through the respiratory tract [11, 17]. The most frequent clinical manifestation of aspergillosis is pneumonia, but aspergillosis may also occur as invasive rhinosinusitis, cerebral infection, or disseminated infection [11, 12, 17].

28.3 Pathogenesis and Host Defense

The risk of infection in patients with cancer is a function of balance between the integrity of host defense mechanisms and the intensity of exposure to potentially pathogenic microorganisms in the host’s environment (especially hospital pathogens).

Microbial invasion and development of infection are facilitated by the presence of comorbidities, immunosuppression, cancer treatment, and damage to anatomic barriers caused by the cancer itself or induced by chemotherapy [5, 9, 18, 19]. Cytotoxic chemotherapy used to treat cancer has potent effects on both humoral and cellular immunities [1, 2]. Cytotoxic regimens used for treating Hodgkin’s and nonHodgkin’s lymphomas, solid tumors of the breast, lung, or germ cells and cancer of the genitourinary tract are in most cases given in cycles lasting weeks to months [1, 2]. These actions damage the host’s defense mechanisms, which are already compromised in many cases by factors related to the underlying cancer (particularly in patients with myeloma, lymphoma, and chronic lymphocytic leukemia). Weakened immune components include the complement cascade and immunoglobulin production, T lymphocytes, monocytes/macrophages, neutrophils, and skin and mucous membranes [1, 2]. Patients with cancer are therefore highly susceptible to almost any type of infection.

Neutropenia is the main immune defect of cancer patients, and the inverse relationship between absolute neutrophil count and infection risk has been known since the 1960s [2]. However, neutropenia is not the only factor influencing the risk of infection. As new chemotherapy regimens and new antibiotics are developed and introduced for therapy or prophylaxis, the pattern of infection risk changes. For example, use of new purine analogues such as fludarabine in patients with chronic lymphocytic leukemia has been associated with an increase in infections with Listeria monocytogenes and Pneumocystis carinii, both associated with T lymphocyte dysfunction, and prophylaxis with trimethoprim–sulfamethoxazole and ciprofloxacin during severe mucositis has led to bacteremia with viridans streptococci [2, 5].

Additionally, underlying conditions such as obstruction of the lumen of a natural body passage (e.g., urinary, biliary, respiratory, digestive tract, or nasolacrimal duct) by cancer impairs the flow of body fluids and secretions, creating conditions that promote microbial growth [1–5, 18]. Cytotoxic chemotherapy damages the epithelial tissue lining, resulting in loss of the integrity of the mucous membrane barrier. Development of mucositis therefore predisposes to infection by the patient’s endogenous commensal flora and colonizing pathogens [2, 5].