Cutaneous Actinomycosis Associated with Anti-TNF-Alpha Therapy: Report of Two Cases

Abstract

Increased susceptibility to infections is among the main safety concerns raised by anti-TNF-α agents. We describe two cases of cutaneous actinomycosis in patients undergoing anti-TNF-α therapy: a 49-year-old female treated with etanercept for rheumatoid arthritis and a 57-year-old female treated with infliximab for psoriasis. Both patients had discharge with the intermittent presence of sulfur granules occurring at the site of previous surgical wounds. Bacteriological culture demonstrated Actinomyces. Since in both cases laboratory findings and medical imaging ruled out visceral actinomycosis, oral antibiotics were introduced without discontinuing anti-TNF-α. The first patient did not relapse after 2 years. The second one did and received a second course of antibiotics combined with transient interruption of the anti-TNF-α therapy. The risk of developing actinomycosis is reported to be similar in immunocompetent and immunocompromised patients, however cases of cutaneous actinomycosis occurring during anti-TNF-α therapy need to be recognized and may be under-reported.

Actinomyces and Related Organisms in Human Infections

“…Sporadic actinomycosis cases have also been reported in this context, including thoracic actinomycosis due to A. graevenitzii (56), rapidly progressing pneumonia due to A. meyeri (93), as well as cutaneous actinomycosis, with one case due to A. neuii subsp. anitratus and another case due to coinfection with A. turicensis and A. urogenitalis (55).…”

“…The disease can also appear as cutaneous actinomycosis, musculoskeletal disease, pericarditis, infection of the central nervous system (CNS), or disseminated disease. Moreover, some actinomycosis cases have been linked to specific conditions, such as osteoradionecrosis or bisphosphonate-related osteonecrosis of the jaws (53,54), the use of anti-inflammatory drugs (55,56), or some hereditary diseases (57,58). Also, unusual presentations of human actinomycosis have been reported, which presents a diagnostic challenge (59).…”

Disseminated cutaneous Actinomyces bovis infection in an immunocompromised host: case report and review of the literature

“…Possible risk factors for cervicofacial and oral actinomycosis include dental procedures, caries, gingivitis, chronic tonsillitis, periodontal disease, otitis or mastoiditis, possibly diabetes, and immunosuppression, malnutrition, and local tissue injuries by tumours, surgery, irradiation, or trauma [ 3 ]. Cutaneous actinomycosis is usually a secondary disease, resulting from either contiguous extension from a deeper source of infection or hematogenous spreading from an extracutaneous (often pulmonary) origin [ 7 ]. In our patient, considering her description, there was cervical involvement at first, with subsequent development of distant cutaneous foci; these were compatible with previous wounds sites as a result of her falls.…”

“…Current assumptions are that actinomycosis can appear in both healthy individuals and immunocompromised hosts [ 3 , 6 ]. Albeit it has been described in patients with HIV [ 8 , 9 ], primary immunodeficiency [ 10 ], haematological malignancies [ 11 ], and individuals under anti-tumour necrosis factor (TNF) agents [ 7 , 12 ], uncertainty remains about which host mechanisms are involved in controlling the infection and if the incidence of actinomycosis is increased in immunocompromised patients. In this case, we consider that the subacute onset and progression of the disease in weeks from a single lesion to multiple disseminated abscesses can possibly be related to the immunosuppression status of the patient, although there have been no reported cases of actinomycosis complicating treatment with azathioprine and mesalazine.…”

Acne inversa complicated by Actinomyces neuii

“…A recent review outlines high response rates in AI patients treated with TNF-α blockers (up to 90 % for Infliximab) but unfortunately also high recurrence rates after discontinuation of this therapy [9]. Two cases of cutaneous Actinomycosis as complication of TNF-α blocker therapy already have been previously reported [10]. Failure to detect superinfections of AI lesions with slow-growing pathogens like Actinomyces spp.…”