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Mycobacterium abscessus
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Jump to navigationJump to search Mycobacterium abscessus complex (MABSC) is a group of rapidly growing, multidrug-resistant non-tuberculous mycobacteria (NTM) species that are common soil and water contaminants. Although M. abscessus complex most commonly cause chronic lung infection and skin and soft tissue infection (SSTI), the complex can also cause infection in almost all human organs, mostly in patients with suppressed immune systems. Amongst NTM species responsible for disease, infection caused by M. abscessus complex are more difficult to treat due to antimicrobial drug resistance.

Contents

 * 1Description
 * 2Physiology
 * 3Differential characteristics
 * 4Genetics
 * 5Pathogenesis
 * 6Management
 * 7Type strain
 * 8Etymology
 * 9See also
 * 10References
 * 11External links

Description[edit]
M. abscessus cells are gram-positive, nonmotile, acid-fast rods about 1.0–2.5 µm long by 0.5 µm wide. They may form colonies on Löwenstein–Jensen media that appear smooth or rough, white or greyish and nonphotochromogenic.

Physiology[edit]
M. abscessus shows growth at 28 °C and 37 °C after 7 days but not at 43 °C. It may grow on MacConkey agar at 28 °C and even 37 °C. It shows tolerance to saline media (5% NaCl) as well as 500 mg/l hydroxylamine (Ogawa egg medium) and 0.2% picrate (Sauton agar medium). Strains of the species have been shown to degrade the antibiotic p-aminosalicylate. M. abscessus has also been shown to produce arylsulfatase but not of nitrate reductase and Tween 80 hydrolase. It shows a negative result for the iron uptake test and no utilisation of fructose, glucose, oxalate or citrate as sole carbon sources.

Differential characteristics[edit]
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, though both species can be differentiated by their hsp65, ITS or rpoB gene sequences.

Genetics[edit]
A draft genome sequence of M. abscessus subsp. bolletii BDT was completed in 2012. Since then, a large number of strains from this subspecies have had their genomes sequenced, leading to a clarification of subspecies boundaries. In 1992, M. abscessus was first recognised as a distinct species. In 2006, this group was separated into three subspecies: abscessus, bolletii and massiliense. In 2011, massiliense and bolletii were briefly merged into a single subspecies, but were subsequently separated again following greater availability of genome sequence data, which showed the three subspecies formed genetically distinct groups.

These distinct groups also correspond to important biological differences. Clinically important differences include differing susceptibilities to antibiotics. M. abscessus subsp. abscessus and bolletii carry a common antibiotic resistance gene which confers resistance to macrolide antibiotics, while massiliense is thought to carry a non-functional copy, and is therefore more susceptible to antibiotics and more easily treated.

Pathogenesis[edit]
M. abscessus can cause lung disease, skin infections, central nervous system infections, bacteremia, eye infections, and other, less common diseases.

Chronic lung disease occurs most commonly in vulnerable hosts with underlying lung disease such as cystic fibrosis, bronchiectasis, and prior tuberculosis. Clinical symptoms of lung infection vary in scope and intensity but commonly include chronic cough, often with purulent sputum. Haemoptysis may also be present. Systemic symptoms include malaise, fatigue, and weight loss in advance disease. The diagnosis of M. abscessus pulmonary infection requires the presence of symptoms, radiologic abnormalities, and microbiologic cultures.

M. abscessus can cause skin infections in immunodeficient patients, patients who have recently undergone surgery, tattooing or acupuncture, or after exposure to hot springs or spas. It can be associated with middle ear infections (otitis media).

The incidence of M. abscessus infections appears to be increasing over time. Outbreaks of M. abscessus have been reported in hospitals and clinical settings worldwide. While outbreaks of major clinical concern involve transmission (most likely indirect transmission) between vulnerable patients such as those receiving lung transplants or being treated for cystic fibrosis, outbreaks have also been reported at clinics providing cosmetic surgery, liposuction, mesotherapy and IV infusion of cell therapy, anthough these are more attributable to contaminated disinfectants, saline and instruments than contact between patients.

Phage therapy
A study from 2019 supported the capability of phages in killing resistant bacteria unable to be treated with antibiotics. Research laboratories came together in order to find these phages by collecting, isolating, and exposing them to resistant Mycobacterium abscessus that had been isolated from a patient in London.

In vitro
A bacteriophage known as Muddy had proved effective at killing the patient’s distinct Mycobacterium abscessus strain (GD01), while phages like ZoeJ and BPs had reduced capabilities at infecting GD01. A mixture of phages, Muddy and engineered versions of ZoeJ and BPs, though, completely infected and killed GD01.

In vivo

A cocktail of bacteriophages, Muddy, ZoeJ, and BPs, effectively killed a strain of Mycobacterium abscessus in vitro. The potential this showed encouraged the commencement of patient treatments towards the GD01 infection. Every 12 hours, the patient received a treatment of the bacteriophage cocktail.

One day of treatment showed high bacteriophage levels in the bloodstream. This suggested that they were being released into the bloodstream and replicating to infect bacteria. No significant side effects were reported. The right phages were found for this patient, but each strain of Mycobacterium abscessus is sensitive to different phages.

Type strain[edit]
The type strain of M. abscessus, most commonly referred to as ATCC19977, was isolated in 1953 from a human knee infection presenting with abscess-like lesions, leading to the strain being named "abscessus". The strain wasn't recognised as a distinct species until 1992, however, when DNA hybridisation work identified it as genetically distinct from its relative, M. chelonae. The genome of GDthe type train was published in 2009.

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

Etymology[edit]
From the Latin ab- (“away”) + cedere (“to go”), an abscess is named for the notion that humors leave the body through pus. Mycobacterium abscessus was first isolated from gluteal abscesses in a 62-year-old patient who had injured her knee as a child and had a disseminated infection 48 years later. The species M. bolletii, named after the late microbiologist and taxonomist Claude Bollet, was described in 2006.

See also[edit]

 * MCAG group

References[edit]
This article incorporates public domain text from the CDC as cited


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