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Mycobacterium haemophilum is a rarely encountered pathogen that is difficult to identify given its unique growth requirements. It is most often seen in adult patients who are immunosuppressed due to advanced HIV or haematological malignancy. Our case highlights a typical presentation of an atypical pathogen in a patient with rheumatoid arthritis receiving anti-tumour necrosis factor therapy. This case represents an important patient population in whom this previously rare infection is increasingly common., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2022. No commercial re-use. See rights and permissions. Published by BMJ.)

A 19-year old woman with acute myeloid leukemia presented with newly observed liver lesions during ongoing consolidation therapy. Due to unexplained cholestasis during induction, biliary duct drainage was performed. Microbiologic and histologic examinations revealed the presence of atypical mycobacteria, namely Mycobacterium abscessus. With an appropriate antiinfective regime which was continuously administered using a portable pump in the outpatient setting, further mycobacterial spread during simultaneous chemotherapy-associated neutropenia was prevented. Despite multiple bacterial resistance mechanisms, proper treatment of leukemia with curative intention could be ensured.

Mycobacterium haemophilum is a slow growing, aerobic, fastidious mycobacterium requiring hemin and a temperature of 30-32° C for optimal growth that is ubiquitous in nature. Disease in immunocompromised adults typically manifests as skin lesions such as papules, pustules and ulcerations. This organism also causes lymphadenitis in immunocompetent children. Antitumour necrosis factor-α (anti-TNF-α) therapy with agents such as infliximab, etanercept and adalimumab is increasingly being used for immunosuppression in patients with various autoimmune conditions. These agents are known to place patients at increased risk for tuberculosis and other granulomatous diseases. However, little is known about illness caused by M haemophilum in patients on immunosuppression with anti-TNF-α therapy. We describe a case of disseminated M haemophilum manifesting as skin lesions in a 72-year-old man with rheumatoid arthritis on infliximab and methotrexate.

Objective: In North America, tuberculosis and nontuberculous mycobacterial (NTM) disease rates associated with antitumour necrosis factor α (anti-TNFα) therapy are unknown., Methods: At Kaiser Permanente Northern California, the authors searched automated pharmacy records to identify inflammatory disease patients who received anti-TNF therapy during 2000-2008 and used validated electronic search algorithms to identify NTM and tuberculosis cases occurring during anti-TNF drug exposure., Results: Of 8418 anti-TNF users identified, 60% had rheumatoid arthritis (RA). Among anti-TNF users, 18 developed NTM and 16 tuberculosis after drug start. Anti-TNF associated rates of NTM and tuberculosis were 74 (95% CI: 37 to 111) and 49 (95% CI: 18 to 79) per 100 000 person-years, respectively. Rates (per 100, 000 person-years) for NTM and tuberculosis respectively for etanercept were 35 (95% CI: 1 to 69) and 17 (95% CI: 0 to 41); infliximab, 116 (95% CI: 30 to 203) and 83 (95% CI: 10 to 156); and adalimumab, 122 (95% CI: 3 to 241) and 91 (95% CI: 19 to 267). Background rates for NTM and tuberculosis in unexposed RA-patients were 19.2 (14.2 to 25.0) and 8.7 (5.3 to 13.2), and in the general population were 4.1 (95% CI 3.9 to 4.4) and 2.8 (95% CI 2.6 to 3.0) per 100, 000 person-years. Among anti-TNF users, compared with uninfected individuals, NTM case-patients were older (median age 68 vs 50 years, p<0.01) and more likely to have RA (100% vs 60%, p<0.01); whereas, tuberculosis case-patients were more likely to have diabetes (37% vs 16%, p=0.02) or chronic renal disease (25% vs 6%, p=0.02)., Conclusions: Among anti-TNF users in USA, mycobacterial disease rates are elevated, and NTM is associated with RA.

Rapid growing mycobacteria pose as a serious emerging threat for patients treated with TNF-α blockers. We report a case of a progressive and fatal pulmonary infection with M. abscessus in a patient previously treated with infliximab for Crohn's disease and review seven other previously reported patients. Five out of eight patients were female. The patients were treated with either anti-TNF-α antibodies or TNF-α blocking receptor. The diagnosis of RGM came in the first 6 months after initiation of TNF-α blockers in five out eight patients. The two patients with M. abscessus lung infection died in spite of antibiotic treatment, whereas the other patients with skin affection and lever affection due to M. Fortuitum had a resolution of their symptoms with discontinuation of TNF-α blockers and antibiotics.

Objective: Transitional cell carcinoma of the bladder is commonly treated with intravesical BCG. We report a cutaneous complication of BCG after therapy in 66-year-old male 4 years after initiating treatment., Materials and Methods: A case review including pathological slides, laboratory data, and radiographic findings., Results: Biopsy findings showed an ill defined granulomatous process with chronic inflammation and necrosis., Conclusion: The patient was managed on antituberculous therapy for a period of 6 months with resolution of symptoms.

Silica exposure results in an increased lifelong risk of developing mycobacterial pulmonary infections. To date, there are no animal models that replicate this finding to permit assessment of the mechanisms underlying susceptibility to mycobacterial infection. To test the hypothesis that prior silica exposure increases risk of mycobacterial infection, we intratracheally (I.T.) administered silica, a control dust (Al(2)O(3)) or saline into mechanically ventilated C57BL/6 mice. Later, the mice received Mycobacterium avium or Mycobacterium tuberculosis I.T. Mice were sacrificed at defined time points and mycobacteria in lung homogenates were quantified. M. avium or M. tuberculosis infection was markedly increased in silica-exposed mice compared with mice exposed to either Al(2)O(3) or saline beginning 3 wk after silica exposure. Similarly, lung sections from silica-exposed mice had many more acid fast bacilli(+) (AFB(+)) organisms than from control mice. Alveolar macrophages (AMs) from bronchoalveolar lavage of silica-exposed mice also revealed a higher number of mycobacteria compared with mice treated with Al(2)O(3) or saline. In addition, passive transfer of AMs from silica-exposed mice to control mice increased M. tuberculosis susceptibility. These results indicate that silica exposure converts mycobacteria-resistant mice into mycobacteria-susceptible mice via a process that likely involves a new population of AMs that are more susceptible to mycobacterial infection.

We report on a patient who was chronically treated with steroids. She simultaneously developed pulmonary nocardiosis as well as a soft tissue infection and osteomyelitis by mycobacterium abscessus. Both infections are rare, but more frequently occur in immunocompromised hosts. The patient was healed after 12 month of adequate antibiotic treatment.

A case of fatal pulmonary Mycobacterium abscessus infection in a 56-year-old man is reported. The patient had a longstanding history of seropositive, nodular rheumatoid arthritis with severe joint manifestations that had been treated with a regimen of prednisone, leflunomide, and etanercept. He presented to our facility with complaint of productive cough, persistent fevers, pleuritic chest discomfort, and dyspnea at rest. The patient was admitted to hospital, placed in isolation, a left-sided chest tube was inserted (left pneumothorax identified), and sputum acid-fast bacteria stains and cultures were obtained. Fluorochrome stains demonstrated numerous acid-fast bacteria, and M. abscessus was recovered from the culture media. He was treated with a regimen of amikacin, cefoxitin, and clarithromycin. He initially responded well, and was discharged home with this regimen. He remained afebrile with decreased cough and sputum production until 15 days after discharge when he was again admitted to hospital, with acute onset dyspnea and right-sided chest discomfort (right pneumothorax identified). He ultimately expired, due to overwhelming pulmonary infection, 20 days after readmission to hospital. Autopsy revealed acid fast bacilli in the setting of numerous, bilateral, necrotic, granulomatous, cavitary pulmonary lesions. Based on its mechanism of action, we propose an association between the use of etanercept, a tumor necrosis factor alpha (TNF-alpha) inhibitor, and this case of fatal pulmonary mycobacterial infection. We recommend that physicians exercise cautious clinical judgment when initiating etanercept therapy in persons with underlying lung disease, especially in communities in which mycobacterial organisms are highly prevalent. We also advise physicians to maintain a high level of vigilance for late onset granulomatous infection in persons using etanercept.