Although
Nocardia species are a rare cause of intracranial abscess and represent only 1% to 2% of all cerebral abscesses, its mortality rate (31%) is considerably greater than that of other agents that can cause cerebral abscesses (<10%) [
12]. In this context, an accurate diagnosis and early treatment are challenging. Initial combination therapy with two active agents is recommended for patients with disseminated or severe nocardiosis [
1]. Empirical therapy should consider the local ecology (e.g., particular strains, trends in antimicrobial susceptibility) and be adapted after the antibiotic susceptibility testing. However, these susceptibility tests may not always be reliable, as shown by the contradictory results of TMP-SMX susceptibility trends. Uhde
et al. reported that among 765
Nocardia isolates submitted to the American Center for Disease Control and Prevention in Atlanta, Georgia from 1995 to 2004, 61% were resistant to SMX, and 42% were resistant to TMP-SMX [
7]. In a 2011 study of 186
Nocardia species isolated from patients in Spain, Larruskain
et al. reported that 16.1% were resistant to TMP-SMX [
8]. A recent report from Canada stated that 43% of the 157 of
Nocardia isolates recovered from Quebec (1988 to 2008) were resistant to TMP-SMX [
9]. By contrast, other researchers have reported a low incidence of resistance to TMP-SMX. Brown-Elliot
et al. stated that among 552 susceptibility results submitted for review, only 14 isolates (2.5%) were identified as sulfonamide-resistant, with three isolates resistant to TMP-SMX and 11 resistant to SMX [
13]. These results are strikingly similar to the low incidence (2%) of sulfonamide resistance observed by Lai
et al. in a study of
Nocardia isolates in Taiwan [
14]. The disparity among the reported data, even in the same country, is of interest because it suggests that factors other than geographic location may play a major role in the susceptibility patterns reported; the most probable factor is a difference in methodology or interpretation. The exchange of organisms between two or more accredited laboratories has been proposed as a way to enhance the accuracy of susceptibility testing [
13]. Despite this recommendation, a recent multisite study by Conville
et al. found that there was a lack of reproducibility for the sulfonamide MIC results, especially when testing
N. wallacei and even within a particular reference laboratory [
6]. Among the reasons for this variability discussed by the authors was the difficulty associated with obtaining a homogeneous organism suspension or inoculum because of the clumping ability of
Nocardia species. Of interest, this study indicated that the disk diffusion test for sulfonamides was useful for validating the MIC results obtained by broth microdilution. In our case, the results of these two susceptibility tests were contradictory for sulfonamides.
N. wallacei is expected to be susceptible to TMP-SMX and resistant to amikacin [
6]. Isolates reported to be resistant to sulfonamides have nonetheless been successfully treated with sulfonamides [
9]. However, rare clinical reports have described the treatment failure of
Nocardia with TMP-SMX [
15]. In the present case, the clinical response to TMP-SMX was discordant with the results of the initial
in vitro susceptibility test. Recently, large microbiological studies have raised concerns regarding the limits of interpretation of the TMX-SMX susceptibility test results. This is the first case of disseminated infection caused by
N. wallacei that demonstrates the conflict between the
in vitro resistance to sulfonamides and the clinical response to TMP-SMX.