Breast TB accounts for fewer than 0.1% of all breast pathologies [4] and has been reported as 3–4.5% of breast pathologies requiring surgery in developing countries [5]. Multipara and women practicing lactation between the ages of twenty and forty are often affected. Breast TB can be either primary or secondary; however, primary breast TB is extraordinarily rare because the breast parenchyma is impervious against the tubercular bacillus [6]. The primary type of tubercular inflammation is caused by the extension of infection through abrasions within the skin of the breast or through cracks within the breast nipples. The secondary type is caused by the retrograde unfurling of the infection from infected axillary nodes, or by direct spread from tissue within the ball-and-socket joint of the shoulder, costo-chondral cartilage, ribs, sternum or pleural membranes adjacent to the ductal glandular breast tissue [6].
The clinical presentation is variable and ranges from a spectrum of multiple painless lesions that may be adhering to the skin or the chest wall, multiple discharging sinuses, skin inflammation and associated nipple retraction or skin thickening and axillary inflammation or nodal formation. This might cause diagnostic predicament because of similitude with cancer or bacterial breast infection.
In 1952, McKeown and Sir Geoffrey Wilkinson classified tuberculosis of the breast into 5 totally different types: nodular, mastitis obliterans, sclerosing, disseminated and acute military type of inflammation [7]. Caseous nodular type of inflammation is the commonest kind. It presents as a pain-free, oval, well-defined, slow growing, non-vascular hypoechoic mass, mimicking the looks of a fibroadenoma within the early stages of the disease. Later, it evolves to become a fistula within the nipple-areolar complex or on the skin and could closely remind of cancer [7].
Radiologically, tuberculosis of the breast has 3 crucial appearances: nodular, diffuse and sclerosing [8].
On ultrasonographic examination, the nodular type of tubercular inflammation presents as lesion/lesions which take the shape of an indistinctly bordered, hypoechoic, heterogeneous mass which might mimic the looks of a slowly growing fibroadenoma and hence is classified as BIRADS three lesions [9]. Diffuse type of the mastitis shows multiple hypoechoic masses which are not well defined, while the sclerosing type shows exaggerated echogenicity of the breast parenchyma without a typical mass formation; the tissue echogenicity here is reflective of edematous breast tissue and inflammation. Various other common appearances include necrosis of the axillary nodes with caseous pathology with conglomeration, focal or diffuse skin thickening or fistula formation. If there is abscess formation which fistulizes to the skin, the fistula tract may additionally be visible with ultrasound [10].
Computerized tomography (CT) and magnetic resonance imaging (MRI) are considered higher diagnostic modalities and helpful with the analysis of deep retro-mammary localization of the breast lesions and associated chest wall involvement. Communication of the fistula tract with pleural membranes, bone and underlying deep soft tissues of the chest can be determined accurately with these imaging modalities.
Biopsy constitutes the gold standard for categorization of the lesions as they show necrotizing inflammation with granulomatous and Langerhans’s cells. These also show predominance of acid fast tubercular bacilli (AFB) diagnosed with the Ziehl-Neelsen stain, thus confirming the diagnosis [11].
There is no medical treatment specific to tubercular mastitis with anti-tubercular treatment forming the backbone of treatment strategy lasting for about six to eighteen months. With emerging resistant strains, the treatment is extended until twenty four months. Surgery (lumpectomy or mastectomy) is additionally a possibility once there is no response to medical treatment betting on the surgeon’s preference [12]. Abscesses can be effectively treated with ultrasound-guided external evacuation.