitis media"
and "chronic mastoiditis" was provided, but the patient (a 10year-old boy) had a secondary subdural empyema and meningitis [7]; amikacin-susceptible M fortuitum was cultured from
both empyemic pus and CSF. The patient was treated with
intravenous, intrathecal, and intraventricular amikacin for .....,4
months and underwent abscess drainage procedures and placement of a ventriculoperitoneal shunt. The infection was ultimately eradicated.
Although these four case reports document well the occurrence and spectrum of severity of otic infections due to
M fortuitum, most of the reports predate the availability of
newer antibiotics with potent activity against this organism
(e.g., imipenem, clarithromycin, and the fluoroquinolones). In
addition, in two ofthe cases [2, 5], the authors seem to advocate
the use of isoniazid, a drug that is inappropriate for the treatment of infections due to M fortuitum [8].
Although a high percentage of Mycobacterium abscessus
isolates from patients with otic infections have been reported
to be resistant to amikacin [1, 3], to our knowledge, amikacinresistant isolates of M. fortuitum have not been recovered from
patients with otic infections, and these isolates appear to be
quite rare overall among clinical isolates of this species [9].
Unfortunately, these findings of broad susceptibility to amikacin may not apply to M. fortuitum isolates from patients
with otic infections who have had previous treatment with
aminoglycoside-containing otic drops. Since our patient had
never been treated with systemic aminoglycosides before amikacin therapy was administered but had received treatment with
both topical neomycin and gentamicin, the possibility exists
that there was a selection effect of prior therapy with topical
aminoglycosides on aminoglycoside-resistant mutants [1, 3].
The combination of amikacin and cefoxitin is the regimen
most often recommended as initial parenteral therapy for serious infections due to M. fortuitum, including mastoiditis [3,
10]. On the basis of our case and the cumulative published
experience, however, we believe that amikacin should probably
not be relied on as the foundation of empirical therapy for
serious otic infections due to rapidly growing mycobacteria.
We would, therefore, consider adding clarithromycin to empirical therapy with the combination of amikacin and cefoxitin to
increase the likelihood that an active antibiotic is being used
from the outset.
1996;22 (June)