Figure 23–32 Model for the evolution of pandemic strains of influenza virus by recombination. Influenza A virus is a natural pathogen of birds, particularly waterfowl, and it is always present in wild bird populations. In 1918, a particularly virulent form of the virus crossed the species barrier from birds to humans and caused a devastating worldwide epidemic. This strain was designated H1N1, referring to the specific forms of its main antigens, hemagglutinin (H) and neuraminidase (N). Changes in the virus, rendering it less virulent, and the rise of adaptive immunity in the human population, prevented the pandemic from continuing in subsequent seasons, although H1N1 influenza strains continued to cause serious disease every year in very young and very old people. In 1957, a new pandemic arose when three genes were replaced by equivalent genes from an avian virus (green bars); the new strain (designated H2N2) was not effectively cleared by antibodies in people who had previously contracted only H1N1 forms of influenza. In 1968, another pandemic was triggered when two genes were replaced from another avian virus; the new virus was designated H3N2. In 1977, there was a resurgence of H1N1 influenza, which had previously been almost completely replaced by the N2 strains. Molecular sequence information suggests that this minor pandemic may have been caused by an accidental release of an influenza strain that had been held in a laboratory since about 1950. In 2009, a new H1N1 swine virus emerged that had derived five genes from pig influenza viruses, two from avian influenza viruses, and one from a human influenza virus. As indicated, most human influenza today is caused by H1N1 and H3N2 strains.
protein synthesis,penicillins 30S ribosome inhibitors protein synthesis,sulfonamides presence of vancomycin, shut down the normal pathway for bacterial cell wall synthesis, and produce a different type of cell wall.
Drug-resistance genes acquired by horizontal transfer frequently come from environmental microbial reservoirs. Nearly all antibiotics used to treat bacterial infections today are based on natural products produced by fungi or bacteria. Penicillin, for example, is made by the mold Penicillium, and more than 50% of the antibiotics currently used in the clinic are made by Gram-positive bacteria of the genus Streptomyces, which reside in the soil. It is believed that microorganisms produce antimicrobial compounds, many of which have probably existed on Earth for hundreds of millions of years, as weapons in their competition with other microorganisms in the environment. Surveys of bacteria taken from soil samples that have never been exposed to antibiotic drugs used in modern medicine reveal that the bacteria are typically already resistant to about seven or eight of the antibiotics widely used in clinical practice. When pathogenic microorganisms are faced with the selective pressure provided by antibiotic treatments, they can apparently draw upon this immense source of genetic material to acquire resistance.
Like most other aspects of infectious disease, human behavior has exacerbated the problem of drug resistance. Many patients take antibiotics for symptoms that are typically caused by viruses (flu-like illnesses, colds, sore throats, and earaches) and these drugs have no effects. Persistent and chronic misuse of antibiotics can eventually result in antibiotic-resistant normal flora, which can then transfer the resistance to pathogens. Antibiotics are also misused in agriculture, where they are commonly employed as food additives to promote the growth and health of farm animals. An antibiotic closely related to vancomycin was commonly added to cattle feed in Europe; the resulting resistance in the normal flora of these animals is widely believed to be one of the original sources for vancomycin-resistant bacteria that now threaten the lives of hospitalized patients.