Resistant strains of bacteria are continuing to increase, both in number and variety, but no significantly different new antibiotics are yet available. The main research efforts at present are directed to looking at variants on the molecular structure of existing antibiotics, rather than to substances which act in a fundamentally different way. The WHO is extremely alarmed by this situation and have stated that 'the time for complacency is over'. The fear is that, within quite a short time span, we shall no longer be able to rely on antibiotics. The worst case scenario is a return to the 1930s when infections which we presently regard as trivial, were dealt with by surgery, including amputation.
Background
A hopeful development has recently been reported from researchers in Glasgow, who have discovered that the venom of certain tropical frogs contains substances which are active against some strains of drug-resistant bacteria. The hope is that these molecules may provide a starting point for a whole new series of antibiotics, possible alternative to antibiotics concerns the use of bacteriophages, which infect and destroy specific bacteria. In the Republic of Georgia, for example, it appears that 'phages' are being routinely prescribed and that they are effective. The phages, each specific to a particular bacterium, are in the first place isolated from sewage water.
It is important that students appreciate that antibiotics do not directly bring about mutation; rather, they provide an environment favouring the natural selection of resistant strains which arise spontaneously. In the absence of competition, resistant strains rapidly become predominant, the resistance genes being passed on to daughter cells during reproduction. The genes conferring antibiotic resistance are located on the bacterial chromosome, and on plasmids. An ability to produce an enzyme which breaks down the antibiotic is one of several different ways in which bacteria become resistant.
Background
Other mechanisms underlying development of resistance include preventing the entrance of antibiotics, causing them to be pumped out if they do enter, and interfering with their ability to bind with their target site.
A particularly worrying development is the emergence of pathogens which combine resistance to a variety of different antibiotics, the multi drug-resistant bacteria.
Background
Multi antibiotic-resistance happens because small lengths of DNA, called transposons which may carry a variety of antibiotic resistance genes, can move from the bacterial chromosome to plasmid or virus DNA which can be freely exchanged between bacteria. The rapid rise in the number of these multi antibiotic- resistant strains has been encouraged by the widespread, indiscriminate and sometimes totally inappropriate use of antibiotics, both medically and in farming.
Antibiotics are given to livestock as a matter of routine, to protect the animals from infection or to treat infection. They also increase their growth rate (live weight gain) by limiting the gut microbial populations which would otherwise utilise some of the food given to the animal. This practice has resulted in the selection of resistant bacteria in these animals. Harmless gut bacteria have become reservoirs for multi resistance plasmids. These bacteria may be able to colonise other organisms, including humans and the plasmids may be transferable to pathogenic bacteria found in humans, making treatment with particular antibiotics ineffective.
Examples of multi antibiotic-resistance are provided by the MRSA strains of Staphylococcus aureus. This organism occurs commonly on the skin and , especially, in the nostrils, where it often does little or no harm. If it invades the body however, it can cause potentially lethal conditions such as septicaemia, meningitis and osteomyelitis. MRSA stands for methicillin resistant Staphylococcus aureus, methicillin being an antibiotic developed in the late 1950s which was effective in killing Staphylococcus aureus, the organism by that time having already become resistant to penicillin G and to almost every other available antibiotic. In the case of strain MRSA 16, only one effective antibiotic, vancomycin, remains, and this has serious side effects on humans. Staphylococcus aureus is easily transferred from the skin of one hospital patient to another and it can be fatal if it enters the bloodstream, or the site of a surgical operation. Resistant strains are controlled with great difficulty and, in many hospitals, incoming patients are screened, and those carrying the bacterium on their skin are isolated. Hospitals maintain stocks of vancomycin in case of need for this 'drug of last resort'.
One strain of Enterococcus is totally resistant to all antibiotics. Although this has a relatively low virulence, except in the frail or elderly, transfer of its resistance genes Staphylococcus aureus has been achieved in the laboratory and so could conceivably occur in nature. Indeed, in 1997, a strain of MRSA resistant even to vancomycin was reported from Japan; this is a very worrying development.
Resistance is also appearing amongst Mycobacterium tuberculosis. At one time around 10 antibiotics were effective against this organism but now, doctors are sometimes down to the last 2 or 3 in their armoury.