Mechanisms of antibiotic resistance

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Mechanisms of antibiotic resistance

block exam 1.5.

block exam 1.5.

Anatomy of the pharynx and esophagus
Anatomy of the oral cavity
Anatomy of the salivary glands
Anatomy of the tongue
Abdominal quadrants, regions and planes
Anatomy of the abdominal viscera: Esophagus and stomach
Anatomy of the abdominal viscera: Small intestine
Anatomy of the abdominal viscera: Pancreas and spleen
Anatomy of the abdominal viscera: Large intestine
Anatomy of the abdominal viscera: Liver, biliary ducts and gallbladder
Anatomy of the anterolateral abdominal wall
Gallbladder histology
Esophagus histology
Stomach histology
Small intestine histology
Colon histology
Liver histology
Pancreas histology
Thymus histology
Spleen histology
Lymph node histology
Introduction to the immune system
Cytokines
Innate immune system
Complement system
T-cell development
B-cell development
MHC class I and MHC class II molecules
T-cell activation
B-cell activation and differentiation
Cell-mediated immunity of CD4 cells
Cell-mediated immunity of natural killer and CD8 cells
VDJ rearrangement
B- and T-cell memory
Antibody classes
Selective immunoglobulin A deficiency
Complement deficiency
Bacterial structure and functions
Bacillus cereus (Food poisoning)
Escherichia coli
Salmonella (non-typhoidal)
Vibrio cholerae (Cholera)
Campylobacter jejuni
Helicobacter pylori
Viral structure and functions
Hepatitis B and Hepatitis D virus
Hepatitis A and Hepatitis E virus
Hepatitis C virus
Norovirus
Rotavirus
Giardia lamblia
Mechanisms of antibiotic resistance
Cell wall synthesis inhibitors: Penicillins
Miscellaneous cell wall synthesis inhibitors
Inflammation
Contracting the immune response and peripheral tolerance
Prebiotics and probiotics
Hepatitis
Diarrhea: Clinical

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The discovery of antibiotics is one of the most important advancements in clinical medicine and public health. It has laid the foundation for a number of other advancements including the ability to perform surgeries more safely and reduction of infant and maternal mortality rates.

Many antibiotics are derived from other bacteria or fungi. For example, penicillin, secreted by the fungus Penicillium, can kill bacteria.

This is because microbes use antibiotics to fight off other microbes. But the use of antibiotics, and, more broadly, antimicrobials, which includes medications that target not only bacteria, but also viruses and fungi, has exploded in recent years.

Antimicrobials have been used on an industrial scale, partially because of overprescription in humans, but more so because of routine use in farm animals!

In fact, a good number of antimicrobials are excreted from humans and animals unchanged, and these get flushed into waste water, which allows pathogens to be perpetually exposed to antimicrobials. In response to this enormous selective pressure, many pathogens have become highly resistant to antimicrobials.

Now when it comes to bacteria, generally speaking, there are four mechanisms for how they become resistant to antimicrobials.

The first mechanism is antibiotic inactivation or modification, which is where bacteria develop specific enzymes that destroy and inactivate antimicrobials.

One example is beta lactamase, which is a bacterial enzyme that destroys antimicrobials that contain a beta lactam ring, like penicillins and cephalosporins. As a result, bacteria that produce beta lactamases are immune to the action of many beta lactam antibiotics.

The second mechanism is the alteration of a target, or binding site. An antibiotic that cannot bind anywhere is rendered useless.

Summary

The mechanisms of antibiotic resistance can be broadly classified into four categories. First, there is enzymatic modification of the antibiotic includes beta-lactamases, which cleave the beta-lactam ring in penicillins and cephalosporins, and other (e.g. AmpC) enzymes, which hydrolyze most beta-lactams except.

The second mechanism of antibiotic resistance is alteration of the target site on the bacterial cell wall. This involves the production of altered penicillin-binding proteins (PBP), which decrease the affinity of the antibiotic for its target.

Third, bacteria may use efflux pumps, which prevent a variety of antibiotics from accumulating in the bacteria cell, by pumping them out of the bacterial cell. Finally, since some antibiotics (e.g. sulfonamides) work by inhibiting the synthesis of molecules that are vital to the bacteria survival like folic acid, bacteria may just stop producing these molecules, and scavenge for folic acid from the environment instead.