Eggs and larvae of Microplitis rufiventris Kok. (Braconidae: Hymenoptera) were exposed to two sublethal concentrations (0.2 and 0.4 ppm) of the chitin synthesis inhibitor lefenuron, by feeding treated artificial diet to their hosts, Spodoptera littoralis (Boisd.) (Noctuidae: Lepidoptera) larvae. Each concentration was initiated during the egg stage or different instars of the parasitoid larvae. Between 4.3 and 33.8% of parasitoid larvae in lefenuron-treated hosts showed morphological and developmental abnormalities. The effect of the compound on the developmental rate and sensitivity of the parasitoid larvae varied according to the parasitoids' age at treatment; the egg stage and older parasitoid larvae were more tolerant to the compound than the first instars. In all treated hosts the developmental rate of the parasitoid was lower than that of controls. The lower lefenuron concentration (0.2 ppm) was more effective at disrupting the development of young parasitoid larvae than the higher one. Delayed or latent effects of the compound were evident in non-emergence of parasitoid adults that were exposed to the compound as first instars. Reduced sensitivity of old parasitoid larvae could be compatible with survival of the parasitoid in integrated control programme of S. littoralis.

The chitin synthesis inhibitor lefenuron [N-{2,5-dichloro-4-(1, 1, 2, 3, 3, 3-hexafluoropropoxy)-phenylaminocarbonyl}-2, 6-difluorobenzamide] was found to have a negative effect on the encapsulation responses of Spodoptera littoralis larvae towards supernumeraries of Microplitis rufiventris parasitoid. Superparasitised hosts fed on compound-free diet showed strong encapsulation reaction (ca. 40.8%) to surplus parasitoid larvae having scars of physical combat. Treated hosts exhibited a significant reduction in either capsule thickness or encapsulation rate to the excess parasitoid larvae. Even when a capsule was formed, it had a thinner haemocy tic layer than tha t of control hosts. Studies on the differential haemocyte counts showed that failure of treated larvae to encapsulate injured surplus parasitoid larvae could be attributed to the following factors: (1) disturbance in plasmatocytes-granular cells (GR) ratio, e.g. abnormal increase in GR levels possibly causing faint haemocytic reaction to injured parasitoid larva(e); (2) the parasitoid surface becoming less attractive to the granulocytes and plasmatocytes; (3) the haemocytes involved in capsule formation (granulocytes, plasmatocytes) losing their ability to spread out over the surface of parasitoid larvae; and (4) the blood cells of the treated host failing to recognise wounded larvae as foreign bodies. Reduced encapsulation capacity might be due to a secondary effect(s) of IGR treatment inducing a suppression of adhesive activity of the plasmatocytes. These results may be useful for improving our understanding of insect immune reaction and/or manipulating parasitoids activity against nonhabitual Parasitoida.

Rates of virus-induced mortality and values of the LC50 and LT50 showed that, in general, parasitism by Microptitis rufiventris Kok. increased the susceptibility of the Egyptian cotton leafworm, Spodoptera littoralis second-instar larvae to its nuclear polyhedrosis virus (SLNPV). By comparing the LC50 values, data revealed that virus-infected parasitized larvae were ca. 3.5 and 4.8 times more susceptible to SLNPV than virus-infected unparasitized ones at 8 and 12 days post-infection, respectively. Also, in virus-infected unparasitized larvae, the time required to attain a 50% mortality was significantly longer than that in virus-infected parasitized ones.