Disseminated Mycobacterium kansasii infection with cutaneous lesions in an immunocompetent patient

Zhang, Miaomiao; Feng, Mei; He, Jian‐Qing

doi:10.1016/j.ijid.2017.07.006

Cited by 7 publications

(12 citation statements)

References 31 publications

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“…The most common cutaneous forms of acquisition of NTM involve direct inoculation via trauma (33), postsurgical infections (42), or iatrogenic acquisition with indwelling medical devices, plastic surgery, cosmetic procedures, or prosthetic implants (24,42). Mycobacteria may seed the skin and soft tissues during systemic dissemination in immunosuppressed individuals (24,25,37,(42)(43)(44). There is some evidence of potential human-to-human transmission of Mycobacterium abscessus subsp.…”

Section: Mycobacterial Species As Human Pathogensmentioning

confidence: 99%

“…M. kansasii infection manifests predominantly as pulmonary disease. Cutaneous involvement of M. kansasii is usually present in immunocompromised hosts and sometimes with concomitant pulmonary disease or disseminated disease (24,37). Cutaneous infection may present as nodules, pustules, verrucous lesions, erythematous plaques, ulcers, and abscesses ( Fig.…”

Section: Mycobacterium Kansasiimentioning

confidence: 99%

“…This infection may occur among immunocompetent and immunocompromised hosts, including those with HIV infection/AIDS or with renal transplantation. Similarly to M. tuberculosis, M. kansasii expresses ESAT-6 and CFP-10 analogs, and therefore IFN-␥ release assays (IGRAs) are not useful in distinguishing this infection from M. tuberculosis infection (37). M. kansasii is susceptible to isoniazid, rifampin, ethambutol, clarithromycin, fluoroquinolones, and aminoglycosides but is intrinsically resistant to pyrazinamide (37,119).…”

Section: Mycobacterium Kansasiimentioning

confidence: 99%

“…Similarly to M. tuberculosis, M. kansasii expresses ESAT-6 and CFP-10 analogs, and therefore IFN-␥ release assays (IGRAs) are not useful in distinguishing this infection from M. tuberculosis infection (37). M. kansasii is susceptible to isoniazid, rifampin, ethambutol, clarithromycin, fluoroquinolones, and aminoglycosides but is intrinsically resistant to pyrazinamide (37,119). Susceptibility testing is recommended only for rifampin given the fact that the best clinical outcomes are associated with rifampin susceptibility (37,119).…”

Section: Mycobacterium Kansasiimentioning

confidence: 99%

“…M. kansasii is susceptible to isoniazid, rifampin, ethambutol, clarithromycin, fluoroquinolones, and aminoglycosides but is intrinsically resistant to pyrazinamide (37,119). Susceptibility testing is recommended only for rifampin given the fact that the best clinical outcomes are associated with rifampin susceptibility (37,119).…”

Section: Mycobacterium Kansasiimentioning

confidence: 99%

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Cutaneous Mycobacterial Infections

et al. 2018

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SUMMARY Humans encounter mycobacterial species due to their ubiquity in different environmental niches. In many individuals, pathogenic mycobacterial species may breach our first-line barrier defenses of the innate immune system and modulate the activation of phagocytes to cause disease of the respiratory tract or the skin and soft tissues, sometimes resulting in disseminated infection. Cutaneous mycobacterial infections may cause a wide range of clinical manifestations, which are divided into four main disease categories: (i) cutaneous manifestations of Mycobacterium tuberculosis infection, (ii) Buruli ulcer caused by Mycobacterium ulcerans and other related slowly growing mycobacteria, (iii) leprosy caused by Mycobacterium leprae and Mycobacterium lepromatosis, and (iv) cutaneous infections caused by rapidly growing mycobacteria. Clinically, cutaneous mycobacterial infections present with widely different clinical presentations, including cellulitis, nonhealing ulcers, subacute or chronic nodular lesions, abscesses, superficial lymphadenitis, verrucous lesions, and other types of findings. Mycobacterial infections of the skin and subcutaneous tissue are associated with important stigma, deformity, and disability. Geography-based environmental exposures influence the epidemiology of cutaneous mycobacterial infections. Cutaneous tuberculosis exhibits different clinical phenotypes acquired through different routes, including via extrinsic inoculation of the tuberculous bacilli and dissemination to the skin from other sites, or represents hypersensitivity reactions to M. tuberculosis infection. In many settings, leprosy remains an important cause of neurological impairment, deformity, limb loss, and stigma. Mycobacterium lepromatosis, a mycobacterial species related to M. leprae, is linked to diffuse lepromatous leprosy of Lucio and Latapí. Mycobacterium ulcerans produces a mycolactone toxin that leads to subcutaneous tissue destruction and immunosuppression, resulting in deep ulcerations that often produce substantial disfigurement and disability. Mycobacterium marinum, a close relative of M. ulcerans, is an important cause of cutaneous sporotrichoid nodular lymphangitic lesions. Among patients with advanced immunosuppression, Mycobacterium kansasii, the Mycobacterium avium-intracellulare complex, and Mycobacterium haemophilum may cause cutaneous or disseminated disease. Rapidly growing mycobacteria, including the Mycobacterium abscessus group, Mycobacterium chelonei, and Mycobacterium fortuitum, are increasingly recognized pathogens in cutaneous infections associated particularly with plastic surgery and cosmetic procedures. Skin biopsies of cutaneous lesions to identify acid-fast staining bacilli and cultures represent the cornerstone of diagnosis. Additionally, histopathological evaluation of skin biopsy specimens may be useful in identifying leprosy, Buruli ulcer, and cutaneous tuberculosis. Molecular assays are useful in some cases. The treatment for cutaneous mycobacterial infections depends on the specific pathogen and therefore requires a careful consideration of antimicrobial choices based on official treatment guidelines.

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