| Mycobacteroides abscessus | |
|---|---|
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| GD01 strain ofMycobacteroides abscessus isolated from patient | |
Scientific classification | |
| Domain: | Bacteria |
| Kingdom: | Bacillati |
| Phylum: | Actinomycetota |
| Class: | Actinomycetia |
| Order: | Mycobacteriales |
| Family: | Mycobacteriaceae |
| Genus: | Mycobacteroides |
| Species: | M. abscessus |
| Binomial name | |
| Mycobacteroides abscessus (Moore and Frerichs 1953) Gupta et al. 2018[1] | |
| Type strain[2] | |
| ATCC 19977 CCUG 20993 CIP 104536 DSM 43491 DSM 44196 Hauduroy L948 JCM 13569 L948 NCTC 13031 TMC 1543 | |
| Subspecies | |
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| Synonyms[1] | |
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Mycobacteroides abscessus (formerlyMycobacterium abscessus[1]) is a species of rapidly growing,multidrug-resistant,nontuberculous mycobacteria (NTM) that is a common soil and water contaminant. AlthoughM. abscessus most commonly causeschroniclung infection and skin and soft tissue infection (SSTI), it can also cause infection in almost all human organs, mostly in patients with suppressedimmune systems.[3] Amongst NTM species responsible for disease, infection caused byM. abscessus complex are more difficult to treat due toantimicrobial drug resistance.[4]
Mycobacteroides abscessus cells areGram-positive, nonmotile,acid-fast rods about 1.0–2.5 μm long by 0.5 μm wide. They may form colonies onLöwenstein–Jensen medium that appear smooth or rough, white or greyish, andnonphotochromogenic.[citation needed]
Abscessus is named forabscesses. It is aLatin word derived fromab- ("away") +cedere ("to go") because it was the ancient medical notion that a manifestation of thefour humors was forpus to leave the body.M. 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 speciesM. bolletii, which was first described in 2006, is named after the late eminent French microbiologist and taxonomist Claude Bollet.[citation needed]
M. abscessus shows growth at 28 °C and 37 °C after 7 days, but not at 43 °C. It may grow onMacConkey agar at 28 °C and even 37 °C.It shows tolerance to saline media (5% NaCl) and 500 mg/Lhydroxylamine (Ogawa egg medium) and 0.2%picrate (Sauton agar medium). Strains of the species have been shown to degrade the antibioticp-aminosalicylate.M. abscessus has also been shown to producearylsulfatase, but not ofnitrate reductase and Tween 80 hydrolase.It shows a negative result for the iron uptake test and no use offructose,glucose,oxalate, orcitrate as sole carbon sources.[citation needed]
M. abscessus andM. chelonae can be distinguished fromM. fortuitum orM. peregrinum by their failure to reducenitrate and to take up iron.Tolerance to 5% NaCl in Löwenstein-Jensen medium, tolerance to 0.2% picrate in Sauton agar, and non-use of citrate as a sole carbon source are characteristics that distinguishM. abscessus fromM. chelonae.M. abscessus andM. chelonae sequevar I share an identical sequence in the 54-510 region of16S rRNA, though both species can be differentiated by theirhsp65,ITS orrpoBgene sequences.[citation needed]
A draft genome sequence ofM. abscessus subsp.bolletii BDT was completed in 2012.[5] Since then, a large number ofstrains from this subspecies have had theirgenomes 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:M. a. abscessus,M. a. bolletii, andM. a. massiliense. In 2011, the latter two were briefly merged into a single subspecies,[6] but were subsequently separated again following greater availability of genome sequence data, which showed the three subspecies formed genetically distinct groups.[7][8] It has been proposed thatM. bolletii andM. massiliense be reinstated as unique species.[9]
These distinct groups also correspond to important biological differences. Clinically important differences include differing susceptibilities to antibiotics.M. a. abscessus andM. a. bolletii carry a commonantibiotic resistance gene, which confers resistance tomacrolideantibiotics, whileM. a. massiliense is thought to carry a nonfunctional copy, so is more susceptible to antibiotics and more easily treated.[7]
M. abscessus can causelung disease, skin infections,central nervous system infections,bacteremia, eye infections, and other, less common diseases.[7]
Chronic lung disease occurs most commonly in vulnerable hosts with underlying lung disease such ascystic fibrosis,bronchiectasis, and priortuberculosis. 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 includemalaise,fatigue, and weight loss in advanced disease.[10] The diagnosis ofM. abscessus pulmonary infection requires the presence of symptoms, radiologic abnormalities, andmicrobiologic cultures.[citation needed]
M. abscessus can cause skin infections in immunodeficient patients, patients who have recently undergone surgery,tattooing, oracupuncture, or after exposure tohot springs or spas.[7] It can be associated with middle-ear infections (otitis media).[11]
The incidence ofM. abscessus infections appears to be increasing over time.[7][12] Outbreaks ofM. abscessus have been reported in hospitals and clinical settings worldwide.[13] 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, although these are more attributable to contaminated disinfectants, saline and instruments than contact between patients.[7]
A study from 2019 supported the capability ofphages in killing resistant bacteria unable to be treated with antibiotics.[14] Research laboratories came together to find these phages by collecting, isolating, and exposing them to resistantM. abscessus that had been isolated from a patient in London.[14]
A bacteriophage known as Muddy had proved effective at killing the patient’s distinctM. abscessus strain (GD01), while phages like ZoeJ and BPs had reduced capabilities at infecting GD01.[14] A mixture of phages, Muddy and engineered versions of ZoeJ and BPs, though, completely infected and killed GD01.[14]
A cocktail of bacteriophages, Muddy, ZoeJ, and BPs, effectively killed a strain ofM. abscessus in vitro.[14] The potential this showed encouraged the commencement of patient treatments towards the GD01 infection.[14] Every 12 hours, the patient received a treatment of the bacteriophage cocktail.[14]
One day of treatment showed high bacteriophage levels in the bloodstream.[14] This suggested that they were being released into thebloodstream and replicating to infect bacteria.[14] No significant side effects were reported.[14] The right phages were found for this patient, but a different strain may be sensitive to different phages.[14]
The type strain ofM. abscessus, most commonly referred to as ATCC 19977, was isolated in 1953 from a human knee infection presenting with abscess-like lesions, leading to the strain being named "abscessus".[15] The strain wasn't recognised as a distinct species until 1992, however, whenDNA hybridisation work identified it as genetically distinct from its relative,M. chelonae.[16] The genome of the type train was published in 2009.[17]
This article incorporates public domain text from the CDC as cited