Lyle A. Weed

Infection of synovial tissues by mycobacteria other than Mycobacterium tuberculosis.

An additional six cases of mycobacterial infection other than by Mycobacterium tuberculosis and involving synovial structures are reported. Follow-up is included on a previously reported case. Five of the patients in the present series had involvement of tendon sheaths of the hand, wrist, and forearm. The causative microorganism was Runyon Group III (Battey bacillus) in two and Mycobacterium avium in two others; one tendon-sheath infection was due to Mycobacterium kansasii. An elbow was infected with Mycobacterium kansasii and a prepatellar bursa, with Mycobacterium fortuitum. We believe surgical excision of involved synovial tissue to be very important; antibacterial treatment is of importance in selected cases.

Infection of Tendon Sheaths, Bursae, Joints, and Soft Tissues by Acid-Fast Bacilli Other than Tubercle Bacilli

Twelve cases are reported in which tendon sheaths, joints, bursae, or soft tissue were infected with unclassified species of mycobacteria other than Mycobacterium tuberculosis. The subchondral bone of the femur was involved in one, and the subcutaneous soft tissue alone in one case. The organism or organisms causing the infections are culturally different from Mycobacterium tuberculosis var. hominis or var. bovis. They are not Mycobacterium avium, Mycobacterium balnei , or Mycobacterium ulcerans. They are not virulent for guinea pigs in the usual sense. They would appear to belong to a large group of organisms some of which are recognized as pathogens in the lungs. In addition, they are usually insensitive to para-aminosalicylic acid, isonicotinic acid hydrazide, and streptomycin, even though the infection has not been previously treated with these agents. Pathologically, they produce granulomata that are quite similar microscopically to those of tuberculosis or brucellosis. Operative incisions, accidental puncture wounds or those resulting from injections, and small lacerating wounds may represent the mode of entry of the organisms. Pre-existing rheumatoid arthritis may be a factor in allowing the proper host-invader relationship to exist, or this factor may he coincidental with the intra-articular injections that rheumatoid patients often receive. Accurate diagnosis is dependent on close cooperation of surgeon, surgical pathologist, and microbiologist. Treatment is of necessity surgical, with reliance on adequate excision of diseased tissue. Antibacterials are not helpful in most instances because of insensitivity of the organisms to drugs.

Chronic Draining Sinuses of the Chest Wall

Microbiologic investigation, including histologic examination of excised tissue, is important to establish the etiologic diagnosis and, together with special radiologic examinations such as sinography, provides the basis for specific treatment.

Chlamydia and non-specific urethritis.

Chlamydia organisms were found in 42 per cent of patients with non-specific urethritis and these organisms probably were the cause of the urethritis. Contact is by venereal means. The drug of choice is 500 mg. tetracycline every 6 hours for 10 days.

Chronic Localized Brucellosis of the Spleen

Chronic localized brucellosis of the spleen possibly may exist as a clinical entity apart from detectable brucellar involvement of other reticuloendothelial organs. Apparently the infection may be restricted to the spleen in some cases, and antibiotic therapy may eradicate the infection in other organs but not in the spleen. Six cases are reported, and a series of 10 cases is reviewed.

SOUTH AMERICAN ELASTOMYCOSIS: FURTHER OBSERVATIONS ON A CASE PREVIOUSLY REPORTED

Following the patients discharge from the Mayo Clinic in January, 1954, we had our next opportunity of seeing him during June, 1956. From 1956 to 1962 his progress was followed through frequent correspondence. He was seen at the Mayo Clinic for the last time during the fall of 1962. His terminal illness was caused by widespread metastasis from carcinoma of the left mainstem bronchus, and he died in May, 1963, more than 15 years after he presumably first acquired South American blastomycosis.