Studies on cannibalism by Heliothis armigera (Hubn.) larvae on nuclear polyhedrosis virus (NPV)-infected larvae and feeding on virosed cadavers indicated that feeding was significantly higher on 4-day-old virosed cadavers followed by 1-day-old cadavers than on healthy or NPV-infected living larvae. The data revealed that cannibalism was significantly higher on NPV-infected (3 days post inoculation) larvae than either healthy larvae or those which had been just inoculated. However, the extent of feeding was higher on healthy larvae (cannibalistic feeding) than on cadavers. Significantly more number of larvae became infected by NPV when they fed on NPV-killed cadavers than on NPV-infected living larvae. Some of the larvae which had fed on either virosed cadavers or NPV-infected larvae survived. But, the disease was expressed in the pupal stage. Pupal mortality was significantly higher in larvae which fed on NPV-inoculated larvae (3 days post inoculation). The multiple choice test to find out the feeding preference of the larvae showed that the larvae had a greater preference to feed on virosed cadavers than either the healthy larvae or the host plant. The role of cannibalistic behaviour in the dissemination of the virus disease under field conditions is discussed.

An additive effect was obtained after treatment of Spodoptera littoralis (Boisd.) larvae with a combination of Bacillus thuringiensis and nuclear polyhedrosis virus (NPVs). The NPVs was the more pathogenic followed by B. t., cytopathologically. Simultaneous application of B. t. and NPVs affected the midgut cells by causing a very specific appearance of cell hypertrophy with some deposits of B. t. crystals on the fourth day of infection as shown by scanning electron microscopy. Transmission electron microscopy showed that the vegetative cells and spores of B. t. entered the midgut epithelial cells followed by the virus. It is possible that the initial destruction caused by the B. t. toxin facilitated penetration and entry of the virus.

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.

Third instar larvae of Spodoptera litura (Fab.) treated with polyhedrosis virus at dosages above 3.2 × 107 polyhedra inclusion bodies (PIB)/ml produced over 90% mortality. The LC50 was 2.3 × 104 PIB/ml. The estimated median lethal time (LT50) was 7.4 and 6 days at the lowest and highest dosages, respectively.

Polyhedra were observed in the epidermal cells, tracheal matrix, muscles and all nuclei of tissues of the virus treated larva 48–72 hr after treatment.

A nuclear polyhedrosis virus isolated from the Egyptian cotton leafworm, Spodoptera littoralis, was found to infect termite castes of Kalotermes flavicollis. Laboratory studies indicated that no specific trend toward mortality responses among the different individuals of termites was noted. All test castes of termites, young, middle-sized, old and reproductive nymphs, and soldiers, were quite equal in their response to the virus infection, regardless of whether the virus concentration was high or low; a concentration of 6.4 × 108 polyhedra/ml, killed only 64% of the treated individuals, while the dosage of 6.4 × 107 polyhedra/ml produced over 90% mortality. Also, thesame trend of response was recorded with the survivors which received challenge doses of NPV suspension each 9 or 10 days. On the other hand, these results revealed that if the NPV is used to control termites, periodic applications would be more efficacious thanone treatment. Virus symptoms were recorded in all affected insects.

Tests on the quantitative adsorption of polyhedra of nuclear polyhedrosis virus of Heliothis armigera to black and red soil showed an increase in the adsorption of polyhedra with an increase in the amount of soil. The increase was higher in the red soil than black soil, but the number of polyhedra adsorbed per unit weight of soil decreased as the amount of soil increased; the rate of decrease being faster in black soil than in red soil. The adsorption of polyhedra of nuclear polyhedrosis virus of Heliothis armigera is discussed based on certain physico-chemical properties of both red and black soils.

Field observations were carried out on a natural outbreak of a nuclear polyhedrosis virus of the armyworm Spodoptera exempta. Records were kept in four study sites with varying larval density, vegetation cover, and climatic conditions. Biotic factors influencing disease outbreaks were also noted. Initial mortality was recorded 11 days after larval outbreak, and the highest mortality occurred 10 days later. The epizootic was highest in sites of high larval density, wide fluctuations of daily temperatures (range 16.2°C), and high relative humidity. Rainfall was recorded in all disease outbreak sites. An acridid Acrotylus patruelis fed on larval cadavers in the field. Polyhedral inclusion bodies recovered from the gut of A. patruelis caused disease when fed to third instar S. exempta larvae in the laboratory. Predation on larvae by the pied crow Corvus albus in some observation sites reduced larval numbers, and may have prevented NPV from rising to epizootic levels in such areas. In sites of high polyhedrosis incidence, the disease led to larval population collapse in 3 weeks following disease outbreak.

The susceptibility of third-instar Spodoptera exempta (Walk.) to a heat-treated nuclear polyhedrosis virus was tested in the laboratory. The polyhedral suspension was purified by differential centrifugation and heat-treated at temperatures that ranged from 20 to 90°C for 10–30 min. The LT50 ranged from 108.4 hr for virus heated at 50°C (10 min) to 162.2 hr for virus heated at 80°C (10 min). The fiducial limits to the LD50s were calculated at 0.95 probability.