The study (CONVERT) by Griffith and colleagues (pp. We can continue the current treatment regimen in hopes of slowing progression, try to “strengthen” the regimen by adding additional antibiotics (none of which are approved for treatment of MAC), offer surgical resection, or simply stop treatment and hope for the best.Įnter the Mad Hatter to the rescue. When patients fail therapy, we have few options for treatment. However, even today, treatment success rates average only 66% among patients with macrolide-susceptible disease who take the American Thoracic Society recommended regimen ( 9) for at least a year ( 10). It was not until the availability of macrolides that we began to see improvement in treatment outcomes ( 10). Today, these organisms, as well as at least 10 other species ( 8), are collectively referred to as Mycobacterium avium complex or MAC.Įarly experience with treating MAC pulmonary disease was fraught with failure ( 9). Eventually, these causative organisms were identified as Mycobacterium avium ( 6), followed by identification of Mycobacterium intracellulare in 1949 ( 7). However, it was not until the 1930s that the causative strains were identified as human pathogens ( 1– 3), and by 1942, only 25 cases of human avian tuberculosis had been reported ( 4, 5). Probable human cases of “avian tuberculosis” were reported as early as the late 1880s. The cause of this disease was an “avian” mycobacteria. Once upon a time, 1868 to be exact, someone noticed that chickens developed “tuberculosis” ( 1). When I used to read fairy tales, I fancied that kind of thing never happened, and now here I am in the middle of one!įairy tales do come true.
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