The antibiotic susceptibility of Escherichia coli has changed significantly from 1970 to the present day, primarily due to the emergence of antibiotic resistance. Over the past few decades, antibiotic resistance in E. coli has increased dramatically, posing challenges for treatment and leading to more complex and serious infections.

Oral Antibiotics (Per Os) for E. coli UTIs :

• Ampicillin
• Amoxicillin/clavulanate
• Cefuroxime
• Trimethoprim/sulfamethoxazole
• Ciprofloxacin
• Fosfomycin
• Nitrofurantoin

Parenteral Antibiotics (IV or IM) for E. coli infections:

• Cefoxitin
• Cefotaxime
• Gentamicin
• Meropenem
• Amikacin
• Piperacillin/tazobactam
• Tigecycline

Here’s a comparison of antibiotic susceptibility in E. coli between the 1970s and today:

1970s Antibiotic Susceptibility in E. coli

General Susceptibility: In the 1970s, E. coli was generally susceptible to a wide range of antibiotics, including commonly used classes like penicillins, cephalosporins, and aminoglycosides.

Penicillins: Although many strains of E. coli were susceptible to penicillins (e.g., ampicillin, amoxicillin), some strains carried the β-lactamase enzyme, which provided resistance to this class of antibiotics. However, resistance was still relatively uncommon at this time.
Cephalosporins: E. coli strains were typically susceptible to first-generation cephalosporins (e.g., cephalexin, cefazolin), which were commonly used for treating UTIs.
Aminoglycosides: Drugs like gentamicin and amikacin, used for severe infections, were generally effective against E. coli.
Sulfonamides and Trimethoprim: These were commonly used for treating UTIs caused by E. coli, and resistance to these drugs was relatively low at the time.

In summary, during the 1970s, E. coli infections could generally be treated with a wide range of antibiotics, and antibiotic resistance was much less common.

Current Antibiotic Susceptibility in E. coli (2020s)

Over the past few decades, the antibiotic susceptibility profile of E. coli has undergone significant changes due to antibiotic misuse, overuse, and selective pressure. Resistance has emerged in many antibiotics that were once highly effective, and this has complicated the treatment of infections.

Key Changes:

• Increased Resistance to β-lactam Antibiotics (Penicillins and Cephalosporins):
  Extended-Spectrum β-Lactamases (ESBLs): In recent years, a major mechanism of resistance in E. coli is the production of ESBLs, enzymes that can break down extended-spectrum cephalosporins (like ceftriaxone or cefotaxime) and penicillins (piperacillin/tazobactam). This has led to the increased resistance of E. coli to penicillins and third-generation cephalosporins.
• Carbapenem Resistance: In some cases, E. coli has developed resistance to carbapenems (e.g., imipenem and meropenem), which are considered last-line treatments for multi-drug-resistant infections. The presence of carbapenem-resistant E. coli (CRE) is now a significant global health threat.
• Fluoroquinolone Resistance: Fluoroquinolones (e.g., ciprofloxacin and levofloxacin) were once highly effective for treating E. coli infections, including UTIs. However, over the years, there has been a significant rise in fluoroquinolone resistance due to mutations in target enzymes like DNA gyrase and topoisomerase IV. This resistance is particularly concerning because fluoroquinolones are often used to treat UTIs caused by resistant strains of E. coli.
• Trimethoprim-Sulfamethoxazole Resistance: Trimethoprim-sulfamethoxazole (TMP-SMX), a combination antibiotic commonly used for UTIs, has also faced growing resistance in E. coli. The resistance can occur through mutations in the enzymes targeted by the drugs, making this combination less effective in some regions.
• Aminoglycoside Resistance: Aminoglycosides (e.g., gentamicin, amikacin and tobramycin) are still effective against E. coli in many cases, but resistance has been increasing due to modification enzymes that inactivate the antibiotic.
• Increased Multidrug Resistance (MDR): Many modern E. coli strains are multidrug-resistant (MDR), meaning they are resistant to several classes of antibiotics. This can make treating infections more difficult and may require the use of more toxic or less effective drugs.
• Rise of Colistin Resistance: Colistin was often used as a last-line antibiotic for multidrug-resistant infections, including those caused by E. coli. However, colistin resistance has emerged in some regions, which complicates treatment options further. Resistance mechanisms, such as mcr-1 gene for colistin resistance, have been found in E. coli.