"Microbial Genetics" is an outstanding example of a paper on infections. In Escherichia coli and other forms of enteric bacteria, the sucrose operon is necessary for the transport and metabolism of sucrose. SucroA, sucrose, and SucroC are the three adjacent structural genes that make up the operon. The availability of glucose and sucrose is one of the factors that regulate the sucrose operons. Normally, the sucrose operon allows for the effective digestion of sucrose to glucose. Sucrose can be the source of energy to the cell through the production of enzyme α -nucleosidase.
In this regard, it would be unnecessary to produce the enzyme if there is no sucrose available or if the glucose is readily available in the cell. The sucrose operon uses a two-part control mechanism to ensure that the cell uses energy, therefore, producing α -sucrosidase, α -sucrose permease and thiosucroside transacetylase. This achievement is also enabled by the sucro repressors which stop the production in the absence of sucrose. The sucro repressor proteins structure consists of three regions; a DNA binding region, the tetramerization region and the core region. The Catabolite activator protein that assists in production in the absence of glucose also terminates the production of enzyme α -nucleosidase.
In positive control, the regulatory proteins can bind to the activator binding site in the presence of sucrose. The cell ‘ senses’ the presence of sucrose. d the activator turns on genes in response. The sucrose operon consists of sucrose, sucrose, and sucrose structural genes, a promoter, a terminator, a regulator, and an operator. SucroA encodes α -sucrosidase, an intracellular enzyme that cleaves the sucrose disaccharide into glucose. SucroB encodes for α -sucrose permease, a membrane-bound transport protein that pumps sucrose into the cell.
SucroC encodes thiosucroside transacetylase that transfers acetyl group from acetyl-CoA to α -sucrose. The genes undergo transcription in the pathogens only when the environment in the host is rich with sucrose. Under these conditions, the genes in the pathogen are triggered and attach themselves to the epithelium of the host (Busby & Ebright, 2001). Antibiotics resistance in an immigrant from India with XDR-TB Antibiotic resistance is when bacteria become resistant to antibiotic drugs that were previously effective for the treatment of infections caused by it. Therefore standard treatments become ineffective and infections persist which increases the risk of spreading to others. Pathogens become resistant to bacteria replicate erroneously.
Bacteria develop resistance through several mechanisms. These include drug activation and modification, alteration of the target site and metabolic pathway, and reduced drug accumulation. This resistance may be spontaneous or genetically induced. The use and misuse of antibiotics accelerate the emergence of drug-resistant strains. Poor infections control practices and inadequate sanitary conditions and inappropriate handling encourage the spread of antibiotics resistance. The emergence of Multidrug resistance progressed to extensively drug-resistant status (XDR-TB) which is resistant to the second line of drugs and totally drug-resistant (TDR-TB).
Extensively drug-resistant status tuberculosis (XDR-TB) is common in high risk of infection of HIV. XDR-TB has also be observed frequently and found in many inpatient TB patients. If undiagnosed it poses a risk for transmission for other people in the community. High mortality rates have been observed among patients with drug resistance TB infection. Mycobacterium tuberculosis has become resistant to drugs such as isoniazid, rifampin, and other antibiotics (Shah, Robinson, & Cagielski, 2008). In the management of drug-resistant TB, an early approach is recommended.
For instance, immigrants should be actively screened for potential cases of TB. Poor infrastructure and mismanagement of individuals with TB in third-world countries have been associated with multidrug resistance TB. Moreover, the use of antibiotics should be controlled especially in countries with low and middle income. The practitioners should care for TB patients using international standards (Kanchan, 2011).
Kanchan, A. (2011). Rapid diagnosis of Extensively Drug-Resistant Tuberculosis by Use of a Reverse Line Blot Hybridisation Assay. Journal of Clinical Microbiology, 2546-2551.
Shah, N. S., Robinson, V. C., & Cagielski, J. P. (2008). Extensivley drug resistant tuberculosis. JAMA, 300(18), 2153-2160.