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Mycobacterium Chelonae

  • Author: Alfred Scott Lea, MD; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Oct 06, 2015
 

Background

Mycobacterium chelonae belongs to the family of nontuberculous mycobacteria (NTM) classified in the rapidly growing mycobacteria (RGM), Runyon group IV that are nonpigmented. RGM typically show visible colonies on solid growth media within 1 week.[1] M chelonae is further grouped in the M chelonae-abscessus group that encompasses Mycobacterium immunogenum, Mycobacterium massiliense, and Mycobacterium bolletii, in addition to M chelonae and M abscessus.

In 1992, M chelonae became its own species based on previous genomic studies.[2, 3] Hence, when researching and reviewing the literature prior to 1992, M abscessus and M chelonae were considered the same organism or subspecies within the M chelonae-abscessus group, which complicated its taxonomy. In addition, further identification of the newer species M massiliense and M bolletii and the proper taxonomy surrounding these 2 species and others cause the taxonomy of this group to be a dynamic process.[4, 5]

M chelonae, along with M abscessus, are considered the most drug resistant of the NTM group, which leads to difficulty when treating infections these organisms. It is important to establish that M chelonae is the pathogen causing a particular infection . The severity of disease and the patient’s underlying medical condition also influence therapy. M chelonae tends to respond better to treatment regimens since is lacks the erm gene that confers macrolide resistance in M abscessus strains.[6] Most information about treatment recommendations are based upon in vitro laboratory observations, clinical anecdotes, retrospective observational series, and expert opinion. Optimal therapeutic interventions and their duration, as well as outcomes data, are not firmly established based upon large, controlled, evidence-based experimental studies.

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Pathophysiology

M chelonae, like many NTM, are ubiquitous in the environment and have been isolated from both natural and potable freshwater sources, soil, contaminated solutions, and reptiles.[7] The organism can grow in distilled and unsupplemented water. It is hydrophobic and adheres to surfaces, owing to the structure and make up of its mycolic acids resulting in biofilm formation.[8, 9] Like most RGM, it is resistant to chlorine and some industrial grade detergents (ie, glutaraldehyde) commonly used in hospital settings.[10] Household water heaters are favorable growth environments owing to the stagnant water and its elevated temperature.[11]

M chelonae causes disease sporadically, as well as in patients with identifiable risk factors, owing to its hardiness, resistance to chemical and antimicrobial degradation, and ubiquitous environmental presence.

M chelonae most commonly causes infection of the skin and skin structures where infections can be classified as a localized cellulitis, as a subcutaneous abscess, or as disseminated disease.[12] According to some series, as many as 75% of patients with disseminated disease are initially colonized with M chelonae, and skin trauma is thought to be the etiology for cutaneous invasion.[13, 14]

Accidental penetrating trauma, particularly when associated with pedicure salons and footbaths are well-known risk factors for disease. Initial reports of NTM cutaneous infection associated with tattoos occurred in 2003. M chelonae has caused outbreaks of skin infections associated with tattoo parlors and has been found in contaminated tattoo ink.[15] Disseminated infection is associated with organ transplants, diabetes mellitus, malignancy, long-term corticosteroid administration, immunosuppressant therapy, and tumor necrosis factor-alpha (TNF-α) inhibitors.[15, 16]

Healthcare-associated M chelonae infections have been associated with surgical infections of all types, complicating eye, otolaryngologic, chest, abdominal, cardiovascular, reconstructive, cosmetic, and orthopedic procedures. Any intervention involving injectable foreign materials, artificial prostheses, and implantable devices (eg, pacemakers, prosthetic valves) are at risk.[17] Surgical site infections have ranged from sternal wound infections associated with the bone wax to plastic and reconstructive surgical infections linked to contaminated water or marking solution.[18, 19] These infections have been associated with acupuncture and mesotherapy in South America.[20] M chelonae has caused peritonitis and dialysis catheter infections in peritoneal dialysis patients.[21] It causes intravascular catheter infections of all types and is particularly common in the immunocompromised patient.

The eye is the second most common site of M chelonae infection. The organism is known to cause dacryocystitis, canaliculitis, conjunctivitis, scleritis, endophthalmitis, and keratitis.[22] Risk factors for infection include both accidental and surgical trauma, laser in situ keratomileusis (LASIK), penetrating keratoplasty (PK), and all procedures involving retained biomaterial.[23] Additional risk factors include the presence of contact lens, corticosteroid use, and human immunodeficiency virus (HIV) infection.

Pulmonary disease with M chelonae is uncommon, and other atypical mycobacteria such as M avium complex (MAC), M kansasii, and M abscessus are the more likely lung pathogens.[24] When M chelonae has been described as the causative pathogen, it usually occurs in patients with severe underlying lung disease such as cystic fibrosis or bronchiectasis, patients with significant gastroesophageal disorders, or in patients with signs of connective-tissue disorders such as mitral valve prolapse (MVP), scoliosis, and pectus excavatum.[25]

Musculoskeletal involvement with M chelonae is also uncommon, but is associated with penetrating trauma. Both osteomyelitis and granulomatous tenosynovitis have been reported without any known preceding trauma.[12, 26] Prosthetic joint infections with M chelonae have been described.[27]

Sinusitis and otitis media secondary to M chelonae has been reported.[28] Cases associated with prior surgery, topical corticosteroid usage, and pressure equalization (PE) tube insertion have been described.[18, 29] M abscessus is the more likely atypical organism to cause otitis media.

Bacteremia is usually associated with fever, with or without chills and sweats. Shock and multisystem organ failure is unusual. Patients typically possess intravascular catheters, dialysis catheters, biliary stents, or prosthetic heart valves and are usually immunocompromised.

Immune defects such as autoantibodies to specific interleukins (ILs), interferon-gamma (INF-γ), and IL or INF receptor deficiencies have been reported and are risk factors for disseminated NTM, in addition to known risk factors such as HIV infection, long-term steroid use, immunosuppressives, and TNF-α inhibitors.[25, 29, 30]

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Epidemiology

Frequency

United States

M chelonae and the other RGM are not reportable infections in the United States, and the true prevalence is unknown. Most of the NTM have been shown to have geographic variation in the United States. M chelonae can occour anywhere in the United States, but the prevalence of M chelonae/abcessus cases is increased cases in the southern and coastal states of Florida, Georgia, Louisiana, and Texas.[1, 25]

The first national survey evaluating the prevalence of NTM in the United States was done between 1981 and 1983, and it showed an annual disease prevalence of 1.78 NTM cases per 100,000 persons, with M chelonae/abcessus reported as 0.08 case per 100,000 persons.[31] NTM lung disease in hospitalized patients was studied from 1998 to 2005 in 11 states and showed increasing prevalence with age in men and women, with some variation between states.[32] In Oregon from 2005 to 2006, individuals meeting a strict case definition for NTM disease were studied, with a reported annualized prevalence of 7.2 cases per 100,000 persons. In that study, M chelonae prevalence was 0.2 case per 100,000 persons, with the majority of cases isolated from skin and soft tissue infections.[33]

Overall, it appears that NTM prevalence is increasing in certain populations and geographic areas throughout the country, but the degree to which M chelonae specifically contributes is uncertain. It represents a smaller percentage of these infections than other NTM species.

International

The global epidemiology of pulmonary NTM infections has been reviewed, with limited reported information about M chelonae.[34] The incidence and prevalence of NTM varies considerably, and M chelonae has been reported in South America, Australia, Taiwan, China, Japan, Canada, Korea, Germany, Italy, France, Switzerland, the United Kingdom, and The Netherlands.[1]

A 2-year review of NTM isolates in a South Korean medical center was evaluated for clinical relevance. Approximately one fourth of 1548 isolates from 794 patients were found to be clinical significant, with M chelonae representing 29 isolates from 25 patients. Of those, only 6 patients (3%) were determined to be definite or probable NTM infection based on American Thoracic Society (ATS) and British Thoracic Society (BTS) guidelines.[35]

A national Australian survey in 2000 reported that all 22 M chelonae pulmonary isolates were not considered pathogens, while the organism was considered pathogenic in 17 of 131 soft-tissue isolates.[36]

Mortality/Morbidity

Mortality from localized or systemic infection with M chelonae is rare but may result from disseminated disease or surgical complications.

Race

M chelonae infection has no clear racial predilection.

Sex

M chelonae infection has no clear sexual predominance.

Age

M chelonae has no clear age predilection, although increased age is frequently identifiable based on associated risk factors and associated events (ie, cardiac surgery, TNF-α inhibitor administration).

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Contributor Information and Disclosures
Author

Alfred Scott Lea, MD Associate Professor of Medicine, Department of Medicine, Division of Infectious Diseases, University of Texas Medical Branch School of Medicine

Alfred Scott Lea, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, Infectious Diseases Society of America, Texas Medical Association, Harris County Medical Society, American College of Certified Wound Specialists

Disclosure: Nothing to disclose.

Coauthor(s)

Jeana L Benwill, MD Assistant Professor, The University of Texas Health Science Center at Tyler

Jeana L Benwill, MD is a member of the following medical societies: Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Aaron Glatt, MD Chief Administrative Officer, Executive Vice President, Mercy Medical Center, Catholic Health Services of Long Island

Aaron Glatt, MD is a member of the following medical societies: American College of Chest Physicians, American Association for Physician Leadership, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Infectious Diseases Society of America, International AIDS Society, Society for Healthcare Epidemiology of America

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Additional Contributors

Klaus-Dieter Lessnau, MD, FCCP Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital

Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

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Cutaneous lesions from Mycobacterium abscessus. Courtesy of K. Galil, US Centers for Disease Control and Prevention.
 
 
 
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