Vol. 21, No. 2
THE JOHNS HOPKINS MICROBIOLOGY NEWSLETTER
Tuesday, January 22, 2002

1. Provided by Karen Fujii, Division of Outbreak Investigation, Maryland Department of Health and Mental Hygiene.

The patient was a 49-year-old Caucasian female with cystic fibrosis who was admitted to the Johns Hopkins Hospital (March, 2001) for a progressive dyspnea over the past several months. Her chest x-ray showed diffuse interstitial fibrosis, but no definitive evidence of acute infiltrate. Her sputum cultures were positive for methicillin resistant Staphylococcus aureus, Pseudomonas aeruginosa, and Mycobacterium abscessus. She was treated with a 2 week course of intravenous tobramycin and ticarcillin, her pulmonary functions stabilized and improved, and she was discharged feeling well.  Because of her stable pulmonary function tests, it was felt that the M. abscessus isolate was due to colonization, and hence she was not treated for M. abscessus. In the subsequent months she was hospitalized several times for complications of cystic fibrosis. She expired from complications of cystic fibrosis (October, 2001).
 
 

Organism:

M. abscessus is a non-pigmented, rapidly growing, non-spore-forming, non-motile bacillus, belonging to the group IV non-tuberculous mycobacteria (NTM) based on Runyon classification. According to previous taxonomic grouping, M. fortuitum complex included M. fortuitum and M. chelonae, the latter species was further divided into subspecies abscessus and subspecies chelonae. Current taxonomic classification considers the above as three separate species (i.e. M. abscessus, M. fortuitum and M. chelonae). M. abscessus is found in soil and water throughout the world and has been recovered from tap water.

Clinical presentations:

M. abscessus can cause disease in healthy and immunocompromised hosts. The most common infection in immunocompetent host is localized wound or soft tissue infection secondary to direct trauma or surgical procedure. It responds to surgical debridement and/or antimicrobial therapy. Other environmentally acquired infections include pulmonary, bone, ear, and ophthalmologic infections. In immunosuppressed hosts, the organism may cause disseminated cutaneous and/or visceral disease, or rarely present as a fever of unknown origin with intraabdominal lymphadenitis. Reported nosocomial infections include sternal and mammoplasty wound infections, bacteremia due to contaminated hemodialysis equipment, peritonitis in peritoneal dialysis patients, and prosthetic valve endocarditis.
 
 

M. abscessus and pulmonary infection versus colonization in patients with cystic fibrosis:

The organisms that frequently result in chronic lung infections in cystic fibrosis patients include Pseudomonas aeruginosa, Staphylococcus aureus, Hemophilus influenzae, and less frequently Burkholderia cepacia, and Stenotrophomonas maltophilia. Patients with underlying chronic lung disease, including cystic fibrosis are at increased risk of NTM infections, although distinguishing signs and symptoms of NTM infection from other chronic bacterial pulmonary infections is often difficult.

After M. avium complex, M. abscessus is believed to be the second most common isolates from positive mycobacterial respiratory cultures in patients with cystic fibrosis. Distinguishing colonization from active disease can be challenging. Repeated isolation of the same Mycobacterium species from respiratory cultures, detection of parenchymal involvement by high resolution CT, or presence of granulomas away from necrotic areas on tissue biopsy may be indicative of indolent infection in the absence of clinical symptoms. Furthermore, a long-standing active infection may result in gradual decline in pulmonary functions. However, the progressive nature of lung disease in cystic fibrosis patients further complicates distinction of active subclinical disease from colonization.

In one study, molecular typing of all M. abscessus isolates from 5 cystic fibrosis patients who attended the same clinic each showed a unique genotype, suggesting lack of person-to-person spread of M. abscessus among patients with cystic fibrosis.
 
 

Diagnosis:

M. abscessus is an acid fast bacillus, which can readily grow on blood or chocolate agar in 3-7 days. It can be distinguished from other rapidly growing mycobacteria based on its growth characteristics, biochemical tests, and gas-liquid chromatography analysis of fatty acids and metabolic products.
 
 

Treatment:

In patients with cystic fibrosis, pulmonary infection due to M. abscessus is very difficult to eradicate. The organism is resistant to standard anti-tuberculosis drugs, and is generally susceptible to parentral antibiotics (e.g. amikacin, cefoxitin) and the newer oral macrolides (e.g. clarithromycin). The cumulative experience in the literature suggests that eradication of M. abscessus with antimicrobial agents alone is unlikely, even with aggressive therapy (such as 6 month IV amikacin, and cefoxitin in addition to oral clarithromycin). Surgical resection of localized disease in addition to antimicrobial therapy may achieve eradication of this organism, although very few cystic fibrosis patients are diagnosed at this early stage. Additional concerns regarding antimicrobial therapy include drug toxicity and development of drug resistance.
 
 

References:
1.    Bange FC, Brown BA, Smaczny C, Wallace Jr RJ, Bottger EC. Lack of transmission of Mycobacterium abscessus among patients with cystic fibrosis attending a single clinic. Clin Infect Dis. 2001 Jun 1;32(11):1648-50.

2.    Brown-Elliott BA, Wallace RJ Jr. Clarithromycin resistance to Mycobacterium abscessus.  J Clin Microbiol. 2001 Jul;39(7):2745-6.

3.    Cullen AR, Cannon CL, Mark EJ, Colin AA. Mycobacterium abscessus infection in cystic fibrosis. Colonization or infection? Am J Respir Crit Care Med. 2000 Feb;161(2 Pt 1):641-5.

4.    Mueller PS, Edson RS. Disseminated Mycobacterium abscessus infection manifesting as fever of unknown origin and intra-abdominal lymphadenitis: case report and literature review. Diagn Microbiol Infect Dis. 2001 Jan; 39(1):33-7.

5.    Murry, PR, Baron, EJ, Pfaller, MA, Tenover, FC, Yolken, RH. Manual of clinical microbiology  (7^th edition). 1999. ASM Press, Washington, DC.

6.    Oliver A, Maiz L, Canton R, Escobar H, Baquero F, Gomez-Mampaso E. Nontuberculous mycobacteria in patients with cystic fibrosis. Clin Infect Dis. 2001 May 1;32(9):1298-303.
 

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