The epicuticle of dauer juveniles of the DD 136 strain of Steinernemafeltiae prevents encapsulation of the nematodes in vivo by hemocytes of Galleria mellonella larvae. The chemical composition of the epicuticle, which provides this protection, was determined using fluorescein isothiocyanate-conjugated lectins (concanavalin A, soybean agglutinin, wheat germ agglutinin) in conjunction with carbohydrases, lipase, and proteases. a-Mannose, 3-N-acetyl-D-galactosamine, and f8-N-acetyl-D-glucosamine were detected on the nematode's epicuticle. The absence of these sugars from enzyme-modified epicuticle did not affect hemocyte attachment. There was no evidence of epicuticular glycoproteins. In general, proteolytic enzymes did not alter the dauer juvenile epicuticle such as to elicit hemocyte-mediated encapsulation. Digestion of the epicuticle of dauer juveniles with lipase rendered the nematodes susceptible to hemocyte-mediated encapsulation. Many entomophilic nematodes live part of their lives in the hemolymph of their insect hosts, where the nematode cuticle is the interface between the nematode and the humoral and cellular components of the hemolymph. The function of the cuticle of these nematodes is incompletely known, but studies have shown that aspects of the transcuticular uptake of nutrients by entomophilic parasitic nematodes (Rutherford and Webster, 1974; Chen and Howells, 1979; Gordon et al., 1982) are related to cuticular structure (Nicholas, 1972; Batson, 1979; Platzer and Platzer, 1985). During the parasitic phase, the cuticle thickness of many entomophilic nematodes decreases (Bailey and Gordon, 1973), and in others, an outer microvillar layer develops (Riding, 1970) and functions as a nutrient absorptive layer. These nematodes encounter humoral (phenol oxidases) and/or cellular (hemocyte-mediated encapsulation) nonself resistance systems in the insect hemolymph (Ratcliffe and Rowley, 1979), but the contribution of the nematode cuticle to either resisting or evading these defenses is unknown, despite the reported occurrence of humoral (Welch and Bronskill, 1962; Andreadis and Hall, 1976) and cellular encapsulation (Nappi, 1975; Ratcliffe and Rowley, 1979). Vinson (1977) proposed that in the absence of active suppression of insect defenses, successful insect Received 5 September 1986; revised 3 December 1986; accepted 5 December 1986. * Present address: Department of Entomology, Macdonald College, McGill University, Ste. Anne de Bellevue, Quebec, Canada H9X 1CO. parasitoids would not be encapsulated due to (1) t e acquisition of a coat of host hemolymph components presenting the nonself agent as self, (2) the possession of heterophilic antigens, (3) the possession ofnonreactive surfaces, or (4) molecular mimicry. Evidence of a protective coat, albeit from insect midgut, may explain the reduction of humoral encapsulation of Brugia pahangi mic ofilariae in mosquitoes (Sutherland et al., 1984; Lafond et al., 1985). Entomophilic nematodes are not known to use molecular mimicry, although it may be used by cestodes and ac nthocephala (Lackie and Lackie, 1979) in some insects. The DD136 strain of Steinernema feltiae evades the hemolymph resistance systems of the gr ater wax moth, Galleria mellonella (Lepidoptera) larvae by avoiding nonself recognition (Dunphy and Webster, 1985), but the means by which this is achieved are unknown. The present study examines some of the epicuticular components of sheathed dauer juvenile S. feltiae DD136, and assesses the contribution of these components in evasion of encapsulation by the nematodes in G. mellonella. MATERIALS AND METHODS