The relationship between Gene mutations of Tuberculosis Mycobacterium and rifampicin/ isoniazid drug resistance
Scientific question: Is there a relationship between gene mutations of tuberculosis Mycobacterium and rifampicin/ isoniazid drug resistance?
Null hypothesis: The changes in bacteria’s gene structures of tuberculosis Mycobacterium have no influence on the resistant ability to rifampicin and isoniazid drugs.
Alternative hypothesis: Gene mutation is one of the ways in which tuberculosis Mycobacterium bacteria resist to drugs and survive.
Mycobacterium Tuberculosis is the bacterium for Tuberculosis infection, which primarily affects the lungs, but can affect other organs. In most cases, Tuberculosis occurs in immunocompromised patients, especially those with Acquired Immuno deficiency syndrome (AIDS).
I would plan a preliminary experimental design that involved a number of different test subjects’ cultures to test the positive hypothesis, and as a control. The test subjects would have different classes of Tuberculosis and their response to rifampicin and isoniazid drugs would be tested consistently to check for any changes.
Appropriate experiments would involve researching into the area on previous studies that have been carried out in the area, their outcomes and conclusions.
3/ Critical Evaluation of Scientific Question and Hypotheses with Preliminary Experimental Design
The hypothesis evaluates a specific aspect of the scientific question. The hypothesis seeks to find out an aspect of the mycobacterium tuberculosis resistance to specific tuberculosis drugs rifampicin and isoniazid (Mayers, 2009). Due to the accuracy and attention needed to come up with reliable results for the study, the hypothesis is limited to investigating one variable at a time.
The null hypothesis for this research project addresses the hypothesis of no difference. It is expected that the health of an individual that has tuberculosis should change once they start taking their regimen of rifampicin and isoniazid, and other drugs that are prescribed for patients with this condition (Hazbon et al, 2006).
If the null hypothesis is rejected, the alternative hypothesis offers a logical conclusion; that there is a difference when gene mutation occurs and it leads to resistance of tuberculosis drugs: rifampicin and isoniazid. The alternative hypothesis definitely offers a logical conclusion if it is proven to be correct.
There is minimal likelihood of bias since scientific techniques will be used in coming up with the data used in analysis. Proper data collection and specimen storage techniques will be utilized to ensure maximum accuracy in data classification and interpretation. Drug resistance is a sensitive issue that requires maximum attention and accuracy to come up with reliable scientific data that can be replicated elsewhere under similar conditions, tools, and specimen (Tessema et al, 2012).
For the experimental design to work effectively, the researcher should be patient and proactive to be able to conduct thorough and exhaustive research. The researcher should also be innovative, especially in a case where he/ she has limited resources and therefore has to do with what is available. Data about the molecular structure of the bacterium Tuberculosis mycobacterium and that of the drugs rifampicin and isoniazid drugs would also be required. The structure of the pathogen and of the drugs would be tracked periodically through the experiment to note any changes in gene structure of the bacterium. As the researcher, I will be more proactive, especially in gathering information needed to come up with informed conclusions, such as mutations occurred as a result of deletion or insertion and the enzymes involved in deactivation of rifampicin and ionized drugs (Wright, 2008).
Experimental data required
The specific Mycobacterium tuberculosis enzymes involved in resistance.
Molecular structure of the rifampicin and isoniazid drugs.
Hazbon, M. et al. (2006). Population genetics of isoniazid resistance mutations and evolution of
multidrug resistant Mycobacterium tuberculosis. Antimicrobial agents. 50(8),2640-9.
Mayers, D. (2009). Antimicrobial Drug Resistance. New York: Springer.
Tessema, B., Emmrich, F., Sack, U. & Rodloff, A. (2012). Analysis of gene mutations
with isoniazid rifampicin and ethambutol resistance among Mycobacterium tuberculosis isolates from Ethiopia. 12: 37. Journal of Infectious Diseases. Biomed central. doi:10.1186/1471-2334-12-37.
Wright, A. (2008). Anti tuberculosis drug resistance in the world. Washington: World Health