**4. Resistance on aminoglycosides**

Aminoglycoside drugs have been part of the fight against *E. coli* pathogenic species, however with the changes in the phenotype of the *E. coli* isolates for example the ever-evolving changes in the ESBL structure as well as the genes that the aminoglycoside drugs encode for susceptibility [26].

### **4.1 Aminoglycoside mode of action**

Aminoglycosides are bactericidal agents that inhibit the synthesis of bacterial proteins through the interruption of the ribosomes. They interfere by binding

to the 30S and 50S ribosomal subunits, they inhibit the translocation process of moving the peptidyl-tRNA from the A site to the P site thereby causing mRNA misreading in that way denouncing the translation process forwarding zero protein synthesis, which entails no budding, multiplication and denouncing perpetuation and survival [26].

#### **4.2 Mechanism of resistance on aminoglycoside drugs**

There are more than 50 types of aminoglycosides modifying enzymes which include, acetyltransferases (aac), phosphotransferases (aph) and nucleotidyltransferases (ant), these enzymes are capable of modifying aminoglycosides at their respective drug recognition sites [27]. The main cause of resistance to the aminoglycoside drugs is that more than one aminoglycoside modifying enzymes may be found in a single isolate bringing in a high probability rate of resistance to the drugs [28].

Mancin [28], conducted a population analysis of genetic and enzymatic resistance of *E. coli* to aminoglycosides, they concluded that the genes aac(6′) and aac(3) can cause significant resistance to amikacin and kanamycin. Another study on genes was conducted by Bodendoerfer [29], where they concluded that in Switzerland the most prevalent resistance genes included the aph(3′)-la, aac(3)-lld and aac(6′)-lb-cr, they also alluded that the genes tend to change in their structural arrangement which is a mediated by the action of the transposon mechanisms of the resistant genes. The mechanisms of the jumping gene continues to be a threat to human health, because the transposon genes can be transferred to the next cell through transformation and conjugation processes which will cause the development of more resistant genes prior to transcription and translation, this information has caused migraine headaches to researchers and scientists who are working tirelessly in the attempt of denouncing resistance [29].

### **5. Conclusion**

*E. coli* bacteria continues to be a nuisance in the medical field bringing endless prospects in resistance against the drugs that are used in an attempt of eradicating the bacteria. The bacterial species has so many different forms of isolates that differ from one another both structurally and genetically, hence the drug that is susceptible to one *E. coli* may be found ineffective to another *E. coli* variant species. The review showed that there are many different mechanisms in which *E. coli* strains are becoming more and more difficult to treat, some evolving to possess enzymes that work in a conjunctive manner to denounce the effect of the drug.

The evolution brings forth the production of many different isolates with different protein structures for drug resistance and allows perpetuation and survival. This alarms for continuous assessments to provide information on the drugs and the interference with the pathogenic microorganism, how the bacteria respond in susceptibility, which will act as a fortress in tracing the reason behind resistance tomorrow. Studies are of importance to help and provide practical proof on how to tackle pathogens which will aid in improving health, denouncing long hospital stays and even patients from succumbing to infections caused by the microorganism.

### **Conflict of interest**

The authors declare no conflict of interest.

*Mechanisms of Antimicrobial Resistance of* E. coli *DOI: http://dx.doi.org/10.5772/intechopen.101671*
