The effects of antimicrobial resisters on E.

coli

Streptomycin:
A brief insight into the mechanism of streptomycin.[1] Streptomycin is an
aminoglycoside antibiotic indicated to treat multi drug resistant
mycobacterium tuberculosis and various non-tuberculosis infections.
Streptomycin’s serum half-life is estimated to be 2.5 hours. [2] In prokaryotes,
the 23S rRNA is part of the large subunit (the 50S) that joins with the 30S small
subunit to create the functional 70S ribosome. The ribosome is comprised of 3
RNAs: the 23S, the 16S and the 5S ribosomal RNAs. The 23S and the 5S
associate with their respective proteins to make up the large subunit of the
ribosome, while the 16S RNA associates with its proteins to make up the small
subunit. Streptomycin works by inhibiting protein synthesis by mimicking
codon-anticodon pairing sites.

Penicilin:
[3] Penicillin and other antibiotics in the beta-lactam family contain a
characteristic four-membered beta-lactam ring. Penicillin kills bacteria through
binding of the beta-lactam ring to DD-transpeptidase, inhibiting its cross-
linking activity and preventing new cell wall formation. Without a cell wall, a
bacterial cell is vulnerable to outside water and molecular pressures, which
causes the cell to quickly die. Since human cells do not contain a cell wall,
penicillin treatment results in bacterial cell death without affecting human
cells.

Gram-positive bacteria have thick cell walls containing high levels of

peptidoglycan, while gram-negative bacteria are characterized by thinner cell
walls with low levels of peptidoglycan. The cell walls of gram-negative bacteria
are surrounded by a lipopolysaccharide (LPS) layer that prevents antibiotic
entry into the cell. Therefore, penicillin is most effective against gram-positive
bacteria where DD-transpeptidase activity is highest.

[4]Bacteria reproduce quickly and are prone to genetic mutations when

growing in the presence of environmental pressures, such as an antibiotic.
Over time, genetic mutations that provide a survival advantage may arise in
the bacterial population, allowing bacteria to continue to grow and multiply in
the presence of antibiotic. This leads to the creation of a resistant strain, which
can only be killed using alternative and stronger antibiotics.

The potential for antibiotic resistance increases through repeated or improper

use of an antibiotic. Bacterial strains can become resistant to more than one
antibiotic, leading to the creation of “superbugs” that are extremely difficult to
treat medically.

[1] Block M, (1997)Blanchard DL: Aminoglycosides. (Accessed 25/04/22)

[2] Ying L, Zhu H, Shoji S, Fredrick K: Roles of specific aminoglycoside-ribosome
interactions in the inhibition of translation. RNA. 2019 Feb;25. (Accessed
25/04/22)
[3] http://www.who.int/mediacentre/news/releases/2014/amr-report/en/
(Accessed 24/04/22)
[4] http://www.cdc.gov/getsmart/antibiotic-use/antibiotic-resistance-
faqs.html (Accessed 24/04/22)