We report the case of a 32-year-old female patient with a breastfeeding history from the preceding year. No history of diabetes, immunosuppression, or breast cancer in family, and no evidence of tuberculous contact. Two months before her admission, the patient experienced mastodynia and an inflammatory left breast within a context of fever, all while showing no respiratory signs. Clinical examination showed an inflammatory left breast without skin lesions, notably orange skin, retraction, or nipple flow. The palpation revealed a painless 10/10 cm sitting at the junction of inferior quadrants of the left breast with an ipsilateral mobile painless axillary lymph node of 3 cm. The biological assessment showed an inflammatory anemia (Hb: 10.9 g/dl), neutrophilic leukocytosis of 18000 elements/microl, a polyclonal hypergammaglobulinemia in favor of an inflammatory syndrome on the electrophoresis of serum proteins and an elevation of C-reactive protein (CRP) to 160 mg/l.
Taking into account this clinical presentation, the patient received a sonomammography which showed a left-mammary multilocular collection dissecting the infiltrated fibro-glandular tissue that is associated with a necrotic ipsilateral axillary lymph node (Figure 1).
A magnetic resonance imaging (MRI) scan was conducted to better characterize the lesions and their extensions. The results of the scan revealed mastitis that is of granulomatous origin classified BIRADS IVa (Breast Imaging-Reporting And Data System) according to the American College of Radiology (ACR) with inflammatory axillary lymph nodes (Figure 2).
A Trucut biopsy was performed, the results of which showed neutrophilic cystic granulomatous mastitis with no signs of tumor proliferation (Figure 3). A puncture in the mammary collection was made to search for Mycobacterium tuberculosis through Ziehl-Neelsen staining, culture, and polymerase chain reaction (PCR). The results were negative. Both QuantiFERON-TB Gold and serological brucellosis were also negative. A cervico-thoracoabdominal-pelvic computed tomography scan conducted to search for pulmonary lesions or other deep lymph nodes showed no anomalies. A serological test for human immunodeficiency virus (HIV) also returned negative.
Therapeutically, the patient was put under a non-specific antibiotic treatment based on amoxicillin/clavulanic acid at first, then third-generation cephalosporins alongside metronidazole without improvement. This necessitated the commencement of an antituberculous regimen despite the negative report regarding tuberculosis. This time, the development was characterized by a fistula and the release of serous fluids after two weeks. A few weeks after, there was a total dewatering and disappearance of inflammatory signs (Figure 4).
In light of this very adequate response to antituberculous treatment and, after ruling out brucellosis, we retained the diagnostic of tuberculous mastitis and continued the antituberculous therapy that is based on rifampicin, isoniazid, ethambutol, and pyrazinamide for two months, followed with rifampicin and isoniazid for four more months for a total period of six months. The patient has remained clinically stable after one year of follow-up.