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Antibiotics disrupt vital processes that bacteria need to survive, such as cell wall synthesis, DNA replication, folic acid synthesis, and protein synthesis.
Bacteria can become resistant through several pathways, including genetic mutations, gene transfer (conjugation, transformation, transduction), and natural selection favoring resistant strains.
Finishing prescribed antibiotics is crucial to ensure that all bacteria are eliminated, preventing the survival of resistant strains and reducing the risk of developing superbugs.
Beta-lactams, such as penicillins, target the bacterial cell wall, disrupting its synthesis and leading to cell lysis.
Gram-negative bacteria have an outer membrane that blocks the entry of certain antibiotics, making them inherently more resistant to many drugs.
The zone of inhibition is the clear area around an antibiotic disk where bacteria cannot grow, indicating the effectiveness of the antibiotic against the tested bacteria.
Sulfonamides inhibit folic acid synthesis in bacteria, which is essential for DNA and RNA synthesis, ultimately hindering bacterial growth.
The three main methods of gene transfer in bacteria are conjugation (DNA transfer via pili), transformation (uptake of free DNA), and transduction (DNA transfer by bacteriophages).
Broad-spectrum antibiotics target a wide range of bacteria, making them useful for treating infections when the specific pathogen is unknown, but they can also disrupt normal flora and promote resistance.
The use of antibiotics in livestock feed can contribute to the development of antibiotic-resistant bacteria, which can be transmitted to humans through the food supply.
Tetracyclines inhibit protein synthesis by binding to bacterial ribosomes, preventing the translation of mRNA into proteins necessary for bacterial growth and reproduction.
Gram-positive bacteria have a thick peptidoglycan cell wall, while Gram-negative bacteria have a thin wall and an outer membrane, affecting their susceptibility to antibiotics.
Overprescribing antibiotics can lead to increased antibiotic resistance, making infections harder to treat and resulting in longer illness durations and higher healthcare costs.
Bacterial mating, or conjugation, allows for the direct transfer of resistance genes between bacteria, facilitating the spread of resistance traits within bacterial populations.
Control disks are used in antibiotic susceptibility testing to establish a baseline for normal bacterial growth without antibiotics, allowing for comparison with antibiotic-treated samples.
Antibiotics target specific bacterial processes and structures that viruses do not possess, such as cell walls and ribosomes, making them ineffective against viral infections.
Not completing an antibiotic course can allow surviving bacteria to develop resistance, leading to treatment failure and the potential for more severe infections.
Fluoroquinolones inhibit bacterial DNA replication enzymes, preventing the synthesis of DNA and ultimately leading to bacterial cell death.
Genetic variation can result in some bacteria having natural resistance mechanisms, allowing them to survive antibiotic treatment and reproduce, thereby spreading resistance.
Sharing leftover antibiotics can lead to inappropriate use, increasing the risk of resistance development and reducing the effectiveness of antibiotics for future infections.