Open Access

Mycobacterium goodii endocarditis following mitral valve ring annuloplasty

Annals of Clinical Microbiology and Antimicrobials201716:14

https://doi.org/10.1186/s12941-017-0190-4

Received: 27 July 2016

Accepted: 15 March 2017

Published: 21 March 2017

Abstract

Background

Mycobacterium goodii is an infrequent human pathogen which has been implicated in prosthesis related infections and penetrating injuries. It is often initially misidentified as a gram-positive rod by clinical microbiologic laboratories and should be considered in the differential diagnosis.

Case presentation

We describe here the second reported case of M. goodii endocarditis. Species level identification was performed by 16S rDNA (ribosomal deoxyribonucleic acid) gene sequencing. The patient was successfully treated with mitral valve replacement and a prolonged combination of ciprofloxacin and trimethoprim/sulfamethoxazole.

Conclusion

Confirmation of the diagnosis utilizing molecular techniques and drug susceptibility testing allowed for successful treatment of this prosthetic infection.

Keywords

Mycobacterium goodii Endocarditis Gene sequencing Prostheses related infections

Background

Mycobacterium goodii is a rapidly growing non-tuberculous mycobacterium (NTM) belonging to the Mycobacterium smegmatis [1] group. Its importance has become increasingly appreciated as a pathogen over the last 20 years, with a predilection towards infecting tissues at the site of penetrating injuries. Antibacterial treatment strategies against this pathogen are diverse but reported case cure rates are high. Here we describe what the authors believe to be the second reported case of M. goodii endocarditis ever reported (first time involving a ring annuloplasty).

Case presentation

A 67-year-old Caucasian man, retired financier, with a history of severe mitral regurgitation status post ring annuloplasty repair complicated by right sided hemothorax requiring two reoperations to achieve hemostasis, presented to an outside hospital 3 weeks postoperatively with fever, loss of appetite, and gait disturbance.

On examination the patient vital signs were normal, lungs were clear, a mild 1/6 systolic murmur was appreciated at the apex, and a drain was in place for a groin seroma related to recent left heart catheterization. He had an unsteady gait and exhibited mild left lower extremity weakness (4/5). His brain magnetic resonance imaging showed multiple ring-enhancing lesions in the pons and posterior fossa suggestive of septic emboli. Transthoracic echocardiography showed moderate mitral regurgitation without any vegetation. Blood cultures grew gram-positive rods suspicious for Actinomyces spp. and he was started on vancomycin and ampicillin/sulbactam. He developed a morbilliform cutaneous eruption felt to be related to the ampicillin and was switched to vancomycin/ceftriaxone. A computed tomography scan of the chest (Fig. 1) was done which showed bilateral infiltrates and mild pleural effusions.
Fig. 1

Computed tomography of chest showing bilateral infiltrates and bilateral pleural effusion

The patient was then transferred to our hospital on day 14 for further management. A transesophageal echocardiogram (TEE) (Fig. 2) showed vegetations on the P3 annulus and evidence of ring dehiscence in A2, A3, and P3 areas. He completed penicillin desensitization and was successfully narrowed to penicillin G to be optimally treated for presumptive actinomycotic endocarditis and both vancomycin and ceftriaxone were stopped. On hospital day 18 he underwent mitral valve replacement with a bioprosthetic valve (27 mm. St. Jude prosthesis). Intraoperatively, vegetations were confirmed on the mitral valve and tissue cultures from the explanted native mitral valve suggested a rapid growing mycobacterium rather than an Actinomyces spp. Empiric treatment with meropenem (1 g IV thrice a day)/amikacin (1 g IV per day)/clarithromycin (500 mg oral twice a day)/ciprofloxacin (400 mg IV twice a day) was initiated pending final confirmation and susceptibility testing. On day 21 it was confirmed that the gram-positive isolate was a 100% match to the M. goodii strain (American Type Culture Collection or ATCC #700504) using 16S sequencing (MicroSeq 500 bp 16S rDNA kit), but M. smegmatis could not be ruled out due to a high-level sequence homology [99.5% match to M. smegmatis type strain (ATCC 19420) with two mismatches]. Serial blood cultures sterilized on hospital day 26 and he was transferred to a nursing facility after repeat TEE showed a normally functioning prosthetic mitral valve.
Fig. 2

Trans-esophageal echocardiogram showing mitral valve vegetation in the mid-esophageal plane

On the day following discharge into the rehabilitation facility, the patient developed a maculopapular eruption involving his flanks and back, which progressed to involve his anterior trunk and all four limbs. He presented to the infectious diseases clinic 3 days after discharge where the rash was suspected of being related to the meropenem and tigecycline was substituted; however, he had an acute anaphylactoid reaction (involving dyspnea and hypotension) during the loading dose of tigecycline (100 mg once) which was subsequently replaced with linezolid (600 mg oral twice a day). His susceptibility reports returned which showed the mycobacterium was susceptible to trimethoprim–sulfamethoxazole, amikacin, doxycycline, ciprofloxacin, imipenem, linezolid and resistant to clarithromycin. In accordance, his regimen was changed to ciprofloxacin (500 mg oral twice a day)/trimethoprim–sulfamethoxazole (1 DS tablet oral twice a day).

The patient was ultimately treated with a total of 6 months of therapy. He followed up in infectious diseases clinic on days 61 and 135 and was contacted by phone 137 weeks post valve replacement and there were no complaints or signs of intervening relapse, was highly active and back to all his prior recreational activities.

Discussion

A broad literature search was done from PubMed, Scopus and OvidSP databases containing the search terms M. goodii to try and identify all human infections with this organism. M. goodii was proposed as a new rapidly growing species related to M. smegmatis based on gene sequencing work by Brown et al. [1] in 1999 in continuation to the work done by Wallace et al. [2]. We have summarized to the best of our knowledge all the published reports about M. goodii infections (Table 1) after Brown [1]. A total of 45 cases (including our patient) have been reported to date. Eleven (25%) cases were wound/bone infections due to trauma. Twenty-two (49%) cases were iatrogenic, with eighteen (38%) involving infection of prosthetic materials. Eight (18%) cases were pulmonary, which were strongly associated with histological findings of lipoid or granulomatous pneumonias. Four (9%) cases had unclear clinical diagnosis but were confirmed to be M. goodii microbiologically.
Table 1

Selected M. goodii reported human cases after Brown et al.

Infection type

Age

Sex

Comorbidities

Treatment

Microbial susceptibility

Mitral valve endocarditis complicating ring annuloplasty

67

M

None

Mitral valve replacement, ciprofloxacin + TMP/SMX (6 months)

Susceptible to TMP/SMX, amikacin, doxycycline, ciprofloxacin, imipenem, linezolid

Resistant to clarithromycin

Prosthetic mitral valve endocarditis [8]

76

F

None mentioned

Mitral valve replacement, tigecycline + ciprofloxacin (2 weeks) doxycycline + ciprofloxacin (11 weeks)

Resistant to cefotaxime, erythromycin, clarithromycin

Pacemaker site infection [9]

23

M

Partial AV canal defect repair at 5 years of age

Pacemaker retained, ofloxacin + amikacin (1 month), doxycycline (6 months)

Resistant to clarithromycin

Pacemaker pocket infection [10]

85

M

Ischemic cardiomyopathy

Pacemaker replacement, TMP/SMX (8 weeks)

Susceptible to TMP/SMX, minocycline, imipenem

Pacemaker pocket and bloodstream infection [11]

82

M

None mentioned

Pacemaker removal, amikacin + minocycline

Resistant to clarithromycin, cefoxitin, clindamycin, vancomycin

Pacemaker pocket infection [12]

74

F

Bicuspid aortic valve, hypothyroidism, diabetes mellitus, gastro-esophageal reflux disease, asthma

Pacemaker removal, ciprofloxacin + doxycycline (6 months)

Susceptible to amikacin, ciprofloxacin, doxycycline, imipenem, linezolid, tobramycin and trimethoprim/sulfamethoxazole Resistant to clarithromycin

Ventriculo-peritoneal shunt infection [13]

60

F

Allergy to sulfa drugs

Ventriculoperitoneal shunt removal, imipenem + moxifloxacin (5 weeks), moxifloxacin monotherapy (3 additional months)

Resistant to azithromycin, clarithromycin

Hernia mesh infection with abdominal wall abscess [14]

65

M

None mentioned

Mesh removal, TMP/SMX

Resistant to cefoxitin, clarithromycin

Hernia mesh infection [15]

64

M

None mentioned

Patch removal. Antibacterial treatment not specified

Susceptible to ciprofloxacin, doxycycline and TMP/SMX

Skin graft infection [16]

6

M

None mentioned

TMP/SMX + linezolid (6 months)

Resistant to clarithromycin, amoxicillin/clavulanate

Prosthetic total knee joint infection [17]

44

M

Nicotine dependence, significant ethanol use

Removal of prosthesis, TMP/SMX (stopped after 1 week by patient), minocycline + ciprofloxacin (6 months)

Resistant to clindamycin

Prosthetic total knee joint infection [15]

75

F

None mentioned

Prosthesis replaced

Susceptible to ciprofloxacin, doxycycline and TMP/SMX

Prosthetic total hip joint infection [15]

64

M

None mentioned

Prosthesis replaced

Susceptible to ciprofloxacin, doxycycline and TMP/SMX

Olecranon bursitis following corticosteroid injections [18]

60

M

Diabetes mellitus

Doxycycline + ciprofloxacin (10 weeks)

Resistant to clarithromycin

Postcataract endophthalmitis [19]

67

M

None mentioned

Pars plana vitrectomy + lens removal, intravitreal amikacin × 2 doses

None reported

Aspiration pneumonia [20]

15

F

Rickettsial infection

Laparoscopic Heller myotomy with fundoplication, ciprofloxacin + doxycycline (12 months)

Resistant to clarithromycin

Complicated parapneumonic effusion [21]

66

M

None mentioned

None mentioned

None mentioned

Since there is no available clinical trial or prospective data to guide therapy for this infection, we extrapolated a treatment approach from the accumulated experience with other more common rapid growing NTM species to treat our patient with this incredibly rare disease. Our empiric regimen selection was further made challenging by the development of a second drug eruption and an anaphylactoid infusional reaction, both of which required cessation of drugs and subsequent drug substitution.

Conclusions

Rapid growing mycobacteria should be suspected in trauma or prosthetic related infections not responding to initial empiric therapies. Molecular techniques are rapid and reliable for confirmation of rapid growing mycobacterial infections and are recommended by the Infectious Diseases Society of America guidelines [3]. Once rapid growing mycobacteria are suspected, 16S ribosomal sequencing should be used if available for species level identification. 16S rRNA gene sequences contain hypervariable regions that can provide species-specific signature sequences useful for identification of bacteria [4]. Since M. goodii has the ability to form biofilms [5], prosthesis removal is indicated to achieve cure if feasible. Macrolides should not be included in the empirical/definitive treatment since it has been shown that the organism has intrinsic macrolide resistance conferred by novel rRNA methylase genes erm(38) and erm(39) [6, 7]. This has also been seen widely in the susceptibility testing for the organism. The organism is usually susceptible to sulfonamides, amikacin, doxycycline, imipenem, fluoroquinolones and they should be optimized for dose and duration according to the severity and comorbidities.

Abbreviations

ATCC: 

American Type Culture Collection

rDNA: 

ribosomal deoxyribonucleic acid

TEE: 

transesophageal echocardiogram

Declarations

Authors’ contributions

RP authored the main text and conducted the literature review. MG was the consultant physician, oversaw the management of this patient and edited/revised several versions of the case report and literature review. Both the authors read and approved the final manuscript.

Acknowledgements

We thank David Ryan Peaper for providing the details about the bacterial identification process and Dr. Elise M Meoli for providing the transesophageal echocardiography images.

Competing interests

The authors declare that they have no competing interests.

Availability of data and materials

The production of this manuscript did not involve the production of any data sets.

Consent

Written informed consent was obtained from the patient for publication of this case report.

Consent for publication

The patient in the case report provided both verbal and written consent to access his entire medical record as well as verbally consented to publishing his case in a de-identified manner.

Ethics approval and consent to participate

The study contains exclusively de-identified patient data from a single case report and a retrospective review of previously published human cases, therefore poses no hazard directly or indirectly to any living persons and is exempt from ethics approval.

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors’ Affiliations

(1)
Texas Heart Institute
(2)
Yale School of Medicine

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Copyright

© The Author(s) 2017

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