A 74 years old patient, diagnosed one month prior with giant cells arteritis (GCA), treated with methylprednisolone and azathioprine, presented with a superficial, soft, painless mass on the right frontal scalp region, noticed by the patient to have grown slowly in the previous week. From the medical history we report pulmonary tuberculosis (treated in 1975), Lyme borreliosis treated with intravenous ceftriaxone in March 2013, followed by moderate Clostridium difficile infection. The laboratory tests revealed increased erythrocyte sedimentation rate (ESR=120 mm/hour) and C-reactive protein (CRP=2.05 mg/dl), hyper-potassemia (5.9 mEq/l) and hypo-sodemia (132 mEq/l).
One week before, physical examination had shown an enlarged painful left temporal artery and a previously absent right frontal scar, most probably a cutaneous superficial atrophy due to vasculitis (Figure 1a, b). Therefore, the new frontal mass suggested a hematoma from a vasculitis-injured vessel effraction, or a superficial arterial aneurysm. Ultrasonography, performed with an Esaote MyLab  Five machine with a 10-13 MHz multifrequence linear transducer, showed an aspect compatible with an abscess (Figure 2). A puncture from the scalp collection reveled pus; a drainage tube was inserted for complete evacuation. The microscopic examination revealed Gram-positive long thin branching roads and culture on Colombia blood agar was indicative of Nocardia spp. with white chalky colonies after 3 days of incubation (Figure 3). Because direct inoculation of Nocardia was less probable (no skin lesion was visible and the patient did not recall any injury), disseminated infection was suspected. The cerebral MRI and abdominal CT did not find any abscesses. The pulmonary radiography detected left apical and subclavicular nodules recalling previous healed pulmonary tuberculosis, but also multiple bilateral subclavicular nodular opacities, the latter not present on the x-ray performed one month before, suggestive of possible tuberculosis reactivation or pulmonary nocardiosis. A bronchoscopy with bronchoalveolar aspiration showed the aspect of suppurative bronchitis; culture identified Acinetobacter calcoaceticus, interpreted as colonization and not as infection, as no pneumonia was detected on X-ray findings. Pulmonary CT scan showed the image of a subcarinal mediastinal mass with polycyclic shape, 6 cm in diameter, other mediastinal adenopathies and minimal bilateral pleural effusion. The transbronchial biopsy was not successful, while diagnostic thoracotomy could not be performed, due to the altered status of the patient.
The patient underwent therapy with intravenous imipenem-cilastatin 2g/day for 21 days and Amikacin 1g/day for 14 days for Nocardia infection, associated with tuberculostatic therapy (rifampicin, izoniazide, ethambutol and pyrazinamide). Tuberculostatic therapy was initiated due to the presence of radiologic subclavicular nodular opacities in a patient with immunosuppressive therapy and history of pulmonary tuberculosis and was stopped when cultures for Mycobacterium tuberculosis were reported as negative.
The scalp collection completely resolved after surgical drainage and antibiotic therapy. Therapy for nocardiosis was recommended after discharge with long term trimethoprim-sulfamethoxazole (TMP 10 mg/kg/day), justified by the immunocompromised status and immunosuppressive therapy. However, after 2 months the patient developed drug-induced myelosuppression and a severe and complicated recurrent Clostridium difficile infection that led to multiorgan dysfunction and exitus.