Aspergillosis is caused by molds belonging to the genus Aspergillus. Aspergillus spp. are prototype health-care acquired pathogens associated with dusty or moist environmental conditions. Clinical and epidemiologic aspects of aspergillosis are discussed extensively in another guideline.
Aspergillus spp. are ubiquitous, aerobic fungi that occur in soil, water, and decaying vegetation; the organism also survives well in air, dust, and moisture present in health-care facilities. The presence of aspergilli in the health-care facility environment is a substantial extrinsic risk factor for opportunistic invasive aspergillosis (invasive aspergillosis being the most serious form of the disease). Site renovation and construction can disturb Aspergillus-contaminated dust and produce bursts of airborne fungal spores. Increased levels of atmospheric dust and fungal spores have been associated with clusters of health-care acquired infections in immunocompromised patients. Absorbent building materials (e.g., wallboard) serve as an ideal substrate for the proliferation of this organism if they become and remain wet, thereby increasing the numbers of fungal spores in the area. Patient-care items, devices, and equipment can become contaminated with Aspergillus spp. spores and serve as sources of infection if stored in such areas.
Most cases of aspergillosis are caused by Aspergillus fumigatus, a thermotolerant/thermophilic fungus capable of growing over a temperature range from 53.6°F–127.4°F (12°C–53°C); optimal growth occurs at approximately 104°F (40°C), a temperature inhibitory to most other saprophytic fungi. It can use cellulose or sugars as carbon sources; because its respiratory process requires an ample supply of carbon, decomposing organic matter is an ideal substrate.
Other opportunistic fungi that have been occasionally linked with health-care associated infections are members of the order Mucorales (e.g., Rhizopus spp.) and miscellaneous moniliaceous molds (e.g., Fusarium spp. and Penicillium spp.). Many of these fungi can proliferate in moist environments (e.g., water-damaged wood and building materials). Some fungi (e.g., Fusarium spp. and Pseudoallescheria spp.) also can be airborne pathogens. As with aspergillosis, a major risk factor for disease caused by any of these pathogens is the host’s severe immunosuppression from either underlying disease or immunosuppressive therapy.
Infections due Cryptococcus neoformans, Histoplasma capsulatum, or Coccidioides immitis can occur in health-care settings if nearby ground is disturbed and a malfunction of the facility’s air-intake components allows these pathogens to enter the ventilation system. C. neoformans is a yeast usually 4– 8 μm in size. However, viable particles of <2 μm diameter (and thus permissive to alveolar deposition) have been found in soil contaminated with bird droppings, particularly from pigeons. H. capsulatum, with the infectious microconidia ranging in size from 2–5 μm, is endemic in the soil of the central river valleys of the United States. Substantial numbers of these infectious particles have been associated with chicken coops and the roosts of blackbirds. Several outbreaks of histoplasmosis have been associated with disruption of the environment; construction activities in an endemic area may be a potential risk factor for health-care acquired airborne infection. C. immitis, with arthrospores of 3–5 μm diameter, has similar potential, especially in the endemic southwestern United States and during seasons of drought followed by heavy rainfall. After the 1994 earthquake centered near Northridge, California, the incidence of coccidioidomycosis in the surrounding area exceeded the historical norm.
Emerging evidence suggests that Pneumocystis carinii, now classified as a fungus, may be spread via airborne, person-to-person transmission. Controlled studies in animals first demonstrated that P. carinii could be spread through the air. More recent studies in health-care settings have detected nucleic acids of P. carinii in air samples from areas frequented or occupied by P. carinii-infected patients but not in control areas that are not occupied by these patients. Clusters of cases have been identified among immunocompromised patients who had contact with a source patient and with each other. Recent studies have examined the presence of P. carinii DNA in oropharyngeal washings and the nares of infected patients, their direct contacts, and persons with no direct contact. Molecular analysis of the DNA by polymerase chain reaction (PCR) provides evidence for airborne transmission of P. carinii from infected patients to direct contacts, but immunocompetent contacts tend to become transiently colonized rather than infected.131 The role of colonized persons in the spread of P. carinii pneumonia (PCP) remains to be determined. At present, specific modifications to ventilation systems to control spread of PCP in a health-care facility are not indicated. Current recommendations outline isolation procedures to minimize or eliminate contact of immunocompromised patients not on PCP prophylaxis with PCP-infected patients.
Wednesday, October 22, 2025
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Guidelines for Environmental Infection Control in Health-Care Facilities
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Requirements for Storage of Sterile Materials
