Schistosomatium douthitti: effects of Lymnaea catascopium age on susceptibility to infection

Laboratory-reared Lymnaea catascopium snails (1–269 days old) were exposed individually to different numbers of Schistosomatium douthitti miracidia. Increasing the exposure dosage from 3 to 10 miracidia generally increased infection rates, in some age classes up to 100%. Successful re-exposure of snails not infected after a primary exposure was possible. Neonatal snails were least likely to become infected, primarily because miracidia were not attracted to them. Snails 12–55 days old were most susceptible to infection. Miracidia were readily attracted to these snails, and many were ingested and subsequently penetrated the host esophageal wall. Miracidial penetration of external snail surfaces was rare. Susceptibility of older snails (65–269 days) progressively declined with age. Many miracidia were entangled and immobilized in mucus produced by these snails, and fewer were ingested. No conspicuous host cellular responses to mother sporocysts were observed in any of the snails sectioned. A comparison of susceptibility of deliberately stunted snails and comparably aged controls of normal size indicated that the former were more susceptible.     

Schistosomatium douthitti: Exposure of Lymnaea catascopium to irradiated miracidia

Irradiation of Schistosomatium douthitti miracidia (4000, 5000, or 6000 rad) did not substantially alter their behavior or ability to penetrate their snail host. Treatment with 4000 rad was not sufficient to prevent all miracidia from establishing patent infections in Lymnaea catascopium, although significantly fewer snails exposed to these miracidia shed cercariae than did controls exposed to normal miracidia. Irradiation of miracidia with either 5000 or 6000 rad totally prevented cercarial production. Although destruction of irradiated mother sporocysts by encapsulating amebocytes was occasionally observed, most expanded without concomitant multiplication of germinal cells and embryo production and then collapsed. They generally persisted in this state throughout the period of observation (32 days). Snails sensitized by exposure to irradiated miracidia and challenged 2 or 10 days later with normal miracidia were as likely to develop patent infections as were snails exposed only to normal miracidia. Double sensitization of snails with irradiated miracidia also failed to confer protection upon challenge with normal miracidia. Most challenge sporocysts developed normally, often in close proximity to collapsed irradiated sporocysts.     

Intermediate host specificity in Schistosoma mansoni

Miracidia of Schistosoma mansoni penetrate into many kinds of snails, but development of normal sporocysts takes place only in certain species of Biomphalaria. Different populations of this snail vary greatly in laboratory infection rates with S. mansoni originating from diverse geographic localities. Cross-exposure experiments show that compatibility factors exist in both snails and parasites. Susceptibility of stocks of Biomphalaria to particular strains of S. mansoni is genetically determined and may be modified by selection in the laboratory. In a compatible snail, the sporocyst develops without host tissue reaction; in incompatible snails the early larvae are rapidly surrounded by amebocytes and fibroblasts, and destroyed. This reaction resembles the generalized host cellular response elicited by any foreign body. An individual snail exposed to many miracidia may have both developing and encapsulated sporocysts side by side within its tissues. The weight of current evidence suggests that elicitation or absence of this cellular response resides in the recognition or nonrecognition of the sporocyst as a foreign body. The sporocyst tegument surface, which forms within a few hours after miracidial penetration, may have a molecular conformation identical with that of the snail, or may be able to bind specific host molecules, so that detection and subsequent encapsulation by host cells are averted. Presuming genetic determination of the sporocyst surface structure and of the host cell detection capability, differing infection rates would result from the particular frequencies of relevant genes in the populations concerned.     

Studies on metabolism of lung flukes of the genus Paragonimus. VI. Succinoxidase system in homogenates of eggs, larvae, and adults

The present study was concerned with the succinoxidase system in Paragonimus westermani, Paragonimus ohirai, and Paragonimus miyazakii. Potassium cyanide inhibited the motility of larval and adult forms. Succinate stimulated the reduction of methylene blue by homogenates of embryonated eggs, larvae, and adults, while malonate inhibited the reduction. Reduced cytochrome c was oxidized by the 1,000g supernatant from homogenates of embryonated eggs, larvae, and adults. The supernatant prepared from unembryonated eggs did not oxidize reduced cytochrome c. Succinate stimulated oxygen consumption by the homogenate of adult worms. Oxygen consumption markedly increased in the homogenate of adults when both succinate and cytochrome c were added as substrate to the reaction mixture, while malonate and cyanide inhibited oxygen consumption.     

Schistosoma mansoni: Agglutination of sporocysts,and formation of gels on miracidia transforming in plasma of Biomphalaria glabrata

The resistance or susceptibility of Biomphalaria glabrata strains to strains of Schistosoma mansoni, the human blood fluke, are evidenced by the responses of snail hemocytes to sporocysts of the schistosome, both in vivo and in vitro. It is now reported that living sporocysts of the PR1 strain of S. mansoni agglutinate in the plasma of all tested strains of B. glabrata, in contrast to fixed sporocysts which agglutinate only in plasma from resistant snail strains. The agglutinating activity in resistant plasmas is not divalent cation dependent, and was not inhibited by the 26 carbohydrates and four amino acids tested. In addition, the observation that gelatinous deposits develop on transforming miracidia-sporocysts in B. glabrata plasmas is also reported. Both the agglutination and gel-formation phenomena may facilitate recognition of, and attacks on, sporocysts, thereby contributing to susceptibility and resistance in this host-parasite system.     

Protein kinase C signalling during miracidium to mother sporocyst development in the helminth parasite, Schistosoma mansoni

For schistosomes, development of the miracidium to mother sporocyst within a compatible molluscan host requires considerable physiological and morphological changes by the parasite. The molecular mechanisms controlling such development have not been explored extensively. To begin to elucidate the importance of kinase-mediated signal transduction to this process, the phosphorylation (activation) of protein kinase C (PKC) in larval stages of Schistosoma mansoni undergoing in vitro transformation was explored. Mining of the S. mansoni genomic database revealed two S. mansoni PKC proteins with high homology to human PKCβ and containing the conserved autophosphorylation (activation) site represented by serine 660 of human PKCβ_II. Western blotting with anti-phosphospecific antibodies directed to this site demonstrated that miracidia freshly-hatched from eggs possessed PKC (78 kDa) which was phosphorylated (activated) when miracidia were exposed to phorbol ester, and dephosphorylated (inhibited) following exposure to the PKC inhibitor GF109203X. Miracidia treated with the phospholipase C (PLC) inhibitor U73122 also displayed decreased PKC phosphorylation. S. mansoni PKC was phosphorylated during the initial 24 h development of miracidia into mother sporocysts; after 31 h and 48 h development, phosphorylation was reduced by 72% and 86%, respectively. Confocal microscopy of miracidia revealed phosphorylated PKC associated with the neural mass, excretory vesicle, tegument, ciliated plates, terebratorium and germinal cells; in larvae undergoing transformation for 31 h, phosphorylated PKC was only occasionally detected, being present in regions likely corresponding to the ridge cyton. Inhibition of PKC in miracidia by GF109230X resulted in accelerated transformation, particularly to the postmiracidium stage; ciliated plates were also shed from developing larvae more rapidly. These results highlight the dynamic nature of PKC signalling during S. mansoni postembryonic development and support a role for active PKC in restricting transformation of S. mansoni miracidia into mother sporocysts.     

日本血吸虫毛蚴对钉螺的钻穿及在螺体内的分布和移行

采自安徽省池的钉螺每粒感染５０只湖南株日本血吸虫毛后的组织学观察说明：毛蚴钻穿钉螺有从螺鳃部、头足总后有皮以及实质组织（外套膜、触角和阴茎）等三方面途径,其中以前二者尤为重要;毛蚴进入螺鳃丝后直接进入血液循环系统,从头足表皮进入的毛蚴,除了少数在钻穿部位附近滞留外,多数继续向头足部深层的肌肉和窦状组织间隙移行,以前头足窦、直肠和消化道外的组织间隙以及肾脏为主要的移行部位;从外套膜、触角、阴茎等部位