The responses of Ligia oceanica (L.) (Crustacea: Isopoda) to infection by Maritrema linguilla Jäg. 1908 and Microphallus similis (Jäg. 1900) (Digenea: Microphallidae) and to abiotic implants

Abstract

The initial and principal encapsulation response of Ligia oceanica to Araldite implants and to encysted metacercariae of Maritrema linguilla is hemolymph coagulation followed by limited hemocyte agglutination. Granules secreted by isolated granulocytes and semigranulocytes may catalyze coagulation. Isolated hyaline cells explode and make an insignificant contribution to the initial cyst wall. Later, hemocytes agglutinate and some granulocytes retain their granules which become melanized. Eventually, a wide multilayered hos capsule is formed. Unencysted metacercariae of M. linguilla transplanted from the pleopods into the dorsal hemocoel of another specimen of L. oceanica encyst and become encapsulated but are not damaged by encapsulation. Transplanted encysted metacercariae are also encapsulated and unharmed. Cercariae implanted directly into the dorsal hemocoel, however, fail to encyst, become encapsulated, die, and lyse within the capsule. Implanted cercariae and encysted metacercariae of Microphallus similis are also encapsulated and destroyed in the hemocoel of L. oceanica. The absence of host response to the naturally infecting unencysted parasite in the pleopod sinuses may be attributed to rhythmic movement, mucopolysaccharide secretions and to the retention of excreta within the excretory bladder. Once the excreta is released during cyst formation in the dorsal hemocoel, encapsulation occurs but this does not appear to harm the parasite. On the contrary, considerable growth occurs within the cyst which suggests that the parasite may absorb nutrients released from necrotic hemocytes.