The aim of this study was to determine the impact of biofield treatment on susceptibility patterns of anti-tubercular drugs to XRD and MDR strains of Mycobacterium
. For this purpose we had selected all three generations drugs, which are used to treat both MDR as well as XDR strains (Table 1). The overall alteration of responses (resistance and susceptibility) of antitubercular drugs after biofield treatment against XDR strains of Mycobacterium
with respect to control are presented in Figure 1.
Based on existing literatures isoniazide resistance developed due to loss of catalase activity [19
], transformation of functional katG gene, deletions and mutation of others gene such as InhA [16
]. In this experiment after the biofield treatment resistance property was reduced 26.7% in isoniazide as compared to control; it could be due to some interaction at genetic level. Mono-resistance to isoniazid is quite common and rifampin is rare. Rifampin or rifampicin resistance occurs in Mycobacterium
strains that are also resistant to isoniazid; thus, rifampin resistance can be a surrogate marker for MDR [17
]. More than 96% of the rifampin-resistant in Mycobacterium
strains is due to mutation of gene encoded in β subunit of DNA dependent RNA polymerase (rpoB) [21
]. The study results showed that rifampicin improved susceptibility by three folds and simultaneously, reduced 27.6% resistance properties as compared to control in XDR strains (Table 1). Pyrazinamide is a prodrug that converted to pyrazinoic acid by the enzyme pyrazinamidase, encoded by the pncA gene in Mycobacterium
strains. Mutations in pncA results to lost or reduced pyrazinamidase activity which leads to development of resistance [23
]. In this experiment, after biofield treatment pyrazinamide reduced 31.4% resistance property in XDR strains besides increased susceptibility by four folds in case of MDR strains as compared to control (Table 1).
The main target of ethambutol was mycobacterial embCAB operon that is responsible for cell wall synthesis. Due to mutation of embCAB lead to resistance against ethambutol in Mycobacterium tuberculosis
, but the exact molecular mechanism of resistance in non-tuberculous mycobacteria is still unknown [24
]. In this report, after biofield treatment to the XDR strains, ethambutol decreased 33.33% resistance and simultaneously improved sensitivity about three folds with respect to control in XDR. In case of treated MDR strains, resistance property increased by 50% and susceptibility was reduced sixty six folds with respect to control (Table 1). Resistance of streptomycin was occurred due to mutations in the gene encodes to the ribosomal protein S12, rpsL [25
]. This study results showed that streptomycin susceptibility was enhanced about five folds and concurrently reduced 41.38% resistance in biofield treated XDR strains as compared to control. In MDR strains, resistance property slightly increased and sensitivity was reduced in biofield treated groups as compared to control.
The resistant properties of all the second generation antitubercular drugs such as kanamycin, ethionamide, p-amino salicylates and ofloxacin of XDR strains of Mycobacterium
were reduced by 46.67, 30.44, 53.84 and 26.67%, respectively as compared to control. Among them only kanamycin showed an improvement in susceptibility by twenty folds towards treated XDR strains as compared to control. Ofloxacin improved susceptibility 25.07% and simultaneously reduced resistance also by 25% in treated group of MDR strain as compared to control (Table 1).
Apart from first and second generations antitubercular drugs fluoroquinolones also possess antitubercular activity and it is well accepted by the scientific community. Due to its wide distribution pattern, can easily invade to an intracellular compartment of Mycobacterium
and produce strong effects like macrophages without cross-resistance to antitubercular drugs [26
]. Among them, moxifloxacin resistance to MDR-TB is very low [29
] and highly effective to isoniazide and rifampicin resistance cases. The main targets of its bactericidal actions to DNA gyrase and topoisomerase IV [30
]. This study further indicated that there was a slight reduction of MIC value (0.25-0.12 µg/ml) of gatifloxacin which is similar to moxifloxacin after biofield treatment in Mycobacterium smegmatis
(Table 2). According to George et al. amikacin and kanamycin are highly resistance to Mycobacterium
]. The study results also demonstrated approximately 50% reduction of resistance in both amikacin and kanamycin was found after biofield treatment in XDR strains as compared to control. Besides, the sensitivity potential of amikacin was improved by 33.35% in the treated group as compared to control in XDR strains of Mycobacterium
. Extensive study reports demonstrate that clofazimine is median resistant to MDR-TB [32
]. Basically, it is designed to treat leprosy, but in MDR-TB cases it is extensively used as an alternative to TB regimens. This study results showed that about 75% resistance property of clofazimine was reduced in XDR-TB after biofield treatment as compared to control. Capreomycin is an important and preferable drug in MDR-TB against Mycobacterium smegmatis
. Resistance occurs due to mutation of tlyA gene [33
]. In eight lab isolates out of 30 XDR strains did not show any growth of Mycobacterium tuberculosis
after biofield treatment (Table 1). Biofield treatment might be responsible to do an alteration in microorganism at genetic and/or enzymatic level, which may act on receptor protein. While altering receptor protein, ligand-receptor/protein interactions may alter that could lead to show different phenotypic characteristics [34
]. Based on these data, it is tempting to speculate that certain alteration in terms of antimycobacterial susceptibility happened due to biofield treatment.