Experimental life cycle of Lagochilascaris major leiper, 1910 (Nematoda: Ascarididae) in cats (Felis domesticus)

The life cycle of Lagochilascaris major was studied using eggs collected from a natural clinical case in a domestic cat. Twenty-seven white mice (Mus musculaus), 5 hamsters (Mesocricetus auratus), and 1 vesper mouse (Calomys callosus) were orally inoculated with 800-1,300 embryonated eggs. When examined from 73 to 246 days postinoculation (PI), encysted third-stage larvae were seen in skeletal muscles and less frequently in connective tissue, liver, and lungs. Twenty-two of the 23 cats orally inoculated with 40-430 encysted larvae from these rodents, and necropsied from 1 hr to 185 days PI, became infected. Third-stage larvae were located in the stomach, esophagus, and oropharynx from 1 to 24 hr PI. At 48 hr, larvae, from mainly the fourth stage, were only found, unilaterally or bilaterally, inside a "sac" in the region of the semilunar fold of the palatine tonsil at the base of the tongue. Adult worms were found in this location from 10 to 175 days PI. No fistulated abscess to the outside medium was found. Adult worms were also found in the middle ears of 2 cats showing purulent otitis. Eggs in the ear secretion were under different stages of development. Eggs in feces were first observed on days 14 and 15 PI, and 1 cat shed them until 178 days PI. Six infected cats were treated with fenbendazole at 50 mg/kg of body weight for 3 consecutive days, eliminating all the parasites present in the tonsils. The drug was not effective against the parasites present in the middle ear. No stage of the parasite was found in the tissues of 5 cats given 4,000-5,200 eggs orally and examined after 19 and 50 days PI. This indicates that the life cycle of L. major requires an obligate paratenic host and is characterized by heteroxenic cycle.     

Development of the stomach worm, Obeliscoides cuniculi (Graybill), in lagomorphs, woodchucks and small rodents

The parasitic development of Obeliscoides cuniculi multistriatus Measures and Anderson, 1983 was studied in New Zealand white rabbits (Oryctolagus cuniculus). Third-stage larvae exsheathed within 24 hr. The third molt occurred 3 days and the fourth 8-11 days post-infection. All worms were fifth stage 14 days post-infection. Males were mature at 16 days and copulation occurred in 15-16 days. Females were gravid at 18 days. The prepatent period was 16-22 days. The patent period was 61-118 days and males lived longer than females. All stages were found in the mucosa except the fifth which was found lying on the mucosal surface within a layer of mucus. Petechiae were the only lesions seen in experimentally infected rabbits. Patent infections of O. c. multistriatus were established experimentally in infected woodchucks (Marmota monax), snowshoe hares (Lepus americanus) and cottontail rabbits (Sylvilagus floridanus). Patent infections of O. c. cuniculi were established experimentally in snowshoe hares. Patent infections of O. c. multistriatus did not appear in experimentally infected HPB white (Swiss Webster) mice (Mus musculus). Wistar rats (Rattus norvegicus), H.O.R.F1 Syrian hamsters (Mesocricetus auratus), H.O.R.F1 smooth-haired guinea pigs (Cavia porcellus) and H.O.R.F1 gerbils (Meriones unguiculatus).     

Development of Thelastoma bulhoesi (Oxyurata: Thelastomatida) and the Effect of Thiabendazole on the Unembryonated Egg

The embryological and postembryological development of Thelastoma bulhoesi was determined. Initial cleavage was into unequal cells and occurred within 1-2 hours at 25 C. Cell division was holoblastic but no true morula is formed. Gastrulation occurred at approximately 48 hours by epibolic synectic mechanisms. First-stage larvae were fully developed at 96 hours. The molt to second-stage larvae was initiated in the egg and was completed at hatching. Second-stage larvae were first observed in the host at 11 hours postinfection, third-stage larvae at 18 hours, and fourth-stage larvae at 192 hours. Adult female worms were observed at 32 days. Thiabendazole, in even the lowest concentrations, inhibited the developmem of unembryonated ova.     

Arrested development of the rabbit stomach worm Obeliscoides cuniculi: resumption of development of arrested larvae throughout the course of a single infection

Arrested development of the rabbit stomach worm Obeliscoides cuniculi: resumption of development of arrested larvae throughout the course of a single infection. International Journal for Parasitology 16: 47–54. Twenty rabbits were inoculated once with cold treated L3s of Obeliscoides cuniculi with a high propensity for arrest and killed in pairs at intervals over 234 days post-infection. An exponential decline in numbers of adult worms and arrested larvae was observed. Arrested larvae resumed development at a rate seven times greater than adults were lost and appeared to replenish the adult population. More male than female arrested larvae were intially established in rabbits but males resumed development at a greater rate than females. Egg and larval production were correlated with the number of female worms present at any one time. In a subsidiary study, arrested larvae were recovered from one rabbit and transferred sequentially through two further rabbits. These larvae resumed development at the same rate as larvae in the 20 rabbits. Both studies suggest that resumption of development is an intrinsic characteristic of the larvae themselves and may be genetically controlled.     

Cultivation of excysted metacercariae of Echinostoma caproni (Trematoda) to ovigerous adults on the chick chorioallantois

Excysted metacercariae of Echinostoma caproni were cultivated on the chick chorioallantoic membrane (CAM) maintained at 38.5 +/- 1 C and a relative humidity of 60-65%. Of 59 6-day-old embryos, each inoculated with 25 metacercariae, 29 (49.2%) were infected 2-12 days postinoculation. The total number of worms recovered from the infected eggs was 163 or 22.5% of the 725 inoculated metacercariae. Eggs contained from 1 to 12 (average 5.6) worms per CAM. Worm length increased rapidly from an average of 0.5 mm at 2 days to about 3.0 mm at 6 days postinoculation. Ovigerous worms first were seen on day 8 PI, but fluke eggs did not develop embryos. Worm development in ovo lagged about 1 day behind that of in vivo worms. One worm maintained for 17 days on 2 successive CAMs reached 6 mm in length, contained about 100 eggs in its uterus, and laid an additional 100 eggs on the CAM surface.     

Stage-specific antigens of Nematospiroides dubius Baylis, 1926 (Nematoda: Heligmosomides)

Antigens were identified from Nematospiroides dubius recovered from outbred Quackenbush mice between 4 and 10 days postinoculation (PI). Parasite surface proteins were radioiodinated and extracts of the whole worms were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, transferred to nitrocellulose, and reacted with normal and immune mouse sera followed by an avidin-biotin-peroxidase assay. Antigens ranged between 250,000 and 20,000 molecular weight (MW). A major surface antigen, 60,000 MW, which appeared to be a complex of different antigens, and a 250,000-MW internal antigen were found on fourth-stage (L4) and fifth-stage (L5) larvae 5-10 days PI but not earlier. A group of minor surface antigens (24,000-30,000 MW) were also expressed as larvae molted from L4 to L5, 6 and 7 days PI, but they differed from antigens of similar MW expressed by adult worms. An antigen, 45,000 MW, was detected in worms 5-10 days PI, but it was only expressed on the surface of L5 worms 9 and 10 days PI. We suggest that the antigen(s) common to adults and larvae may account for protective immunity.     

Endocrine changes associated with metamorphosis and diapause induction in the yellow-spotted longicorn beetle, Psacothea hilaris

At 25 degrees C and under a long-day photoperiod, all 5th instar Psacothea hilaris larvae pupate at the next molt. Under a short-day photoperiod, in contrast, they undergo one or two additional larval molts and enter diapause; the 7th instar larvae enter diapause without further molt. The changes in hemolymph juvenile hormone (JH III) titers, JH esterase activity, and ecdysteroid titers in pupation-destined, pre-diapause, and diapause-destined larvae were examined. JH titers of the 5th instar pupation-destined larvae decreased continuously from 1.3 ng/ml and became virtually undetectable on day 13, when JH esterase activity peaked. Ecdysteroids exhibited a small peak on day 8, 1 day before gut purge, and a large peak on day 11, 2 days before the larvae became pre-pupae. The two ecdysteroid peaks are suggested to be associated with pupal commitment and pupation, respectively. JH titers of the 5th instar pre-diapause larvae were maintained at approximately 1.5 ng/ml for 5 days and then increased to form a peak (3.3 ng/ml) on day 11. JH esterase activity remained at a low level throughout. Ecdysteroid levels exhibited a large peak of 40 ng/ml on day 18, coincident with the larval molt to the 6th instar. JH titers of the 7th instar diapause-destined larvae peaked at 1.9 ng/ml on day 3, and a level of approximately 1.1 ng/ml was maintained even 30-60 days into the instar, when they were in diapause. Ecdysteroid titers remained approximately 0.02 ng/ml. Diapause induction in this species was suggested to be a consequence of high JH and low ecdysteroid titers.     

Infectivity, growth, and distribution of Echinostoma caproni (Trematoda) in the ICR mouse

Host-parasite interactions of the intestinal trematode Echinostoma caproni were studied in ICR laboratory mice. All of 40 mice, each fed 25 metacercarial cysts of Echinostoma caproni, were infected 1-20 wk postinfection (PI) with a mean of 17.2 worms/host. At 24 and 29 wk PI only 2 of 6 mice (33%) were infected, with a mean of 4.2 worms/host. Mean body area of worms increased rapidly to about 5 mm2 by week 2, increased less rapidly to 8.8 mm2 by week 12, plateaued until week 24, and then declined. Mean dry weight of worms increased rapidly to about 0.5 mg by week 2, less rapidly to 1.4 mg by week 12, and then plateaued until week 24 PI. From 1 to 8 wk PI most worms localized in the jejunum and ileum; later most worms were in the jejunum and duodenum. Considerable differences were seen in the growth and distribution of E. caproni in the ICR mouse compared with previous studies on this echinostome species in the NMRI mouse.     

Nematospiroides dubius: arrested development of larvae in immune mice.

When immune NIH mice were killed 10 days after a challenge infection with Nematospiroides dubius, approximately 10% of the inoculated larvae were recovered from the intestinal lumen, irrespective of the dose administered. When such mice were treated with cortisone from Day 10 for a period of 8 to 14 days and were subsequently killed for worm counts, it was found that they had significantly more worms than the immune control mice killed on Day 10. During the week following the beginning of treatment with cortisone there was little change in the low worm burdens in immune mice. However, 9 to 11 days after this treatment worm counts indicated that worms were accumulating in the intestinal lumen, and concurrently eggs were recorded in the feces of the mice. These observations indicated that a period of 9 to 11 days was required after the initiation of cortisone treatment on Day 10 for the worms in immune mice to complete their development to the adult lumen-dwelling stage. It is suggested that the larvae in the challenge infection became arrested early in their development in the intestinal wall and that growth resumed only after cortisone treatment. When treatment with cortisone was initiated later after challenge, it was still effective in reactivating arrested worms, but the lower worm recoveries in these mice indicated that the arrested larvae were being slowly rejected by the host. In subsequent experiments it was established that the arrested larvae of N. dubius were insusceptible to the activity of pyrantel embonate, an anthelmintic which is 99% effective against adult worms in the intestinal lumen. The mechanism whereby the larvae of N. dubius became arrested in immune mice and subsequently resumed their development after cortisone treatment is discussed.     

Experimental Oesophagostomum bifurcum in monkeys

OESOPHAGOSTOMUM BIFURCUM: larvae, cultured from human stools collected in northern Ghana, were used to establish experimental infections in monkeys. A patent infection was established in a rhesus monkey (Macaca mulatta) and this infection was used to generate larvae to inoculate additional monkeys. In all, 17 animals were inoculated. Thirteen of 15 animals developed antibodies to the infection between 19 and 62 days post inoculation (PI); two animals had a positive response before inoculation. Four of ten animals developed patent infections between 88 and 134 days and passed eggs in the faeces. Egg shedding was consistent in only one animal, but at low levels of one or two eggs per 2 mg direct smear, and extended over a 400 day period. In the other three animals, egg shedding was sporadic and of only 2-4 weeks duration. In seven animals necropsied between 19 and 22 days PI, one to 17 early fourth-stage larvae were recovered from nodules in the bowel wall; in an eighth animal examined at 314 days, six immature adult worms (early fifth stage) were recovered from nodules in the bowel wall. The morphological features and growth of these recovered larvae are described. Three animals were inoculated with larvae that had been dried for one week at 28 degrees C; two animals began shedding eggs at 128 and 134 days PI, respectively. The present results suggest that the parasite obtained from humans is poorly adapted to lower primate hosts, and supports the concept that Oesophagostomum bifurcum found in humans and monkeys in the same geographical region of northern Ghana and Togo are distinct and that the infections in humans are not likely to represent zoonotic infections acquired from monkeys.     

Brugia malayi,Brugia pahangi, and Brugia patei: Pulmonary pathology in jirds, Meriones unguiculatus

The chronological development of pulmonary lesions due to subperiodic Brugia malayi and related species was studied in the jird, Meriones unguiculatus. Major pathologic changes included (1) granulomas induced by larvae and adults, (2) obstructive endarteritis, and (3) chronic interstitial inflammation with degenerating microfilariae. The majority of pulmonary granulomas were initiated near the time of the final molt, about 30 days postinoculation, followed by involution and formation of residual vascular lesions over the next several months. A minority of granulomas arose about sexually mature adult worms and showed a characteristic sequence of development along the length of these worms. Ultrastructural observations suggested that within granulomas internal structures of the worm underwent an autolytic-like disintegration, while the cuticle remained intact. A material, presumably of parasitic origin, then appeared between the cuticle and adherent epitheloid and giant cells and was subsequently phagocytized by these cells. Obstructive endarteritis appeared to peak at about the time of the final molt, and became largely fibrotic by 125 days postinoculation; electron microscopy of the subintimal infiltrates revealed a variety of cells including inflammatory cells and others interpreted as modfied cells of vascular origin (smooth muscle cells and two types of endothelial cells).Parasitological data suggested that both larvae and adults migrated to the lungs and that mating occurred here, rather than in peripheral sites of development. In terms of development, reproduction and survival, the pulmonary arteries of the male jird offered a suitable alternative for the localization of these primarily lymphatic filariae; our results thus suggest that the pulmonary localization of these worms should not be considered indicative of an aberrant mode of development. The failure of female jirds to develop detectable peripheral microfilaremia was associated with a high rate of infertility among female worms, rather than pulmonary sequestration or destruction of microfilariae.     

Experimental infection of Dirofilaria immitis in raccoon dogs

Canine heartworm (Dirofilaria immitis) is a nematode that naturally parasitizes in the pulmonary arteries and the right ventricle of domestic dogs (Canis familiaris) as final hosts. Japanese raccoon dogs (Nyctereutes procyonoides viverrinus) also are known to be susceptible to infection by the parasite. However, prevalence of this infection among free-ranging raccoon dogs is low and so is the worm burden. To examine the susceptibility of the raccoon dog to D. immitis infection, 3 raccoon dogs and 2 beagles were inoculated 4 times with 25 third-stage larvae (L3s) of D. immitis at 3-wk intervals. Worms were recovered from 2 raccoon dogs and both domestic dogs. The average percentage of recovery (2.3%) of the raccoon dogs was almost 10 times lower (24.5%) than that of the domestic dogs, but there was no significant difference in the body length of worms recovered from 2 types of hosts. To examine microfilaremia, 2 raccoon dogs were infected with 100 L3s. Microfilaremia was observed for 180 days postinoculation (PI) but disappeared at about 300 days PI. The raccoon dog was mildly susceptible to infection with D. immitis, but surviving worms developed and matured normally.     

Effects of albendazole against larval and adult Angiostrongylus cantonensis in rats

Effects of albendazole against larval and adult stages of Angiostrongylus cantonensis in rats were examined. (1) A single oral dose of albendazole of 10, 50 or 100 mg/kg at 7 or 14 days post-infection (PI) showed that the use of drug at 7 days PI was more effective in the larval infection. Rats treated 7 days PI showed significant reductions in the relative wet weight of heart and lungs (g/100 g body wt.), the mean total number of recovered worms and the mean body length of worms, as compared to those in the non-treated control. Similarly, visual morbidity assessment of the lung-tissues revealed a marked reduction in pathological changes in the rats treated 7 days PI. (2) Following two or three successive oral doses of 100 mg/kg at weekly intervals from 6 weeks PI, the first-stage larvae in rat feces completely disappeared 2 weeks post-treatment (PT) and this disappearance lasted during the experiment. In rats treated once, however, larval output reappeared from 3 weeks PT. Both histological sections of the rat lung-tissues and the recovered female worms showed degenerative changes in the female reproductive systems.     

Depletion of eosinophils by anti-IL-5 monoclonal antibody treatment of mice infected with Trichinella spiralis does not alter parasite burden or immunologic resistance to reinfection.

Mechanisms of parasite killing by eosinophils are widely studied and are often implicated in mediating resistance to parasitic infection, especially in conjunction with specific antibodies. Evidence for the eosinophil as an anti-parasite killer cell in vivo is limited and may not justify the belief that eosinophils engage and/or kill infective helminths. We reexamined this question in a mouse model of trichinosis in which antisera to eosinophils were previously used to show the requirement for eosinophils in resistance to this nematode. The current studies used mAb to IL-5 to suppress eosinophil levels in CF1 mice infected with Trichinella spiralis. In mice given a primary infection and injected with an isotype control mAb or left untreated, the medullary and peripheral blood eosinophil numbers peaked at 3 wk postinfection (PI) and returned to baseline levels by 4 wk PI. Peripheral blood eosinophil numbers in infected mice injected with anti-IL-5 were maintained at levels below those of uninfected normal mice through 4 wk of infection. Histologically, there was a prominent eosinophil accumulation in infected, untreated, or control-mAb-treated mice associated with nurse cell complexes containing infective juveniles in skeletal muscle at 3 and 4 wk PI. This was largely eliminated in mice treated with anti-IL-5 mAb. However, the number of muscle stage juvenile worms recovered 3 and 4 wk PI after acid pepsin digestion was unaffected by eosinophil depletion. Challenge infections, in which mice were infected at day 0 with 125 muscle stage worms and challenged at day 28 PI with 350 muscle stage worms, developed peak eosinophil numbers in bone marrow and peripheral blood 3 wk after primary infection and 2 wk after challenge infection in mice receiving either no treatment or control mAb. In challenged mice receiving anti-IL-5 mAb, medullary and peripheral blood eosinophil numbers remained at or below those of uninfected animals. Although all groups exhibited significant resistance measured as muscle stage worm burdens 56 days PI, eosinophil depletion did not affect resistance of muscle worm recovery. These results suggest that eosinophils are not essential in the control of T. spiralis in either primary or challenge infections of CF1 mice. This in vivo study illustrates the questionable value of in vitro killing assays to assign effector function to any single inflammatory cell type.     

Development of Trichosomoides nasalis (Nematoda: Trichinelloidea) in the murid host: evidence for larval growth in striated muscle fibres

Trichosomoides nasalis (Trichinelloidea) is a parasite of Arvicanthis niloticus (Muridae) in Senegal. Female worms that harbour dwarf males in their uteri, occur in the epithelium of the nasal mucosa. Young laboratory-bred A. niloticus were either fed females containing larvated eggs or intraperitoneally injected with motile first-stage larvae recovered from female uteri. Both resulted in successful infection. Organs examined during rodent necropsy were blood and lymphatic circulatory systems (heart, large vessels, lymphnodes), lungs, liver, kidneys, thoracic and abdominal cavities, thoracic and abdominal muscular walls, diaphragm, tongue, and nasal mucosa. Development to adult nasal stages took three weeks. Recovery of newly hatched larvae from the peritoneal fluid at four-eight hours after oral infection suggests a direct passage from the stomach or intestinal wall to the musculature. However, dissemination through the blood, as observed with Trichinella spiralis, cannot be excluded even though newly hatched larvae of T. nasalis are twice as thick (15 μm). Developing larvae were found in histological sections of the striated muscle of the abdominal and thoracic walls, and larvae in fourth moult were dissected from these sites. Adult females were found in the deep nasal mucosa where mating occurred prior to worms settling in the nasal epithelium. The present study shows a remarkable similarity between T. nasalis and Trichinella species regarding muscle tropism, but the development of T. nasalis is not arrested at the late first-larval stage and does not induce transformation of infected fibres into nurse cells. T. nasalis seems a potential model to study molecular relations between trichinelloid larvae and infected muscle fibres.     

Effects of PGE1 or PGE2 and/or acetazolamide on expulsion of Nippostrongylus brasiliensis from rats

PGE1 and PGE2 have been reported to enhance natural expulsion of Nippostrongylus brasiliensis, a nematode parasite, from the intestine of the rat. Mucus production may also be a key element of worm rejection. Our study attempts to determine if 1) PGE1 or PGE2 alter the normal course of infection with N. brasiliensis in rats, 2) a known mucous enhancing drug, acetazolamide, can augment the rate of worm expulsion, and 3) combinations of prostaglandins and acetazolamide affect N. brasiliensis in the rat. Rats were inoculated with approximately 1,000 infective larvae of N. brasiliensis. Animals were administered, intraduodenally, one of the following: 0.2 ml 0.9% NaCl; 0.2 ml 100% ethanol; 250 micrograms PGE1/0.2 ml 100% ethanol; 250 micrograms PGE2/0.2 ml 100% ethanol; 250 micrograms acetazolamide/0.2 ml 100% ethanol; 250 micrograms PGE1 or PGE2 + 250 micrograms acetazolamide/0.2 ml 100% ethanol. These solutions were given in a single bolus on day 6 postinoculation (PI) or twice daily on days 6-9 PI. Following these treatments the number of parasite ova per gram feces per day for days 6-10 PI and numbers of worms present at necropsy on day 10 PI were determined. Treatment with prostaglandins or acetazolamide or both failed to adversely affect egg deposition by adult female worms or the number of worms in the small intestine. These results do not support the involvement of prostaglandins in the expulsion of N. brasiliensis from the host intestine.     

Kinetics of primary and secondary infections with Strongyloides ratti in mice

Dawkins H. J. S. and Grove D. I. 1981 Kinetics of primary and secondary infections with Strongyloides ratti in mice. International journal for Parasitology11: 89–96. The kinetics of infection with S. ratti were quantitated in normal and previously exposed C57B1 /6 mice. In primary infections, larvae penetrated the skin rapidly and were seen in peak numbers 12 h after infection. By 24 h after infection, larval numbers had declined appreciably and there was a slow decrease in numbers thereafter. Larvae were first observed in the lungs at 24 h and maximal recovery occurred at 48 h. It is thought that larval migration through the lungs is rapid. Worms were first seen in the intestines two days after infection. Maximum numbers were seen on the fifth day and worm expulsion was complete by day 10. Two moults took place in the small intestine during days 3 and 4 after infection. Rhabditiform larvae were first noted on the fourth day after infection. Mice exposed to S. ratti four weeks previously had significantly less larvae in the skin 4 and 12 h after infection but by 24 h there was no difference when compared with mice with primary infections. Peak recovery of larvae from the lungs occurred 24 h after infection; significantly less larvae were recovered on days 2 and 3 when compared with normal mice. There was a marked reduction in the adult worm burden in the gut; the number of worms recovered was less than one fifth of that seen in primary infections. Those worms which did mature were less fecund and were expelled from the intestines within 7 days of infection. It is suggested that in previously exposed animals, the migration of larvae from the skin is hastened, many of these larvae are destroyed in the lungs and that expulsion of worms which do mature in the intestines is accelerated.     

Efficacy of ivermectin against Parelaphostrongylus andersoni (Nematoda, Metastrongyloidea) in white-tailed deer (Odocoileus virginianus)

Ivermectin was injected subcutaneously at 200 and 400 micrograms/kg of body weight into seven white-tailed deer (Odocoileus virginianus) in an attempt to control the muscle nematode Parelaphostrongylus andersoni. Counts of first-stage larvae in feces dropped to zero at 17 to 18 days posttreatment. Larvae reappeared in feces 1.5 to 6 wk later in six deer. Four deer were treated again approximately 9 wk after the first treatment; larval counts dropped to zero in 12 to 18 days. Larvae reappeared in low numbers 45 to 55 days after the second treatment. Because deer were held indoors on cement and the prepatent period of these worms is approximately 2 mo, the reappearance of larvae was not due to reinfection by accidental ingestion of gastropod intermediate hosts. Results suggest that ivermectin at dosages of 200 or 400 micrograms/kg of body weight suppressed larval production by adult female nematodes for several weeks or destroyed first-stage larvae in the lungs.     

Intestinal Transit Time During Infection with Eimeria nieschulzi in Rats*

SYNOPSIS. Experiments were designed to test whether or not intestinal transit time increases significantly during severe coccidiosis in the rat. Intraduodenal catheters were surgically implanted into 25 rats. Six to 12 days after surgery 11 rats were inoculated orally with 10⁴ sporulated oocysts of Eimeria nieschulzi Dieben, and 11 were inoculated with 10⁶ oocysts; 3 rats were retained as uninfected controls. At 2, 4, 8, 9, and 16 days postinoculation (PI) Na₂⁵¹CrO₄ was injected through the catheter into the duodenum of fasted rats and allowed to progress through the small bowel for 15 min, at which time the rats were killed. The distribution of ⁵¹Cr in the gut was plotted as a function of gut length. The leading edge of radioactivity traversed 70% of the gut length in controls, and ～ 50–60% in parasitized rats on days 2, 4, 8, and 9 PI. Also, a reflux of gut contents, as evidenced by radioactivity in the stomach, occurred early (PI days 2 & 4) in rats infected with 10⁴ oocysts and throughout patency in rats infected with 10⁶ oocysts. A 2nd study was undertaken to determine if chemically induced suppression of gut transit time during early infection would enhance infectivity as measured by increased parasite fecundity. Nine rats were injected subcutaneously with an antidiarrheal agent, Loperamide®, known to slow small bowel motility significantly. Another group of 9 control rats was injected with the ethanol-propylene glycol solvent. Ten min after injection, all rats were inoculated per os with 10⁴E. nieschulzi oocysts. The daily number of oocysts discharged/rat was followed from PI days 5–11. Patency began for all rats on PI day 7. The total number of oocysts discharged by the drugged rats as compared with controls was not significantly different.     

Age of adult worms of Echinostoma caproni does not affect development of miracidia

The effect of the age of adult Echinostoma caproni on egg development was studied. The percentage of fully developed miracidia was determined in eggs derived from adult worms obtained from laboratory mice at 2, 4, 6, and 8 wk postinfection (PI). Regardless of the age of worms from which the eggs were obtained, the percentage of fully developed miracidia was always >90%, and 60-80% of the eggs hatched. Several previous studies have shown that eggs derived from 2- to 4-wk-old E. caproni yielded miracidia that infected Biomphalaria glabrata snails. Results of the present study on E. caproni were in marked contrast to previous results with Echinostoma friedi, for which viable eggs were not obtained at 2 and 3 wk PI and maximal infectivity of miracidia in snails was obtained from eggs derived from worms collected at 8 and 9 wk PI. Further studies are needed to determine if the egg viability of other species in the "revolutum" group follow that of E. caproni or E. friedi.