Scrofuloderma: causes, symptoms, diagnosis, and treatment

Scrofuloderma, also known as tuberculosis cutis colliquativa, is caused by mycobacterium tuberculosis invasion in the skin through local lymphatic tuberculosis, bone or joint tuberculosis lesions, or directly through lymphatic vessels, mainly in the neck, followed by the upper chest, underarms, and groin, with long duration.


Mycobacterium tuberculosis causing this disease is mostly mycobacterium hominis, merely mycobacterium bovis. Scrofuloderma is generally secondary to lymphatic tuberculosis, bone tuberculosis, or joint tuberculosis. Mycobacterium tuberculosis spreads directly from infected lesions or through hematogenous dissemination and lymphatic vessels. Living conditions, sanitary conditions, and immunity are associated with the occurrence and development of the disease.

Signs and Symptoms

The predilection site is the neck and upper chest, followed by the axillary region and groin, mostly in the buttocks of children if caused by bone and joint tuberculosis. Most patients have lymphatic or bone and joint tuberculosis. The initial clinical manifestations are several, soy sized, solid, painless, movable, sharply demarcated, skin colored, subcutaneous nodules, with normal skin surface temperature. With the development of inflammation, nodules can fuse into plaques, raised and adhered to the skin. The skin above the nodules is bluish red, then caseous necrosis and softening in the center of the nodules occurs, and the skin turns to deep red. The skin gradually thins and is ruptured, forming sinus tracts with destroyed base. Pus with caseous substances is discharged, and the pus contains mycobacterium tuberculosis. New infections in the nearby lymph nodes cause enlargement, softening, and necrosis, forming new sinus tracts. If the skin surface is necrotic, a large ulcer can be formed. The edges of the ulcer are purplish red, irregular, undermined, with deep base, with not fresh granulation tissue on the surface, with little exudate. Cicatrization can cause irregular adhesion and fibrosis in some areas. Funicular scars are a feature of this disease and can be used to diagnose the disease even in many years.

The disease develops slowly. Patients generally have no systemic symptoms. Positive results in tuberculin test are present.


In the epidermis, acanthosis, cellular edema, with or without vacuolization, and hyperpigmentation in the basal layer are visible. Tuberculous infiltration or tuberculosis infiltration in the deep dermis or subcutaneous tissue is present. Mycobacterium tuberculosis can be found. The epidermis and upper dermis are often ruptured and with ulceration. When the lesion is matured, tuberculous granulomatous changes, composed of multinucleated giant cells and epithelioid cells, can be seen. Caseous necrosis in the center and peripheral lymphocytic infiltration, sometimes surrounded by solid connective tissue, are present. Collagen and elastin are destroyed in the lesion, and blood vessels and lymphatic vessels are less common, but many new blood vessels and lymphatic vessels are visible at the edges. In secondary infection, massive neutrophil infiltration in the upper dermis is present, and pyogenic bacteria can be found. In the recovery stage, proliferation and fibrosis of granulation tissues results in scars.


On the basis of ulcers and sinus tracts in the skin due to perforation of lymphatic tuberculosis or bone and joint tuberculosis, long duration, typical tuberculosis granuloma in histopathological examinations, and acid-fast bacilli, diagnosis is not difficult.


Small localized lesions can be surgically resected. For unruptured abscesses, pus can be taken out with a sterile syringe, and isoniazid or amikacin can be injected. Topical isoniazid powder or ointment can be applied to the ruptured abscesses.

Systemic anti-tuberculosis treatment should be more than 6 months.

First-line anti-tuberculosis drugs include isoniazid (INH), rifampicin (RIF), pyrazinamide (PZA), and ethambutol (EMB). These drugs should be treated in combination.

Second-line anti-tuberculosis drugs are often used in drug-resistant tuberculosis patients or patients unable to tolerate first-line drugs, mainly including aminoglycosides and fluoroquinolones, such as streptomycin, kanamycin, amikacin, capreomycin, levofloxacin, and moxifloxacin. Aminoglycosides are only for parenteral use.

Other second-line drugs include ethionamide, cycloserine, and para-aminosalicylic acid, with anti-tuberculosis effect weaker than first-line drugs, with strong toxicity, but effective against drug-resistant tuberculosis.

Bedaquiline, delamanid, and sutezolid are new anti-tuberculosis drugs and are usually reserved for extensively drug-resistant tuberculosis, or patients unable to tolerate other second-line drugs.