Bacterial Infections

Bacteria are the most frequent cause of pulmonary infections in immunocompromised patients. Jain et al., in a study evaluating 104 intensive care unit (ICU) patients with lung infiltrates, found that 49% of episodes were bacterial infections.⁴ The specific bacterial etiology of pulmonary infections in immunocompromised patients differs in frequency depending on underlying immune defects. Encapsulated organisms such as Streptococcus pneumoniae and Haemophilus influenzae are particularly common in patients with immunoglobulin defects, such as those suffering from multiple myeloma or in patients with chronic lymphocytic leukemia. Infections caused by penicillin-resistant S. pneumoniae are on the rise,⁵ and prophylactic use of antibiotics against gram-negative bacteria in patients with neutropenia has favored the emergence of Staphylococcus aureus infections (including methicillin-resistant [MRSA]) and multi-resistant gram-negative bacilli (Pseudomonas aeruginosa, Acinetobacter spp., and Stenotrophomonas maltophilia.)⁶ Epidemiologic studies have shown that Legionella pneumonia is more prevalent in the ICU host, particularly in renal transplant recipients and patients with lymphoma. It is important to consider that 15% to 30% of cases of bacterial pneumonia are mixed bacterial/opportunistic infections,¹ a finding of particular therapeutic importance in patients who do not respond to what was initially considered to be appropriate specific antibiotic treatment.

Fungal Infections

Aspergillus spp. are some of the most common microorganisms causing pneumonia in the ICU patient. Since neutrophils are the key cells in defense against Aspergillus, neutropenic patients, particularly HSCT recipients, are at special risk for this infection. Among recipients of solid-organ transplants, the incidence of invasive pulmonary aspergillosis (IPA) is highest after lung transplantation. A steady increase in documented cases of IPA after organ transplantation has been reported.⁷ It is estimated that aspergillosis is found in 30% of patients with protracted severe neutropenia.⁸

Although mortality associated with IPA in IC patients has historically been as high as 80%, during the past 2 decades, the outcome of this infection seems to be changing. Early detection of infection using antigen-specific diagnostic techniques based on serum detection of either galactomannan or beta-D-glucan, two constituents of fungal cell walls, may improve diagnosis, particularly in patients with leukemia and HSCT recipients. Recent reports suggest that detection of galactomannan in bronchoalveolar lavage fluid might be more sensitive than detection in serum.⁹ Diagnosis of invasive fungal diseases with the use of polymerase chain reaction (PCR) assay, although promising, is currently investigational.¹⁰ Implementation of thoracic computed tomography (CT) scan in patients at high risk for invasive pulmonary aspergillosis may improve outcome.¹¹ Prompt institution of azoles appears to have resulted in improved survival.¹²

Candida species colonize the respiratory tract and are often recovered from pulmonary specimens in ICU patients, but are only considered truly pathogenic if fungemia occurs or lung tissue invasion can be demonstrated. With expanded use of new antifungal therapies, an increased incidence of infections due to Candida krusei and Candida glabrata has been reported. Other fungi that can infect immunocompromised patients as a result of environmental exposures (e.g., Penicillium purpurogenum,¹³ Scedosporium prolificans¹⁴) can cause lethal infections.

A marked decrease in the incidence of Pneumocystis jiroveci pneumonia has been found recently, primarily owing to use of specific prophylaxis in patients at risk and the use of highly active antiretroviral therapy (HAART) in human immunodeficiency virus (HIV)-infected patients. In a recent report, P. jiroveci infection was documented in 2.5% of patients undergoing allogeneic HSCT. The majority of cases occurred late in the course following HSCT (median 14.5 months)¹⁵ and with a CD4⁺ count less than 200 cells/mm³.

Mycobacterium Infections

There has been a marked decrease in pulmonary tuberculosis in HIV-infected patients with the introduction of HAART.¹⁶ However, remarkable geographic differences in the incidence of pulmonary tuberculosis in such patients have been reported.¹⁷ A high level of suspicion is necessary to diagnose pulmonary tuberculosis in ICU patients; tuberculosis should be particularly considered in patients with T-cell defects (see Table 68-1). The typical radiologic pattern is often replaced by diffuse, basal, or miliary infiltrates as well as mediastinal lymph nodes. Although sputum analysis is a good noninvasive test for mycobacterium staining, most patients will undergo bronchoscopy, with a diagnostic yield of more than 90%.

Different PCR techniques have been developed to try to circumvent the problem of diagnostic delay in tuberculosis; however, false-positive results in patients shedding nonviable microorganisms limit the clinical use of these techniques. Atypical mycobacterial infections, particularly Mycobacterium avium complex, were previously common in HIV patients with less than 50 CD4⁺ cells/mm³. However, since the introduction of HAART, the incidence of these infections has dropped significantly. With the exception of lung transplant patients, atypical mycobacterial infections are rare in SOT recipients.