Figure 23–12 acquisition of a viral envelope. (A) Electron micrograph of an animal cell from which six copies of an enveloped virus (Semliki forest virus) are budding. (B) Schematic drawing of the envelope assembly and budding processes. The lipid bilayer that surrounds the viral capsid is derived directly from the plasma membrane of the host cell. In contrast, the proteins in this lipid bilayer (shown in green) are encoded by the viral genome. (A, courtesy of M. Olsen and
G. Griffith.)
Figure 23–13 effective control of a viral disease through vaccination. The graph shows the number of cases of poliomyelitis reported per year in the United States. The arrows indicate the timing of the introduction of the Salk vaccine (inactivated virus given by injection) and the Sabin vaccine (live attenuated virus given orally).
The mechanisms through which pathogens cause disease are as diverse as the pathogens themselves. Nonetheless, all pathogens must carry out certain common tasks: they must gain access to the host, reach an appropriate niche, avoid host defenses, replicate, and exit from the infected host to spread to an uninfected one. In this section, we examine the common strategies that many pathogens use to accomplish these tasks.
Pathogens Overcome Epithelial Barriers to Infect the Host
The first step in infection is for the pathogen to gain access to the host. A thick covering of skin protects most parts of the human body from the environment. The protective boundaries of some other human tissues (eyes, nasal passages, respiratory tract, mouth, digestive tract, urinary tract, and female genital tract) are less robust. In the lungs and small intestine, for example, the barrier is just a single monolayer of epithelial cells. Nonetheless, all these epithelia serve as barriers to infection.
Wounds in barrier epithelia allow pathogens direct access to unoccupied niches within otherwise sterile host tissues. This avenue of entry requires little in the way of pathogen specialization, and many members of the normal flora can cause serious illness if they enter through such wounds. Staphylococci from the skin and nose, or Streptococci from the throat and mouth, are two examples of opportunistic bacterial pathogens that are responsible for many serious infections resulting from breaches in epithelial barriers. The recent emergence of bacterial strains of Staphylococcus that are resistant to the antibiotics commonly used for treatment (for example, methicillin-resistant Staphylococcus aureus, or MRSA, which infects up to 50,000,000 people worldwide) is of particular concern. Papillomaviruses, which cause warts and cervical cancer, also take advantage of breaches in epithelial barriers.
Primary pathogens, however, need not wait for a wound to gain access to their host. One efficient way for such a pathogen to cross the skin is to catch a ride in the saliva of a biting arthropod. A diverse group of bacteria, viruses, and protozoa has developed the ability to survive in insects and then use them as vectors to spread from one mammalian host to another. As discussed earlier, the Plasmodium protozoan that causes malaria develops through several forms in its life cycle, including some that are specialized for survival in a human and others that are specialized for survival in a mosquito (see Figure 23–9). Viruses that are spread by insect bites cause yellow fever and Dengue fever, as well as many kinds of viral encephalitis (inflammation of the brain). These viruses replicate in both insect cells and mammalian cells, as required for their transmission by an insect vector.