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The 8-methoxy fluoroquinolones (gatifloxacin, moxifloxacin) may be effective in some rapidly growing mycobacterial infections [ 43 ]. Tigecycline, available only in an intravenous preparation, appears to have good in vitro activity, and susceptibility testing can be performed in reference laboratories. Preliminary clinical studies indicate that its use may be limited by its adverse effect profile, most notably nausea. Linezolid often shows some degree of in vitro response, and if used, there may be some benefit from concomitant pyridoxine administration for prevention of cytopenia (but not peripheral neuropathy) [ 44 ]. When risks for VIII cranial nerve toxicity or renal dysfunction preclude systemic aminoglycoside treatment, inhaled therapy (e.g., amikacin) can be tried, but there have been no controlled trials. Each agent has its own unique toxicity profile, and drug-drug interactions require close monitoring and informing patients of potential risks. On the horizon, newer agents hold some promise, and the field of treatment for rapidly growing mycobacteria may benefit from testing of newer antituberculous agents [ 45 , 46 ].

In vitro susceptibility testing and guidelines of the Clinical and Laboratory Standards Institute [ 47 ] for microbroth dilution using a panel of antimicrobial agents, including macrolides, aminoglycosides, fluoroquinolones, cefoxitin, imipenem, linezolid, tigecycline, doxycycline, minocycline, and trimethoprim-sulfamethoxazole, should guide therapy. There are no results of controlled trials of treatment of rapidly growing mycobacterial infection. Although spontaneous healing of skin infection without antibiotics has been reported, most experts recommend antibiotics, usually in combination to avoid emergence of resistance [ 48 ]. Severe infections sometimes require cooperative management between those with infectious disease expertise and surgical colleagues to ensure adequate debridement of necrotic tissue. Therapy needs to be individualized. With such recalcitrant infections, it is strongly recommended that foreign bodies be removed.

Appropriate antibiotics are given for varying periods of time depending on disease severity and location. Skin and soft tissue infections may be successfully treated in 3–6 months with excellent chance for cure when medication either with or without concomitant surgical debridement is used. Pulmonary disease due to M. abscessus is currently considered “managed” but not cured. Most experts in the field practice intermittent intravenous therapy: intravenous imipenem or cefoxitin for 1 or 2 months plus a macrolide. Intravenous amikacin may also be used adjunctively in this pulsed fashion as long as there are no contraindications, such as renal insufficiency or evidence of damage to cranial nerve VIII. For the periods in between the pulsed intravenous therapy, “holding” regimens of a macrolide plus a quinolone may be helpful, even if in vitro susceptibility results reveal resistance to the quinolones. Pulmonary disease due to M. fortuitum generally has a much better outcome and in many cases can be considered cured after therapy for 12–24 months with at least 2 or 3 antibiotics with in vitro susceptibility. A commonly used regimen might include sulfamethoxazole, moxifloxacin, and minocycline. Antibiotics, both intravenous and oral, are administered as symptoms dictate. Short courses of intravenous antibiotics for 1–2 months plus an oral macrolide with a continuation phase using an oral macrolide and quinolone for 6–12 months is a regimen that is commonly used by experts in the field. Aminoglycosides are typically given during initial therapy for 2–8 weeks and longer if bone or other recalcitrant infection exists. For pulmonary disease due to M. abscessus , inhaled amikacin may also be considered but has not been used in clinical trials. Table 2 highlights recommendations for treatment of infection due to rapidly growing mycobacteria. A typical regimen for skin and soft tissue infection due to rapidly growing mycobacteria is intravenous imipenem or cefoxitin combined with amikacin as initial therapy accompanied by a macrolide.

Hypotheses that identify impairments as the cause of disabilities and functional losses are even easier to generate. If a person cannot walk following a CVA, for example, it would be incorrect in the HOAC II to hypothesize that the cause is damage to the motor cortex. Although this may be true, the quantification of the type and extent of pathology is not observable and measurable by physical therapists. The diagnostic hypothesis may be that the person cannot walk because he or she lacks the ability to generate sufficient quadriceps femoris muscle force during stance. In this example, the problem is a functional deficit, and the hypothesis relates the functional deficit to an impairment. The testing criteria will be the amount of force the therapist believes the patient needs to be able to generate to eliminate the problem (ie, to walk). Had the hypothesis identified a pathology (damage to the motor cortex), the pathology could not be measured by physical therapists, and, more importantly, the intervention is not designed to change the pathology, but rather the impairment and disability that the pathology caused. In addition, the pathology (as measured with magnetic resonance imaging, for example) would likely be unchanged, even though the intervention successfully dealt with the impairment or functional limitation.

The critical elements of hypotheses are that they deal with elements that would be affected by the intervention and that they must be sufficiently clear to allow for the generation of testing criteria. The testing criteria that therapists generate must represent pathology, impairments, or functional loss that can be measured in clinical practice. As discussed earlier, when a previously undiagnosed pathology is hypothesized to be present, consultation with or referral to a physician may be required to confirm the hypothesis. A problem may have more than one underlying cause, and, in these cases, the therapist may generate multiple hypotheses. The therapist also would generate testing criteria for each hypothesis. This might occur, for example, when weakness and a lack of coordination are hypothesized to be the reasons why a person can no longer ambulate independently.

Physical therapists, like many other health care professionals, share beliefs about what is happening and what may happen to their patients. Some of these beliefs are based on data that identify risk factors, factors that once eliminated should reduce the possibility of future negative health outcomes. The Framingham study, for example, identified many risk factors for cardiovascular disease. 14 Epidemiological studies of this type are usually the means for justifying interventions designed to eliminate risk factors. Unfortunately, data often are lacking for beliefs that health care professionals have about risk factors.

On what data do physical therapists act? The question is a legitimate patient management and resource allocation query. Without evidence to support the value of elimination of risk factors, the possibility of excessive intervention exists. Too little intervention for risk factors also is a possibility. The HOAC II provides a mechanism for therapists to use either epidemiological data or theoretical constructs to justify interventions aimed at reducing risk factors. The former is data based or evidence based, whereas the latter uses argumentation and logic that should have some scientific basis. Evidence-based arguments are preferred. 15

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