Host biology Aspects unique to pediatric patients

Anatomical considerations are important throughout infancy, but particularly in preterm neonates. Due to the reduced thickness of the skin, the use of medical devices and the moist environment, preterm neonates have a particular susceptibility to developing primary cutaneous aspergillosis and zygomycosis [1, 2]. Similarly, the extremely tenuous gastrointestinal wall structures lead to a unique propensity to primary invasive gastrointestinal mold infections with precipitous perforation, a pattern that is relatively uncommon in other settings [3, 4]. The comparably small diameter of blood vessels provides a nidus for catheter-associated Candida thrombophlebitis, -thrombosis, and endocarditis [5-8]; life-threatening Candida laryngitis and epiglottitis may occur in immunocompromised infants and young children for similar anatomical reasons [9-12].

In neonates, physiological differences such as the larger fractional water content, the smaller plasma protein fraction, relatively larger organ volumes, and the functional immaturity of hepatic metabolism and renal excretion result in considerable differences in drug distribution, metabolism, and elimination as compared to a standard healthy adult [13-15]. The still incomplete blood-brain barrier, in addition to its pharmacological consequences on drug penetration, may also be one reason for the enhanced risk of neonates to develop meningoencephalitis, an otherwise unusual complication of invasive Candida infection [16, 17]. Infants and younger children continue to exhibit differences in the relative proportion of body water, adipose tissue, and organ volumes; of note, as compared to the age-related, decreasing organ function in adult individuals, the functional reserve of both hepatic and renal function is generally larger [15].

Specific immunological characteristics in neonates include a functional immaturity of mono- and polymorphonuclear phagocytes and T lymphocytes [18] as well as a possibly increased susceptibility to the immunosup-pressive effects of glucocorticosteroids [4], which may render them susceptible to nosocomially acquired opportunistic mycoses. The yet-developing cellular immunity may also explain the occurrence of overwhelming infections by Histoplasma capsulatum [19, 20] and possibly other endemic fungi in infants [21]. The pediatrician may also become confronted with neonates and infants who present with superficial or invasive fungal infections as one of the first manifestations of a congenital T cell immunodeficiency [22, 23]

or of chronic granulomatous disease [24, 25]. In older children and adolescents, genetic illnesses such as cystic fibrosis or B cell disorders, which lead to chronic recurrent airway infection and lung destruction, may result in fungal airway disease including allergic bronchopulmonary aspergillosis, aspergilloma, and sometimes, invasive mould infections [26, 27].

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