Bacteria can become resistant to antibiotics when the drugs are used too often or when patients do not take their medication appropriately. A few strong bacteria survive and reproduce, giving rise to new generations of resistant organisms. Doctors have to keep moving through a limited arsenal of antibiotics as more and more types of bacteria learn to outsmart the drugs that were once used to destroy them.
Bacteriologists are currently faced with a relentless increase in the resistance of bacteria to bactericidal drugs, and some of the most difficult epidemics of resistant bacteria arise in hospitals, as so-called iatrogenic diseases. The problem is exacerbated by excessive use of antibiotics. Although antibiotics attack bacteria rather than viruses, there are still many doctors willing to prescribe broad-spectrum antibiotics to patients with ill-defined symptoms that are almost certain viral in origin. The veterinary industry has also contributed by using antibiotics freely on farm animals so that there are low-grade residues in human food.
Soon after penicillin came into use in the 1940s, microbiologists began to find resistant strains emerging as a simple result of selective evolution. In 1967, the first penicillin-resistant forms of Pneumococci, which causes pneumonia, meningitis and middle-ear infections in children, was discovered in Papua New Guinea. Within a decade it began to produce epidemics in South African hospitals and is now a global problem. Pharmaceutical researchers managed to avert a crisis over penicillin resistance by discovering new classes of antibiotics – cephalosporins, tetracyclins, aminoglycosides, and carbapenems. As bacteria became resistant to one drug, doctors could prescribe another. This has become more difficult. Now biotechnologists are working on alternative bacteriocidal drugs, such as natural defensive anti-bacterial peptides produced by living creatures such as frogs, insects, sharks and bacteria themselves. These molecules, which go by various names such as bacteriocins, magainins and cercropins, work in a quite different way to conventional antibiotics. They destroy the cell walls of the bacteria from the outside rather than interfere with their inner chemistry, and so are much more difficult to develop resistance to. However, one limitation with most anti-bacterial peptides is that they are broken down by the digestive system and so cannot be taken by mouth.
Antibiotic resistance is growing worldwide, particularly in the developing world. Recent incidences include the emergence and spread of antibiotic-resistant Salmonella typhi, more virulent strains of Shigella, which causes dysentery, and other infectious epidemic organisms. One strain of E. coli is so virulent that only 10 bacteria can make a human ill. In 1996 the strain infected 8,5000 people in Japan, killing eight, and 400 people in Scotland, killing at least 16.
Even when antibiotic-resistant infections are not deadly, they are costly to treat and debilitating to patients. Doctors now must often treat patients with a series of antibiotics before finding one that is effective.
More than 90% of strains of Staphyloccous aureus bacteria, a common cause of hospital "staph" infections, are now resistant to penicillin. and some to other antibiotics, e.g. methicillin-resistant Staphylococcus aureus (MRSA). More than 30% are resistant to all antibiotics except vancomycin. In 1998 in New York, a man in his 70's died after being infected by vancomycin-resistant "staph" (VRS, still rare). Vancomycin-resistant enterococcus (VRE) also causes intractable wound infections.
The ulcer-causing bacterium Helicobacter pylori is increasingly resistant to two of the antibiotics commonly used to treat it in the USA. In 2001, it was reported that resistance to metronidazole occurred in 35% of patients and resistance to clarithromycin occurred in about 11% of cases. Women and younger patients were more likely to be resistant to the antibiotics. Resistance was found in 50% of those over 20 years but in only 31% of those 71 years and older. The researchers suggest that higher resistance among women may be related to the use of metronidazole for gynaecologic infections.
A strain of the bacterium Salmonella enterica – a frequent culprit in post-picnic cases of diarrhoea – has acquired resistance to fluoroquinolones, a class of antibiotics commonly used against it. The newly strengthened bug was discovered when researchers investigated an outbreak of salmonella infection in two Oregon nursing homes that persisted for two years. The discovery is troubling for two reasons, said Dr. Fred Angulo, a medical epidemiologist with the CDC. First, salmonella has not caused an outbreak in a health care institution since the 1960s; better infection-control procedures had kept the bacterium at bay, but its freshly acquired resistance allowed it to evade these precautions. Second, the bug in this outbreak has been traced to a hospital in the Philippines where one Oregon patient was treated for a stroke before being returned to the United States. The same resistant bug had been seen in this country only once before, in 1994, in a New York resident who had also visited the Philippines. In other words, one hospital halfway around the world caused two drug-resistant infections, several years apart, on opposite U.S. coasts.