Specificity of natural resistance to trematode infections in Biomphalaria glabrata.
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Biomedical subjects
Publications and source records attributed to D Heyneman.
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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.
Formation of an amebocyte aggregate in the ventricular cavity of Biomphalaria glabrata can be induced 30 hr or more after a single infection by irradiated or (less frequently) by normal Echinostoma lindoense miracidia. The resulting amebocyte mass frequently encapsulated and destroyed the developing E. lindoense sporocysts within the ventricle. The constituent amebocytes of the capsule correspond in vitro and by staining characteristics to circulating amebocytes of uninfected snails, but with additional inclusion bodies, increased mucopolysaccharide, acid phosphatases, and lipid-positive staining reactions. Mitotic activity, rapid growth, and later regression of the amebocyte-producing organ (located between the posterior mantle epithelium and anterior pericardial endothelium) follow the growth and regression sequence of the ventricular capsule. Though peripheral foci of secondary amebocyte production have been found and were previously known, the amebocyte-producing organ appears to be the primary amebocyte source responsible for the snails' rapid intraventricular sporocyst encapsulation.
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.
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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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.
An epizootic of reptilian amebiasis seems to have caused the death of 15 to 16 large and valuable captive snakes (boas, pythons, and anacondas) occupying one of 5 large display dioramas in the Steinhart Aquarium of the California Academy of Science, Golden Gate Park, San Francisco. Subsequent review of previous snake deaths in the colony indicated that of 464 snakes that had died since early 1969, 89 snakes had intestinal or hepatic lesions, and 80 of these snakes had pathologic features which involved severe intestinal ulceration, hemorrhage, and massive enteritis, with or without hepatic necrosis and destruction, condition compatible with Entamoeba invadens infection. The present epizootic began in November, 1972, with the death by acute enteritis of a red-tailed boa constrictor (Boa constrictor amarali) and was followed by the loss of 15 other large boids and pythonids. The affected snakes became immobile, refused to feed, and began to die 10 weeks after the death of the red-tailed boa. Seven boa constrictors, 4 pythons, and 4 anacondas from the same diorama died during the ensuing 10 weeks. Entamoeba invadens trophozoites were identified in the stool of the remaining living snake, a 3-m boa constrictor, and in the liver and the intestinal tissue of 1 of the dead boas examined microscopically. The parasite was also found in the stool of a giant Burmese python (Python molurus bivittatus) that died in the adjacent diorama and in the tissues of a blue-tongued skink (Tiliqua scincoides), separately housed, that died of enteritis during this period. Amebic cysts were recovered from turtle and alligator fecal samples taken from a central "swamp," or reservoir, draining the dioramas, water that is returned to the snake display areas after passage through a biological sand-gravel filter and ultraviolet radiation exposure. Cultures from these stools were positive and proved lethal to an experimentally infected boa constrictor. Treatment of the surviving snake in the affected diorama with metronidazole at the dose rate of 275 mg/kg proved rapidly effective; toxicosis was not observed. Other snakes and lizards suspected of having the infection were similarly treated and returned to normal behavior and feeding patterns. Epidemiologic considerations review the probable mode of introduction and spread of this highly lethal snake pathogen and recommendations are made for avoiding infection, prophylactic treatment, and handling of similar epizootics when they do occur among captive reptiles in aquariums, zoos, and research laboratories.
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