Chloramphenicol Cause Damage To The Human Body

found that both the drug and the bacteria use enzymes as their defense and attack

The misuse and overdose of the antibiotics increase the resistance problem. It can cause these bacteria to

Antibiotics target specific structure or process of the cell. Such as, inhibition of cell wall synthesis, Inhibition of protein synthesis, Injury to plasma membrane, & Inhibition of nucleic acid synthesis. These drugs include, such as B lactam drugs that are bactericidal & kill bacteria by interfering with the synthesis of the cell wall, Polymyxin B drugs that injures the plasma membrane allowing the cell to burst. Tetracycline & Chloramphenicol that are bacteriostatic drugs, and inhibits protein synthesis. Fluoroquinolones & Rifamycin that are bactericidal drugs & interfere with the synthesis of nucleic acid. The pathogens can develop resistance against these drugs that are used to treat them. Resistance to antibiotics can be acquired by mutation

This is injected straight directly into the veins. Medicines are rapidly absorbed into the body. This can only be performed by a doctor or trained nurse.

These mutations, no matter what process that has led to their occurrence, block the action of antibiotics by interfering with their mechanism of action (1). Currently, antibiotics attack bacteria through one of two mechanisms. In both mechanisms the antibiotic enters the microbe and interferes with production of the components needed to form new bacterial cells. Some antibiotics act on the cell membrane, causing increased permeability and leakage of cell contents. Other antibiotics interfere with protein synthesis in cells. They block one or more of the steps involved in the transformation of nucleic acids into proteins.

Many antibiotics work by attaching themselves to their target and preventing it from interacting with other molecules inside the cell. In this case resistance comes from when the protein mutates and therefore changes arrangement of the protein. This means that the protein the antibiotic is attempting to counteract is either no longer there or has changed in structure. Therefore, the antibiotic can no longer bind to the protein as it can no longer recognise it. This means the antibiotic cannot carry out its function and so is ineffective.

In most cases the reactions are mild and if they do occur then first-hand you should consult the medicine box/bottle/DOMAR where it will state any possible side effects on the leaflet or possibly on the main label ir you see on some pain medication ‘’Caution-May make sleepy do not operate heavy machinery’’ etc.

This is because antibiotics work differently to destroy an essential function of bacteria. From a biochemical or physical perspective, there are 3 main factors that contribute to the resistance. The first factor is that bacterium will alter its cell wall so that the antibiotic cannot penetrate it. Another factor includes bacteria producing enzymes that can break down the antibiotics before they can work. The third factor is that certain bacteria have developed mechanisms known as efflux pumps, which are able to generate antibiotics from the bacterial cell before they have a chance to exert any effect. The last effect is when the bacteria's antibiotic target site is altered which causes the antibiotic to be unable to bind itself to it, which is essential for the antibiotic to have an effect on the bacteria. The genetics of bacteria also play a large role in antibiotic resistance. Bacteria, like other living organisms, possess DNA that codes for the proteins and enzymes it requires for survival. Changes to the DNA can result in alterations in the final proteins or enzymes, which in turn can lead to antibiotic resistance. An example is the acquisition and accumulation of resistance genes from bacteria

This is given through a vein (intravenously). This medicine decreases the risk of damage to the heart.

Antibiotics are developed for the treatment of bacterial infections due to their effective clinical properties (Appendix Fig. 2). They are extensively utilized for the inhibition of bacterial; DNA, RNA, proteins and cell wall synthesis (reference). However, the efficiency of treating bacterial infections has vastly deteriorated because of the ongoing emergence of multi-drug resistant pathogens (Appendix Fig. 3 & Table 1-8) (reference). The prolonged use and misuse of antibiotics have resulted in the evolution of bacteria attaining mechanisms which, prevent antibiotics from binding to their molecular targets (Appendix Fig. 4) (reference).

One big factor in the resistance bacteria show towards antibiotics is antibiotic concentration. Usually, if large amounts of an antibiotic are attacking a bacteria it will stop the multiplication process and even kill it off, but if there is small amounts of antibiotic it will allow the bacteria to continue to spread. You can find many bacteria in a jelly-like biofilm which provides a shield to them.

The protein-synthesizing machinery in mitochondria and chloroplasts resemble prokaryotes. This is shown through their ribosomal RNA and the structure of the ribosomes. The ribosomes are similar in size and structure to bacterial ribosomes. fMat is always the first amino acid that is in the mitochondria and chloroplasts transcripts. The antibiotics that act by blocking protein synthesis in bacteria also block protein synthesis in mitochondria and chloroplasts. These antibiotics do not interfere with protein synthesis in the cytoplasm of the eukaryotes. The inhibitors that effect the protein synthesis of eukaryotic ribosomes do not change the protein synthesis of the bacteria, mitochondria, or chloroplasts.

Applications outside the intestine are called parenteral. One form is an injection, which can be subcutaneous (under the skin), intramuscular (into a muscle), or intravenous (into a vein). Parenteral administration of an antibiotic is used when a physician requires a strong, quick concentration of the antibiotic in the bloodstream. Manufacture.

Although the antibiotic may cure or prevent some infections, bacteria can transform, causing a new line of bacteria to form which can become resistant to the current antibiotics. The authors also take into consideration the delivery system of the drug. They have their own input on how the delivery should be and what previous procedures are lacking.

The widely used growth promoters are Antibiotics. It can be defined as any medicines that destroy or inhibit bacterial growth and are administered at a low sub-therapeutic dosage (Hughes and Heritage, 2004).