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Nail care and nail cosmetics
Published in Archana Singal, Shekhar Neema, Piyush Kumar, Nail Disorders, 2019
Cuticles are softened by either applying a chemical cuticle remover (alkaline substance like 0.4% sodium or potassium hydroxide) or soaking in warm water. Once soft and malleable, the cuticles are pushed proximally and/or clipped away with a metal or wood implement. This is the most damaging step in the whole procedure as it predisposes the nail folds to environmental insult and secondary infections. Use of unsterilized instruments can help transmit fungal and viral infections from one nail to another, and from one person to another. Pedicure tubs in which hands and feet are soaked have been reported to cause Mycobacterium fortuitum infections from a nail salon in California.6
Tuberculosis of the Temporal Bone
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
Tuberculosis is a chronic granulomatous infection caused by Mycobacterium tuberculosis. Other mycobacteria such as Mycobacterium bovis, Mycobacterium avium and Mycobacterium fortuitum can also cause infection referred to as ‘atypical tuberculosis’ or non-tuberculous mycobacterium (NTM) (see also Chapter 37, Cervicofacial infections). While tuberculosis (TB) is predominantly pulmonary, 12–15% of reported cases of TB involve extrapulmonary sites.1 Rarely the temporal bone may be involved with TB – tuberculous otitis media or tuberculous otomastoiditis.
Clarithromycin
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Mycobacterium fortuitum isolates are usually susceptible to clarithromycin in in vitro testing, but they often contain the inducible macrolide resistance gene (erm), and therefore macrolides should be used in treatment of M. fortuitum with caution (Brown et al., 1992; Nash et al., 2005).
Bacteria Associated with Granulomatous Lobular Mastitis and the Potential for Personalized Therapy
Published in Journal of Investigative Surgery, 2022
Xin-Qian Li, Hong-Li Wu, Jing-Ping Yuan, Tian-gang Liu, Sheng-Rong Sun, Chuang Chen
Nontuberculous mycobacteria have been identified in GLM, including Mycobacterium abscessus and Mycobacterium fortuitum. Four cases of breast infection associated with M. abscessus have been reported in the literature, three of which involved subjects diagnosed with GLM. Potentially effective antimicrobials include a combination of triple anti-tuberculosis drugs, clarithromycin, linezolid, tigecycline and amikacin [51–54]. In our centre, M. abscessus was identified in a Vietnamese patient with GLM. The patient was given rifampin, but her condition worsened a week later. We then changed the antibiotic to levofloxacin, and the pus reduced in volume and became thinner within three weeks. Two months later, the mass was impalpable. In GLM patients, M. fortuitum often has a history of nipple piercing [55,56], although its presence without foreign body piercing in the breast has also been described [57].
Response surface modeling integrated microtiter plate assay for Mycobacterium fortuitum biofilm quantification
Published in Biofouling, 2021
Ayushi Sharma, Jitendraa Vashistt, Rahul Shrivastava
Biofilm formation is a major factor involved in boosting M. fortuitum infections (Schulze-Röbbecke et al. 1992). The bacterium forms biofilms under both low- and high-nutrient conditions (Hall-Stoodley et al. 1998). Complications associated with its attachment to polypropylene sutures and medical implants, such as mammaplasty prostheses and prosthetic heart valves, were documented previously (Zamora et al. 2007). Mycobacterium fortuitum has been recognized as a robust pathogen (Kawamoto et al. 1999) whose eradication from hospital settings is difficult because of its adherence potential (Zamora et al. 2007) and resistance to biocides such as silver nitrate, phenol, and hydrogen peroxide (Bardouniotis et al. 2001). This bacterium exhibits intrinsic resistance to the first-line antituberculous drugs pyrazinamide, ethambutol, rifampicin, and isoniazid (El Helou et al. 2013). In addition to its sensitivity to macrolides, it has been known to carry the inducible erythromycin methylase (erm) gene, with the possibility of conferring resistance to macrolides (clarithromycin) (Nash et al. 2005). Hence, monotherapy of M. fortuitum with macrolides is not recommended (De Groote and Huitt 2006). Its biofilms exhibit a pronounced resistance profile against ciprofloxacin, amikacin, and clarithromycin, which are commonly used to treat infections caused by the mycobacterium (Ortíz-Pérez et al. 2011).
New therapeutic strategies for Mycobacterium abscessus pulmonary diseases – untapping the mycolic acid pathway
Published in Expert Review of Anti-infective Therapy, 2023
Matthéo Alcaraz, Thomas E. Edwards, Laurent Kremer
These encouraging results also prompted to investigate the effect of NITD−916 in other NTM. Mycobacterium fortuitum (Mfor) represents another rapidly-growing mycobacteria encountered in patients [114]. This opportunistic pathogen is highly resistant to a large variety of antibiotics, including β-lactams, aminoglycosides, macrolides, tetracyclines, or anti-TB drugs [115,116]. As is the case for Mabs, none of the currently used drugs relies on the MA pathway in Mfor. This difficulty to clinically cure Mfor infections emphasizes the need for new molecules to include in the drug regimen. Since InhA from Mfor (InhAMFO) shares 88.5% identity with InhAMTB and 90% identity with InhAMAB, it was hypothesized that NITD−916 could also inhibit InhAMFO. NITD−916 exhibited very low MICs against several clinical isolates of Mfor [117] and strong antimycobacterial activity against Mfor-infected macrophages. Remarkably, the molecule was very active in a zebrafish model of Mfor infection. Particularly, in this animal model, a short time of treatment (1 day) was sufficient to significantly reduce global bacterial loads, to limit physiopathological symptoms such as cords and abscesses which are often associated with the severity of the disease. This also led to a strong protective effect of the embryos against killing by Mfor [117]. As for Mtb or Mabs, NITD−916 drastically inhibited the de novo synthesis of MA in an InhA-dependent manner. Supporting these results, the resolution of the crystal structure of the ternary complex InhAMFO-NAD-NITD−916 confirmed the direct binding of NITD−916 with InhAMFO [117].