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Only when a microorganism has successfully established a site of infection in the host does disease occur, and little damage will be caused unless the agent is able to spread from the original site of infection or can secrete toxins that can spread to other parts of the body. Extracellular pathogens spread by direct extension of the focus of infection through the lymphatics or the bloodstream. Usually, spread by the bloodstream occurs only after the lymphatic system has been overwhelmed by the burden of infectious agent. Obligate intracellular pathogens must spread from cell to cell; they do so either by direct transmission from one cell to the next or by release into the extracellular fluid and reinfection of both adjacent and distant cells. Many common food poisoning organisms cause pathology without spreading into the tissues. They establish a site of infection on the epithelial surface in the lumen of the gut and cause no direct pathology themselves, but they secrete toxins that cause damage either in situ or after crossing the epithelial barrier and entering the circulation.
Most infectious agents show a significant degree of host specificity, causing disease only in one or a few related species. What determines host specificity for every agent is not known, but the requirement for attachment to a particular cell-surface molecule is one critical factor. As other interactions with host cells are also commonly needed to support replication, most pathogens have a limited host range. The molecular mechanisms of host specificity comprise an area of research known as molecular pathogenesis, which falls outside the scope of this book.
While most microorganisms are repelled by innate host defenses, an initial infection, once established, generally leads to perceptible disease followed by an effective host adaptive immune response. This is initiated in the local lymphoid tissue, in response to antigens presented by dendritic cells activated during the course of the innate immune response (Fig. 10.2, third and fourth panels). Antigen-specific effector T cells and antibody-secreting B cells are generated by clonal expansion and differentiation over the course of several days, during which time the induced responses of innate immunity continue to function. Eventually, antigen-specific T cells and then antibodies are released into the blood and recruited to the site of infection (Fig. 10.2, last panel). A cure involves the clearance of extracellular infectious particles by antibodies and the clearance of intracellular residues of infection through the actions of effector T cells.
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