Antibiotic resistance

When the early antibiotics such as penicillin and streptomycin went into use, individual general and species of bacteria tended either to be susceptible to them. As antibiotics have been widely used, broadening the definition to include antiprotozoal, antifungal and antiviral drugs, organisms once exquisitely sensitive to specific drugs are no longer effective. In some cases, there may be partial resistance, so extremely high dosage levels, usually parenteral, may work, but in such cases, it is probably a matter of time until fully resistant forms emerge.

Development of resistance

At the microbial level, this may be due either to the antibiotic therapy allowing the survival of naturally resistant organisms of the species, or of the transfer of resistance genetic factors among bacteria. It is not, as once thought, a matter of natural selection, where a few organisms within a species randomly mutate, become resistant, and thus better equipped for survival.

Other mechanisms, not yet fully understood in the ecology, include the transfer of resistance genes among totally different species

Human activities promoting antibiotic resistance=

A number of organisms have developed resistance to antibiotics resistant to them. Assorted human actions cause much of the development of resistance, with reasons ranging to overprescribing antibiotics in situations where they are unlikely to help, to patients stopping therapy when they feel better but still have an active bacterial infection, to the use of antibiotics as agricultural growth stimulants.

Treating resistant forms

When a form was found resistant, especially if the mechanism of resistance was known, a variant of the same class of antibiotics might be useful.

Bacterial resistance to the penicillins

For example, the earliest example of bacterial resistance to penicillins was bacterial production of an enzyme called penicillinase, or, more precisely, penicillin beta-lactamase, which breaks a chemical bond in the key lactam structure of penicillin molecules.

Among the first responses were the synthesis of penicillins, such as methicillin, which protected this bond. In time, however, methicillin did not work on some bacteria, beginning with Staphylococcus aureus. Since S. aureus is an important pathogen, common in wound infection but also appearing in systemic disease. methicillin-resistant staphylococcus aureus ('MRSA) became a matter of close surveillance by infectious disease specialists.

In serious infections with MRSA, the "last resort" tended to be vancomycin. Since vancomycin, for systemic infections, must be administered intravenously, it was relatively easy to restrict it to controlled hospital use, only for specific strains. Eventually, vancomycin resistance was seen among staphylococci; acquired resistance was first oberved in Enterococci.