Different modes of immune reactions of insect vectors of human and animal diseases to nematode and protozoan parasites, fungi, bacteria, viruses and to other biological materials e.g. xenografts are discussed in this paper. Since most of the insect vectors of diseases are adult dipterans with low numbers of circulating haemocytes, their mode of defence against metazoan parasites and fungal pathogens is primarily by means of humoral encapsulation, with little haemocyte participation. Although earlier workers reported that humoral capsules in dipterans were formed without direct participation by haemocytes, this paper reveals increasing evidence of cellular involvement in the formation of humoral capsules, both at the initial and terminal stages of the encapsulation process. The role of phenoloxidase system in non-self recognition and in the process of melanization of haemolymph and capsules formed around parasites and fungal pathogens is also discussed. Immune defence of insect vectors against bacterial invasion by means of haemocytic reactions e.g. phagocytosis and nodule formation and by synthesis and release of humoral antibacterial factors e.g. lysozyme, attacins and cecropins is described and compared with similar reactions reported to occur in other insects. The role of lectins in defence of insect vectors against the parasites they transmit e.g. sandflies against Leishmania, blackflies against Onchocerca and tsetse against Trypanosomes is discussed and the possible mechanisms by which some parasites evade recognition and attack by the vector immune systems are also briefly discussed.

Epidinocarsis lopezi proved to be an efficient biological control agent of the cassava mealybug (CM), Phenacoccus manihoti, despite apparently low parasitization rates. Laboratory experiments indicated that its killing power at higher temperatures was two to three times higher than the per cent mummy formation suggested. Following an attack by an E. lopezi female some CM hosts were killed through host feeding and some through successful development of the parasitoid larva, processes which both benefit the parasitoid. If the host was found unsuitable, no egg was laid, and the CM survived the attack. Other CM died from the wasp attack without forming a mummy. This mortality is attributed to mutilation and unsuccessful larval development of E. lopezi. Most ovipositions induced a defence reaction by the host that lead to melanization. This process involved mainly wound tissue, sometimes partial encapsulation of the tail end of the parasitoid larva, and infrequently complete and fatal encapsulation of the parasitoid larva.