Aortic Endograft Infection with <i>Mycobacterium chimaera</i> and <i>Granulicatella adiacens</i>, Switzerland, 2014

Plate, Andreas; Kohl, Thomas A.; Keller, Peter M.; Majer, Sabine; Fulchini, Rosamaria; Strahm, Carol; Medugno, Cristoforo; Rančić, Zoran; Husmann, Lars; Sax, Hugo; Niemann, Stefan; Hasse, Barbara

doi:10.3201/eid2409.180247

Cited by 4 publications

(3 citation statements)

References 11 publications

(15 reference statements)

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“…AST of environmental M. chimaera isolates recovered from HCUs is important because whole-genome sequencing studies have linked the majority of invasive M. chimaera infections to strains recovered from contaminated HCU devices globally (4). Treatment of invasive M. chimaera infections associated with OHS has been challenging (14,16,17,29). Like other NTM species, M. chimaera appears to be an effective biofilm producer (30).…”

Section: No Of Isolates B With Mics Ofmentioning

confidence: 99%

Antimicrobial Susceptibility of Clinical and Environmental Mycobacterium chimaera Isolates

Mok

Hannan

Nölke

et al. 2019

Antimicrob Agents Chemother

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Mycobacterium chimaera is a slow-growing nontuberculous Mycobacterium species belonging to the Mycobacterium avium complex (MAC). It has been identified globally as the cause of a large outbreak of cardiovascular infections following open heart surgery, but it can also cause respiratory infections in individuals with underlying structural pulmonary disease. Invasive M. chimaera infections are associated with poor clinical responses, and the optimal antibiotic treatment regimen for these infections is not known. In this study, the drug susceptibility profiles of clinical and environmental M. chimaera isolates for antimicrobial agents that are commonly considered for treatment of MAC infections were determined. All M. chimaera isolates were susceptible to clarithromycin, with a median MIC of 2 μg/ml, while 98% (85/87 isolates) were susceptible to amikacin. Twenty-five percent of isolates (22/87 isolates) had intermediate susceptibility and 52% (46/87 isolates) were resistant to moxifloxacin. Similarly, 39% of isolates (34/87 isolates) had intermediate susceptibility and 39% (34/87 isolates) were resistant to linezolid. MIC breakpoints derived from the literature were used to determine resistance to rifampin (16/87 isolates [18%]), ethambutol (10/87 isolates [11%]), rifabutin (2/87 isolates [2%]), and streptomycin (1/87 isolates [1%]). In conclusion, our results showed that clarithromycin, amikacin, rifabutin, and streptomycin had the best activity against M. chimaera isolates, while susceptibility rates were lower for rifampin and ethambutol. In contrast, there was a high prevalence of isolates that were not susceptible to moxifloxacin or linezolid. While factors in addition to antibiotic susceptibility may determine the outcomes of treatment of M. chimaera infections, our results should inform the selection of antimicrobials as part of the overall therapeutic strategy.

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Section: No Of Isolates B With Mics Ofmentioning

confidence: 99%

Antimicrobial Susceptibility of Clinical and Environmental Mycobacterium chimaera Isolates

Mok

Hannan

Nölke

et al. 2019

Antimicrob Agents Chemother

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“…Mizoguchi et al [13] reported an endovascular device infection with an iliopsoas abscess caused by Mycobacterium tuberculosis var. bovis after intravesical bacillus Calmette-Guérin therapy; Shaikh et al [14] reported an aortic graft infection with a Mycobacterium avium complex in a patient with a human immunode ciency virus infection; and Plate et al [15] reported an aortic endograft infection with Mycobacterium chimaera associated with an outbreak in the high-care units. To the best of our knowledge, this is the rst report of aortic endograft infection with MMA.…”

Section: Discussionmentioning

confidence: 99%

Aortic endograft infection by Mycobacterium abscessus subsp. massiliense with acquired clarithromycin resistance is associated with unreported gene mutations: A case report

Akiyama

Iwamoto

Kamada

et al. 2023

Preprint

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Background Mycobacterium abscessus subsp. massiliense (MMA) comprises a group of non-tuberculous, rapidly growing mycobacteria. Although MMA can cause pulmonary diseases, surgical site infections, and disseminated diseases, aortic endograft infection has not been reported. Here, we describe the first case of aortic endograft infection caused by MMA. Case presentation Two months after stent-graft insertion for an abdominal aortic aneurysm, an 85-year-old man was admitted with fever and abdominal pain and was diagnosed with aortic endograft infection. Despite 14 days of meropenem and vancomycin intravenous administration, periaortic fluid pooling increased as compared to that before antibiotic administration. The abscess was drained, and fluorescent acid-fast staining of the abscess fluid revealed bacilli. The organism was identified as MMA by genetic testing. Intravenous imipenem–cilastatin (IPM/CS), amikacin (AMK), and oral clarithromycin (CAM) were administered. After 2 months, oral CAM and sitafloxacin were administered because the abscess had decreased in size. However, after 6 weeks, the abscess increased in size again. Antimicrobial susceptibility testing of the drainage fluid from the abscess resulted in the isolation of an MMA strain that had acquired resistance to CAM. Intravenous IPM/CS, AMK, and oral linezolid were added to the treatment regimen along with oral CAM and STFX. However, he was not fully cured and died 6 months later. Neither the full-length erythromycin ribosome methyltransferase (erm)(41) gene nor the rrl or rpIV gene mutations were found by Sanger sequencing in the pre- and post-treatment strains. Whole-genome sequence analysis of the post-treatment strain revealed mutations in genes with no previous reports of association with macrolide resistance. Conclusions Aortic endograft infection caused by MMA strain is extremely rare; nonetheless, MMA should be suspected as the causative microorganism when broad-spectrum antimicrobials are ineffective.

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“…Mizoguchi et al [ 13 ] reported an endovascular device infection with an iliopsoas abscess caused by Mycobacterium tuberculosis var. bovis after intravesical bacillus Calmette – Guérin therapy; Shaikh et al [ 14 ] reported an aortic graft infection with a Mycobacterium avium complex in a patient with a human immunodeficiency virus infection; and Plate et al [ 15 ] reported an aortic endograft infection with Mycobacterium chimaera associated with an outbreak in the high-care units. To the best of our knowledge, this is the first report of aortic endograft infection with MMA.…”

Section: Discussionmentioning

confidence: 99%

Aortic endograft infection by Mycobacterium abscessus subsp. massiliense with acquired clarithromycin resistance: a case report

Akiyama,

Iwamoto,

Kamada

et al. 2023

BMC Infect Dis

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Background Mycobacterium abscessus subsp. massiliense (MMA) comprises a group of non-tuberculous, rapidly growing mycobacteria. Although MMA can cause pulmonary diseases, surgical site infections, and disseminated diseases, aortic endograft infection has not been reported. Here, we describe the first case of aortic endograft infection caused by MMA. Case presentation Two months after stent-graft insertion for an abdominal aortic aneurysm, an 85-year-old man was admitted with fever and abdominal pain and was diagnosed with aortic endograft infection. Despite 14 days of meropenem and vancomycin intravenous administration, periaortic fluid pooling increased as compared to that before antibiotic administration. The abscess was drained, and fluorescent acid-fast staining of the abscess fluid revealed bacilli. We conducted genetic tests on the genes hsp65, rpoB, and sodA, performed Whole Genome Sequencing (WGS), and identified the organism as MMA. Intravenous imipenem–cilastatin (IPM/CS), amikacin (AMK), and oral clarithromycin (CAM) were administered. After 2 months, oral CAM and sitafloxacin were administered because the abscess had decreased in size. However, after 6 weeks, the abscess increased in size again. Antimicrobial susceptibility testing of the drainage fluid from the abscess resulted in the isolation of an MMA strain that had acquired resistance to CAM. Intravenous IPM/CS, AMK, and oral linezolid were added to the treatment regimen along with oral CAM and STFX. However, he was not fully cured and died 6 months later. Neither the full-length erythromycin ribosome methyltransferase (erm)(41) gene nor the rrl or rpIV gene mutations were found by Sanger sequencing in the pre- and post-treatment strains. Whole-genome sequence analysis of the post-treatment strain revealed mutations in genes with no previous reports of association with macrolide resistance. Conclusions Aortic endograft infection caused by MMA strain is extremely rare; nonetheless, MMA should be suspected as the causative microorganism when broad-spectrum antimicrobials are ineffective.

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Aortic Endograft Infection with Mycobacterium chimaera and Granulicatella adiacens, Switzerland, 2014

Cited by 4 publications

References 11 publications

Antimicrobial Susceptibility of Clinical and Environmental Mycobacterium chimaera Isolates

Antimicrobial Susceptibility of Clinical and Environmental Mycobacterium chimaera Isolates

Aortic endograft infection by Mycobacterium abscessus subsp. massiliense with acquired clarithromycin resistance is associated with unreported gene mutations: A case report

Aortic endograft infection by Mycobacterium abscessus subsp. massiliense with acquired clarithromycin resistance: a case report

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