The IgE system exists because the same events which lead to often-life threatening complications of allergy, in presence of parasites are helpful in their elimination.
The tissue injury mediated via this hypersensitivity (type I) occurs due to the mediators released by mast cell degranulation due to IgE being synthesised in atopic individuals towards normal environmental particles. The effects are also due to further immune cells being recruited by the mediators. In case of parasites, this IgE is supposed to help in their elimination and not cause tissue injury, justifying its evolution as a defence mechanism.
How does this happen? If release of the mediators is a part of the pathway, even if the degranulation is localised in the vicinity of the parasite, the mediators will spread systemically or atleast in the nearby tissues with the same consequences as in the case of non-parasite activation of these events.
What then is the ultimate cause beneath there being tissue injury if the stimulation is unintended but there being none when the stimulation is directed and intended? Or is there some injury in the latter case also, in which case the classification of this response in absence of a parasite into hypersensitivity i only because there is no positive effect in this case, while there was some benefit accompanying the deleterious effects in the former case? Is the presence of a parasite and possible localised degranulation the only difference between these cases?