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NAME: Aspergillus spp.

SYNONYM OR CROSS REFERENCE: Aspergillosis, farmer’s lung, A. fumigatus, A. flavus, A. niger, A. nidulans, A. terreus Footnote 1.

CHARACTERISTICS: The genus Aspergillus belongs to the class Euascomycetes of the Phylum Ascomycota Footnote 1. They consist of anamorphic (asexual) species with known or presumed telomorphic forms in the family Trichocomaceae Footnote 1. The genus Aspergillus includes seven subgenera, each containing several species Footnote 1. Aspergillus spp. contain approximately 184 species, 40 of which have been reported to cause human or animal infections Footnote 1. Aspergillus spp. reproduce by producing conidia on uniseriate or biseriate phialides Footnote 1. Aspergillus colonies grow rapidly, producing white, green, yellow, or black colonies Footnote 1.


PATHOGENICITY/TOXICITY: Aspergillus spp. includes many species, about 40 of which have been implicated in human or animal infections Footnote 1. Aspergillosis is a common term used to describe infections caused by different species of Aspergillus Footnote 1. Most cases of aspergillosis are caused by A. fumigatus, with A. flavus and A. niger being the second most common pathogenic Aspergillus spp. worldwide Footnote 1. Diseases caused by Aspergillus spp. include clinical allergies (allergic bronchopulmonary aspergillosis, rhinitis, Farmers’s lung), superficial and local infections (cutaneous infections, otomycosis, tracheobronchitis), infections associated with damaged tissue (aspergilloma, osteomyelitis), and invasive pulmonary and extrapulmonary infections Footnote 1. Invasive infections due to Aspergillus spp. occur mainly in immunocompromised individuals and are the most severe forms of infections caused by Aspergillus spp. Footnote 1. Invasive aspergillosis is most commonly caused by A. fumigatus, but other species such as A. flavus, A. nidulans, and A. terreus have also been reported to cause invasive infections Footnote 1. Invasive infections primarily involve the sino-pulmonary tract, with lung being the most common site of invasion Footnote 2. Clinical signs suggestive of invasive sinusitis include fever, facial pain, headache, asymmetric facial swelling, epistaxis, proptosis, cranial nerve abnormalities, ischemia of the palate, and bone erosion Footnote 2. Fever, cough, and dyspnea are the most common but non-specific symptoms of invasive pulmonary aspergillosis Footnote 2. Vascular invasion may also occur and may manifest as pleural chest pain Footnote 2. If left untreated, hematogenous dissemination involving any organ may occur. The most serious condition is the involvement of the CNS, leading to seizures or stroke Footnote 2.

EPIDEMIOLOGY: Aspergillus spp. are found worldwide, and widely distributed in the environment Footnote 3. Aspergillus spp. are rare causes of disease in humans, and occur primarily in immunocompromised individuals Footnote 3. Invasive infections caused by Aspergillus spp. have been associated with high rates of morbidity and mortality especially in immune compromised individuals such as transplant patientsFootnote 1, Footnote 4. In the United States, the number of aspergillosis related deaths in immunocompromised individuals increased from 0.04 deaths per 100,000 people in 1980 to 0.15 deaths per 100,000 people in 1997 Footnote 5. The incidence of invasive Aspergillus in patients with acute leukemia was reported to be 12.7 %, with a death rate of 13% in the year 2006 in United States Footnote 6. Compared to 2003, the mortality associated with invasive aspergillosis in acute leukemia patients has decreased from 24%, and the incidence has increased from 5.8%.

HOST RANGE: Humans, cows, dolphins, birds, and horsesFootnote 1, Footnote 7.

MODE OF TRANSMISSION: Inhalation of airborne conidia, through contaminated water (exposure to conidia during showering), and nosocomial infections (hospital fabrics and plastics may serve as importance source of Aspergillus spp.)Footnote 1, Footnote 2, Footnote 8, Footnote 9.


INCUBATION PERIOD: 2 days – 3 months Footnote 9.

COMMUNICABILITY: No evidence of human to human transmission Footnote 9.


RESERVOIR: Conidia of Aspergillus are present in decomposing organic matter and soil Footnote 2. Water and food may also act as reservoirs of transmission of Aspergillus spp. Footnote 8.




DRUG SUSCEPTIBILITY/RESISTANCE: Aspergillus spp. are resistant to itraconazole Footnote 10. Some A. fumigatus isolates have been reported to be resistant to voriconazole and posaconazole and echinocandins Footnote 10. This organism is susceptible to voriconazole and amphotericin B Footnote 2.

SUSCEPTIBILITY TO DISINFECTANTS: A. niger and A. fumigatus are sensitive to 0.5% alkaline solution of glutaraldehyde Footnote 11. A. niger is also sensitive to 0.125% butyl paraban ester Footnote 12. A 1:50 dilution of a phenolic disinfectant containing 15% 2-phenylphenol and 6.3% 4-ter-amylphenol has shown to be effective against A. fumigatus but not A. niger Footnote 12. Aspergillus spp. are also susceptible to sodium hypochlorite and cupric sulphate Footnote 8.

PHYSICAL INACTIVATION: Conidia are generally heat resistant Footnote 3 ; however, treatment at 60oC for 45 minutes has been reported to completely inactivate A. niger, and A. flavus conidia Footnote 8. A. fumigatus, considered to be the most pathogenic species, cannot be completely inactivated by this procedure, although its initial concentration is reduced by 3 logs. Microwave irradiation at 800 watts for 90 seconds to 2 minutes is also effective in inactivating conidia A. fumigatus and A. flavus Footnote 8.

SURVIVAL OUTSIDE HOST: Can survive in soil and decomposing vegetation Footnote 2.


SURVEILLANCE: Monitor for symptoms. Diagnosis of infection is made by direct examination of Aspergillus hyphal elements and hyphal morphology in routine KOH Aspergillus preparations or in tissue sections stained with fungal stainsFootnote 1, Footnote 9, Footnote 13. Detection of Aspergillus antigen (galactomanan or 1,3-β-D-glucan) or antibodies in serum or other body fluids or a positive skin test result, or PCR can also be usedFootnote 1, Footnote 2, Footnote 10, Footnote 13.

Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID/TREATMENT: The guidelines of the Infectious Diseases Society of America recommend the use of voriconazole as the primary therapy for invasive aspergillosis Footnote 2. Amphotericin B deoxycholate can also be used as initial therapy Footnote 2. Amphotericin B lipid complex and Caspofungin are used for patients who are intolerant of conventional amphotericin B therapy Footnote 2. Debridement is required for local aspergillosis such as sinusitis, cutaneous disease and osteomyelitis Footnote 2.


PROPHYLAXIS: Prophylaxis for Aspergillus spp. is recommended for those at risk of invasive aspergillosis, such as those with graft vs. host disease or neutropenic patients with acute myeloid leukaemia or myelodysplastic syndrome Footnote 10.


LABORATORY-ACQUIRED INFECTIONS: None reported so far Footnote 14.

SOURCE/SPECIMENS: Sputum, biopsy material, transtracheal aspirates, blood, soilFootnote 1, Footnote 2.

PRIMARY HAZARDS: Inhalation of air contaminated with Aspergillus spores Footnote 14.



RISK GROUP CLASSIFICATION: Risk group 2 Footnote 15. This risk group applies to the genus as a whole, and may not apply to every species within the genus.

CONTAINMENT REQUIRMENT: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures Footnote 16. These containment requirements apply to the genus as a whole, and may not apply to each species within the genus.

PROTECTIVE CLOTHING: Lab coat. Gloves when direct skin contact with infected materials or animals is unavoidable. Eye protection must be used where there is a known or potential risk of exposure to splashes. Footnote 16.

OTHER PRECAUTIONS: All procedures that may produce aerosols, or involve high concentrations or large volumes should be conducted in a biological safety cabinet (BSC). The use of needles, syringes, and other sharp objects should be strictly limited. Additional precautions should be considered with work involving animals or large scale activities Footnote 16.


SPILLS: Allow aerosols to settle, then, wearing protective clothing, gently cover the spill with absorbent paper towel and apply appropriate disinfectant, starting at the perimeter and working towards the center. Allow sufficient contact time before clean up Footnote 16.

DISPOSAL: Decontaminate all wastes that contain or have come in contact with the infectious organism by autoclave, chemical disinfection, gamma irradiation, or incineration before disposingFootnote 16.

STORAGE: The infectious agent should be stored in leak-proof containers that are appropriately labeled Footnote 16.


REGULATORY INFORMATION: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.

UPDATED: October 2010

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of Canada

Although the information, opinions and recommendations contained in this Pathogen Safety Data sheet are compiled from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.

Copyright ©
Public Health Agency of Canada, 2010


Footnote 1
Verweij, P.E. and Brandt, M.E. (2007). Aspergillus, Fusarium and other opportunistic moniliaceous fungi. In P. R. Murray (Ed.), (9th ed., pp. 1802-1838). Washington D.C.: ASM Press.
Footnote 2
Segal, B. H. (2009). Aspergillosis. New England Journal of Medicine, 360(18), 1870-1884.
Footnote 3
Ryan, K. J. (2004). Candida, Aspergillus, and Other Opportunistic Fungi. In Ryan, K.J. and Ray, C.G. (Ed.), Sherris Medical Microbiology (4th ed., pp. 659-668). USA: McGraw-Hill.
Footnote 4
Weber, D. J., & Rutala, W. A. (1996). Use of Metals as Microbicides in Preventing Infections in Healthcare. In S. S. Block (Ed.), Disinfection, Sterilization, and Preservation (5th ed., pp. 415-430). Philadelphia P.A.: Lipincott Williams and Wilkins.
Footnote 5
McNeil, M. M., Nash, S. L., Hajjeh, R. A., Phelan, M. A., Conn, L. A., Plikaytis, B. D., & Warnock, D. W. (2001). Trends in mortality due to invasive mycotic diseases in the United States, 1980-1997. Clinical Infectious Diseases, 33(5), 641-647.
Footnote 6
Pagano, L., Caira, M., Picardi, M., Candoni, A., Melillo, L., Fianchi, L., Offidani, M., & Nosari, A. (2007). Invasive aspergillosis in patients with acute leukemia: Update on morbidity and mortality - SEIFEM-C report [6]. Clinical Infectious Diseases, 44(11), 1524-1525.
Footnote 7
Tell, L. A. (2005). Aspergillosis in mammals and birds: Impact on veterinary medicine. Medical Mycology, 43(SUPPL.1), S71-S73.
Footnote 8
Araujo, R., Gonçalves Rodrigues, A., & Pina-Vaz, C. (2006). Susceptibility pattern among pathogenic species of Aspergillus to physical and chemical treatments. Medical Mycology, 44(5), 439-443.
Footnote 9
American Academy of Pediatrics.Committee on Infectious Diseases. (2009). Red book (28th ed.). Elk Grove Village, IL: American Academy of Pediatrics. Retrieved from STAT!Ref
Footnote 10
Erjavec, Z., Kluin-Nelemans, H., & Verweij, P. E. (2009). Trends in invasive fungal infections, with emphasis on invasive aspergillosis. Clinical Microbiology and Infection, 15(7), 625-633.
Footnote 11
Scott, E. M., & Gorman, S. P. (1996). Glutaraldehyde. In S. S. Block (Ed.), Disinfection, Sterilization, and Preservation (5th ed., pp. 361-381). Philadelphia P.A.: Lipincott Williams and Wilkins.
Footnote 12
Goddard, P.A. and McCue, K.A. (1996). Phenolic Compounds. In S. S. Block (Ed.), Disinfection, Sterilization, and Preservation (5th ed., pp. 255-281). Philadephia P.A.: Lipincott, Williams and Wilkins.
Footnote 13
Patterson, T.F. and Patterson, J.E. (1996). Fungistatic and fungicidal compounds for human pathogens. In S. S. Block (Ed.), Disinfection, Sterilization, and Preservation (5th ed., pp. 617-639). Philadelphia P.A.: Lipincott Williams and Wilkins.
Footnote 14
Schell, W. A. (2006). Mycotic agents of human disease. In Flemming, D.O., and Hunt, D.L. (Ed.), Biological Safety: Principles and practices (4th ed., pp. 163-178). Washington, D.C.: ASM Press.
Footnote 15
Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of Canada, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009, (2009).
Footnote 16
Public Health Agency of Canada. (2004.). The Laboratory Biosafety Guidelines. (3rd ed.). Ottawa.: Public Health Agency of Canada.