Antibiotic resistance is the ability of a microorganism to withstand the effects of an antibiotic.
The resistance has come about through gene action or plasmid exchange between bacteria of the same species. If a bacterium carries several resistance genes, it is called multiresistant or, informally, a superbug.
Essentially this process is natural selection in action. The antibiotic action is an environmental pressure, those bacteria which have a mutation allowing them to survive will live on to reproduce. They will then pass this trait to their offspring, which will be a fully resistant generation.
Several studies have demonstrated that patterns of antibiotic usage greatly affect the number of resistant organisms which develop. Overuse of broadspectrum antibiotics, such as second and third generation cephalosporins, greatly hastens the development of methicillin resistance, even in organisms that have never been exposed to the selective pressure of methicillin per se. Other factors contributing towards resistance include incorrect diagnosis, unnecessary prescriptions, improper use of antibiotics by patients, and the use of antibiotics as livestock food additives for growth promotion.
Staphylococcus aureus (Staph aureus) is one of the major resistant pathogens. Found on the mucous membranes and the skin of around a third of the population it is extremely adaptable to antibiotic pressure. It was the first bacterium in which penicillin resistance was found, in 1947 just four years after the drug started being mass-produced. Methicillin was then the antibiotic of choice. MRSA (methicillin-resistant Staphylococcus aureus) was first detected in Britain in 1961 and is now "quite common" in hospitals. Responsible for 37% of fatal cases of blood poisoning in the UK in 1999, up from 4% in 1991. Half of all S. aureus infections in the US are resistant to penicillin, methicillin, tetracycline and erythromycin.
This left vancomycin as the only effective agent available at the time. A new class of antibiotics, oxazolidinones, became available in the 1990s, and the first commercially available oxazolidinone, linezolid, is comparable to vancomycin in effectiveness against MRSA. However, VRSA (Vancomycin Resistant Staphylococcus Aureus) was first identified in Japan in 1997 and has since been found in hospitals in England, France and the US.
VRSA is also termed GISA (glycopeptide intermediate staphylococcus aureus) or VISA (Vancomycin intermediate staphylococcus aureus), indicating resistance to all glycopeptide antibiotics.
Enterococcus faecium is another superbug found in hospitals, penicillin resistance was seen in 1983, vancomycin resistance (VRE) in 1987 and linezolid resistance (LRE) in the late 1990s.
Penicillin-resistant pneumonia (or pneumococcus, caused by Streptococcus pneumoniae) was first detected in 1967 as was penicillin-resistant gonorrhea. Resistance to penicillin substitutes is also known beyond staph aureus. By 1993 Escherichia coli was resistant to five fluoroquinolones variants. Mycobacterium tuberculosis is commonly resistant to isoniazid and rifampin and sometimes universally resistant to the common treatments. Other strains offering some resistance include Salmonella, Campylobacteria, and Streptococci.
Vaccines do not suffer this problem. This is because a vaccine enhances the body's natural defenses. An antibiotic operates in place of the body's normal defenses. However, while theoretically promising, actual antistaphylococcal vaccines have shown limited efficacy, because of immunological variation between staphylococcus species, and the limited duration of effectiveness of the antibodies produced. Development and testing of more effective vaccines is underway.
See also: tuberculosisVaccines are Better
