Bacteria and archaebacteria, the most abundant single-celled organisms, are commonly 1-2 ^m in size. Despite their small size and simple architecture, they are remarkable biochemical factories, converting simple chemicals into complex biological molecules. Bacteria are critical to the earth's ecology, but some cause major diseases: bubonic plague (Black Death) from Yersinia pestis, strep throat from Streptomyces, tuberculosis from Mycobacterium tuberculosis, anthrax from Bacillus anthracis, cholera from Vibrio cholerae, food poisoning from certain types of E. coli and Salmonella.
Humans are walking repositories of bacteria, as are all plants and animals. We provide food and shelter for a staggering number of "bugs," with the greatest concentration in our intestines. Bacteria help us digest our food and in turn are able to reproduce. A common gut bacterium, E. coli is also a favorite experimental organism. In response to signals from bacteria such as E. coli, the intestinal cells form appropriate shapes to provide a niche where bacteria can live, thus facilitating proper digestion by the combined efforts of the bacterial and the intestinal cells. Conversely, exposure to intestinal cells changes the properties of the bacteria so that they participate more effectively in digestion. Such communication and response is a common feature of cells.
The normal, peaceful mutualism of humans and bacteria is sometimes violated by one or both parties. When bacteria begin to grow where they are dangerous to us (e.g., in the bloodstream or in a wound), the cells of our immune system fight back, neutralizing or devouring the intruders. Powerful antibiotic medicines, which selectively poison prokaryotic cells, provide rapid assistance to our relatively slow-developing immune response. Understanding the molecular biology of bacterial cells leads to an understanding of how bacteria are normally poisoned by antibiotics, how they become resistant to antibiotics, and what processes or structures present in bacterial but not human cells might be usefully targeted by new drugs.
▲ FIGURE 1-4 Plasmodium organisms, the parasites that cause malaria, are single-celled protozoans with a remarkable life cycle. Many Plasmodium species are known, and they can infect a variety of animals, cycling between insect and vertebrate hosts. The four species that cause malaria in humans undergo several dramatic transformations within their human and mosquito hosts. (a) Diagram of the life cycle. Sporozoites enter a human host when an infected Anopheles mosquito bites a person 1. They migrate to the liver where they develop into merozoites, which are released into the blood 2|. Merozoites differ substantially from sporozoites, so this transformation is a metamorphosis (Greek, "to transform" or "many shapes"). Circulating merozoites invade red blood cells (RBCs) and reproduce within them 3. Proteins produced by some Plasmodium species move to the surface of infected RBCs, causing the cells to adhere to the walls of blood vessels. This prevents infected RBCs cells from circulating to the spleen where cells of the immune system would destroy the RBCs and the Plasmodium organisms they harbor. After growing and reproducing in RBCs for a period of time characteristic of each Plasmodium species, the merozoites suddenly burst forth in synchrony from large numbers of infected cells 4|. It is this event that brings on the fevers and shaking chills that are the well-known symptoms of malaria. Some of the released merozoites infect additional RBCs, creating a cycle of production and infection. Eventually, some merozoites develop into male and female gametocytes 5, another metamorphosis. These cells, which contain half the usual number of chromosomes, cannot survive for long unless they are transferred in blood to an Anopheles mosquito. In the mosquito's stomach, the gametocytes are transformed into sperm or eggs (gametes), yet another metamorphosis marked by development of long hairlike flagella on the sperm 6. Fusion of sperm and eggs generates zygotes 7|, which implant into the cells of the stomach wall and grow into oocysts, essentially factories for producing sporozoites. Rupture of an oocyst releases thousands of sporozoites 8; these migrate to the salivary glands, setting the stage for infection of another human host. (b) Scanning electron micrograph of mature oocysts and emerging sporozoites. Oocysts abut the external surface of stomach wall cells and are encased within a membrane that protects them from the host immune system. [Part (b) courtesy of R. E. Sinden.]
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