The pathology associated with lymphatic filariasis results from a complex interplay of the pathogenic potential of the parasite, the immune response of the host, and external ('complicating') bacterial and fungal infections.
While genital damage (particularly hydroceles) and lymphoedema / elephantiasis are the most recognizable clinical entities associated with lymphatic filarial infections, there are much earlier stages of lymphatic pathology and dysfunction whose recognition has only recently been made possible through ultrasonographic and lymphoscintigraphic techniques. For example, ultrasonography has identified massive lymphatic dilatation around and for several cm beyond adult filarial worms which, though they are in continuous vigorous motion, remain 'fixed' at characteristic sites within lymphatic vessels.
Histologically, dilatation and proliferation of lymphatic endothelium can be identified, and the abnormal lymphatic function associated with these changes can be readily documented by lymphoscintigraphy. Interestingly, despite the earlier paradigm that pathology associated with lymphatic filarial diseases was primarily the result of immune-mediated inflammatory responses, all of these changes can occur in the absence of such overt inflammatory responses and, even by themselves, can lead to both lymphoedema and hydrocele formation. The immune system during the development of this 'non-inflammatory pathology' is to keep itself 'down-regulated' through the production of contra-inflammatory immune molecules; specifically, the characteristic mediators of Th2-type T-cell responses (IL-4, IL-5, IL-10) and antibodies of the IgG4 (non-complement-fixing) subclass that serve as "blocking antibodies". Such adaptations do, of course, serve to promote the biological principle of parasitism in which a satisfactory balance between parasite 'aggressiveness' and host responsiveness must evolve to maintain this special relationship.