Nontuberculous mycobacteria NTM is a group of bacteria, normally found in soil and water and some domestic and wild animals, that can cause severe lung disease.
Unlike tuberculosis TB , which is spread from person to person, nontuberculous mycobacteria NTM infections are not considered contagious. The nontuberculous mycobacteria NTM causes are still under investigation. Although the bacteria is found easily in water and soil, they do not affect most people. Transmission occurs when a person inhales droplet nuclei containing M. Caused by a mutation, cystic fibrosis CF isn't contagious , but one serious complication definitely is: infection with Mycobacterium abscessus , an obscure agent related to the microbe that causes tuberculosis.
How do you treat Mycobacterium Abscessus? What are the symptoms of Mycobacterium? Mycobacteria are a type of germ. There are many different kinds. The most common one causes tuberculosis.
At other times, they can cause lung symptoms similar to tuberculosis: Cough. Weight loss. Coughing up blood or mucus.
Weakness or fatigue. Fever and chills. Night sweats. Lack of appetite and weight loss. Is Mac disease fatal? However, the damage already done to the lungs cannot be cured bronchiectasis.
The breathing tests also called pulmonary function tests are abnormal in most patients with bronchiectasis. How can you prevent Mycobacterium? This promotes spreads to other tissues and extracellular replication that results in abscess formation and tissue damage Bernut et al. The rough morphology is also associated with increased apoptosis leading to increases in extracellular bacteria and promotion of cord formation Bernut et al.
Interestingly, CFTR CF transmembrane conductance regulator defects, such as those seen in CF, has been associated with impaired NADPH oxidase production which leads to increase intracellular growth and reduce neutrophil chemotaxis, compromising granuloma integrity Bernut et al.
The absence of glycopeptidolipid GLP , a molecule in the outer surface of the cell wall, has been associated with rough colony morphology. Defects in the mmpL4b gene are associated with the loss of GLP, leading to conversion to a rough phenotype showing morphological plasticity Nessar et al.
The GLP loss unmask lipoproteins that produce a strong inflammatory response Nessar et al. This correlates with the fact that hypervirulence has been observed in the rough morphology vs smooth morphology Bernut et al. Intramacrophage survival of the smooth morphology is also explained by phago-lysosomal fusion block and resistance to apoptosis, the phagosome shows membrane disruption at early stages of infection leading to phagosome- cytosol communication and phagosomal escape allowing extracellular replication Bernut et al.
Cord formation is a unique and new immune evasion mechanism in MABC infection. The three subspecies of MABC are separated based on multilocus sequencing of housekeeping genes Harris and Kenna, The reference strain ATCC contains a full genome sequence of 5. It includes an Kb full-length prophage, five insertion elements, and a 23 Kb- mercury resistance plasmid, which has been associated with infection in young patients with CF Cortes et al.
The resistant plasmid is highly similar to an episome present in M. Marinum , suggesting that these species may have exchanged the plasmid Medjahed et al. MABC contains unique genes not present in other mycobacteria that appear to have been acquired by horizontal gene transfer from different species such as pseudomonas sp.
These shared genes are thought to contribute to the pathogenesis of Pseudomonas sp. Updates reveal that there are two presentations of NTM pulmonary infections. One is an upper lobe fibrocavitary form while the other is a nodular bronchiectatic form NB.
The upper lobe fibrocavitary form is characterized by cavitary lesions similar to tuberculosis and usually occurs in older males with underlying lung disease Shin et al. It is rapidly progressive and can lead to lung destruction in a short period of time Sohn et al. The nodular bronchiectatic form is seen in the middle lobe of the right lung and lingula in the left lung. This form typically is present in nonsmoking postmenopausal women as bilateral bronchiectasis with small nodular opacities and tends to have a much slower course over time Sohn et al.
In CF patients, infection leads to an unexpected decline in lung function. This infection is particularly important in adolescents as it can cause the largest loss of potential years of life Ravnholt et al. Resistance updates reveal that the molecular mechanism responsible for macrolide resistance is the expression of an erythromycin ribosome methylase, erm gen.
Other resistance molecular mechanisms include the rrs gene responsible for resistance in aminoglycosides, a class A beta-lactamase associated with resistance to most Beta-lactams only cefoxitin and imipenem are useful , and enzymatic inactivation of most tetracyclines except tigecycline.
The principal mechanisms of antibiotic resistance are described in Table 2. The mechanism responsible for inducible macrolide resistance is the expression of an erythromycin ribosome methylase, erm 41 gene, in the presence of macrolides Koh et al. This methylase transfers one or two methyl groups to adenine in the peptidyl region of 23S rRNA, preventing clarithromycin binding Nessar et al.
Mutations in the rrl gene encoding the 23S rRNA peptidyl transferase are also associated with acquired macrolide resistance Choi et al. Spontaneous single mutations in the rrs gene encoding the 16S rRNA are responsible for resistance to aminoglycosides Nessar et al. Nucleotide variation at the quinolone resistance determining region QRDR confers resistance to fluoroquinolones Kim et al. MABC hydrolyzes several members of cephalosporins and carbapenems, reducing its activity Luthra et al.
This change is associated with high levels of resistance to doxycycline; however, tigecycline resists inactivation explaining its good activity in vitro Luthra et al. Due to difficulties in differentiating between colonization from MABC isolates and true disease, clinical, radiologic, and microbiologic criteria are required for diagnosis Ryu and Daley, A direct smear of the respiratory specimen should be examined using a fluorescent method with higher sensitivity than conventional stains like Ziehl-Neelsen; however, microscopy alone cannot distinguish between mycobacterial species and viable or non-viable specimens Somoskovi, Diagnostic updates suggest that culture is mandatory in all cases for diagnosis Cortes et al.
Growth is necessary for precise identification, with molecular methods being the gold standard for identification Jones et al. Genotyping methods can be used to assess strain relatedness allowing outbreaks recognition. Commonly used methods are pulsed-field gel electrophoresis PFGE , multilocus sequencing, and methods based on minisatellite sequences variable number tandem repeats VNTR and amplified fragment length polymorphism Somoskovi, PFGE has been the standard method for differentiating strains within the complex Howard, WGS offers a higher degree of resolution than other genotyping methods providing crucial information about transmission events Harris and Kenna, Therapeutic updates suggest that in vitro antimicrobial testing in broth microdilution assay is required; incubation for 14 days is necessary to rule out inducible resistance for macrolides Somoskovi, ; Jones et al.
Clinical and Laboratory Standards Institute CLSI guidelines recommend minimal inhibitory concentration MICs for susceptibility testing using a panel of 10 antimicrobials: amikacin, cefoxitin, clarithromycin, ciprofloxacin, doxycycline, imipenem, linezolid, moxifloxacin, trimethoprim-sulfamethoxazole, and tobramycin Koh et al.
A study on the clinical impact of differentiating M. Different sputum conversion rates could be explained by local differences in the prevalence of subspecies Pasipanodya et al. Multidrug regimen includes macrolide based combination therapy with two parenteral agents for the initial phase Jeong et al. Initial therapy should be given for at least months, followed by oral macrolide based therapy Koh et al. Recently, the British thoracic society has recommended for the initial phase to include 4 weeks of intravenous amikacin, tigecycline, imipenem when tolerated and oral clarithromycin.
For the continuation phase, nebulized amikacin and an oral macrolide with one to three of the following: linezolid, clofazimine, minocycline cotrimoxazole, and moxifloxacin Haworth et al. The goal is twelve-month sputum culture negativity Thomson and Yew, ; However, recurrence and drug-related toxicity secondary to long term therapy are frequent, making this outcome unrealistic for many patients Lyu et al. One study evaluating outcomes in patients with long term injectable therapy showed adverse effects in Alternative goals include symptomatic improvement and radiographic regression of infiltrates rather than sputum conversion Griffith et al.
Tigecycline combined with clarithromycin also appears synergistic against MABC Additionally, tigecycline has shown good tissue penetration and few severe side effects making long-term therapy with this antibiotic an option Huang et al.
Other antibiotics such as linezolid showed good activity in clinical trials Zhang et al. Recently, a study showed that clarithromycin-nanocapsules reduced colony numbers during MABC infection as they improved delivery of antimicrobial to mycobacteria inside macrophages Anversa Dimer et al. NO has been also used as a promising strategy for treatment in patients with MABC infection and CF as NO kills bacterial cells and disperse biofilms avoiding resistance Chiarelli et al.
Mycobacterium abscessus is not considered contagious from person to person, and usually enters the body through a break in the skin. Infections with Mycobacterium abscessus can often cause serious symptoms. These mycobacteria mostly infect the skin, but can, in rare cases, infect the lungs, especially in those with a history of chronic lung afflictions. It usually spreads through direct physical contact with contaminated areas, rather than through person-to-person contact. Infected persons are, however, generally advised to keep the infection site clean and wash their hands frequently, to avoid bacterial contamination of the environment.
Chronic respiratory conditions, open wounds and lowered immunity are some of the primary risk factors for the contraction of this mycobacterial infection. This bacterium can contaminate medical implements, including hypodermic syringes, so that it often infects those who receive injections or surgical procedures in improperly sanitized surroundings.
Persons infected with this bacterium are generally advised to inform the diagnosing physician of the nature and location of any recent procedures.
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