Mycobacterium goodii endocarditis following mitral valve ring annuloplasty

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).

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.

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.

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.

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.

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.