HSC Section 8_April 2017

Hobson et al

Two of 3 MRSA-infected patients had resolution of their infections, averaging 8.5 6 0.7 weeks of definitive antibio- tic therapy and 12.6 6 0.9 total weeks of antibiotic therapy. One patient infected with MRSA and Acinetobacter died from an infected central catheter while undergoing treatment for MOE. Although the treatment duration was longer for MRSA-infected than for Pseudomonas -infected patients, these differences in duration were not statistically signifi- cant ( P = .18 for total and P = .10 for definitive therapy). None of the MRSA-infected patients underwent surgical intervention beyond debridement of the ear canal. The MRSA-infected patients were treated with intravenous vancomycin. Overall, the 7 patients with documented resolution of non- Pseudomonas infections were treated with antibiotics for an average of 9.3 6 4.5 weeks of definitive antibiotic therapy and 10.4 6 4.6 total weeks of antibiotic therapy. These treatment durations were longer (3.2 and 2.5 weeks, respectively) than those for the Pseudomonas -infected patients but did not reach significance ( P = .09 and P = .25). Six of these 7 patients (86%) received intravenous therapy with nonquinolone antibiotics. Discussion Classically, MOE has been thought to be due exclusively to Pseudomonas infection. In fact, Cohen and Friedman 10 sug- gested the presence of Pseudomonas on cultures as an obli- gatory diagnostic criterion for this disease, though noting that this required further investigation. In 1988, Rubin and Yu 3 performed a literature review of 260 cases of MOE and found that virtually all cases (99.2%) were caused by Pseudomonas . With increasing frequency, however, non- pseudomonal cases of MOE are being reported. Fewer than half (45%) of the patients in our study had cultures that grew Pseudomonas . Similarly, in 2010, Chen et al 7 and Jacobsen and Antonelli 13 reported relatively low proportions of pseudomonal MOE, with only 26.9% and 34% of their respective patients having Pseudomonas isolated in cultures. Commensurate with the decline in Pseudomonas isolates has been a rise of other organisms leading to MOE. 5-7,13 The second most common isolate in our series was S aureus , with 3 isolates being MRSA (15%). To our knowl- edge, there are few reports documenting MRSA as a causa- tive organism in cases of MOE. 7,8 With the evolving microbiology of MOE, it is essential that treatment be tailored to the causative organism(s). Since its introduction in the late 1980s, oral ciprofloxacin has commonly been used as a first-line empiric treatment for MOE. 14 This allowed patients with early-stage disease to be treated empirically in an outpatient setting. Now, how- ever, with the increasing frequency of nonpseudomonal MOE, ciprofloxacin may not always be an effective treat- ment, as it has poor gram-positive coverage and is ineffec- tive against MRSA. Additionally, the incidence of ciprofloxacin-resistant Pseudomonas has been rising. Although there was 1 instance of levofloxacin resistance and not any documented

ciprofloxacin resistance in our Pseudomonas isolates, other investigators have reported an increasing incidence ciprofloxacin-resistant Pseudomonas as a cause of MOE. 14,15 In 2002, Berenholz et al 15 were the first to report MOE caused by ciprofloxacin-resistant Pseudomonas , with 33% of their Pseudomonas isolates being resistant to ciprofloxacin. The clinical features of MOE caused by Pseudomonas and MRSA were similar in many respects (average age of onset, signs and symptoms, etc), but some important differences were noted. Diabetes is a commonly noted comorbidity in patients with MOE and, along with immunocompromised state, is thought to be a risk factor for development of the disease. 3 In our series, all of the Pseudomonas -infected patients had diabetes, whereas only 1 of the 3 MRSA- infected patients did ( P = .046). Additionally, only 55% of the patients with non- Pseudomonas infections had diabetes, which was also significantly less than in the Pseudomonas - infected patients ( P = .04). These findings illustrate the point that a diagnosis of MOE must be considered in any patient with refractory otitis externa, even in those without diabetes. Furthermore, it suggests that atypical organisms, such as MRSA, should be suspected in patients without diabetes who present with MOE. There were important limitations of this study worth men- tioning. First, the study was retrospective in nature, and data were limited to the available records. Additionally, the patient population was heterogeneous in terms of prior ther- apy and the manner in which cultures were obtained. It is possible that prior therapy would eradicate organisms that would have otherwise have been detected on culture. This means that potentially pathogenic organisms (in isolation or as a part of a polymicrobial infection) may have been eradi- cated or rendered undetectable by culture prior to presenta- tion to our offices in some instances. Furthermore, ear-swab culture may not always be reflective of the pathogenic organ- ism infecting the temporal bone in MOE. Although the spe- cific role of culture method has not been investigated in MOE, discordance between swab and bone culture has been shown for diabetic foot osteomyelitis. 16 For this reason, we recommend tissue biopsy in cases in which there is poor or no response to ear-swab culture–directed therapy. Additionally, the choice of antibiotic was based on the preference of the treating neurotologist in conjunction with an infectious disease specialist. Many patients were treated with intravenous antibiotics, while sensitivities sug- gested that an oral antibiotic could have been used. Because MRSA is a rare organism to cause MOE, there are few data guiding treatment of this offending organism. It is worth noting that 1 of our MRSA-infected patients was being treated with oral trimethoprim-sulfamethoxazole at the time of presen- tation and culture. Although sensitivities indicated that the organism was susceptible to this antibiotic, the patient’s infec- tion was not responsive to this treatment. The infection was resolved with intravenous vancomycin treatment. In general, treatment durations were planned for 6 weeks and extended as needed on the basis of clinical or radio- graphic evidence of persistent or progressive disease. It is

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