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Biomedical subjects

K J Lie

Publications and source records attributed to K J Lie.

At least 37 records · Page 2Linked to original sources
PubMed1977

Failure of irradiated Echinostoma audyi and Hypoderaeum dingeri to sensitize Lymnaea rubiginosa snails.

Attempts to induce acquired resistance in Lymnaea rubiginosa snails against the echinostomes Echinostoma audyi and Hypoderaeum dingeri by means of irradiated miracidia were unsuccessful, although Lie and coworkers using similar methods had recently sensitized Biomphalaria glabrata against Echinostoma lindoense (1975a). In contrast to the B. glabrata-E. lindoense system, in Lymnaea rubiginosa the amebocytic response to irradiated parasites was slow: irradiated E. audyi sporocysts were encapsulated 15 to 28 days and H. dingeri sporocysts 20 to 27 days postexposure. No obvious enlargement of the amebocyte-producing organ was seen. No resistance was demonstrable to subsequent homologous challenge. Development of acquired resistance to a trematode infection in snails may be related to the speed with which the snails destroy the irradiated sporocysts.

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PubMed1976

Studies on resistance in snails. 3. Tissue reactions to Echinostoma lindoense sporocysts in sensitized and resensitized Biomphalaria glabrata.

The resistance of Biomphalaria glabrata snails that have been sensitized by various levels of irradiated or nonirradiated Echinostoma lindoense miracidia increased after a second challenge infection with nonirradiated miracidia of the same species. This was demonstrated by increased suppression of migrating capacity of invading sporocysts, an accelerated host tissue reaction, and a greater tendency of snail amebocytes to flatten while attacking the parasite. Three methods of elimination of invading sporocysts were observed: (1) encapsulation by amebocytes followed by destruction of the sporocysts; (2) expulsion of the sporocyst through the host epithelium after its encapsulation in the subepithelial tissues; (3) blockade of the parasite's entry into subepithelial tissues by a localized amebocyte aggregation. The basic mechanism of host snail response to a single or a repeated challenge infection appears to be similar, though an anamnestic reaction is evident in the accelerated response following a second challenge exposure.

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PubMed1976

Studies on resistance in snails. 5. Tissue reactions to Echinostoma lincloense in naturally resistant Biomphalaria glabrata.

Laboratory-raised juvenile albino Biomphalaria glabrata snails show a wide range of natural resistance to a single infection with 50 or 100 miracidia of Echinostoma lindoense. In the most resistant snails all sporocysts are destroyed in peripheral tissues soon after miracidial penetration. In less resistant snails some sporocysts reach the heart where they are encapsulated. In fully susceptible snails, all sporocysts rapidly migrate to the heart, where they mature and continue to develop. The greater part of our B. glabrata colony consists of snails in which sporocysts reaching the heart will survive, but in which a varying number of sporocysts will be destroyed in the tissues. These snails are usually considered susceptible, as they do become infected. Tissue reactions induced by sporocysts following a single infection in naturally resistant snails are similar to reactions in snails with an acquired resistance. In fully susceptible snails, the amebocyte-producing organ remains small and inactive. It is slightly to moderately stimulated in partially resistant snails in which destruction of sporocysts occurs in the tissues and surviving larvae are found in the ventricle. In snails in which amebocyte aggregates or capsules develop in the ventricle, the organ becomes markedly enlarged. Migration of sporocysts in the snail appears not to be continuous, as periodic rests seem to occur. Migration follows intrusion of the sporocyst through the tissues, induced by bodily distension and contraction, and then proceeds within the arteries against the blood flow, passing from one endothelial attachment site to another, possibly aided by negative pressure during ventricular diastole.

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PubMed1976

Studies on resistance in snails. 6. Escape of Echinostoma lindoense sporocysts from encapsulation in the snail heart and subsequent loss of the host's ability to resist infection by the same parasite.

Formation of amebocyte aggregates in the ventricular cavity of Biomphalaria glabrata, induced by developing sporocysts of Echinostoma lindoense, does not always result in destruction of the parasites, as the sporocysts occasionally escape encapsulation in the heart. When this occurs, a remarkable loss of protective capacity follows and the host snails become highly susceptible to reinfection with the same species--even more so than in control susceptible snails exposed for the first time. Although the amebocyte-producing organ is considerably enlarged after a first infection and shows numerous mitoses, the amebocytes produced by snails harboring an "escaped" infection in the heart appear unable to attack the parasites of the first or of the second exposure. Instead, the amebocytes produced accumulate in the loose connective tissues between the liver lobuli, where early developmental stages of the parasites do not occur. These amebocytes apparently have lost their ability to recognize the parasites as foreign.

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PubMed1976

Studies on resistance in snails. 7. Evidence of interference with the defense reaction in Biomphalaria glabrata by trematode larvae.

Echinostoma lindoense sporocysts that develop from irradiated miracidia normally are destroyed by amebocyte capsules in the ventricle of Biomphalaria glabrata within 10 days postexposure. The survival period of these ventricular sporocysts was considerably longer in snails that also harbored normal sporocysts of E. lindoense, Paryphostomum segregatum, or Schistosoma mansoni. Protection of irradiated E. lindoense sporocysts by the same of different trematode species is presumed to be the result of an active process by which normal sporocysts interfere with capsule formation and protect themselves and other trematode larvae from encapsulation. Homologous protection was stronger than heterologous.

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PubMed1975

The life cycle of Echinoparyphium ralphaudyi sp. n. (Trematoda: Echinostomatidae).

The life cycel and morphology of Echinoparyphium ralphaudyi sp. n. is described. Natural infections were found in Bulinus truncatus from Egypt, Ethiopia, and the Yemen Arab Republic, and later in B. forskalii and B. sericinus from Ethiopia. Sporocysts develop near the places of miracidial entry into the snail (the head-foot region, mantle edge, pseudobranch, and antennae). Rediae occur mainly in the ovotestis and in tissues anterior to the liver. The first cercariae are released 24 days postexposure. Metacercariae encyst in various freshwater snails and are localized in the pericardial sac and the posterior part of the kidney. Adult worms live in the small intestine of a variety of experimental animals: hamsters, rats, mice, chicks, ducklings, pigeons, and finches.

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