Nocardia is an intracellular pathogen with the potential to cause life-threatening disease, particularly in immunocompromised patients. Based on long-term data (nine years, 2000 patients), the incidence of Nocardia infection has been estimated at 0.01% in patients taking adalimumab.1
The diagnosis of Nocardia is often limited by clinical suspicion and local expertise of the diagnostic laboratory.2
Case Description A 36 year old male with a history of Crohn’s disease, on chronic adalimumab therapy, presented to the emergency department after he sustained a forehead laceration while working in his backyard. The wound was cleansed in standard fashion and sutures placed. Later, during suture removal, he was noted to have a small single draining pustule. He was then prescribed a seven day course of oral trimethoprim-sulfamethoxazole.
Over the course of several days, he developed tender lymphadenopathy and fever prompting cessation of adalimumab and subsequent hospitalization. Wound cultures were obtained and subsequently grew Nocardia arthritidis.
Due to the development of a persistent cough, a computed tomography (CT) of his chest demonstrated multiple pulmonary nodules, some with cavitation. He was subsequently treated with a combination of intravenous (IV) trimethoprim-sulfamethoxazole and meropenem with improvement of his pustules and near complete resolution of the pulmonary nodules on subsequent imaging.
Tumor necrosis factor (TNF) is a cytokine produced by activated monocytes, macrophages and T lymphocytes involved in cell-mediated immunity. TNF interacts with other cytokines, including interferon-delta, to generate an immune response to intracellular pathogens such as Myobacterium tuberculosis, Listeria, Histoplasma and Nocardia. Disruption of this pathway by anti-TNF medications, such as adalimumab, may increase rates of infection by such organisms.3
Nocardia are soil-borne, gram-positive, facultative intracellular bacteria. They are ubiquitous and found worldwide in dust, sand, soil and bodies of water. Respiratory transmission is presumed to be via contact with dust particles contaminated by the organism.4
Nocardia has a predilection for the lungs due to its ability to aerosolize, but infection may also occur via the skin or central nervous system.5,6
Cutaneous infections typically occur through open wounds contaminated with soil. Lesions may manifest as localized abscesses and mimic infection from pyogenic bacteria. Infection may also spread to regional lymph nodes and mimic sporotrichosis.2
The laboratory diagnosis of Nocardia requires a high level of suspicion, since these organisms are slow-growing and may lead to premature disposal of cultures. Histologically, Nocardia are strictly aerobic bacteria with branching filamentous structures. Standard blood cultures are rarely found to be positive. Confirmation and speciation require specialized polymerace chain reaxtion (PCR) testing.4
Initial antibiotic therapy includes IV trimethoprim- sulfamethoxazole for a minimum of three weeks. After three weeks, patients without immune dysfunction may be switched to oral trimethoprim-sulfamethoxazole until infection resolution. For those who are immunocompromised, duration of treatment may be extended beyond six months.7
The prognosis is poor (mortality rate >50%) for immunocompromised patients with disseminated nocardiosis, even those treated with appropriate antibiotics.5,8
Cutaenous Nocardiosis should be considered in inflammatory bowel disease patients on anti-TNF therapy presenting with atypical or difficult to treat cutaneous infections to ensure timely diagnosis and treatment.