Walter T. Hughes

Aspergillosis is caused by a monomorphic mold and may occur in several diverse disease forms. The clinical features depend on whether the infection results in colonization only, in hypersensitivity to the organism (allergic aspergillosis), or in invasive mycotic disease, which is found predominantly in the immunosuppressed host.


Of the some 300 Aspergillus species, the most common ones affecting humans are A. fumigatus and A. flavus. Other species involved in infections include A. niger, A. oryzae, A. glaucus, A. nidulans, A. restrictus, A. sydowi, A. terreus, A. versicolor, A. candidus, A. ustus, and A. amstelodami.


Aspergillus is ubiquitous in the environment in most parts of the world and may be found in soil, hay, compost piles, decaying vegetation, water, flour, house dust, bedding, food, chemical solutions, medications, surgical dressings, fireproofing material, shower stalls, and potted plants.

Allergic bronchopulmonary aspergillosis has been reported as a complication of asthma and cystic fibrosis. Invasive aspergillosis is found predominantly in the immunocompromised host.

Human-to-human and animal-to-human transmission are not known to occur. Host factors for susceptibility are of prime importance in the acquisition of the infection. At high risk are individuals with malignancy; organ transplant recipients; and patients with acquired immunodeficiency syndrome (AIDS), chronic granulomatous disease, and other immune deficiency disorders.

Nosocomial aspergillosis has been associated with airborne and waterborne organisms in the hospital environment of immunosuppressed patients. The high density of organisms associated with building construction and in fireproofing materials has been related to outbreaks of pulmonary aspergillosis in hospitalized patients. Furthermore, primary cutaneous aspergillosis may occur under surgical dressings and at Hickman catheter sites. Infrequently, invasive aspergillosis of the lung, sinuses, brain, and bone occurs in otherwise normal individuals.


Allergic Aspergillosis

Allergic bronchopulmonary aspergillosis begins with the inhalation of Aspergillus conidia (spores). In a genetically susceptible (HLA-DR restriction) asthmatic patient or one with cystic fibrosis, the spores develop into hyphal forms as the bronchi become colonized. A local inflammatory reaction develops. Antigens of the hyphae react with IgE, IgG, and IgA antibodies as the response escalates to damage of the bronchial wall and infiltration with eosinophils. Antigen-specific CD4 Th2-like T lymphocytes produce increased levels of interleukin (IL)-4 and IL-5. The bronchial wall is infiltrated with mononuclear cells and eosinophils. Mucus and exudate, along with segments of the fungus, may fill the bronchi. The lung parenchyma may become involved with granulomatous reactions. Vasculitis is an uncommon finding with this type of pulmonary aspergillosis, and the lack of an acute neutrophil response is compatible with a delayed hypersensitivity response.

Invasive Aspergillosis

The pathogenesis of invasive aspergillosis differs considerably from that of allergic aspergillosis. Although pulmonary aspergillosis is found occasionally in presumably otherwise normal individuals, the usual host for any invasive form of the disease is one whose immune system has been compromised. Normally, inhaled Aspergillus conidia that reach the paranasal sinuses and lung are ingested and digested by polymorphonuclear leukocytes or alveolar macrophages. If this arm of the defense mechanism is impaired, as it is in patients with chronic granulomatous disease (in whom oxidative intracellular killing is impaired) and in patients with other phagocytic defects or quantitative deficits, the organism may colonize and develop hyphal and invasive forms. With this type of host-parasite relationship, the outcome often is hemorrhagic infarction and necrosis.

The pathologic pattern appears to be related, to some extent, to the severity of immunocompromise. A fibrosing granulomatous reaction or chronic, nonspecific inflammatory response may be found in an otherwise healthy patient. A severely compromised host exhibits massive hyphal invasion of blood vessels and no granulation tissue. In some patients, the
infection may localize with formation of a cavity—the aspergilloma. The cavity is occupied partially by a ball of Aspergillus hyphae. Rarely, a chronic, necrotizing, granulomatous pneumonia is seen around a central zone of infarct-like necrosis of parenchyma resulting from angioinvasive aspergilli. These lesions tend to be found in the upper lobes. Paranasal sinuses infected with this fungus may exhibit a spectrum of tissue responses similar to the pattern described for the lung, or the site may be colonized only, with hypertrophy of the sinus mucosa.

Jul 24, 2016 | Posted by in ORTHOPEDIC | Comments Off on Aspergillosis

Full access? Get Clinical Tree

Get Clinical Tree app for offline access