Disseminated Cutaneous Mycobacterium Chelonae Infection

Charles L. Kane, MPH, Albert L.Vincent, PhD, John N. Greene, MD, and Ramon L. Sandin, MD, H. Lee Moffitt Cancer Center & Research Institute, Tampa, Fla.


Cancer Control. 2000;7(2) 

In This Article


M. chelonae is a rapidly growing, nontuberculous mycobacterium that is ubiquitous and usually causes infection following incidental environmental inoculation. It was first isolated in 1903 from a sea turtle, Chelona corticata. This free-living saprophyte has since been isolated from water, soil, and dust. In 1905, a similar, rapidly growing atypical, M. ranae, was isolated from frogs and later renamed M.fortuitum by Da Costa in 1938.[4] Sharing metabolic traits, these two were linked in the M.fortuitum-chelonae complex. Later, M. chelonae was found to be more resistant to amikacin, sulfonamides, and doxy-cycline than M. fortuitum, and the two were again disassociated and recognized as separate species.[5] In 1953, M. abscessus was isolated from a human joint and was also initially thought to be M. chelonae until DNA homology between the two organisms was shown to be only 35%.[6] Since the 1980s, M. abscessus and M. chelonae have generally been regarded as separate species, although some authors continue to treat them both as a single species, which is taxonomically incorrect.

The characteristic presentation of M. chelonae in immunocompromised patients is a disseminated cutaneous infection.[6,8] Localized cellulitis or abscess is typical in the immunocompetent host. Transmission is through direct environmental inoculation rather than person to person, and the incubation period is typically 4 to 6 weeks.[9] Infection may appear most commonly as a disseminated or localized cutaneous infection (eg, cellulitis, subcutaneous abscess), and less commonly as osteomyelitis, pneumonitis, lymphadenitis, corneal ulcers, postinjection abscesses, catheter-related infections, or postsurgical endocarditis.[1,6,7,8,9,10,11,12,13,14] Involvement secondary to catheter placement is unusual but has been described in hemodialysis and peritoneal dialysis, while peristomal infection has been described in tracheostomy patients.[8] Sporotrichoid progression involving an extremity has been rarely described. It is more likely seen in M. kansasii or M. marinum infections.[15,16] Because of the variable clinical and therapeutic considerations, culture identification and in vitro susceptibility testing are important in directing treatment.

In a clinical trial by Wallace et al,[17] clarithromycin alone proved to be adequate treatment against disseminated cutaneous infections. Since the early 1990s, multiple case reports have affirmed clarithromycin as the drug of choice for M. chelonae cutaneous infections. [8,16,17,18,19] Resistance developed in one partially compliant patient on single drug therapy of clarithromycin [17] and has also been reported elsewhere.[20,21] Accumulated experience reported in the literature supports multidrug therapy for nontuberculous mycobacterial infections.[8,16,17,19,20] Most standard antimycobacterials, including ethambutol, pyrazinamide, and isoniazid, exhibit little to no effect against rapidly growing mycobacteria.[22] The probability of in vitro susceptibility of M. chelonae for the most effective antimicrobial agents are as follows: clarithromycin (100%), tobramycin (100%), amikacin (80%), imipenem (60%), doxycycline (25%), and ciprofloxacin (20%).[22] In our patient, clarithromycin and rifampin were the initial treatments chosen because culture results did not identify M. chelonae until later in the course of treatment. One study used a combination of ofloxacin, ethambutol, and doxycycline, which led to complete resolution in 6 weeks.[23] However, treatment lengths may vary greatly; the clarithromycin and rifampin regimen used for our patient led to a satisfactory outcome over 7 months. The recommended treatment period is 6 months despite possible clearing of lesions.[17] The afore-mentioned susceptibilities, together with cases supporting successful combination therapies composed of less conventional drugs, highlight the fact that there is considerable variability of response among isolates and provide further support for obtaining in vitro susceptibility. A refractory case of disseminated cutaneous M. abscessus infection was recently treated with interferon gamma (IFN-gamma).[24] It seems a mutation in the IFN-gamma receptor gene renders some patients more susceptible to mycobacterial infection,[25] which may justify the use of IFN-gamma if conventional therapy fails.


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