Fig. 6.46 A-F Skeletal coccidioidomycosis in the lower limb. A, B A lytic lesion in the lateral tibial condyle. C Ill-defined lesions in the lower end of the femur medially, and in the patella. D A granuloma causing destruction on both sides of the first metatarsophalangeal joint, with an associated soft tissue mass. There are early lesions in the distal phalanx and the proximal end of the first metatarsal. E A more "punched-out" lytic lesion in the proximal end of the fifth metatarsal. F Almost complete destruction of the mid-tarsal bones and the proximal ends of the first four metatarsals, with soft tissue swelling. (D courtesy of Dr. J. P. McGahan et al and AIR, 1981)

Clinical Characteristics

The cutaneous form of infection (Fig. 6.49) is the commonest, developing as a subcutaneous nontender nodule I week to 6 months after inoculation. The skin becomes blackened (and the lesion may be mistaken for anthrax) and then ulcerates, resembling a gumma. In some localities, 75% of the infections are on the upper limbs. In most patients the regional lymph nodes enlarge and multiple nodules form along the lymphatics: these nodules may become indurated and may eventually ulcerate, but other lymphatics become acutely inflamed. The skin lesion may persist for many years, and some do not develop lymphatic spread, remaining without change, localized where they started. This is the most common pattern in children, where the infection may be found on the face and the early lesion can resemble verrucous warts. There is an uncommon mucocutaneous infection, involving the nose, mouth pharynx, and even the vocal cords.

In other patients, the cutaneous infections may spread directly to underlying bones or joints and there may be an effusion into a joint. Tenosynovitis often affects the elbows of knees. However, systemic spread may also occur without any apparent initial cutaneous or pulmonary lesions. This usually occurs in immunodepressed patients, who have not only multiple hard subcutaneous nodules but infection in the bones, viscera, heart, and even meninges. The clinical symptoms depend on the site of the infection.

When the lungs are involved (which is in less than 20% of cases), the clinical complaints are of general malaise, chronic cough with sputum, and hemopty sis, accompanied by fever, dyspnea, and chest pain, Eventually there may be chest wall involvement, with infection of the ribs and draining sinuses, but this occurs less commonly than in actinomycosis or nocardiosis. Apart from the draining sinuses, pulmonary sporotrichosis is indistinguishable from other granulomatous infections, such as tuberculosis, sarcoidosis, and histoplasmosis capsulati. Some patients with pulmonary infection may be asymptomatic.

Imaging Diagnosis

There are no specific or diagnostic imaging findings in sporotrichosis.

The primary lung infection is progressive and usually bilateral and destructive, with either cavitation or consolidation. The lesions are often apical and mistaken for tuberculosis. The infection can be localized and nodular, or segmental, or there may be miliary spread which becomes confluent in patches. If the infection persits, thin-walled cavities appear and there will be fibrosis. If untreated, this becomes a massive density with central necrosis and cavitation. Pleural effusion and pleural thickening may occur, but are not very common: the infection may spread into the chest wall and cause osteomyelitis of the ribs, with sinus tracts and fistulae.Mediastinal lymphadenopathy is common, and may be the presenting feature. The hilar lymph nodes enlarge rapidly and may compress a bronchus. This is most often mistaken for primary tuberculosis or sarcoidosis, or lymphadenopathy from one of the other mycotic infections. The diagnosis cannot be made by imaging, but needs appropriate skin and laboratory tests.

Computed tomography and MRI will demonstrate mediastinal lymphadenopathy and the pulmonary lesions, but there are no specific findings.

Skeletal involvement is common (Fig. 6.50), usually underlying the cutaneous and subcutaneous lesions: occasionally there is no obvious primary site. Bone infection causes an intense periosteal reaction and destructive osteomyelitis, with lytic lesions in the metaphyses. Neighboring joints develop infections by direct spread, with effusions and destruction of the articular surfaces and periarticular tissue. There can be serious skeletal involvement even without symptoms, and scintigraphy is useful to detect these cases, particularly in the spine in patients with severe infections. Systemic spread is usually a complication of pulmonary infection. Although almost any organ or site may be involved, there are no specific imaging findings allowing the diagnosis of sporotrichosis.