FUNGAL INFECTIONS
Fungal infections may be superficial, e.g. oral thrush, skin/nail mycosis, etc. or invasive, involving fungemia or systemic tissue disease. While superficial fungal infections are common, invasive disease is rare except in immunocompromised children.
This chapter deals with three important fungal infections—candidiasis, aspergillosis and cryptococcal meningitis. Others, e.g. histoplasmosis (H.capsulatus) blastomycosis (B.dermatitidis), coccidiomycosis (C. immitis), and mucormycosis are extremely rare in Indian children.
Candidiasis is the commonest human fungal infection due to C. albicans, though non-albicans species are emerging as important pathogens for invasive disease. As candida is a common colonizer of gut, respiratory tract and vaginal flora, the term candidiasis usually refers to superficial overgrowth or invasive systemic disease. High-risk factors: Candidiasis is the commonest opportunistic infection in immunocompromised children and those on prolonged antibiotics, though also seen in normal newborns (as oral thrush or diaper dermatitis) and adolescent females (as vulvovaginitis).
Clinical spectrum of candidiasis depends on the risk factors and usually include:
Oral candidiasis (thrush) is commonest candidal infection, seen in: (a) normal newborns and infants lt;3 months, (b) prolonged antibiotic therapy, (c) prolonged use of steroid inhalers, and (d) immunocompromised children. Clinically, it is characterized by superficial white plaque on oral mucosa, tongue and palate that leaves punctate bleeding on removal (Ch 14.3.3).
Diaper dermatitis presents as confluent popular erythema with red satellite pustules over diaper area. It is common in infants on antibiotics, chronic diarrhea or contact dermatitis.
Systemic (invasive) candidiasis is seen in: (a) extreme preterms/low birth weight newborns, (b) immunocompromised states, and (c) after prolonged vascular/ urinary catheterization.
Infection form colonized sites may spread directly (esophageal candidiasis, candiduria) or hematogenously, to produce systemic illness, e.g. pneumonia, meningitis and candidemia.Chronic mucocutaneous candidiasis is a heterogeneous group of T-cell defects, characterized by persistent/ recurrent mucocutaneous candidiasis, usually associated with endocrinopathies, e.g. Addison's disease and other autoimmune disorders. Invasive disease is rare and treatment is prolonged topical antifungal therapy.
Diagnosis of superficial candidiasis is largely clinical, while invasive disease may be confirmed by: (a) direct demonstration of yeast cells/hyphae from skin/mucosal scrapping, or (b) fungal cultures from blood, CSF or urine. In catheter-related cases, removed catheter-tip should always be cultured to confirm the source of infection.
Treatment: Superficial candidiasis is treated with topical anti-fungal preparations, e.g. miconazole, clotrimazole, nystatin or gentian violet, apart from supportive measures, e.g. frequent change of diapers and topical steroid creams, if severe inflammation is present.
IV Liposomal Amphotericin (5 mg/kg/d for 2-3 weeks after last positive culture) is the drug of choice for invasive candidiasis. A second antifungal-Flucytosine or Fluconazole may be added in CNS/renal disease.
Fluconazole is not effective against many non-albicans strains.
Aspergillosis refers to a group of diseases, usually caused by Aspergillus fumigatus. Infection is acquired by inhalation of spores (conidia), present in soil/decaying plants or rarely by wound contamination.
Risk factors for aspergillosis include: (a) inherent atopic states (asthma), (b) heavy/prolonged exposure (Farmer's lung), (c) chronic lung disease (allergic bronchopulmonary aspergillosis), and (d) immunocompromised host, e.g. HIV, neutropenia or malignancies (invasive disease).
Clinically, it may present as: (a) non-invasive disease pulmonary or sinus aspergilloma or otomycosis, (b) invasive pneumonia or disseminated aspergillosis, and (c) hypersensitivity syndromes, e.g.
asthma, bronchopulmonary aspergillosis, etc.Diagnosis depends on: (a) clinical suspicion, (b) presence of fungal mycelia/hyphae in tissue lesions or sputum on microscopy/culture, and (c) allergy tests, e.g. skin test, specific IgE levels or radioallergosorbent test (RAST) in hypersensitivity syndromes.
Treatment of choice is: (a) IV/PO voriconazole or liposomal Amphotericin B in invasive disease, (b) topical antifungals and steroids in non-invasive disease, and (c) steroids for hypersensitivity manifestations; along with supportive therapy. Duration of therapy depends on the site of infection, severity of disease and clinical response. Cryptococcosis (C. neoformans) is the second commonest fungal infection in HIV +ve population, after candidiasis. Infection is acquired by inhalation of spores, present in soil or vegetations contaminated by bird-droppings.
Clinically, sub-acute meningitis is the commonest feature of invasive disease in immunodeficient children, followed by sepsis-like syndrome, lymphonodular disease, cutaneous ulcers/warts and skeletal disease. Cryptococcosis is extremely rare in immunocompetent individuals, except asymptomatic/progressive pneumonia in heavily-exposed adults, e.g. pigeon breeders or bird-traders.
Diagnosis rests on clinical suspicion in immunodeficiency state, supported by latex agglutination test in serum or CSF (titers gt;1:32). Confirmation requires recovery of fungus on CSF/serum culture or in biopsy tissues.
Treatment of choice for invasive cryptococcosis, (e.g. meningitis) is IV Amphotericin B, with/without Flucytosine till complete response, followed by lifelong maintenance therapy with Fluconazole. Mild cases limited to lung involvement may be treated with oral Fluconazole.
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