![]() ![]() marinum should be incubated at 28 to 30☌. The optimal temperature for most cultures for NTM is between 28 and 37☌ with rare exception ( M. However, culture would still be necessary to identify a specific organism and determine specific antimicrobial susceptibility (see below) ( Drage et al., 2010). Histopathology of tissue specimens obtained from skin biopsy may yield additional helpful information, as certain morphological characteristics, such as granulomatous changes, lymphohistiocytic infiltrate, as well as special stains for AFB may indicate mycobacterial infection. In many cases, the NTM, especially the RGM, may be more sensitive to the AFB decolorization procedure and may not stain at all with fluorochrome stains, so negative smears do not necessarily mean that NTM, especially RGM, are not present in a clinical sample ( Griffith et al., 2007). The Gram stain will not reliably detect mycobacteria. ![]() The recommended method for staining clinical specimens is the fluorochrome technique. Swabs are not recommended for sample collection because they often result in limited culture material, decreasing chances for recovery of NTM. Aseptic collection of as much fluid as possible by needle aspiration or surgical procedures is recommended. In terms of specimen collection for laboratory evaluation, potential sources of contamination, such as tap water, should be avoided, because environmental mycobacteria may be present. NTM have been recently implicated in skin and soft tissue infections following pedicure, mesotherapy, laser resurfacing, breast augmentation, tattoos, implants and fillers, body piercings, liposuction, Mohs micrographic surgery, punch biopsies, and injections. The incidence of NTM infections related to cosmetic procedures is on the rise and increasingly becoming a public health concern. kansasii are the most common isolates in the US, with reports of all three most common in the Southeastern United States ( Griffith et al., 2007). The most common clinical manifestations of NTM infection in the United States include pulmonary disease, lymphatic disease, skin and soft tissue infections, and disseminated disease. An increased risk of NTM infections is therefore theoretically plausible during TNF inhibitor therapy, and most experts recommend treating and controlling known NTM infections in this setting. IFN-ƴ and IL-12 control mycobacteria through the up-regulation TNF α, made predominantly by monocytes/macrophages. Tumor necrosis factor α (TNF) plays a critical role in control of infection by intracellular organisms, as evidenced by well-documented risk of reactivation tuberculosis in patients receiving TNF inhibitor therapy ( Keane, 2004). ![]() As such, deficiencies or abnormalities in this positive feedback loop, acquired or genetic, increase the risk of NTM infections ( Griffith et al., 2007). Similar to other intracellular pathogens, NTM are phagocytized and killed by normal functioning macrophages in response to IFN-ƴ production, up-regulated by interleukin-12 (IL-12). An abnormal immune system, involving, for example, a decline in CD4 + T cell count or macrophage dysfunction, is prone to NTM infection. There have been no documented cases of human-to-human or animal-to-human transmission. ![]() NTM-related infections are acquired through environmental exposures. Tap water is the primary reservoir for human transmission, but NTM are also found in soil, animals, vegetable matter, and birds ( Mandell et al., 2009). These organisms are found worldwide and are ubiquitous in the environment. The NTM group of organisms consists of more than 125 species, defined as mycobacteria species other than M. ![]()
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