alone is often inadequate, and needle or surgical drainage is recommended. Pulmonary infections with rifampin-susceptible M. kansasii isolates have been shown to respond well to a prolonged regimen of isoniazid (300 mg/d), rifampin (600 mg/d), ethambutol (15 mg/kg/d), and pyridox- ine (50 mg/d) for at least 12 to 18 months. 13 As in HIV-associated MAC infections, the duration of therapy should also be dictated by the immune status of the patient. Clinical recovery should be monitored closely as resistance to rifampin can lead to failure of treatment and resistance to other drugs. 13 If failure of the initial regimen does occur, a new three-drug regimen based on susceptibilities should include clarithromycin or azithromycin, moxifloxacin, ethambutol, sulfa- methoxazole, or streptomycin. 13 For patients who are co-infected with HIV, additional information must be considered. Combination antiretroviral therapy and the agents used for the treatment of M. kansasii have associated side effects and may also inter- act with each other when used concomitantly. Importantly, rifabutin is known to interact less with combination antiretroviral therapy than rifampin. 14 The interplay of preexisting comor- bidities must also be taken into account. Since
Figure D: A thin-pour agar plate (Hardy Diagnostics) with a Myobacterium kansasii sample grown from a broth culture of the aspirate of myxoid- appearing fluid drawn from right subacromial-subdeltoid bursa. Heterogeneously yellow hue is indicative of a photochromogen. Identification of organism as Mycobacterium kansasii was confirmed by DNA probe of RNA target (GEN-PROBE).
they are superficial andmost frequently exposed to trauma. 10 This presentation is in contrast to that of M. tuberculosis , which, due to its propensity for hematogenous spread, does not show preference for particular bursae. 10 One patient, described by Barham and Hargreaves, presented with monoarticular M. kansasii bursitis contracted through local trauma and direct inoculation. 8 In contrast, three cases of polyarticular M. kansasii bursitis described by Mathew et al. were thought to result from hematogenous spread. Interestingly, all three patients were immunocompromised secondary to immunosuppres- sive therapies. The only patient described with M. kansasi i subacromial bursitis was predisposed to infection second- ary to articular manifestations of dermatomyositis. The patient initially presented with cutaneous nodules on his forearms that later spread to the subacromial bursa, a result of hematogenous dissemination. 7 M. tuberculosis is the only other mycobacteria that has been demonstrated to infect this particular bursa, though neither of the two cases described were in HIV-infected patients. 11 All of these infections oc- curred in the absence of trauma. 7, 11 MANAGEMENT Guidelines for the treatment of M. kansasii joint infec- tions currently do not exist due to the uncommon nature of this condition, and guidelines regarding disseminated nontuberculous mycobacterial infections are similar to those for pulmonary infections. Clinical experience has shown that with other infectious causes of bursitis, antibiotic treatment
isoniazid is a known hepatotoxic drug, liver enzymes should be closely monitored, and patients must be educated to strictly avoid alcohol. Since the majority of HIV patients with disseminated M. kansasii infections present with very lowCD4 counts, the possibility of IRIS must be considered as well. Currently, no guidelines exist recommending when to discontinue combination antiretroviral therapy, and clinical judgment must be used in these situations. Steroids should be used to treat any inflammatory symptoms that appear. Combination antiretroviral therapy should only be discontinued in the presence of life-threatening inflammatory conditions that do not respond to steroids. 15 DISCUSSION OF CASE Our patient’s case is significant for multiple reasons. First, his presentation was more indolent than the cases described in the available literature. His lack of pain or inhibition of his daily activities contrasts with the other cases, in which patients directly sought medical attention for their joint complaints. In addition, the patient’s physical exam showed no signs of acute inflammation such as pain, warmth, or erythema – all of which were present in the other cases of M. kansasii joint infections, even those with deficient immune status. 3 Immunocompromised patients are susceptible to less-common pathogens and often pres- ent with unusual symptoms and findings. It is imperative that physicians have a low threshold to further investigate the cause of an arthropathy, whether it be monoarticular or
J La State Med Soc VOL 166 July/August 2014 185
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