Microbial Genetics Issues - Essay Example

In Escherichia coli and other forms of enteric bacteria, the sucrose operon is necessary for the transport and metabolism of sucrose. SucroA, sucroB, 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 operon.

Normally, the sucrose operon allows for the effective digestion of sucrose into glucose. Sucrose can be the source of energy to the cell through the production of the enzyme α-glucosidase. In this regard, it would be unnecessary to produce the enzyme if there is no sucrose available or if 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 sucrose repressor which stops the production in the absence of sucrose. The sucrose repressor protein 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-glucosidase. 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 and the activator turns on genes in response.

The sucrose operon consists of sucroA, sucroB, and sucrose structural genes, a promoter, a terminator, a regulator and an operator. SucroA encodes α-nucleosidase, 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 the 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).

Antibiotic resistance is when bacteria become resistant to antibiotic drugs that were previously effective for the treatment of infections caused by them. Therefore standard treatments become ineffective and infections persist which increases the risk of spreading to others. Pathogens become resistant to bacteria and 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 antibiotic resistance.

The emergence of Multidrug resistance progressed to extensively drug-resistant status (XDR-TB) which is resistant to the second line of drugs and drug-resistant (TDR-TB). Extensively drug-resistant status tuberculosis (XDR-TB) is common with a high risk of infection of HIV. XDR-TB has also been observed frequently and found in many inpatient TB patients. If undiagnosed it poses a risk for transmission to 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 to 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).