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Chapter 22 : Acquired Immunity: Chronic Bacterial Infections
Category: Immunology; Clinical Microbiology
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This chapter discusses what happens when the immune response is capable of controlling a bacterial pathogen but not eliminating it. In this case, acquired immunity is defined not as the response capable of eliminating the pathogen but the response that allows survival of the host. The presence of ongoing infection and inflammation is likely to severely interfere with the generation of acquired specific memory. In this chapter the authors have consider the acquired cellular response to bacterial challenge with a focus on members of the genus Mycobacterium. The chapter focuses on the elements of the acquired immune response that mediate both immunity as well as the immunopathologic consequences that are often concomitant with expression of immunity to chronic bacterial pathogens. More recent studies, made possible by the development of tools capable of dissecting the nature of the T-cell response during an infection, have highlighted the truly complex nature of acquired immunity. The nature of the inflammatory response to Mycobacterium tuberculosis in the absence of acquired immune response suggests that the pathogen makes use of the acquired response to generate the damage required for transmission. The relative importance of cytokine cross-regulation, regulatory T-cell control, and the active cytotoxic activity of the bacteria in regulating the acquired response to Mycobacterium ulcerans has yet to be fully defined.
Chronic bacterial infection influences the host immune response. When the acquired cellular response of the host rapidly eliminates an invading bacterial population, it rapidly contracts and a memory population capable of rapidly responding to reinfection is generated (a). In a chronic infection (b), there are several potential outcomes for the host response that depend upon bacterial burden, the level of immunosuppression from the bacteria, the extent of immunoregulation, and the inflammatory environment. The response could maintain a high level (long dashed line, A), fluctuate in response to bacterial number (dot/dash line, B), contract to a level capable of controlling bacterial growth (short dash, C), or become depleted as the bacterial infection persists (short to long dash, D). In tuberculosis, it appears that curve C is the pattern of host response; however, curve D may also apply as the infected host ages.
Chronic infection allows for increased transmission. A bacterial pathogen with multiple transmission strategies such as Y. pestis can afford to grow rapidly and kill one host (the human) as the alternative hosts provide a reservoir and the possibility of further spread. In contrast, in the absence of an alternative vector for transmission, it is advantageous for bacteria to persist within a host and thereby maximize the exposure of the infected host to target hosts (e.g., M. tuberculosis).
The nature of acquired immune response to chronic bacterial infection. The nature and extent of the acquired cellular response to chronic bacterial infection depend upon a variety of factors. The nature of the bacterial stimulus will determine the initial and extended activation of the acquired response by determining the levels of APC activation and inflammatory cytokines. The ability of the bacteria to affect the architecture and function of the lymph node as well as the site of infection greatly influences the continued activation of the acquired specific responses as well as defines the ability of the protective cellular response to be expressed.