Mermithid parasites of larval diptera probably resemble M. nigrescens in obtaining dietary amino acids by stimulating the catabolism of proteins within the host fat body (Gordon, 1981). In addition to the reduction of most protein fractions, significant decreases also occurred in hemolymph glucose in parasitized blackflies; however, blood trehalose concentrations were not affected (Gordon et al., 1978). Glycogen reserves were shown to be similarly reduced in the fat body of mermithid- parasitized simuliids (Condon and Gordon, 1977). Gordon et al. (1979) found that parasitism did not significantly affect either the overall concentration of lipids or relative proportions of the lipid fraction in the hemolymph of mosquitoes. Mermithid parasitism of mosquitoes and simuliids caused almost complete degeneration of host fat body tissue. All storage metabolites, including glycogen, within the fat body may directly or indirectly be utilized by the developing nematode.
Responses are somewhat different in larger hosts with longer periods of parasitism. Protein in the fat body of grasshoppers parasitized by M. nigrescens was depleted after 2 weeks; corresponding reductions in proteins were not recorded from the hemolymph until I week later. The third week of infection represented a period of maintenance and reconstruction of fat body soluble proteins, but corresponding effects were not found for hemolymph proteins until the fourth week of infection (Gordon et al., 1978).
Gordon and Webster (1971) found that the overall level of amino acids in the hemolymph of adult female grasshoppers was not affected by mermithid parasitism, but the content of amino acids within the fat body was significantly reduced. Parasitism by M. nigrescens resulted in glucose levels remaining low for the first 4 weeks of parasitism relative to trehalose, but no significant difference for glucose levels when compared to unparasitized controls. Trehalose levels dropped and remained low for much of the parasitic period. These data suggested that the nematode modifies its host's metabolism to favor production of small molecules such as glucose and amino acids from carbohydrate and protein reserves and that the host cell's ability to sequester nutrients is impaired during parasitism (Rutherford and Webster, 1978).
Craig and Webster (1974) found that ecdysone levels in locusts were unaffected by M. nigrescens and attributed the inhibition of molting in parasitized insects to depletion by the nematode of precursors required by the host for protein and cuticle synthesis. However, ovaries of parasitized locusts were unable to sequester vitellogenic proteins available within the hemolymph, suggesting endocrine dysfunction in the host (Gordon, 1981).
Major modifications of the host's metabolism by mermithid parasitism are manifested in host tissue degeneration and retarded development including resorption or suppression of oocyte development. As a result, hosts are usually prevented from maturing to the adult stage or when they do they are generally unable to-,reproduce.
Hosts are occasionally able to prevent parasite development by either cellular or humoral responses. The most common cellular response is encapsulation. Poinar et al. (1979b) reported that Culex territans responded to the development of parasitic juveniles of R. culicivorax by covering the 2- to 3-day-old parasites with blood cells. These nematodes failed to complete development. A more frequent condition, melanotic encapsulation, was reported in Diabrotica beetle larvae attacked by F. leipsandra. Host hemocytes lysed on the cuticle of the nematode soon after it entered the host, and within 6-8 hours an inner layer of melanin had formed around the nematode (Poinar, 1979).
Similar responses were observed for larvae of Psorophoraferox, Aedes triseriatus, and Anopheles quadrimaculatus to the R. culicivorax. However, some 70 species of mosquitoes have not elicited this type of defense response to R. culicivorax (Petersen and Chapman, 1979). Recently, Gaugler et al. (1984) reported an encapsulation response when Empidomermis sp. entered larvae of Aedes stimulans if the nematodes were unable to migrate to the host's head and enter central nervous tissue. After pupation, the nematodes dropped back into the hemocoel where they no longer elicited a host defense reaction. This response may be common in mermithids that enter the larval stage but fail to mature until the host reaches the adult stage. Also, Harlos et al. (1980) noted that Culicimermis sp. entered the nerve tissue of Aedes vexans larvae and later developed in adult hosts; Petersen (unpublished data) observed a similar response in Ae. sollicitans when parasitized by P. culicis.
Humoral responses, noncellular components of the insect's hemolymph which have an adverse effect on nematode development (Poinar, 1979), may account for the host resistance observed in Aedes intrudens and Aedes provocans to an Empidomermis sp. when no discernible host response was observed, which was unlike the encapsulation response this nematode elicited in Ae. stimulans (Gaugler et al., 1984).
Another type of humoral response may be that observed when blackflies were subjected to the mosquito mermithid R. culicivorax. The mermithid initiated development in early-instar ;Iackflies, and direct host reaction to this unnatural parasite was not observed; eventually, however, both nematode and host died (Poinar, 1979).
Physical and behavioral responses also influence parasitism by mermithids. Host age, especially in aquatic insect hosts, has been shown to have a considerable effect on host susceptibility. Refractiveness because of age appears to be caused by the thicker cuticle in older larvae (Petersen and Willis, 1970). In the laboratory, as a result of mass-rearing practices for R. culicivorax, where exposed but uninfected hosts were retained to supply the next generation, the host mosquitoes were found to have become measurably less susceptible to the nematode after some 100 generations. No evidence of humoral defense mechanisms were found and the mode of defense was not determined (Petersen, 1978a). In a similar buildup of refractiveness in An. quadrimaculatus to S. Petersen, it was reported that less susceptible hosts were more active and aggressive in attempting to remove attacking preparasites (Woodard and Fukuda, 1977).