Mold management of wetted carpet.

This study evaluated the growth and removal of fungi on wetted carpet using newly designed technologies that rely on physical principles of steam, heat, and fluid flow. Sixty samples of carpet were embedded with heat-treated house dust, followed by embedding, wearing with a hexapod, and wetting. Samples were inoculated using a liquid suspension of Cladosporium sphaerospermum prior to placement over a water-saturated foam pad. Incubation times were 24 hr, 7 days, and 30 days. Cleaning was performed using three methods; high-flow hot water extraction, hot water and detergent, and steam. Fungal loading increased from approximately 1500 colony forming units per area (CFU/cm(2)) in 24 hr to a maximum of approximately 10,200 CFU/cm(2) after 7 days with a slight decline to 9700 CFU/cm(2) after 30 days incubation. Statistically significant differences were found among all three methods for removal of fungi for all three time periods (p < 0.05). Steam-vapor was significantly better than the alternative methods (p <0.001) with over 99% efficiency in mold spore decline from wetted carpet after 24 hr and 30 days, and over 92% efficiency after 7 days. The alternative methods exhibited lower efficiencies with a decline over time, from a maximum of 82% and 81% at 24 hr down to 60% and 43% at 30 days for detergent-hot water and high-flow, hot water extraction, respectively. The net effect of the mold management study demonstrates that while steam has a consistent fungal removal rate, the detergent and high-flow, hot water methods decline in efficiency with increasing incubation time.

Inactivation of dust mites, dust mite allergen, and mold from carpet.

Carpet is known to be a reservoir for biological contaminants, such as dust mites, dust mite allergen, and mold, if it is not kept clean. The accumulation of these contaminants in carpet might trigger allergies or asthma symptoms in both children and adults. The purpose of this study is to compare methods for removal of dust mites, dust mite allergens, and mold from carpet. Carpets were artificially worn to simulate 1 to 2 years of wear in a four-person household. The worn carpets were inoculated together with a common indoor mold (Cladosporium species) and house dust mites and incubated for 6 weeks to allow time for dust mite growth on the carpet. The carpets were randomly assigned to one of the four treatment groups. Available treatment regimens for controlling carpet contaminants were evaluated through a literature review and experimentation. Four moderately low-hazard, nondestructive methods were selected as treatments: vacuuming, steam-vapor, Neem oil (a natural tree extract), and benzalkonium chloride (a quaternary ammonium compound). Steam vapor treatment demonstrated the greatest dust mite population reduction (p < 0.05) when compared to other methods. The two physical methods, steam vapor and vacuuming, have no statistically significant efficacy in inactivating dust mite allergens (p = 0.084), but have higher efficacy when compared to the chemical method on dust mite allergens (p = 0.002). There is no statistically significant difference in the efficacy for reducing mold in carpet (p > 0.05) for both physical and chemical methods. The steam-vapor treatment effectively killed dust mites and denatured dust mite allergen in the laboratory environment.

Fungi and allergic lower respiratory tract diseases.

Asthma is a common disorder that in 2009 afflicted 8.2% of adults and children, 24.6 million persons, in the United States. In patients with moderate and severe persistent asthma, there is significantly increased morbidity, use of health care support, and health care costs. Epidemiologic studies in the United States and Europe have associated mold sensitivity, particularly to Alternaria alternata and Cladosporium herbarum, with the development, persistence, and severity of asthma. In addition, sensitivity to Aspergillus fumigatus has been associated with severe persistent asthma in adults. Allergic bronchopulmonary aspergillosis (ABPA) is caused by A fumigatus and is characterized by exacerbations of asthma, recurrent transient chest radiographic infiltrates, coughing up thick mucus plugs, peripheral and pulmonary eosinophilia, and increased total serum IgE and fungus-specific IgE levels, especially during exacerbation. The airways appear to be chronically or intermittently colonized by A fumigatus in patients with ABPA. ABPA is the most common form of allergic bronchopulmonary mycosis (ABPM); other fungi, including Candida, Penicillium, and Curvularia species, are implicated. The characteristics of ABPM include severe asthma, eosinophilia, markedly increased total IgE and specific IgE levels, bronchiectasis, and mold colonization of the airways. The term severe asthma associated with fungal sensitization (SAFS) has been coined to illustrate the high rate of fungal sensitivity in patients with persistent severe asthma and improvement with antifungal treatment. The immunopathology of ABPA, ABPM, and SAFS is incompletely understood. Genetic risks identified in patients with ABPA include HLA association and certain T(H)2-prominent and cystic fibrosis variants, but these have not been studied in patients with ABPM and SAFS. Oral corticosteroid and antifungal therapies appear to be partially successful in patients with ABPA. However, the role of antifungal and immunomodulating therapies in patients with ABPA, ABPM, and SAFS requires additional larger studies.

Hypersensitivity pneumonitis secondary to residential exposure to Aureobasidium pullulans in 2 siblings.

BACKGROUND: Hypersensitivity pneumonitis (HP) is an immune-mediated hypersensitivity reaction to a variety of inhaled particles that may lead to acute, subacute, or chronic interstitial pneumonitis and possibly end-stage lung disease. Avian antigens most commonly cause HP in children, but fungi have also been implicated. OBJECTIVE: To describe a 15-year-old girl and her 6-year-old brother who developed HP from residential exposure to Aureobasidium pullulans. METHODS: Allergy skin testing, serum precipitating antibodies, pulmonary function testing, chest radiography, chest computed tomography, bronchoalveolar lavage, and a home survey for possible causative antigens were performed. RESULTS: Both patients lived on a horse farm and had fatigue, weight loss, cough, and dyspnea. The siblings had restrictive patterns on pulmonary function tests, with decreased diffusion capacity of carbon monoxide, ground-glass opacities on high-resolution chest computed tomography, and serum precipitins to A pullulans. Bronchoalveolar lavage in the girl demonstrated lymphocytosis, with a preponderance of CD8+ T cells and natural killer cells. Symptoms improved after the children vacated the home and recurred on repeated exposure in both patients. Home evaluation revealed extensive mold contamination, with A pullulans counts of 659, 329, and 71 CFU/m3 in the boy's bedroom, the girl's bedroom, and outdoors, respectively. CONCLUSIONS: The diagnosis of HP in these siblings is supported by the clinical history, the diagnostic findings, and the recurrence of symptoms on repeated exposure. These cases represent the second report of HP resulting from nonoccupational exposure to A pullulans in North America and the first report in children.