An Impact of Biofield Treatment: Antimycobacterial Susceptibility Potential Using BACTEC 460/MGIT-TB System

What is it about?

The aim was to evaluate the impact of biofield treatment modality on mycobacterial strains in relation to antimycobacterials susceptibility. Mycobacterial sensitivity was analysed using 12 B BACTEC vials on the BACTEC 460 TB machine in 39 lab isolates (sputum samples) from stored stock cultures. Two American Type Culture Collection (ATCC) strains were also used to assess the minimum inhibitory concentration (MIC) of antimicrobials (Mycobacterium smegmatis 14468 and Mycobacterium tuberculosis 25177). Rifampicin, ethambutol and streptomycin in treated samples showed increased susceptibility as 3.33%, 3.33% and 400.6%, respectively, as compared to control in extensive drug resistance (XDR) strains. Pyrazinamide showed 300% susceptibility as compared to control in multidrug resistance (MDR) strains. Isoniazide did not show any improvement of susceptibility pattern against treated either in XDR or MDR strains of Mycobacterium as compared to control. Besides susceptibility, the resistance pattern of treated group was reduced in case of isoniazide (26.7%), rifampicin (27.6%), pyrazinamide (31.4%), ethambutol (33.43%) and streptomycin (41.3%) as compared to the untreated group of XDR strains. The MIC values of few antimicrobials were also altered in the treated group of Mycobacterium smegmatis. There was a significant reduction observed in MIC values of linezolid (8.0 to 2.0 µg/ml) and tobramycin (2.0 to 1.0 µg/ml); however, very slight changes occurred in the remaining antimicrobials of treated samples. There was no change of MIC values in the strain of Mycobacterium tuberculosis after biofield treatment. Biofield treatment effect on Mycobacterium against anti-tubercular drugs might be due to altered ligand-receptor/protein interactions at either enzymatic and/or genetic level with respect to anti-mycobacterium susceptibility and MIC values of antimicrobials.

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Why is it important?

Global tuberculosis control is facing major challenges now days. Multidrug resistance of Mycobacterium tuberculosis (MDR-TB) has recently become a serious public health burden. Extensively drug resistant TB (XDR-TB; MDR resistance plus resistance to a fluoroquinolones and an aminoglycoside and to at least one of the three injectable drugs kanamycin, capreomycin and amikacin) is a form of tuberculosis which is now a serious threat to human life. Antimycobacterial susceptibility testing is necessary for the proper treatment of patients with tuberculosis through a multiple drug regimen. The key reasons for the development of MDR-TB are due to ongoing bacterial mutation and early discontinuation of treatment [1]. Drug resistance in M. tuberculosis are attributed to random mutations in the mycobacterial genome. All wild type population of M. tuberculosis contain a few mutant strains that are resistant to one of the drugs. These drug resistant strains emerge and become a dominant clone of the population when chemotherapy is intermittent or otherwise inadequate. Tuberculosis has become a threat in the modern era of antimicrobial warfare, because its unique characteristics give it enormous potential for developing resistance to even the strongest antimicrobials [2]. There are various major lacunas associated with currently used directly observed treatment short course (DOTS) regimen in both MDR as well as XDR-TB. The duration and complexity of treatment result in non-adherence, which leads to sub-optimal response like failure, relapse and ultimately developed resistance. Manifestation of adverse effects of anti-TB drugs also contributes a problem of non-adherence. Co-infection of TB and HIV is a problem by itself and prophylactic therapy of latent TB (TB infection without symptoms) with isoniazid is also associated with problems of non-adherence [3-5]. Based on above lacunas there is an urgent need for an alternative way to improve tuberculosis therapy by either enhancing the application of existing agents by means of some alternative strategy or introducing new drugs. Biofield treatment is an alternative approach which may be useful to improve these lacunas associated with mycobacterial resistance. The human biofield’s is the energetic matrix that surrounds the human [6]. It directly links with the cellular activity that allows the DNA to communicate faster than light and maintain intelligence in the organisms [7]. According to universal principles of Maxwell's equations and the principle of reciprocity, it defines electromagnetic connections related to the human biofield [8]. Afterward, Harold Saton Burr had performed the detailed studies on the correlation of electric current with physiological process and concluded that every single process in the human body had an electrical significance [9]. According to Rivera-Ruiz et al. 2008, reported that electrocardiography has been extensively used to measure the biofield of human body [10]. Thus, the cumulative effect of bio-magnetic field and electric field surrounds the human body is defined as biofield. The energy associated with this field is considered as biofield energy and it can also be monitored by using electromyography (EMG) and electroencephalogram (EEG) [11]. Mr. Mahendra Trivedi’s biofield treatment (The Trivedi effect®) has been known to transform the unique structural, physical and chemical properties of materials [12,13], improved the productivity of crops [14,15] and altered characteristic features of microbes [16-19]. Recently, the BACTEC Mycobacteria Growth Indicator Tube System (BACTEC 960/MGIT), a newly developed non-radiometric, fully automated, and continuous monitoring system, has been introduced as an alternative to the radiometric BACTEC 460 for growth and detection of mycobacteria. BACTEC 960/MGIT is a suitable tool for the detection of M. tuberculosis and other mycobacterial species, comprising wide variations in diagnostic performance [20]. The aim of this study was to determine the impact of biofield treatment on XRD and MDR strains of Mycobacterium against susceptibility patterns of antitubercular drugs.

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