The patterns of tissue reactions described above are useful guidelines for analyzing microscopic features of infectious processes, but in practice it must be remembered that different types of host reactions often occur at the same time. For example, the lung of a patient with AIDS may be infected with CMV, which causes cytolytic changes, and, at the same time, by Pneumocystis, which causes interstitial inflammation. Similar patterns of inflammation also can be seen in tissue responses to physical or chemical agents and in other inflammatory conditions of unknown cause. Finally, in immunocompromised individuals, the absence of a host inflammatory response frequently eliminates some of the histologic clues about the potential nature of infecting microorganism(s). Because of this potential for mixed infections and/or lack of host response, other diagnostic tests for infection in addition to pathologic examination are essential to make a definitive diagnosis.
Inherited or acquired defects in immunity (Chapter 5) often impair only part of the immune system, rendering the affected individuals susceptible to specific types of infections.
Patients with antibody deficiency, as in X-linked agammaglobulinemia, contract severe bacterial infections by extracellular bacteria and a few viral infections (rotavirus and enteroviruses).
Patients with T-cell defects are susceptible to infections with intracellular pathogens, notably viruses and some parasites.
Patients with deficiencies in early complement components are particularly susceptible to infections by encapsulated bacteria, such as S. pneumoniae, whereas deficiencies of the late components of complement are associated with Neisseria infections.
Deficiencies in neutrophil function lead to increased infections with S. aureus, some gram-negative bacteria, and fungi.
Individuals with inherited deficiencies in specific components of innate and adaptive immunity sometimes show selective susceptibility to particular infections. These patterns reveal the essential roles of different molecules in mediating protective immunity to specific microorganisms. For example, patients with mutations in signaling molecules downstream of several TLRs are prone to pyogenic bacterial diseases, particularly with S. pneumoniae infections. Impaired TLR3 responses are associated with childhood HSV encephalitis. Inherited defects in IL-17 immunity (such as mutations in STAT3, a transcription factor needed for Th17 cell generation) are associated with chronic mucocutaneous candidiasis.
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Acquired immunodeficiencies have a variety of causes, the most widely known being infection with HIV, which causes AIDS (Chapter 5). HIV infects and kills CD4+ helper T lymphocytes, leading to profound immunosuppression and a multitude of infections. Other causes of acquired immunodeficiency include infiltrative processes that suppress bone marrow function (e.g., leukemia), immunosuppressive drugs (such as those used to treat certain autoimmune diseases), and hemopoietic stem cell transplantation. Diseases of organ systems other than the immune system also can make patients susceptible to disease due to specific microorganisms. Individuals with cystic fibrosis and impaired respiratory clearance commonly get infections dominated by Pseudomonas aeruginosa. Lack of splenic function in individuals with sickle cell disease makes them susceptible to infection with encapsulated bacteria such as S. pneumoniae. Burns destroy skin, removing this barrier to microbes, allowing infection with pathogens such as P. aeruginosa. Finally, malnutrition impairs immune defenses.