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Ü. R. Korkmaz et al.
young children. In 1959, Witting and Glasser outlined the epidemiological link
between childhood viral bronchiolitis and the later development of repeated
wheezing and/or asthma [81]. Since then, numerous studies have indicated the
relationship between asthma and RSV [82–84]. The follow-up at age 18years,
involving 46 of 47 subjects with RSV and 92 of 93 controls, revealed that
severe early RSV bronchiolitis is linked to a higher prevalence of persistent
allergic asthma into early adulthood, with small airway dysfunction (LCI)
associated with current asthma and airway inflammation [85]. Early-life severe
RSV infection has been linked to the onset of childhood wheezing illnesses
during infancy and the development of childhood asthma [86]. However, to
definitively determine causality, the effect of interventions that prevent, delay,
or reduce the severity of the initial RSV infection on childhood asthma needs
to be investigated.
The mechanisms linking these viruses to asthma development are distinct,
with RV generally a risk for later atopic asthma, while RSV is more likely to be
associated with later nonatopic asthma [71]. Another notable difference is that
in children hospitalized for lower respiratory tract illness, while RSV is frequently detected until about 12months of age, RV becomes more common in
older children [87]. Makrinioti et al. performed the rst meta-analysis that
directly compares between-virus differences in the magnitude of virus-recurrent
wheeze and virus-childhood asthma outcomes [88]. The preschool wheeze and
childhood asthma development association comparison between RSV- and
RV-induced bronchiolitis analysis shows that the RV-induced bronchiolitis
group was more strongly associated with the risk of developing wheeze and
childhood asthma [88].
Other commonly identied viruses include human bocavirus (hBOV) and human
metapneumovirus (HMPV), with detection rates reaching 10–25%, followed by the
parainuenza virus, adenovirus, coronavirus, and inuenza virus, each generally
accounting for less than 10% [71].
Nasal biopsy analysis from 49 children infected with HMPV showed that infection is a leading cause of respiratory tract infection in the rst years of life [89, 90].
Moreover, an association was observed between infection with HMPV and the diagnosis of an asthma exacerbation [90]. However, the connection between HMPV
infection and asthma was intriguing. Conicting reports exist on a potential link
between this infection and asthma [91]. Nevertheless, the existence of a correlation
between the presence of a virus and symptoms of respiratory tract disease does not
necessarily imply a causal relationship.
In addition, scientists highlighted the possible relationship of hBOV wheezy
infection with nonspecic markers of atopy in Polish children [92]. Another report
highlighted that 11.6% of hospitalized children with exacerbations of asthma were
infected with Bocavirus [93].
Epidemiologic studies indicated that H1N1 induces severe complications in the
lower respiratory tract, including bronchitis pneumonia, and atelectasis even in
atopic children without any history of either an asthma attack or asthma treatment [94].
8 Respiratory Microbiome
105
8.5 Mycobiome
Research conducted by Charlson et al. (2012) identied fungal communities in
BAL and oropharyngeal wash (OW) samples obtained from six healthy individuals.
The fungal communities observed in the OW samples of these healthy volunteers
were predominantly composed of fungal species already recognized in the oral cavity, with Candida and Aspergillus being notable examples [95]. Fungi identied in
BAL specimens from these subjects exhibited fewer fungal quantities compared to
samples from OW [95]. Numerous sequence reads were linked to the genera
Davidiellaceae, Aspergillus, Penicillium, and Polyporales, implying that fungal
inhabitants are present at a diminished density in the alveolar regions of the lungs in
contrast to the upper respiratory tract [96]. Continuous exposure to fungal allergens
may contribute to fungal colonization which potentially promotes a major shift in
bacterial microbiome and exacerbates the challenges in managing asthma symptoms clinically [97]. Fungi are a well-recognized source of indoor and outdoor allergens for individuals with atopic disease. The predominant associations involve three
distinct fungal groups: Ascomycota, Basidiomycota, and Deuteromycota [67].
Fluctuations in seasons can lead to heightened spore production from fungi, contributing to worsened asthma symptoms and increased pediatric morbidity [98]. A
study revealed a correlation between seasons and changes in the composition of
fungal microbiota in samples from children with respiratory illnesses [49]. An
increase in respiratory symptoms during the spring was linked to an increase in
Malassezia, whereas those occurring in the fall were associated with an enrichment
of allergenic fungi, Candida and Cladosporium [49].
Numerous studies have explored the correlation between exposure to fungi, sensitization, and the exacerbation of asthma in childhood. In particular, lamentous
fungal species belonging to the Aspergillus, Alternaria, Cladosporium, Penicillium,
and Didymella genera (in the phylum Ascomycota) generate spores that can serve as
allergens, potentially triggering bronchial asthma in individuals with atopic tendencies [99–101]. Among them, Alternaria is one of the most well-studied airborne
fungi in terms of allergic potency [102]. Although Alternaria spp. typically exist in
lower atmospheric concentrations compared to other airborne allergenic spores,
they exhibit the highest sensitization rate among atopic patients, estimated to range
from 13% to 17% [103]. Analysis of BAL pellets from children who underwent
bronchoscopy indicated that Rhodosporidium, Pneumocystis, Leucosporidium, and
Rhodotorula were substantially increased in severe asthmatic individuals compared
with nonasthmatic. In contrast, Davidiella, Cryptococcus, and Sterigmatomyces
were more prevalent in the nonasthmatic individual [57]. Tham etal. have shown
that the risk of child and adolescent asthma hospitalization is linked to exposures to
various outdoor fungal spore types, including Alternaria, Leptosphaeria,
Cladosporium, Sporormiella, Coprinus, and Drechslera [104]. This association is
particularly notable in individuals sensitized to Cladosporium [104]. Although
informative and providing a detailed account of microbial characteristics in these
asthmatic groups, these studies do not establish a causal relationship between the
identied airway mycobiome signatures and the development of asthma. In a study
106
Ü. R. Korkmaz et al.
involving 280 children from Boston, exposure to Alternaria in classrooms was
linked to prolonged asthma symptoms in children already sensitized to Alternaria.
This association was observed in comparison to sensitized children exposed to
lower levels of Alternaria in classrooms over 2 weeks [105]. Another study by
Welsh etal. (2016) examined sputum cultures from children with acute exacerbation or stable asthma and discovered elevated concentrations of Aspergillus fumiga-
tus in the sputum of children experiencing exacerbation, indicating a potential role
of this fungal species in asthma manifestations [106].
Aspergillus, a genus of mold that includes various species of fungi, is associated
with hypersensitivity respiratory disorders, conditions include Aspergillus-induced
asthma, allergic bronchopulmonary aspergillosis (ABPA), allergic Aspergillus
sinusitis (AAS), and hypersensitivity pneumonitis [107]. In 1953, the most extensively documented case of asthma linked to fungal was ABPA, initially identied as
a distinct entity that develops following sensitization to mostly A. fumigatus allergen [63]. The prevalence of ABPA is on the rise, it is impacting 1–3% of all asthmatics globally [108]. In individuals with asthma, fungal spores are entangled within
the thick and adhesive secretions that typically characterize the airways [107]. This
continuous exposure can exacerbate asthma, potentially leading to a more severe
manifestation of the condition [108].
While fungal spores are prevalent in substantial quantities outdoors, they are also
commonly found in indoor environments, primarily resulting from mold growth
facilitated by ventilation systems that assist in their dispersion [68, 69]. A more
recent issue has arisen with the recognition that numerous households contain signicant quantities of fungi. In multiple studies conducted across Europe, Canada,
and the United States, ndings revealed the presence of mold in homes ranging
from 15% to 36% [70–74]. A study conducted on 640 infants from Cincinnati elevated that the presence of major mold caused the likelihood of recurrent wheezing
by nearly two-fold in infants, ve-fold in infants sensitized to food or aeroallergens,
and six-fold in aeroallergen-sensitized [75]. A prospective birth cohort study suggested a direct relationship between the amount of indoor fungal exposure and the
incidence of respiratory tract infection in the rst year of life [76].
Evidence from the experimental mouse model indicates that prevalent fungal
colonizers in the gut can inuence the immune system, potentially making the host
more susceptible to allergic airway inammation. Changes in the mycobiome
induced by antibiotic treatment and the intestinal increase of Candida albicans
[109, 110], Candida parapsilosis [111], or Wallemia mellicola [112] have been
associated with heightened severity of allergic airway inammation in mice. In
addition, the expansion of lamentous fungi (Aspergillus amstelodami, Epicoccum
nigrum, and Wallemia sebi) subsequent to antifungal treatment exacerbated allergic
airway responses in animal research [113, 114]. Furthermore, a study analyzing
fecal samples from infants who later developed the atopic/wheeze phenotype
revealed a higher proportion of total sequenced fungal reads, a signicant increase
in fungal 18S recovered DNA, and an overrepresentation of Pichia kudriavzevii at
3 months of age [115]. These ndings suggest a correlation between early gut
8 Respiratory Microbiome
107
fungal overgrowth and the subsequent development of asthma, uncovering fungal
alterations associated with heightened susceptibility to asthma by school age.
These investigations highlighted the signicant role of fungi in exacerbating
asthma, affecting both children and adults. The origins of this impact are often
traced back to immune sensitization during infancy or childhood. However, not
every encounter with fungi leads to asthma-inducing sensitizations. Like bacteria,
some fungal exposures may be protective, highlighting the complex interplay
between specic fungal species’ immunogenicity and host immune susceptibilities.
Although not all fungal exposures negatively affect immune development, certain
genera, such as Alternaria and Aspergillus, consistently correlate with sensitization
in asthmatics and increased asthma severity. Improvements are still needed in fungal taxonomic databases, as well as in bioinformatics algorithms capable of effectively accommodating the greater variability in read length and the increased
frequency of genetic insertions and deletions within the regions commonly utilized
in most mycobiome sequencing approaches.
The microbiome represents a new frontier in respiratory medicine, and further
research is needed to elucidate the potential mechanisms underlying the pathophysiological processes of airway disease other than asthma in pediatric and adult populations. Not only bacteria but also fungi and viruses are collectively linked to clinical
outcomes, including periods of exacerbation, severity of disease, and response to
treatment. In the future, the development of personalized microbiota-based therapies may help alleviate clinical symptoms and decelerate the progression of airway
disease using the integration of data regarding microbiota with technological
advances such as next-generation sequencing and omics.
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Ü. R. Korkmaz et al.
Communication withSick Children
BurakÇakir, AlbertoAdalid, andÖznurBilaç
9.1 Introduction
Childhood is referred to as the rst 18-year period of life, and this period can be
examined in subgroups. The rst month of life is considered the newborn period,
while the ages of 0–2 are referred to as the infancy period. Subsequently, the period
can be divided into early childhood and preschool age. The school age is followed
by the adolescent (teenage) period, and an individual who has reached the age of 18
is considered an adult.
9.2 Essential Features ofCommunication withChildren
inChildhood
9
The behavioral and cognitive development of children generally follows a specic
sequential order. However, the pace of development can vary from child to child,
being either slow or rapid [1]. Life, growth and development are interconnected,
therefore communication should encompass all three aspects [2]. The manner of
communication should be age-appropriate for the child, which is a fundamental
principle. Another fundamental principle is recognizing the presence of the family
in the relationship established with the child [3].
B. Çakir
Uşak University Training and Research Hospital, Uşak, Turkey
A. Adalid
Private Psychoanalystand Psychotherapist, Mexico City, Mexico
Mexican Association of Group PsychoanalyticPsychotherapy (AMPAG),
Mexico City, Mexico
Ö. Bilaç (*)
Manisa Celal Bayar University Hospital, Manisa, Turkey
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2024
H. Yüksel et al. (eds.), Pediatric Airway Diseases, Comprehensive ENT,
https://doi.org/10.1007/978-3-031-74853-0_9
113