Respiratory Treatment and Prevention (Advances in Experimental Medicine and Biology)

(caused mainly by slow growers) remains a sub-
ject of discussions (van Ingen et al. 2012b).
There are important discrepancies between mini-
mum inhibitory concentrations (MICs) measured
inin vitroconditions and the activity of the
respective drug observed in vivo (van Ingen
et al.2012a). For theMycobacterium aviumcom-
plex, the susceptibility testing of macrolides only
(i.e., clarithromycin) is currently recommended,
since this testing has been clinically validated
(CLSI 2011 ; Wallace et al. 1996 ). ForMycobac-
terium kansasii, the initial testing should include
only rifampicin. Rifampicin resistant isolates
have been observed in patients who fail to
respond to treatment with rifampicin-based regi-
men (Wallace et al. 1994 ).
For rapid growers, relationship between MICs
and clinical outcome has been studied for several
drugs such as tobramycin, co-trimoxazole,
cefoxitin, and doxycycline. However, these
drugs have been tested mostly in extrapulmonary
diseases and the key drugs, including amikacin
and macrolides, have not been included (Wallace
et al. 1985 ). MIC of any drug other than that
mentioned above should be interpreted with cau-
tion, and an expert consultation before applying
non-standard therapy is recommended.

5 Treatment of Non-Tuberculous
Mycobacterial (NTM)
Pulmonary Diseases

The clinical and radiographic picture of NTM as
well as treatment are often akin to that of
TB. However, antibiotics are used more fre-
quently than antituberculotics. The main cause
of chemotherapy failure is undoubtedly the pri-
mary resistance of NTM to most classical

antituberculotics. Furthermore, time between

the identification of a pathogen and commence-

ment of therapy is rather long in most cases.

Except for the pulmonary forms of the disease

caused byM. kansasii, the long-term treatment

with antituberculotics of lung lesions is

ineffective.

In contrast to TB, diagnosis of NTM lung

disease does not necessarily require specific

treatment. The final decision concerning pharma-

cotherapy requires an individual approach

depending on a specific NTM species, patient

acceptance, tolerance and compliance, and treat-

ment goals, for instance, a reduction of

symptoms or sputum conversion. Treatment

options include an observation of the disease

course with the best possible pulmonary care, a

course of antibiotics given in a constant or inter-

mittent dosage regimen, and sometimes intrave-

nous therapy for several months or surgical

treatment (Griffith et al. 2007 ).

There are several issues typical for NTM

which influence the effectiveness of antibiotic

therapy. Thein vitrosusceptibility testing often

does not provide a good guidance for an effective

in vivoresponse to antibiotics. One of the most

important therapeutic goals is to avoid the emer-

gence of macrolide resistant Mycobacterium

aviumcomplex infections (Griffith et al. 2007 )

orM. abscessus(Koh et al. 2011 ) strains during

therapy. The primary goal of treatment is a

12-month period of sputum culture negativity

while on therapy. The recommended treatment

regimens for selected NTM respiratory

pathogens are listed in Table1. However, these

multi-drug regimens may lead to significant

pharmacokinetic interactions. In particular,

rifampicin reduces the serum levels of

macrolides and moxifloxacin in patients with

Table 1 Recommended treatment regimens for NTM respiratory pathogens

Mycobacterial species Drugs

M. avium complex macrolide, rifamycins, ethambutol

M. kansasii rifampicin, ethambutol, izoniazid

M. xenopi macrolide, rifamycins, ethambutol

M. chelonae aminoglycosides, macrolide

M. abscessus amikacin, cefoxitin, imipenem, tigecycline, linezolide, macrolide

M. fortuitum amikacin, cefoxitin, sulfonamides

22 I. Porvaznik et al.