Chapter 1 Infection

We do not know whether infectious bioterrorism will

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exposed or immunized and are thus vulnerable to its reintroduction. We do not know whether infectious bioterrorism will work on the scale contemplated by its perpetrators, but in the case of anthrax we do know that sophisticated systems have been designed to attempt it. We hope never to learn whether bioterrorism will work on a large scale. Pathogenesis Once a potential pathogen reaches its host, features of the organism determine whether or not disease ensues. The primary reason why pathogens are so few in relation to the microbial world is that being a successful pathogen is very complicated. Multiple features, called virulence factors, are required to persist, cause disease, and escape to repeat the cycle. The variations are many, but the mechanisms used by many pathogens are now being dissected at the molecular level. The first step for any pathogen is to attach and persist at whatever site it gains access. This usually involves specialized surface molecules or structures that correspond to receptors on human cells. Because human cells were not designed to receive the microorganisms, the pathogens are usually exploiting some molecule important for essential functions of the cell. For some toxin-producing pathogens, this attachment is all they need to produce disease. For most pathogens, it just allows them to persist long enough to proceed to the next stage—invasion into or beyond the mucosal cells. For viruses, invasion of cells is essential, because they cannot replicate on their own. Invading pathogens must also be able to adapt to a new milieu. For example, the nutrients and ionic environment of the cell surface differs from that inside the cell or in the submucosa. Some of the steps in pathogenesis at the cellular level are illustrated in Figure 1–6. Persistence and even invasion do not necessarily translate immediately to disease. The invading organisms must disrupt function in some way. For some, the inflammatory response they stimulate is enough. For example, a lung alveolus filled with neutrophils responding to the presence of Streptococcus pneumoniae loses its ability to exchange oxygen . The longer a pathogen can survive in the face of the host response, the greater the compromise in host function. Most pathogens do more than this. Destruction of host cells through the production of digestive enzymes, toxins, or intracellular multiplication is among the more common mechanisms. Other pathogens operate by altering the function of a cell without injury. Some of these actions are understood at a molecular level. Diphtheria is caused by a bacterial toxin that blocks protein synthesis inside the host cell. Details of the molecular mechanism for this action are illustrated in Figure 1–7. Some viruses cause the insertion of molecules in the host cell membrane, which cause other host cells to attack it. The variations are diverse and fascinating.
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Immunity Although the science of immunology is beyond the scope of this book, understanding the immune response to infection (see Chapter 2) is an important part of appreciating pathogenic mechanisms. In fact,
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