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The association between environment and fungal disease

The association between environment and fungal disease. Malcolm Richardson University Hospital of South Manchester, and The University of Manchester, UK. Fungi are in the air. Public concern. ”Exorcising a mold monster” ”Attack on the killer mold”

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The association between environment and fungal disease

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  1. The association between environment and fungal disease Malcolm Richardson University Hospital of South Manchester, and The University of Manchester, UK

  2. Fungi are in the air

  3. Public concern ”Exorcising a mold monster” ”Attack on the killer mold” ”It’s everywhere. Tales about rampant toxic mold get plenty of attention, but science tells a less dramatic story” ”The mold rush” ”One in four homes in the UK is infested with toxic mould”

  4. Public concern: Europe • Smaller scale than US • High public awareness • Regional • Limited research • Limited funding: • EU: MOULDARRAY: Co-Operative Award: Holland, Finland, UK, Denmark, Sweden

  5. Patients live in mouldy houses:exposure to Aspergillus and more......

  6. Exposure in the garden

  7. The tsunami and Sakseniae vasiformis

  8. 42 days LAMB Snell & Yavakoli 2007; 119: 448-449

  9. Key issues • Air as a source of human infection • Water as a source of human infection • Other environmental sources of human infection • Hospital versus community acquisition of infection • Molecular strain typing of Aspergillus species

  10. Aw < 0.80, ERH <80% Aw < 0.80-0.90, ERH <80-90% Aw >0.90, ERH >90% water Aw: Minimum water activity level at 25°C ERH: Equilibrium relative humidity

  11. Evaluate Potential or Actual Mould-related Health Issues We have to establish the cause-effect relationship between indoor amplification of fungi and the health problem of the building resident or hospital patient.

  12. Indoor Events 1.Intrusion and condensation of water. 2. Impact of conidium or spore from air. 3.Germination of conidium or spore. 4.Penetration of substrate. 5.Development of vegetative hyphae. 6. Translocation of nutrients. 7. Development of aerial hyphae.

  13. Indoor Events(continued) 8. Coordination of conidiogenesis or ascocarp formation, melanin biosynthesis, mycotoxin production. 9. Release of Volatile Organic Compounds.

  14. Indoor Events (continued) 10. Liberation and air dispersal of conidia, spores, hyphal fragments, cell wall pieces, melanin particles. 11. Inhalation, skin contact 12. Absorption of mycotoxins. 13. Antigen challenge.

  15. Relationship Between Health and Indoor Moulds exposure from mould growth indoors indoors background exposure from all sources and agents outdoors individual’s health and genetics Baseline health status Final health status Effect of indoor exposure

  16. Exposure and Disease 1. exposure a. inhalation of conidia, spores, hyphae, cell wall components, mycotoxins, MVOCs.     b. contact by conidia, spores, hyphae, cell wall components, mycotoxins, MVOCs.     c. ingestion of conidia, spores, hyphae, mycotoxins.

  17. Exposure and Disease (continued) 2. Disease a.Allergic • alveolitis, anaphylaxis, asthma, conjunctivitis, dermatitis, hypersensitivity pneumonitis, rhinitis, rhinosinusitis, sinusitis b.irritant

  18. Exposure and Disease (continued) c.Mycotoxicosis 1). fungal volatile organic compounds • mycotoxin biosynthetic pathway 2). mycotoxins and other secondary metabolites • inhalation, ingestion, skin contact

  19. Exposure and Disease (continued) d.Invasive 1). exceptionally rare 2). immunocompromised patients 3). aspergillosis 4). invasive sinusitis

  20. Thought Process • Is there amplification of the fungus indoors? • What species has been identified growing within the structure? • Are there signs and symptoms compatible with: • a. allergic fungal disease? • b. fungal toxicosis? • 4. What is the residents past medical • history for: • a. respiratory disease? • b. allergic disease? • c. sinusitis?

  21. Thought Process (continued) 5. Have mycotoxins been detected in: a. building materials? b. air samples? 6. Is serology an option? 7. Is skin testing an option?

  22. Thought Process (continued) 9. Is there mould count data for the outdoor air: a. daily and seasonal data (weather reports and summaries) b. intensity of mould counts during investigation 10. What are the levels of other allergens such as pollen, mites?

  23. Hospital demolition Hansen et al. JHI 2008; 70: 259-264.

  24. Heavy excavation! Nihtinen et al. 2007 BMT

  25. Benet et al. CID 2007; 45: 682-686.

  26. Key statements • “a significant relationship between environmental fungal contamination in haematology wards and the incidence of IPA” • “a straightforward association between environmental modification and decreased IA incidence”

  27. Six links in the nosocomial infection chain • The causative agent: environmental moulds • Mode of transmission: air, water, food • Susceptible host: high risk patients • Portal of entry: respiratory tract, skin • Portal of exit: person to person transmission • Reservoir: air, water

  28. Source of Aspergillus

  29. Air as a source of human infection • Inhalation: most common portal of entry • Temporal association between hospital-based outbreaks and construction • Very little data on base-line concentrations • Longitudinal studies show no correlation between sporadic cases of IA and changes in spore count

  30. Concentrations of airborne Aspergillus compared to the incidence of invasive aspergillosis: lack of correlation • 54-week air sampling period • A. fumigatus and A. flavus: mean 1.83 cfu m-3 • Individual samples: maximum: 11.6 cfu m-3 • No correlation with season or ward • 6 cases of IPA during sampling period • No association with fluctuations in air count Conclusion: “the available data do not provide a firm link between hospital exposure and an increased incidence of aspergillosis” Hospenthal et al., Medical Mycology 1998.

  31. Toxic mould in the hospital setting Growth: 1-2 mm per hour!

  32. ASPERGILLOSIS

  33. Invasive aspergillosis

  34. Aspergillus: Time to diagnosis of aspergillosis after BMT Graft versus host disease 20 18 16 14 12 10 8 6 4 2 0 Neutropenia Wald et al. J Infect Dis 1997;175:1459 Cases 10 20 30 40 50 60 70 80 90 100 110 120 130 140 150 160 170 Days after transplant

  35. Nosocomial Due to break in, or contamination of hospital water system Due to break in HEPA filtration system Due to construction or demolition work in the hospital Community-acquired Due to housing quality Due to occupational activities Due to leisure activities Due to exposure to Aspergillus spores (minimum effective dose not known) Nosocomially vs. community-acquired IA Praz-Christinaz et al. Transplant Infect Dis 2007; 9: 175-181

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