Forgot your password?

Please enter your username or email address. Instructions for resetting the password will be immediately emailed to you.
Reset Password

Return to login form 

Please note: While some information will still be current in a year, other information may already be out of date in three months time. If you are in any doubt, please feel free to ask.

Risk of infection with CF germs in asthma

Dear expert team,

I am a father with CF. My daughter has infantile bronchial asthma.

Do my Pseudomonas germs have any effect on my daughter’s asthma?

Many thanks for your support.

Kind regards.
Dear questioner,

You have CF, are colonized with P. aeruginosa, and are worried that this germ could negatively affect your daughter’s asthma.

To begin with, in contrast to CF, P. aeruginosa is not primarily associated with the clinical picture of bronchial asthma. Therefore there is hardly any detailed data for asthmatics on possible effects of colonization with P. aeruginosa, which in this present case cannot be ruled out entirely.

Usually, P. aerguinosa only causes respiratory infections in case of immunosuppression or pre-existing lung disorders such as cystic fibrosis, bronchiectasis, chronic obstructive pulmonary disease (COPD) and ciliary dyskinesia.

Bronchial asthma does not belong to the group of diseases in which P. aeruginosa plays a particular role. Asthma is a chronic, inflammatory disease of the respiratory tracts in which hypersensitivity (Th2 immune response) to various stimuli is prominent. Since the term “asthma” can refer to many different clinical pictures and I do not have any detailed information on your daughter (e.g. age), I can only answer the question broadly.

Apart from hypersentivity of the respiratory tracts, infections can play a certain role in asthma as well. Apparently, infantile infections from viruses can increase the later development of asthma. Additionally, infections in asthma patients can cause exacerbations, i.e. acute impairment. Here, various viral infections are by far the most significant. Bacterial germs occur much less frequently as causes of exacerbations; if so, it is predominantly the prevalent germs of respiratory infections which also appear in healthy people, such as H. influenzae, S pneumoniae, M catarrhalis, S. aureus, mycoplasmae or chlamydia. P. aeruginosa is therefore not predominant, since the conditions in the respiratory tracts are apparently not very favorable for this germ.

Very rarely though, P. aeruginosa can also be proven in asthma from samples of the respiratory tracts (Fayon et al, 1999). A transmission of P. aeruginosa to your daughter is therefore unlikely but cannot be ruled out entirely, particularly with regard to the high number of germs in CF patients and the close contact between family members. Furthermore, heavy mucus production, increased obstruction of the respiratory tracts or bronchiectases the way they occur, for instance, after a long-time progression of asthma, can promote P. aeruginosa colonization. The exact effects depend on many factors and are hard to predict.

Apart from allergens and other germs, however, P. aeruginosa is only one among many possible factors that can influence asthma. According to experimental data, the antigenes of P. aeruginosa bacteria cause a Th1 immune response and thus do not directly reinforce the hypersensitivity that is responsible for asthma (Allard et al, 2009). Since the casual contact between father and daughter has to be assessed more strongly than the residual risk of a Pseudomonas transmission that cannot be ruled out, I only consider it necessary to abide by the hygiene measures CF patients are usually familiar with (hand hygiene when in contact with secretions of the respiratory tracts, preparation of inhalators, etc.)

Kind regards
Michael Hogardt

M Fayon, J Just, H Vu Thien, T Chiba, L Pascual, G Sandouk and A Grimfeld. Bacterial flora of the lower respiratory tract in children with bronchial Asthma. Acta Pädiatr 88, 1999.

J B. Allard, L Rinaldi, M Wargo, G Allen, S Akira, S Uematsu, M E. Poynter. Th2 Allergic Immune Response to Inhaled Fungal Antigens is Modulated By TLR-4-Independent Bacterial Products. Eur J Immunol.