Question

Describe the class of antimicrobial drugs in E.coli  and why they are effective in destroying these microbes and why is this particular drug more effective based on their structure. What is the mode of action for viral or eukaryotic infection? Antibiotic resistance can also be described here, if applicable to the organism. Include how it relates to the information covered in class- which chap number and what was taught

Answer 1

Ans=A wide range of antimicrobial agents effectively inhibit the growth of E. coli. The β-lactams, fluoroquinolones, aminoglycosides and trimethoprim-sulfamethoxazole are often used to treat community and hospital infections due to E. coli

why=β-lactams disrupt cell wall synthesis by binding to and inhibiting the penicillin-binding proteins essential for transpeptidation and carboxypeptidation reactions in cell wall peptidoglycan synthesis. Fluoroquinolones interfere with DNA supercoiling and promote DNA gyrase-mediated double-stranded DNA. The aminoglycosides bind irreversibly to the 50S subunit of the 70S bacterial ribosomes. Sulfonamides and trimethoprim interfere with bacterial folic acid synthesis by inhibiting tetrahydropteric acid syntheses and dihydrofolate reductase, respectively.

Resistance = b-lactam antibiotics, especially the cephalosporins and b-lactam-b-lactamases inhibitor combinations, are major drug classes used to treat community-onset or hospital-acquired infections caused by E. coli,especially due to the ExPEC pathotype . Among E coli, b-lactamase production remains the most important contributing factor to b-lactam resistance. b-lactamases are bacterial enzymes that inactivate b-lactam antibiotics by hydrolysis, which results in ineffective compounds .

Resistance to aminopenicillins (e.g. ampicillin) and early-generation cephalosporins (e.g. cefazolin) among E. coli is often mediated by the production of narrow-spectrum b-lactamases such as TEM-1, TEM-2 and to a lesser extent SHV-1 enzyme. Most importantly among E. coli, is the increasing recognition of isolates producing the so-called “newer b-lactamases” that causes resistance to the expanded-spectrum cephalosporins and/or the carbapenems. These enzymes consist of the plasmid-mediated AmpC b-lactamases (e.g. CMY types), extended-spectrum b-lactamases (e.g. TEM, SHV, CTX-M types), and carbapenemases (KPC types, metallo-b-lactamases (MBLs) and OXA-types) . CMY, CTX-M, and NDM types of b-lactamase are mostly responsible for the emerging resistance to the β-lactam antibiotics among E. coli .The VIM, IPM, KPC and OXA-48 β-lactamases had been described in various members of the Enterobacteriaceae (especiallyKlebsiella spp.) and are not yet commonly encountered among E. coli.

The up regulation of efflux pumps and plasmid-mediated resistance mechanisms (e.g. qnr determinants) can reduce fluoroquinolone susceptibilities in E. coli, however high level resistance to the fluoroquinolones typically requires 1-2 point mutations within the quinolone resistance determining regions of gyrA and parC, the chromosomal genes encoding for DNA gyrase and topoisomerase IV respectively .

Resistance to aminoglycosides may develop because of impaired uptake and aminoglycoside phosphorylation, although enzymatic modification by acetylation of an amino group is considered the most common mechanism. The genes encoding for enzymatic modification of aminoglycosides are often part of class I integrons (30). A variant of aminoglycoside acetyltransferase aac(6’)-Ib , named aac(6’)-Ib-cr are very prevalent among antibiotic resistant E. coli (69). AAC(6’)-Ib-cr has the additional ability to acetylate fluoroquinolones with unprotected amino nitrogen on the piperazine ring that includes norfloxacin and ciprofloxacin.

Trimethoprim-sulfamethoxazole resistance results from alterations of different substrate enzymes or their overproduction, loss of bacterial drug-binding capacity, and decreased cell permeability.

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