Effect of exposure to Echinostoma itliei miracidia on growth and survival of young Biomphalaria glabrata snails

Kuris A. M. 1980. Effect of exposure to Echinostoma liei miracidia on growth and survival of young Biomphalaria glabrata snails. International Journal for Parasitology10: 303–308. Exposure to miracidia of Echinostoma liei resulted in increased mortality and reduced growth of 1–2 mm albino Biomphalaria glabrata snails whether or not the snails became infected. Growth rates for infected and exposed but uninfected snails were significantly more variable than growth rates of unexposed snails. Retarded growth and increased mortality were detected as rapidly as seven to nine days after exposure. Neither growth nor survivorship of 4–6 mm snails was altered upon exposure to or infection by E. liei.     

Failure of Echinostoma lindoense to reinfect snails already harboring that species.

In Biomphalaria glabrata snails already harboring Echinostoma lindoense, attempts at reinfection with the same trematode species failed when the interval between exposures was 6 days or more. With 2 days between exposures, the experimental snails were as susceptible to reinfection as the control snails. Between these limits, the reinfection failure rate increased with the exposure interval. Failure to reinfect the snails was probably due to cannibalism, young sporocysts from the second infection being swallowed by predatory rediae from the first infection. Development of sporocysts in successfully reinfected snails was normal.     

DEVELOPMENT OF ACCESSORY SEXUAL ORGANS IN BIOMPHALARIA GLABRATA (PLANORBIDAE) IN RELATION TO TIMING OF INFECTION BY SCHISTOSOMA MANSONI: CONSEQUENCES FOR ENERGY UTILIZATION PATTERNS BY THE PARASITE

The growth rates of ovotestis and individual accessory sexualorgans (ASO) of Biomphalaria glabrata snails were studied forcontrols and for immature and mature snails infected with Schistosomamansoni. The infection of immature B. glabrata strongly delaysgrowth of the ovotestis and inhibits the development of theaccessory sexual organs. There is no significant differenceup to 2 weeks post infection in the volume of the ovotestisand the ASO between mature infected B. glabrata and controlsnails. From 3 to 4 weeks post infection there was a reductionin the volume of the ovotestis and the ASO of infected matureB. glabrata; then growth of the ovotestis, albumen gland andfemale organs was stopped, but the effect of infection was lessconsistent for the male organs. For a parasite, immature andmature snails have to be considered as two different resourceenvironments, each having at infection time a particular patternof resource allocation, towards growth for juvenile and towardsreproduction for adult snails, changing the possible energyutilization patterns which can be used by the trematode. (Received 29 January 1993; accepted 22 April 1993)     

Distribution and variation of hemagglutinating activity in the hemolymph of Biomphalaria glabrata

A sensitive hemagglutination assay utilizing glutaraldehyde-fixed trypsinized calf erythrocytes (GTC) is described to test for agglutinin levels in hemolymph and albumen gland extracts from nine populations of Biomphalaria glabrata, and from B. straminea and B. obstructa. High levels of GTC-reactive hemagglutinin were found in all snail populations. There was no correlation between hemagglutinin titer and innate resistance of B. glabrata strains to Schistosoma mansoni. However, an increase in hemagglutinin titer occurs in B. glabrata M-RLc snails infected with Echinostoma lindoense and in snails sensitized and reexposed to this parasite.     

Location of Biomphalaria glabrata (Say) by miracidia of Schistosoma mansoni Sambon in natural standing and running waters on the West Indian Island of St. Lucia

Upatham E. S. 1973. Location of Biomphalaria glabrata (Say) by miracidia of Schistosoma mansoni Sambon in natural standing and running waters on the West Indian Island of St. Lucia. International Journal of Parasitology3: 289–297. The ability of S. mansoni miracidia to locate B. glabrata in natural ditches and streams was investigated. Miracidia located and infected snails at distances of 9–14 and 97-54 in horizontally in standing and running waters respectively. In running water, no infection occurred above a velocity of 13.11 $\text{cm}\text{sec}$. In both types of habitat, infection rates in snails increased with increasing levels of miracidia but decreased as the location of caged snails moved away from the miracidial point of entry. Laboratory experi- ments showed that the number of daughter sporocysts was proportional to the number of miracidia. Judging by the number of daughter sporocysts recovered only a small percentage of miracidia succeeded in locating and penetrating snails (6.8–13-7 % and 1.4–6.2 % in standing and running waters respectively). In standing water, infection may be inhibited by the limited ability of miracidia to move horizontally. In running water, the flow extends significantly the effective scanning capacity of the miracidia, giving them a better chance of coming into contact with snails, which is of importance in the epidemiology of schistosomiasis. Owing to a con- siderable wastage of miracidia and the higher relative efficiency of miracidia at lower densities in detecting snails, control measures such as chemotherapy or provision of safe water supplies designed to lower egg output and reduce contamination may not seriously influence transmission unless S. mansoni egg production or contamination is massively reduced.     

Ribeiroia marini: pathogenesis and larval trematode antagonism in the snail, Biomphalaria glabrata

Larval trematode antagonism between Ribeiroia marini and Schistosoma mansoni was studied in the snail Biomphalaria glabrata. A laboratory-raised Puerto Rican strain of B. glabrata was exposed to single and double infections with given numbers of: (1) embryonated eggs of R. marini from laboratory rats, and (2) miracidia of S. mansoni from mice. Snails were maintained in outside environmental tanks in San Juan, Puerto Rico and larval trematode interactions were examined in a series of five experiments. Snails of all sizes were highly susceptible to single infections with R. marini. Rediae and cercariae caused extensive damage to the digestive gland and ovotestis resulting in premature death of snails. Heavily infected snails were castrated and stopped laying eggs. Snails infected first with S. mansoni were only partly susceptible to superinfection with R. marini given on Day 23. In a reverse experiment, snails infected first with R. marini were only partly susceptible to a second infection with S. mansoni given on Day 23. In simultaneous exposures, snails developed double infections (22%) with R. marini dominant and S. mansoni sporocyst and cercaria production reduced. While R. marini is not a strong direct antagonist against established S. mansoni infections, it has several attributes as a possible biological control agent: hardy eggs easily produced in rats; high infectivity to snails of all ages; and ability to castrate and prematurely kill B. glabrata. The R. marini-rat system described here provides a convenient laboratory and field model for the study of intrasnail trematode antagonism and biological control.     

Resistance to schistosome infection in Biomphalaria glabrata induced by gamma radiation

Two strains of Biomphalaria glabrata were studied with respect to the effects of ionizing radiation on their susceptibility to Schistosoma mansoni infection. Gamma radiation at levels of 3.5 and 5 krad did not induce susceptibility in the resistant S-3 strain, but was found to initiate resistance in the susceptible PR-1 strain. In an attempt to understand the induced resistance in irradiated snails, histopathologic examinations and analyses of snail hemolymph were performed. Results indicated that miracidia invading irradiated snails were quickly surrounded and encapsulated by amoebocytes. Similarly, alterations in the hemolymph of irradiated snails suggested that radiation induced aging. It is suggested that radiation-altered snails may be of value in studying the defense mechanisms of these organisms.     

Schistosoma mansoni: Lysozyme activity in Biomphalaria glabrata during infection with two strains

Levels of lysozyme activity were determined in the hemolymph, digestive gland, and headfoot extracts of M-line stock of snails, Biomphalaria glabrata, during infection with the PR-1 and Lc-1 strains of the trematode, Schistosoma mansoni. At 3 hr postexposure there was a 10-fold increase in the levels of enzyme activity in the hemolymph of snails infected with the Lc-1 strain to which the snail is resistant. This increase was considerably higher when compared to the threefold increase in the PR-1-infected snails. The infection also induced a gradual depletion of lysozyme activity in the headfoot muscles of the two groups of infected snails. There were no changes in the levels of enzyme activity in the digestive gland extracts of the control and the two groups of infected snails. Similar changes in the levels of enzyme activity in the hemolymph and headfoot extracts of infected snails suggest a nonspecific response to a parasite infection and do not indicate that lysozyme is primarily responsible for the destruction of schistosome parasite in a resistant snail host.     

Positive phototropism is accelerated in Biomphalaria glabrata snails by infection with Schistosoma mansoni

Parasite-induced behavioral changes in their hosts favor to complete the lifecycle of parasites. Schistosome infection is also known to cause physiological changes in infected freshwater snail intermediate hosts. Here, we report, a novel phenomenon in which Schistosoma mansoni, a highly debilitating worm affecting millions of people worldwide, alters the phototropic behavior of Biomphalaria glabrata, the vector snail. S. mansoni-infection enhanced positive phototropism of vector snails and infected snails spent significantly more time in light. Possibly, these behavioral changes help the parasite to be released efficiently from the infected intermediate hosts, and to infect mammalian hosts.     

Comparative mortality studies on Biomphalaria glabrata (mollusca: Pulmonata) exposed to copper internally and externally

Various concentrations of copper in the form of CuSO₄ were injected into the hemocoel of Biomphalaria glabrata, and mortality of this snail was subsequently monitored. The concentrations of copper in the hemolymph of injected snails were calculated, and specimens were incubated in these concentrations. Greater mortality was observed when snails were incubated in concentrations of copper than when they were injected with a sufficient amount of copper to attain these same concentrations in the hemolymph. Injection of copper into the hemocoel of B. glabrata resulted in the formation of a noncellular hemolymph precipitate, most likely denatured proteins, at the injection site, which was most noticeable with higher concentrations of copper. It has been concluded that external concentrations of copper are more cidal to B. glabrata than are internal, i.e., injected, concentrations. These data support the hypothesis that the cidal action of copper on B. glabrata is due to an attack on the mollusc's surface epithelia.     

Effects of UVB on interactions between Schistosoma mansoni and Biomphalaria glabrata

Ultraviolet B (UVB, 280-315 nm) radiation is detrimental to both of larvae of the digenetic trematode Schistosoma mansoni and its snail intermediate host, Biomphalaria glabrata. We explored effects of UVB on three aspects of the interaction between host and parasite: survival of infected snails, innate susceptibility and resistance of snails to infection, and acquired resistance induced by irradiated miracidia. Snails infected for 1 week showed significantly lower survival than uninfected snails following irradiation with a range of UVB intensities. In contrast to known immunomodulatory effects in vertebrates, an effect of UVB on susceptibility or resistance of snails to infection could not be conclusively demonstrated. Finally, exposure of susceptible snails to UVB-irradiated miracidia failed to induce resistance to a subsequent challenge with nonirradiated miracidia, a result similar to that reported previously with ionizing radiation.     

Field studies on the bionomics of the free-living stages of St. Lucian Schistosoma mansoni.

Densities of Schistosoma mansoni miracidia and cercariae in natural habitats in three St. Lucian valleys were monitored over a 3-year period by exposure of sentinel snails, Biomphalaria glabrata, and a cercariometric technique, supplemented by sampling of field snails. Separate measures for control of S. mansoni transmission were under evaluation in two of the valleys. Sentinel snails became infected sporadically and their infection rates per valley ranged from 0·12% to 4·99%. S. mansoni miracidial inoculation rates ranged from 1 to over 4 per infected sentinel snail. Combined rainfall of more than 3 in on the day before any day of sentinel snail exposure interfered with miracidium-snail interaction. Densities of S. mansoni cercariae ranged from 0·05 to 21 per litre of water sampled. The number of cercariae detected in a habitat by cercariometry was directly proportional to the number of infected field snails. Sentinel snail infection rates exhibited a downward and an upward trend, respectively, in the controlled and uncontrolled areas, although the changes were not significant statistically.     

Acquired resistance in snails. Induction of resistance to Schistosoma mansoni in Biomphalaria glabrata

Acquired resistance to Schistosoma mansoni PR-I strain has been induced in Biomphalaria glabrata 442132 strain by infecting the snails with irradiated homologous miracidia. Present and previous results support the hypothesis that acquired resistance to trematodes in snails is an enhancement of the host's natural resistance to the parasite.     

Studies on resistance in snails: Interference by nonirradiated echinostome larvae with natural resistance to Schistosoma mansoni in Biomphalaria glabrata

Most of the genetically selected juvenile Biomphalaria glabrata snails, normally strongly resistant to Schistosoma mansoni, lost their juvenile resistance to this parasite when other trematodes were concurrently present in the snail. Three echinostome species all were able to reduce this genetically controlled juvenile resistance: Echinostoma lindoense, E. paraensei, and e. liei. Subsequently, adult resistance to S. mansoni, clearly present in control snails of the same age and strain that were not doubly infected, failed to develop in most of the snails that also harbored echinostomes. Other snails, selected for resistance as adults to S. mansoni, also usually became susceptible to this parasite following infection with E. paraensei. The capacity of E. paraensei to interfere with the snails' resistance to S. mansoni was greater than that of E. lindoense. Destruction by predation of primary sporocysts of S. mansoni by echinostome rediae prevented completion of development of the S. mansoni infections. In a number of snails all primary S. mansoni sporocysts were consumed before secondary sporocysts could be formed. In most experimental snails, however, some of the schistosomes survived, often as a small number of degenerated secondary S. mansoni sporocysts. The capability of flukes to interfere with the natural defense of snails may be an important phenomenon whereby trematode species survive in their snail hosts.     

Hemocytes of Biomphalaria glabrata: Factors affecting variability

Variability in the hemocyte number of two geographic strains of Biomphalaria glabrata was studied. In each strain a logarithmic increase in hemocyte number associated with increasing shell size was observed. A two fold increase in circulating hemocytes occurred 2 hr following the exposure of a susceptible strain of B. glabrata to miracidia of Schistosoma mansoni. The hemocyte number was dependent on the temperatures at which the snails were maintained.