The Advent of Resistance to Antibiotics
The improper use of antibiotics has given rise to strains of bacteria which have developed resistance to these antibiotics. When patients are prescribed antibiotics, sometimes they do not complete the full course. Although they feel better, they may not have killed the entire population of bacteria to which the drug used was targeted. These pathogenic micro- organisms can then develop a resistance to the drug or develop the capacity to inactivate antibiotics. Eg penicillin resistance can occur when the bacteria develops an enzyme ( β lactamase) which breaks down the structure of penicillin. Antibiotics taken may also have killed off many of the residential intestinal flora and the ensuing lack of competition can lead to an overgrowth of bacteria with resistance to antibiotics. The resistance itself is a genetic mutation that has been brought about by evolutionary stress i.e exposure to antibiotics. The genes which confer resistance to antibiotics are often located in the plasmids of bacteria , which contain DNA independent of chromosomal DNA, and can be passed on in a number of ways in what is called horizontal gene transfer. Bacterial conjugation occurs when bacteria are in direct contact with one another, and genetic material is transferred between them. Transduction occurs when DNA is carried between bacterium via a virus and transfection is the genetic alteration of a cell, brought about by the uptake of genetic material from a cells surroundings through the cell membrane. Eg pinocytosis. This genetic material can then be expressed during cell replication. Through natural selection, the gene that confers antibiotic resistance becomes more prevalent in the offspring of these bacteria. Micro-organisms that have resistance to one type of antibiotic may also come in contact with bacteria with resistance to another type of antibiotic. When these bacteria share genetic information, they give rise to organisms which are resistant to several types of antibiotics, making them very difficult to treat. This is known as multiple drug resistance, and poses a massive threat to the health of the global community. Incompletion of a course of antibiotics is not the only cause of MDR. Prescription of antibiotics where there is no need, eg kidney infection which should be treated with cranberry juice, and the misdiagnosis of conditions ,eg prescribing antibiotics for a viral infection , also compound the problem.
Pathogenesis of MRSA and Clostridium Difficile
Stapplococcal aureus is a common commensal gram positive bacteria resident on normal skin and in the nasal passages of 30% of people. MRSA is no more virulent than the garden variety of the bacteria but is much more difficult to treat due to its multi-drug resistance. Skin infections occur at the site of trauma such as cuts, abrasions, broken skin or damaged hair follicles and are often localised and manifested by lesions, boils or other red and swollen pustulates. Infection becomes more serious when the organism gets inside the body through surgical wounds, especially invasive surgery involving medical implants or prosthetic joints. Once in the bloodstream, MRSA can causes potentially fatal conditions such as septicaemia and abcesses on internal organs. Strains of MRSA may express a number of potential virulence factors. Surface proteins help the bacteria to adhere to host tissue. Other surface proteins called invasins facillitate the entry of the bacteria into a host cell. Surface factors such as capsules and Protein A inhibit the ability of phagocytotic cells to digest the micro-organism. Toxins produced by the bacteria can lyse eukaryotic cell membranes eg α toxin forms pores in membranes and hemolysin destroys erythrocytes. The infection caused by MRSA is a result of the particular toxins produced by the strain. Enterotoxins A-G cause food poisoning and TSST-1 (toxic shock syndrome toxin-1) can cause...