Mucormycosis and invasive aspergillosis are uncommon infections that are almost always limited to immunocompromised hosts, particularly those with hematolymphoid malignancies and profound neutropenia, those undergoing corticosteroid therapy, or following hematopoietic stem cell transplant recipients.
MORPHOLOGYMucormycosisiscausedbytheclassoffungiknownasZygomycetes.Rhizopus andMucor arethetwofungiofmedicalimportancewithintheZygomycetesclass.Theirhyphaearenonseptate andbranchatrightangles;bycontrast,thehyphaeofAspergillus organismsareseptate andbranchatmoreacuteangles(see
Fig.13.42C ).BothzygomycetesandAspergillus causeanondistinctive,suppurative,sometimesgranulomatousreactionwithapredilection for invading blood vessel walls, causing hemorrahage, vascular necrosis and infarction (see
Fig.13.42B
In rhinocerebral and pulmonary mucormycosis, zygomycetes have a propensity to colonize the nasal cavity or sinuses and then spread by direct extension into the brain, orbit, and other head and neck structures. Patients with diabetic ketoacidosis are most likely to develop a fulminant invasive form of rhinocerebral mucormycosis. Pulmonary disease can be localized (e.g., cavitary lesions) or may manifest radiologically with diffuse “miliary” involvement.
Invasive aspergillosis preferentially localizes to the lungs, and infection most often manifests as a necrotizing pneumonia (see
Fig. 13.42B ). Systemic dissemination, especially to the brain, is a complication that is often fatal.
Allergic bronchopulmonary aspergillosis occurs in patients with asthma who develop an exacerbation of symptoms caused by a type I hypersensitivity against the fungus growing in the bronchi. Such patients often have circulating IgE antibodies against Aspergillus and peripheral eosinophilia.
Aspergilloma (“fungus ball”) formation occurs by fungal colonization of preexisting pulmonary cavities (e.g., dilated bronchi or lung cysts, posttuberculosis cavitary lesions). These masses may act as ball valves to occlude the cavity, thereby predisposing the patient to infection and hemoptysis.
Pulmonary disease continues to be the leading contributor to morbidity and mortality in HIV-infected individuals. Although the use of potent anti-retroviral agents and effective chemoprophylaxis has markedly decreased the incidence and has improved outcomes, the plethora of entities involved makes diagnosis and treatment a distinct challenge.
Despite the emphasis on “opportunistic” infections, it should be recognized that bacterial lower-respiratory tract infection caused by the “usual” pathogens is exceedingly common in HIV infection. The implicated organisms include S. pneumoniae, S. aureus, H. influenzae, and gram-negative rods. Bacterial pneumonias in HIV-infected individuals are more common, more severe, and more often associated with bacteremia than in those without HIV infection.
Not all pulmonary infiltrates in HIV-infected individuals are infectious. A host of noninfectious diseases, including Kaposi sarcoma (Chapters 5 and 10), pulmonary non-Hodgkin lymphoma (Chapter 12), and primary lung cancer, occur with increased frequency and must be excluded.