Allergic-type inflammatory reactions to Onchocerca volvulus microfilariae in the skin. The Figure shows effect of treatment with the microflaricidal drug diethylcarbamazine. Pre-treatment skin biopsy (A) shows microfilariae in the dermis with few associated inflammatory cells. After treatment with a single dose of DEC, the dead microfilariae become the focus of an intense inflammatory reaction composed of eosinophilic abscesses in the superficial dermis (B). Clinical appearance of the skin after DEC treatment (C).

Examples of allergic-type reactions to helminth parasites. A. Immediate hypersensitivity reaction to Paragonimus mexicanus antigen extract injected into the forearm of child. B. Cutaneous larva migrans showing serpiginous track of dog hookworm larvae in foot. C. Punctate keratitis in young child infected with Onchocerca volvulus. The punctate opacities are sites of microfilarial death in the cornea and are composed of eosinophil-rich inflammatory infiltrates. The photograph was taken after removal of an onchocercal nodule (bandage). D. Acute papular onchodermatitis in woman infected with O.volvulus. Localized popular eruptions appear periodically in infected individuals representing the sites of ‘spontaneous’ microfilarial death.

Possible effects of Ascaris lumbricoides infection on atopy and asthma. The human response to exposure to A. lumbricoides is likely to be modified by host genetic factors and other factors including the intensity of infection and the age at which first infections occur. Exposure to A. lumbricoides could affect the development of allergen skin test reactivity in 4 ways (shown by paths 1-2-3, 1-2-4-7 and 1-4). Pathway 9-10 represents the effect of chronic infections - a high IgG4/low IgE response to A. lumbricoides or modified Th2 response [reference 1] develops and may lead to the suppression of allergen skin test reactivity. The pathways leading from step1 would be associated with a high IgE/low IgG4 response to A. lumbricoides. Pathway 7 represents the enhancement of allergen skin test reactivity by an unknown mechanism. Exposure to A. lumbricoides could cause or increase asthma symptoms and bronchial hyper-reactivity via enhanced allergen skin test reactivity (paths 7-6, 1-2-3-6, and 1-4-6) or be independent of allergen skin test reactivity (paths 1-5 and 8) or independent of both anti-Ascaris IgE and allergen skin test reactivity (8). Suppression of asthma symptoms and or BHR could occur via path 9-11, although there is very limited evidence in support of this. Shown are published associations from cross-sectional studies and presumed causal directions (arrows). Reference numbers are shown in brackets.