Management of fungal colonization/infection

Ref ID: 19455

Author:

F. M. Muller

Author address:

University Heidelberg, Germany

Full conference title:

6th Trends in Medical Mycology 2013

Date: 11 October 2014

Abstract:

Mutations in CFTR genes result in a defective mucociliary clearance
with production of viscous and sticky bronchial mucus that facilitates
the colonization with airborne bacteria and fungal spores. Fungi can
be routinely detected in the upper and lower respiratory tract includ-
ing the paranasal sinuses of CF-patients. However, they do not neces-
sarily cause infections. Candida spp. are the most common isolated
yeasts, whereas Aspergillus spp., Scedosporium apiospermum, as well as
Exophiala dermatitidis in some countries, are the most frequent
moulds recovered from respiratory specimens. Other Aspergillus spp.,
e.g. Aspergillus flavus, Aspergillus niger, Aspergillus nidulans as well as
Pneumocystis jirovecii and Rasamsonia argillacea are transient coloniz-
ers of the respiratory tract.Fungal colonization of the CF airways has
a prevalence rate ranging from 16 to 56.7%. It follows usually bacte-
rial infections, and is less common in younger children. The mean
age of first isolation of A. fumigatus and S. apiospermum is about 12.3
and 14.1 years, respectively.
A. fumigatus is often isolated in close relationship with P. aerugin-
osa, and these patients have a higher risk of developing chronic P.
aeruginosa infections despite antimicrobial therapy. Persistent A. fu-
migatus infection is associated with an increased risk of pulmonary
exacerbations requiring hospitalization. Therefore, the prevention of
initial colonization with A. fumigatus may postpone the subsequent
development of P. aeruginosa infection. Molecular typing studies
revealed that isogenic Candida and Aspergillus strains can persist for
months to years in the CF respiratory tract, and patient to patient
transmission can occur.
Generally, there is delineation between Candida superficial/mucosal
infections such as thrush, esophagitis, vaginal thrush or skin mani-
festations and candidaemia, organ mycoses and sepsis. A. fumigatus can cause aspergilloma in pre-existing pulmonary
cavities (bronchiectasis), and in chronically obstructed paranasal
sinuses. Other diseases are IgE-mediated allergic rhinitis and asthma,
hypersensitivity pneumonitis, chronic necrotizing pneumonia, and
allergic bronchopulmonary aspergillosis (ABPA). Molds can produce
a biofilm in the lungs which acts as a protective barrier and makes
them unreachable for both the body’s immune defence system as
well as for antifungal drugs.
Mixed fungal and bacterial communities are poorly studied. Some
bacteria can enhance the development of the fungus by secreting
compounds that increase the virulence of the fungus, or alternatively
they will secrete toxins to kill the fungus. Similarly, fungi can secrete
molecules which will regulate the quorum sensing of P. aeruginosa.
Antifungal treatment in CF is currently used to treat candidaemia,
invasive pulmonary aspergillosis, aspergilloma, and proven or sus-
pected allergic bronchopulmonary aspergillosis.
Lately the discussion has focused on whether a longer lasting colo-
nization by A. fumigatus should be treated with antifungal drugs. A
first randomized, placebo-controlled pilot study tested whether CF
patients who were chronically colonized by A. fumigatus would profit
from six months of oral antifungal therapy using itraconazole.
Within the relatively small group of 35 patients, no difference could
be detected between the placebo and the itraconazole group with
regard to pulmonary exacerbations or a decrease in FEV1.
Conclusion: Antifungal treatment of chronic A. fumigatus infection
is not recommended so far. The most appropriate antifungal treat-
ment should not be selected only on the basis of its efficiency to kill
in vitro grown fungal cells, but also on its ability to penetrate the
extracellular matrix in biofilm growth.

Abstract Number: w09-4

Conference Year: 2013

Link to conference website: NULL

New link: NULL

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