Mycobacterium abscessus infection after use of tumor necrosis factor α inhibitor therapy: case report and review of infectious complications associated with tumor necrosis factor α inhibitor use

Mufti, Areej H.; Toye, Baldwin; Mckendry, Robert R.J.; Angel, Jonathan B.

doi:10.1016/j.diagmicrobio.2005.06.006

Cited by 47 publications

(34 citation statements)

References 63 publications

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“…This is consistent with several histopathological studies in humans showing that M. abscessus can cause organized granulomatous lesions with epithelioid giant cells (53). Recent reports of M. abscessus infection after use of inhibitors of tumor necrosis factor (TNF) (40,52) suggested that TNF also contributes to M. abscessus control, as demonstrated for other pathogenic mycobacteria (1,5,38,49).…”

supporting

confidence: 87%

Importance of T Cells, Gamma Interferon, and Tumor Necrosis Factor in Immune Control of the Rapid GrowerMycobacterium abscessusin C57BL/6 Mice

et al. 2007

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Mycobacterium abscessus is an emerging rapidly growing mycobacterium that causes tuberculous-like lesions in humans. We studied the immune control of this organism in C57BL/6 mice challenged intravenously with 10 7 CFU. Bacteria were eliminated from both the spleen and the liver within 90 days, and liver histology showed organized granulomatous lesions. A T-and B-cell requirement was investigated by challenging Rag2 ؊/؊ , Cd3 ؊/؊ , and MT ؊/؊ mice. Rag2 ؊/؊ and Cd3 ؊/؊ mice were significantly impaired in the ability to clear M. abscessus from the liver and spleen, and MT ؊/؊ mice were significantly impaired in the ability to clear M. abscessus from the liver, suggesting that infection control was primarily T cell dependent in the spleen and both T and B cell dependent in the liver. The liver granulomatous response was similar to that of wild-type controls in MT ؊/؊ mice but completely absent in Cd3 ؊/؊ and Rag2 ؊/؊ mice. We studied the involvement of gamma interferon (IFN-␥) and tumor necrosis factor (TNF) by challenging C57BL/6 mice deficient in the IFN-␥ receptor (Ifngr1 ؊/؊ ) and in TNF (Tnf ؊/؊ ). Ifngr1 ؊/؊ mice were significantly impaired in M. abscessus control both in the spleen and in the liver, and granulomas were profoundly altered. The effect was even more substantial in Tnf ؊/؊ mice; they failed to control M. abscessus infection in the liver and died within 20 to 25 days after infection with many hepatic inflammatory foci and major lesions of ischemic necrosis in the liver and kidney. These features were not observed with the closely related species M. chelonae. T-cell immunity, IFN-␥, and TNF are central factors for the control of M. abscessus in C57BL/6 mice, as they are for the control of pathogenic slowly growing mycobacteria.Mycobacterium abscessus is a rapidly growing mycobacterium (RGM) that has emerged as a significant pathogen in humans (6, 21) following its recent recognition as a species distinct from M. chelonae (36). M. abscessus is now recognized as the causative agent of a wide spectrum of human infections, including skin and soft tissue infections (6,21,54,57), lung infections in individuals with or without underlying disorders (e.g., cystic fibrosis) (26, 50), and infections or pseudoinfections related to contaminated medical devices (3,25,57). Disseminated infections have also been reported (11) for immunocompromised patients (organ transplantation, autoimmune disorders, malignancies) (6,28,48) and for subjects with a genetic defect in the interleukin-12 (IL-12)-gamma interferon (IFN-␥) signaling circuit (9). These life-threatening infections are therapeutically problematic because M. abscessus strains are resistant to most antibiotics (6).In light of clinical data, M. abscessus is now considered by many authors to be one of the most pathogenic RGM species (6). However, clear experimental evidence for its pathogenicity is poor; various studies using strains identified as M. fortuitum and M. abscessus showed that both species were lethal for mice following intravenous injection (35,...

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confidence: 87%

Importance of T Cells, Gamma Interferon, and Tumor Necrosis Factor in Immune Control of the Rapid GrowerMycobacterium abscessusin C57BL/6 Mice

et al. 2007

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“…Nontuberculous mycobacterial (NTM) disease has emerged as another mycobacterial infection in patients receiving TNF-a inhibitors, with several reported cases of NTM disease in patients receiving anti-TNF-a therapy [11][12][13][14]. One survey suggested that cases of NTM disease associated with TNF-a inhibitors are twice as frequent as cases of TB associated with anti-TNF-a in the USA [11].…”

Section: Introductionmentioning

confidence: 99%

Mycobacterial diseases developed during anti-tumour necrosis factor-α therapy

Yoo

Kang

et al. 2014

Eur Respir J

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Nontuberculous mycobacterial (NTM) disease and tuberculosis (TB) develop during antitumour necrosis factor (TNF)-a therapy. We compared clinical characteristics and outcomes between the two diseases.A total of 1165 patients were screened for TB and treated with TNF-a antagonists from July 2004 to July 2013 for the following conditions: inflammatory bowel disease (n5422), rheumatoid arthritis (n5320), and ankylosing spondylitis (n5389).TB and NTM disease were diagnosed at baseline screening in four and three patients, respectively, and developed during anti-TNF-a therapy in 19 and six patients, respectively. The incidence rate of TB and NTM disease was 747.7 per 100 000 and 238.2 per 100 000 person-years, respectively. Patients with NTM disease were older, with a greater proportion of females. All cases of NTM disease involved the lung, with rheumatoid arthritis (83.3%) being the most frequent underlying disease. The most common radiological feature was consolidation in NTM disease, and honeycombing was present in two rheumatoid arthritis patients with NTM disease. The most common pathogen was Mycobacterium intracellulare (n53) followed by Mycobacterium avium (n52). Both the NTM and TB group showed favourable outcomes.The clinical characteristics differed between NTM disease and TB that developed on anti-TNF-a agents, but clinical outcomes were favourable in both diseases. @ERSpublications Clinical characteristics differ between nontuberculous mycobacterial disease and TB that develop on anti-TNF-a agents

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“…Evidence from both animal models and humans shows that anti-TNF treatment, in addition to its valuable therapeutic ability to reduce the severity of inflammatory disease, is associated with increased susceptibility to opportunistic infection, particularly TB (19) and other atypical mycobacterial infections (6,24,26). Rapid and lethal reactivation of TB infection has been reported for TNF-deficient mice with high bacterial loads in the lungs, spleen, and liver (5).…”

Section: Discussionmentioning

confidence: 99%

Reduction of Chemokine Secretion in Response to Mycobacteria in Infliximab-Treated Patients

Newton

McDermott

Martineau

et al. 2008

Clin Vaccine Immunol

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The use of anti-tumor necrosis factor (TNF) agents as a treatment for chronic inflammatory conditions has been shown to be associated with an increased risk of developing tuberculosis. We studied the effect of the anti-TNF antibody infliximab on antimycobacterial immunity in 26 patients with rheumatoid arthritis or ankylosing spondylitis by use of an in vitro whole-blood model employing a reporter mycobacterium. Blood samples taken before and 30 min and 7 days after a 2-hour infliximab infusion were compared in terms of their abilities both to suppress luminescence of Mycobacterium bovis bacillus Calmette-Guérin lux and to secrete chemokines and cytokines 24 and 96 h after infection. No immediate effect of infliximab on mycobacterial luminescence was detected using this bioassay, irrespective of whether patients were receiving their first (n ‫؍‬ 14) or maintenance (n ‫؍‬ 12) doses of infliximab. Moreover, no effect on mycobacterial luminescence was detected when blood was taken 7 days after infliximab treatment (n ‫؍‬ 7). By contrast, there was a significant reduction in the chemokines implicated in cellular trafficking, namely, interleukin-8, macrophage-inhibitory protein-1␣ (MIP-1␣), MIP-1␤ (24 h and 96 h), and monocyte chemoattractant protein-1 (MCP-1) (24 h) following BCG lux strain infection in the 30-minute post-infliximab-infusion blood samples (P < 0.05). This effect was sustained by MIP-1␤ and MCP-1 (24 h; P < 0.05) at 7 days after infusion. Our results suggest that the development of tuberculosis in infliximab-treated patients is not directly related to the mycobactericidal effects of TNF but may be due to inhibition of TNF-dependent chemokine gradients disrupting cellular migration necessary to maintain the integrity of the granuloma.

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Mycobacterium abscessus infection after use of tumor necrosis factor α inhibitor therapy: case report and review of infectious complications associated with tumor necrosis factor α inhibitor use

Cited by 47 publications

References 63 publications

Importance of T Cells, Gamma Interferon, and Tumor Necrosis Factor in Immune Control of the Rapid GrowerMycobacterium abscessusin C57BL/6 Mice

Importance of T Cells, Gamma Interferon, and Tumor Necrosis Factor in Immune Control of the Rapid GrowerMycobacterium abscessusin C57BL/6 Mice

Mycobacterial diseases developed during anti-tumour necrosis factor-α therapy

Reduction of Chemokine Secretion in Response to Mycobacteria in Infliximab-Treated Patients

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