Mycobacterium abscessus causes

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]

Overview

Mycobacterium abscessus is a bacterium distantly related to the ones that cause tuberculosis and leprosy. It is part of a group known as rapidly growing mycobacteria and is found in water, soil, and dust. It has been known to contaminate medications and products, including medical devices.

Mycobacterium Abscessus

Taxonomy

Transmission

Infection with M. abscessus is usually caused by injections of substances contaminated with the bacterium or through invasive medical procedures employing contaminated equipment or material. Infection can also occur after accidental injury where the wound is contaminated by soil. There is very little risk of transmission from person to person.

Mycobacterium abscessus is relatively resistant to chlorine and standard desinfectant.[1]

Microscopy

  • Gram-positive, nonmotile and acid-fast rods (1.0-2.5µm x 0.5µm).

Colony characteristics

  • Colonies on Löwenstein-Jensen media may occur as smooth as well as rough, white or greyish and nonphotochromogenic.

Physiology

  • Growth at 28°C and 37°C after 7 days but not at 43°C.
  • On MacConkey agar at 28°C and even 37°C.
  • Tolerance to 5% NaCl and 500mg/l hydroxylamine (Ogawa egg medium) and 0.2% picrate (Sauton agar medium).
  • Positive degradation of p-aminosalicylate.
  • Production of arylsulfatase but not of nitrate reductase and Tween 80 hydrolase.
  • Negative iron uptake test. No utilisation of fructose, glucose, oxalate and citrate as sole carbon sources.

Differential Characteristics

  • M. abscessus and M. chelonae can be distinguished from M. fortuitum or M. peregrinum by their failure to reduce nitrate and to take up iron.
  • Tolerance to 5% NaCl in Löwenstein-Jensen media tolerance to 0.2% picrate in Sauton agar and non-utilisation of citrate as a sole carbon source are characteristics that distinguish M. abscessus from M. chelonae.
  • M. abscessus and M. chelonae sequevar I share an identical sequence in the 54-510 region of 16S rRNA, However, both species can be differentiated by their hsp65 or ITS sequences

Strains

ATCC 19977 = CCUG 20993 = CIP 104536 = DSM 44196 = JCM 13569 = NCTC 13031

Genetics

A draft genome sequence of M. abscessus subsp. bolletii BDT was completed in 2012.[2] More than 25 different strains of this subspecies, including pathogenic isolates, have had their genomes sequenced.[3]

Resistance to Antibiotics

Intrinsic Factors

  • The permeability barrier of the envelope of the myobacterium[4]
  • Low affinity of the antibiotics to their target[4]
  • Drug export systems[4]
  • Neutralization of the antibiotics by cytoplasmic enzymes[4]

Acquired Factors

  • Mutation of the genes that code the antibiotic targets[4]

References

  1. Wallace RJ, Brown BA, Griffith DE (1998). "Nosocomial outbreaks/pseudo-outbreaks caused by nontuberculous mycobacteria". Annu Rev Microbiol. 52: 453–90. doi:10.1146/annurev.micro.52.1.453. PMID 9891805.
  2. Choi, G.-E.; Cho, Y.-J.; Koh, W.-J.; Chun, J.; Cho, S.-N.; Shin, S. J. (24 April 2012). "Draft Genome Sequence of Mycobacterium abscessus subsp. bolletii BDT". Journal of Bacteriology. 194 (10): 2756–2757. doi:10.1128/JB.00354-12.
  3. Davidson, Rebecca M. (December 2013). "Phylogenomics of Brazilian epidemic isolates of Mycobacterium abscessus subsp. bolletii reveals relationships of global outbreak strains". Infection, Genetics and Evolution. 20: 292–297. doi:10.1016/j.meegid.2013.09.012. Unknown parameter |coauthors= ignored (help)
  4. 4.0 4.1 4.2 4.3 4.4 Nessar R, Cambau E, Reyrat JM, Murray A, Gicquel B (2012). "Mycobacterium abscessus: a new antibiotic nightmare". J Antimicrob Chemother. 67 (4): 810–8. doi:10.1093/jac/dkr578. PMID 22290346.


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