An Unusual Cause of Mastoiditis That Evolved

An Unusual Cause of Mastoiditis That Evolved Into Mult
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An Unusual Cause of Mastoiditis That Evolved Into Multiple
Ring-Enhancing Intracerebral Lesions in a Person With HIV
Infection
August 01, 2007
By AIDS Reader [1]
Acute mastoiditis, an infectious inflammatory process in the temporal bone, is an uncommon
complication of otitis medi
Acute mastoiditis is rarely seen today; when it occurs, it typically affects very young or
immunocompromised persons.1 Before the discovery of antibiotics, up to 20% of cases of acute otitis
media evolved into acute mastoiditis that was frequently associated with severe intracranial
complications2 and death.3 In this report, we present a case of advanced HIV infection in a patient in
whom mastoiditis caused by Nocardia asteroides developed. His course was complicated by sigmoid
sinus thrombosis—a rare but potentially fatal complication of mastoiditis.4
CASE SUMMARY
A 42-year-old black man with advanced HIV infection was hospitalized after 2 weeks of right ear pain
and discharge. Pertinent physical findings included swelling and erythema in the right temporal area
and purulent secretion in the right ear canal. The patient had been poorly adherent to his
antiretroviral therapy, and his CD4+ cell count was less than 20/µL. His history included an episode of
Cryptococcus meningitis 2 years before his present hospitalization and also presumptive
Pneumocystis jiroveci pneumonia. He was allergic to sulfa drugs.
Figure 1. CT scan showing erosive changes of the
right temporal bone and bony destruction in the temporal squamosa.
CT scans of the brain and temporal bones revealed focal collections in the subcutaneous tissue of
the right temporal region and erosive changes of the right temporal bone with bony destruction in
the temporal squamosa as well as in the mastoid portion (Figure 1). MRI angiography confirmed
those findings and revealed a thrombosis of the right transverse and sigmoid sinuses. Cultures were
obtained, and surgical debridement was scheduled.
The patient was treated with piperacillin/tazobactam 3.375 g intravenously every 6 hours for 10 days
and then underwent mastoidectomy and drainage of the abscess. Samples of bone tissue and
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An Unusual Cause of Mastoiditis That Evolved Into Mult
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drainage were sent for microbiological studies. The Gram stain and initial cultures were negative,
and the patient was discharged to a skilled nursing facility about 1 week after surgery. The plan was
to continue his antibiotic therapy at the same dosage for several weeks, but the patient left after 1
week at the facility against medical advice. Two weeks after he left the nursing facility, his gait
became unsteady, and his baseline mental status deteriorated. The patient became bedridden and
was brought to our institution for further evaluation.
On physical examination at his second admission, he was alert and oriented to place and person only
and was unable to follow complex commands. He had dysarthria. The strength on the right side of
his body was 3/5 in both upper and lower extremities; the strength on the left side was normal.
There was a decreased sensation on the right side of his body, including his face, with hyperreflexia.
Figure 2. CT scan of the brain demonstrating a
right temporal ring-enhancing lesion and vasogenic edema.
A CT scan of the brain demonstrated a right temporal ring-enhancing lesion with vasogenic edema
and mass effect but without midline shift (Figure 2). Cerebrospinal fluid examination showed 9
white blood cells/µL (normal, 0 to 5), 126 red blood cells/µL (normal, 0), glucose level of 35 mg/dL
(normal, 40 to 70), and total protein level of 283 mg/dL (normal, 15 to 45). Results of India ink
analysis were negative.
Therapy for presumptive CNS toxoplasmosis was started. The patient was treated with clindamycin
600 mg intravenously every 6 hours, pyrimethamine 75 mg orally once daily, and folinic acid 15 mg
orally once daily based on his medical history, physical findings, the brain CT scan, his very low CD4
count, and a positive result for Toxoplasma antibodies in serum.
The patient's health did not improve with this therapy, and his neurocognitive function continued to
deteriorate. New brain imaging studies were obtained 12 days after the initiation of his
anti-Toxoplasma treatment: This brain CT scan showed multiple ring-enhancing lesions within the
right temporal lobe and cerebellum. The MRI scans of the brain also showed multifocal
ring-enhancing lesions within the brain and right mastoid region, with evidence of conglomeration
within the right temporal region (Figure 3). These findings suggested bacterial abscesses. Both
imaging studies showed that the lesions had progressed since the examination performed 12 days
earlier despite treatment for toxoplasmosis.
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An Unusual Cause of Mastoiditis That Evolved Into Mult
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Figure 3. MRI scans of the brain showing
multifocal ring enhancing lesions within the brain and right mastoid region.
Culture results obtained during surgery (about 60 days earlier) became available and were positive
for N asteroides. The samples were collected from the retroauricular abscess, ear discharge, and
right mastoid (after mastoidectomy). The patient began therapy for CNS nocardiosis with
intravenous amikacin 450 mg every 12 hours and intravenous imipenem/cilastatin 500 mg every 6
hours because of his history of allergy to sulfa drugs.
Unfortunately, his condition further deteriorated despite antibiotic therapy, and 5 days later,
multiorgan failure developed. The patient was then transferred to a hospice care facility and died
after 3 days.
DISCUSSION
Acute mastoiditis is an inflammatory process of the mastoid bone and is usually, but not necessarily,
preceded by an episode of acute suppurative or subacute otitis media.5 The evolution of acute
mastoiditis begins when the mucosal lining of the pneumatized cells become inflamed and produce
an exudate. Serosanguineous fluid eventually becomes mucopurulent. The cellular walls of the
pneumatized cells subsequently become demineralized because of increased osteoclastic activity,
pressure of the purulent exudate on the thin bony septa, and ischemia of the septa secondary to
reduced blood flow. As the bony septa break down, small abscess cavities form leading to
coalescence. Finally, the coalescent cells form an empyema, or pus under pressure, which then
escapes to surrounding areas.
Typically, the organisms involved in mastoiditis are the same as those involved in acute otitis
media3,6,7: Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. However,
atypical pathogens, such as in this case, may also be involved. Diagnosis is usually made via CT of
the temporal bones, which shows temporal bone abnormalities and occasionally intracranial
complications.
Treatment of acute mastoiditis depends on the pathological stage at which it is encountered and the
causative organism. Nevertheless, it is generally accepted that surgery and antibiotic therapy are
the cornerstones for the management of mastoiditis-associated intracranial complications.2,4,6,7
Since the beginning of the HIV epidemic, HIV infection has become one of the most common
underlying conditions to predispose to nocardiosis.8 In a study from our institution,9 19 of the 25
cases of nocardiosis seen over 6 years were in HIV-infected patients, and similar to this case, all
involved advanced HIV disease with CD4+ cell counts less than 100/µL.
CNS involvement typically occurs through hematogenous spread, but in some cases it can occur
through contiguous spread, most likely, as in this case, from ear and mastoid infections. The
mortality from Nocardia brain abscess is high, ranging from 40% to 87% despite adequate therapy.10
Delay of treatment is also associated with a poor outcome. Unfortunately, delays in therapy are not
unusual, in part, because of relatively infrequent occurrence of this type of infection, the time
required to culture the organism, and the lack of a "typical" presentation.
Sulfonamides, particularly sulfadiazine and sulfisoxazole, have been the antimicrobial agents of
choice since they were introduced more than 50 years ago.8 Trimethoprim/sulfamethoxazole (TMP/
SMX) is the most frequently used combination to treat this infection despite the absence of
conclusive data supporting the need for this combination (1 part TMP to 5 parts SMX). Treatment
should be aggressive and prolonged if there is CNS involvement or if the patient is
immunosuppressed because the relapse rate is high.
Alternative antimicrobial agents should be considered only for patients who are intolerant of or fail to
respond to sulfonamide therapy. The parenteral drugs currently most active in vitro against the
largest percentage of Nocardia isolates are amikacin and imipenem. Other active drugs include
ampicillin/sulbactam, certain cephalosporins (eg, ceftriaxone and cefotaxime), and linezolid.11
The optimal length of therapy is also unknown, but a common recommendation is that intravenous
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An Unusual Cause of Mastoiditis That Evolved Into Mult
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antibiotics should be given for at least 6 weeks, then switched to oral treatment for a total of 12
months. Some experts suggest that intravenous antibiotic therapy be continued for 12 months,
particularly in immunocompromised patients or when the CNS is involved.8,11,12
Clinicians should include mastoiditis in the differential diagnosis for all patients who have severe ear
pain—especially those who are immunocompromised—because unusual pathogens, such as
Nocardia species, can cause life-threatening infections.
No potential conflict of interest relevant to the article was reported by the authors.
References:
References
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current status. Int J Pediatr Otolaryngol. 2000;56:33-40.
3. Robinson RF, Koranyi K, Mahan JD, Nahata MC. Increased frequency of acute mastoiditis in
children. Am J Health Syst Pharm. 2004;61:304, 306.
4. Ozdemir D, Cakmakci H, Ikiz AO, et al. Sigmoid sinus thrombosis following mastoiditis: early
diagnosis enhances good prognosis. Pediatr Emerg Care. 2005;21:606-609.
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management. Curr Clin Trop Infect Dis. 1995;15:204-229.
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retrospective study (1990 through 2001). Pediatr Infect Dis J. 2003; 22:878-882.
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2004;43:261-267.
8. Lerner PI. Nocardiosis. Clin Infect Dis. 1996;22:891-903.
9. Castro JG, Espinoza L. Nocardia species infections in a large county hospital in Miami: 6 years
experience. J Infect. 2007;54:358-361.
10. Lederman ER, Crum NF. A case series and focused review of nocardiosis: clinical and
microbiologic aspects. Medicine (Baltimore). 2004;83:300-313.
11. Antony S, Stivers M, Rivera J. Endocarditis/endovascular infection associated with Nocardia.
Infect Med. 2006;23:262-266.
12. Gombert ME. Susceptibility of Nocardia asteroides to various antibiotics, including newer
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