Osteomyelitis Due to Mycobacterium goodii in an Adolescent, United States.

Osteomyelitis is a rare clinical manifestation of infection with nontuberculous mycobacteria (NTM). We report an adolescent with femoral osteomyelitis associated with prosthetic material due to an emerging pathogen, Mycobacterium goodii. Application of secA1 and 16S ribosomal RNA gene sequencing reliably determined the NTM species, enabling targeted antimicrobial therapy.

Nontuberculous mycobacteria (NTM) are an emerging cause of human infections, likely because of improved detection methods and an increasing high-risk population (–). Coventional methods to identify NTM species rely on phenotypic characteristics to differentiate the most common species, but these labor-intensive and time-consuming methods delay final identification and appropriate therapy (). Sequencing of 16S rRNA and secA1 (essential secretory protein SecA1) genes provides an accurate and cost-effective method for NTM identification, offering a turnaround time of 1–2 days compared with 2–6 weeks for results from conventional methods ().

M. goodii is a rapidly growing mycobacterium that can be nonpigmented or late-pigmented. Before 1999, the original classification of the 3 species in the M. smegmatis group identified 28 isolates of M. goodii, which most often were associated with posttraumatic wound infections (). Since then, M. goodii has been implicated in infections related to prosthetic devices and penetrating trauma. Three recent reports detail 19 cases of M. goodii infections in patients with a mean age of 60 years (range 6–85 years). Types of infection included prosthetic device or pocket infection (n = 12), wound infection (n = 3), endocarditis (n = 1), pneumonia (n = 2), and endophthalmitis (n = 1) (–). We noted only 3 pediatric cases in the literature: 2 cases of pneumonia, 1 in a 15-year-old girl and 1 in a 7-week-old infant; and 1 soft tissue infection in a 6-year-old boy (,,).

We report a 15-year-old male patient with severe bilateral knee flexion contractures who underwent bilateral femoral extension osteotomies with hardware implantation. Two months later, he had intermittent low-grade fevers, right thigh pain, and surgical wound dehiscence with drainage. Initial laboratory results showed elevated leukocyte count, erythrocyte sedimentation rate, and C-reactive protein (Figure). An incision and discharge was performed but the femoral hardware was retained; 4 days later, a second incision and drainage was performed with primary closure.

Figure

Timeline of laboratory values, surgical interventions, notification of pertinent culture results, and antimicrobial drug therapy in a case of osteomyelitis due to Mycobacterium goodii in an adolescent, United States. White boxes represent periods of hospitalization. Gray arrows indicate dates of surgical intervention with cultures obtained and femoral hardware retained. Solid black arrow indicates surgical intervention with cultures obtained and femoral hardware removed. Shaded arrow indicates interventional radiology aspiration of subcutaneous fluid collection with cultures obtained. Shaded diamond indicates first notification of nontuberculous mycobacterium growth. Solid gray diamond indicates first notification of M. goodii by 16S and secA1 sequencing. Solid black diamond indicates first notification of susceptibility results for M. goodii. AZ, azithromycin; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; Hgb, hemoglobin; NTM, nontuberculous mycobacteria.

Acid-fast bacillus (AFB) cultures were obtained; after 22 days, NTM growth was identified. Empiric therapy was initiated with intravenous (IV) amikacin (15 mg/kg 1×/d), IV cefoxitin (3,000 mg every 8 h), oral azithromycin (250 mg 1×/d), and oral ciprofloxacin (500 mg every 12 h). Two weeks later, the patient underwent a third incision and drainage and hardware was removed because of recrudescent fever and surgical site discharge. AFB tissue cultures from bone again grew NTM. Sequencing of the secA1 and 16S genes from all NTM isolates identified M. goodii (Appendix Figure). The patient’s therapy was modified to oral trimethoprim/sulfamethoxazole (TMP/SMX; 320 mg 2×/d, 6 mg/kg/dose based on TMP component), with continued IV amikacin and oral ciprofloxacin. Antimicrobial susceptibility testing results confirmed susceptibility to TMP/SMX, ciprofloxacin, amikacin, and doxycycline but noted resistance to clarithromycin and cefoxitin. Amikacin was discontinued after a total of 36 days of therapy.

Five months after his last surgical intervention, the patient had clear discharge from his right thigh. A small superficial skin abscess was noted on magnetic resonance imaging. Fine needle aspiration of the fluid collection was performed from which AFB cultures were sterile but universal bacterial 16S rDNA PCR detected M. goodii. Given the potential for antimicrobial resistance, oral doxycycline (100 mg 2×/d) was added to the patient’s antimicrobial drug regimen. The 3-drug regimen was continued for an additional 4 months. Repeat imaging at the end of therapy showed no evidence of fluid reaccumulation, and the patient has not had an infection relapse for 10 months after discontinuation of antimicrobial drug therapy. No other M. goodii infections have been identified at our institution since this case.

NTM osteomyelitis treatment can be challenging. Management strategies include prolonged antimicrobial drug therapy, surgical debridement, and removal of foreign material (). M. goodii usually is susceptible to TMP/SMX, amikacin, ciprofloxacin, imipenem, and doxycycline (). However, M. goodii is intrinsically resistant to macrolides and rifampin, which commonly are used for empirical therapy of NTM infections; early species identification is crucial to ensuring effective and timely treatment (,,). Optimal treatment is unknown, but a combination of >2 active drugs, for a minimum of 6 months, combined with surgical debridement and hardware removal, is recommended to ensure clinical and bacteriological cure and prevent antimicrobial resistance (,).

Our case shows similarities to prior adult reports, specifically prosthetic-associated M. goodii infection, and further highlights the emergence of this pathogen in the pediatric population. Given the repeated culture-positive results from our patient, we do not believe this case was the result of an environmental contaminant. In addition, no other cases of M. goodii infection have been identified at our institution to suggest nosocomial infection, but we cannot definitively exclude this mode of acquisition.

In conclusion, our case highlights M. goodii as an emerging pediatric NTM pathogen. These findings underscore the use of secA1 and 16S rRNA sequencing for rapid species identification to enable timely and effective antimicrobial drug therapy.

Appendix

Phylogenetic tree of mycobacterial isolates by secA1 and partial 16S sequences from a case of osteomyelitis in an adolescent caused by Mycobacterium goodii and sequences from publicly available databases.