Type:
Whole Allergen
Whole Allergen
Whole Allergen
Acremonium kiliense
Inhalation
Cephalothecaceae
Acremonium kiliense
Acremonium kiliense / Cephalosporium acremonium
Storage rot of apples, wilt of rice
The saprophytic fungus mold Acremonium kiliense, also referred to in the literature as Cephalosporium acremonium, can contaminate air, surfaces, and drinking water. Exposure to Acremonium/Cephalosporium spp. has been specifically associated with a range of respiratory and cutaneous allergic conditions including asthma, allergic rhinitis, hypersensitivity pneumonia, acute exogenous allergic alveolitis, chronic pulmonary morbidity, and atopic dermatitis. No allergenic molecules have been characterized from A. kiliense to date, however, an alkaline protease enzyme has been isolated which may have allergenic potential.
Acremonium kiliense is a saprophytic fungus, characterized by light microscopy as a Gram-positive microorganism with septate hyphae (1, 2). Of note, Acremonium is a highly morphologically homogenous genus, so it is difficult to reliably differentiate species from each other, or from other Acremonium-like species (3-5).
Molecular studies have demonstrated that many species in Acremonium are polyphyletic, and Acremonium-like species cluster in different lineages throughout the Ascomycota, mainly in the class Sordariomycetes (2, 4). Due to phylogenetic ambiguities, an unknown portion of the literature on Acremonium kiliense may be based on other Acremonium spp., Cephalosporium spp., or Sarocladium kiliense (2, 6-8).
Taxonomic tree of Acremonium kiliense (9) |
|
---|---|
Domain |
Eukaryota |
Kingdom |
Fungi |
Phylum |
Ascomycota |
Subphylum |
Pezizomycotina |
Class |
Sordariomycetes |
Order |
Hypocreales |
Genus |
Acremonium |
Taxonomic tree of Acremonium kiliense (9) |
---|
Acremonium/Sarocladium spp. are omnipresent and commonly isolated from soil, air, and plant debris (4, 5). Fungal spores are ubiquitous and constitute the largest component of aerobiological particles in the environment, exceeding the concentration of pollen grains (10, 11). Concentrations of spores vary seasonally in response to changing temperature, rainfall, relative humidity, wind, and circadian light patterns, with higher numbers generally in late summer and early autumn (10).
Acremonium spp. have been detected in the air and on the surfaces of pots and growing media in enclosed environments such as greenhouses (12, 13), and isolated from both chlorinated and unchlorinated tap water systems in relatively high frequencies, especially in cooler seasons (11, 14).
Throughout the year, viable Cephalosporium spp. were recovered and cultured, alongside many other fungi genera, from samples of ambient air and house dust collected from homes in North America, contributing to the potentially important role of fungi in producing perennial symptoms of allergy in sensitized patients (15). Bedroom relative humidity was found to correlate with prevalence levels of airborne mesophilic fungal contaminants. Cephalosporium spp. were recovered from 11.3% (17/150) of single-family dwellings in Michigan (USA), a location where artificial humidifiers are routinely used during winter due to very dry ambient air (16).
Fungi are ubiquitous, and as a consequence sensitization can be found throughout the world (10).
Exposure to fungi can occur via inhalation, skin contact, or ingestion (10).
Fungal allergens can elicit respiratory and skin symptoms in sensitized patients, and can also activate the innate immune system and enhance inflammation caused by unrelated allergens (e.g. grass pollen). The prevalence of sensitization to molds is estimated to range from 3‒10% among the general population worldwide but may be higher in atopic individuals (10).
Fungal sensitization is found more often in patients with asthma and may represent a risk factor for developing asthma (10). A study in Chicago (USA) reported that mean levels of mold spores during the pollen season (March 21 to October 31 during four consecutive years), but not levels of tree, grass, or ragweed pollen, were significantly higher on days corresponding with asthma-related deaths than for days on which no deaths occurred (p<0.005) (17).
In most clinical cases the exact etiological agent cannot be specified due to the morphological similarity of many species of Acremonium (3, 4). Additionally, phylogenetic ambiguities may have based an unknown portion of the literature on Acremonium kiliense, other Acremonium spp., Cephalosporium spp., or Sarocladium kiliense (2, 6-8). As a result, the actual incidence of various species of Acremonium/Cephalosporium/Sarocladium in the clinical setting is unknown, and likely to be under-represented (3-5).
A cross-sectional multivariate analysis of preschool children (<7 years of age) in Colombia (South America) identified exposure to Acremonium spp. as an indoor biological contaminant that could be associated with asthmatic respiratory symptoms (18). In the US, one patient within a cohort of 21 atopic patients with symptoms consistent with allergic rhinitis or asthma showed specific IgE against Acremonium strictum (19).
‘Humidifier lung’ has been proposed as an important cause of hypersensitivity pneumonia. One case report described a male ex-smoker (aged 60 years) who was hospitalized with progressive dyspnea and fever and diagnosed with acute respiratory tract infection. Shortly after discharge following successful treatment, the patient was readmitted with recurring symptoms, and diagnosed with hypersensitive pneumonitis with a positive specific precipitin reaction against antibody for Cephalosporium acremonium. The patient in this report recovered after treatment, and no relapse was observed after avoiding the use of a humidifier (20). Various other authors have also reported positive antigen-specific antibodies to Cephalosporium in patients with hypersensitivity pneumonitis, several of which were directly traced back to the use of a humidifier (21-24).
A case report from Germany described a patient (aged 24 years) diagnosed with acute exogenous allergic alveolitis with typical symptoms of unproductive cough, dyspnea on exertion, fever, loss of weight, headache, and limb pains. In this patient, precipitating antibodies were demonstrated against a range of molds including Cephalosporium acremonium, which were traced to pot plant earth and containers at the patient’s home (25).
Cephalosporium spp. were identified as the apparent antigenic source in two cases of significant chronic pulmonary morbidity where symptoms remitted during absence from the home. In Case 1 (female aged 33 years with persistent fever, myalgias, and dyspnea), the source was repeated flooding of the patient’s home with sewer water. Case 2 (female aged 36 years with intermittent coughing, myalgia, malaise, and dyspnea for several years) was traced to a contaminated humidifier. Both patients fully recovered after vacating their homes (24).
In a study evaluating the association between gut mycobiome and atopic dermatitis development in infants aged 9–12 months, the abundance of Acremonium spp. was considerably higher in individuals who had outgrown (recovered) versus those who persisted (still undergoing) (p=0.0023) (26).
Occupational exposure to fungi and its association with allergy was assessed in a survey of employees at a museum in Warsaw (Poland). A total of 85% (88/103) workers reported one or more allergic symptoms including rhinitis (69%), conjunctivitis (70%), and skin symptoms (57%), while 30% of subjects reported developing these symptoms at work following contact with items potentially contaminated with fungi. The species most frequently isolated from investigated exhibits included Penicillium, Aspergillus, Cladosporium, Alternaria, Trichoderma, Acremonium, and Paecilomycese, and sensitization to at least one of these fungal allergens was reported in 30% of subjects (27).
In immunocompetent individuals, Acremonium kiliense/Sarocladium kiliense can cause infections such as dermatophytoses, kerion, onicomycoses, keratitis, and mycetomas (1, 4, 7). Pathogenicity is usually related to inoculation of the fungus via a penetrating injury that often leads to a granuloma formation (28). However, in immunodeficient patients or those with underlying immunological disorders, the fungus can cause pneumonia, arthritis, osteomyelitis, endocarditis, peritonitis, meningitis, and sepsis, especially in the presence of risk factors such as prosthesis, catheters, immunosuppressive therapy, and anatomic disorders (1, 4, 7, 28, 29). These infections are difficult to treat and may have a fatal outcome (5, 6).
A nosocomial outbreak of fungemias in Chile, involving 65 chemotherapy patients in 8 hospitals with mild clinical manifestations, was attributed to Sarocladium kiliense (29). Reports of superficial and subcutaneous Sarocladium infections have been reported worldwide (5). Opportunistic agents including Acremonium kiliense have also been detected in patients with phagocyte disorders. A case report described pneumonia caused by A. kiliense as the first clinical manifestation of chronic granulomatous disease in a child aged 4 months (1).
No allergenic molecules have been characterized from A. kiliense to date (30).
An alkaline protease enzyme has been isolated from A. kiliense (8). Protease activity is a common and important feature of many allergens capable of inducing asthma, and fungal protease allergens have been implicated in the facilitation of allergic sensitization and airway hyperresponsiveness in asthma (31, 32).
No published data is currently available.
Author: RubyDuke Communications
Reviewer: Dr. Christian Fischer
Last reviewed:January 2022