Hymenolepis citelli and H. diminuta: worm burdens in homologous and heterologous infections in rats

Primary and secondary infections of Hymenolepis citelli were followed in CFHB rats. In primary infections of 6, 20, and 50 cysticercoids, over 75% of the worms administered became established and grew. Thereafter, survival depended on the intensity of the primary infection. Acquired resistance to homologous challenge infections could be stimulated in rats by prior infection with H. citelli. The growth of secondary worms decreased as the intensity of the sensitizing infection increased. The protective response waned with time in the absence of the primary worms. Cross-protective responses between H. citelli and H. diminuta occur in rats infected previously with either parasite. Retardation in the growth of secondary worms may have an immunological basis.     

The occurrence and distribution of 5-hydroxytryptamine in Hymenolepis diminuta and H. nana

The presence of 5-HT in Hymenolepis diminuta and Hymenolepis nana was detected by 2 biochemical methods and as yellow fluorescence in a histochemical method. In H. diminuta, 5-HT was found in a concentration of about 1.2 micron/g; this amount did not vary significantly in worms aged 6 to 18 days or more or in various regions of the worm. In H. nana, 5-HT was found in a concentration of about 1.8 micron/g. It was histochemically localized in H. diminuta and H. nana in a pattern similar to that of acetylcholinesterase previously described in these 2 cestodes, and it may be the opposing neuro-transmitter to acetylcholine. The lack of 5-HT in the vestigial rostellum of H. diminuta may be correlated with loss of function of this organ.     

Hymenolepis diminuta and H. nana: cross immunity against the lumen phase in BALB/c mice

When BALB/c mice initially given cysticercoids of Hymenolepis diminuta orally (Day 0) were challenged with eggs or cysticercoids of H. nana, almost all the mice became completely resistant to H. nana challenges from Day 30 onward, and no luminal adults of H. nana were established. There was a tendency for the number of tissue cysticercoids recovered 4 days after egg challenge in immunized mice to be much less than that in control mice (P less than 0.001, Student's t test). However, when these cysticercoids recovered from immune group mice were inoculated into uninfected mice, they matured in the lumen. Thus, the cross immunity to H. nana challenge evoked by an initial prepatent infection with H. diminuta appeared to be directed not against the tissue phase but against the lumen phase of H. nana. When BALB/c mice initially given eggs of H. nana were challenged with H. diminuta, they became resistant to H. diminuta from Day 15 onward. When the mice given eggs of H. nana were treated with a cestocide, praziquantel, at the beginning of the expected luminal development of H. nana and experienced a tissue phase only before challenge with H. diminuta, they showed no resistance to H. diminuta. Thus, the cross immunity to H. diminuta challenge evoked by an initial patent infection with H. nana appeared to be due to the immunogens of the lumen phase of H. nana but not those of the tissue phase. The cross immunity may be, therefore, essentially evoked by the lumen phase of these two phylogenetically closely related species and not by or against the tissue phase of H. nana.(ABSTRACT TRUNCATED AT 250 WORDS)     

Complement-mediated lysis in vitro of newly excysted tapeworms: Hymenolepis diminuta, Hymenolepis microstoma, Hymenolepis nana and Hymenolepis citelli

Bøgh H., Christensen J.P.B. and Andreassen J. 1986. Complement-mediated lysis in vitro of newly excysted tapeworms: Hymenolepis diminuta, Hymenolepis microstoma, Hymenolepis nana and Hymenolepis citelii. International Journal for Parasitology16: 157–161. Newly excysted worms of Hymenolepis diminuta were lysed in 50% normal serum from all 13 animal species tested, including man. Since H. diminuta was neither lysed in complement inactivated serum—by heat or adding EDTA, LPS or CVF—nor in C5-deficient mouse serum, it is concluded that the lysis was associated with the complement cascade. It is shown that H. diminuta can activate the complement system via both the classical and alternative pathway. Furthermore, it is indicated that the lysis is independent of serum antibodies. Hymenolepis nana and H. citelli were also lysed in all normal sera tested, eight and six respectively, while newly excysted worms of H. microstoma were lysed in normal sera from 10 mammals and birds, but not in sera from its hosts, the mouse, rat and golden hamster. This indicates that the complement system of these three species differs from that of the other species tested in such a way that H. microstoma is able to avoid lysis in these sera.     

Hymenolepis nana: immunity against oncosphere challenge in mice previously given viable or non-viable oncospheres of H. nana, H. diminuta, H. microstoma and Taenia taeniaeformis

When mice, previously given oral inoculation with viable oncospheres of the heterologous cestode species (Hymenolepis diminuta, H. microstoma, Taenia taeniaeformis) and the homologous one (H. nana), were challenged with oncospheres of H. nana 4 days after the primary inoculation, they showed strong and complete resistance to H. nana challenge, respectively. However, the resistance was not evoked in mice given either infective eggs of Toxocara canis or non-viable oncospheres of all cestode species examined. Congenitally athymic nude mice given viable oncospheres did not show any resistance to H. nana either. Eosinophil infiltration around cysticercoids of H. nana in the intestinal villi appeared to be more prominent in mice previously given viable oncospheres of H. diminuta than in mice given non-viable oncospheres or PBS only. Some of the eosinophils in the villus harboring cysticercoid(s) of H. nana invaded the epithelia in the former, whereas all eosinophils remained in the lamina propria in the latter. There was almost no eosinophil infiltration in nude mice. Microscopic observations revealed that oncospheres of H. diminuta, which require beetles as the intermediate host like H. microstoma, could invade the mouse intestinal tissue. Therefore, it is strongly suggested that the strong cross resistance to H. nana in mice, induced by oncospheres of all heterologous cestode species, is thymus-dependent and due to oncospheral invasion into the intestinal tissue of mice.     

Lumen phase specific cross immunity between Hymenolepis microstoma and H. nana in mice

, and 1988. Lumen phase specific cross immunity between Hymenolepis microstoma and H. nana in mice. International Journal for Parasitology 18: 1019–1027. When mice inoculated with five cysticercoids of Hymenolepis microstoma were challenged with H. nana, they showed strong resistance to challenges with both eggs and cysticercoids of H. nana from day 20. The immunity became complete from day 30 onward: no tissue cysticercoids or lumenal adults of H. nana were established in these mice. However, when mice were challenged with H. nana 10 or 20 days after 10-day old immature H. microstoma were removed by an anthelmintic, the immunity evoked was directed exclusively against the lumenal phase of the cysticercoid challenge but not the tissue cysticercoids of the egg challenge. When mice experienced the prepatent infection with H. microstoma twice, the immunity evoked was also against the lumenal phase of the egg challenge: the oncospheres developed into tissue cysticercoids but thereafter completely failed to develop into lumenal adult tapeworms. Infection with a single cysticercoid of H. microstoma was shown to be sufficient to evoke immunity against H. nana cysticercoid infections in two strains of mice. Sera from mice which experienced a patent infection with H. microstoma revealed that IgG, IgA, IgM isotypes reacted against oncospheres and cysticercoids of both species, while sera from mice which experienced two prepatent infections reacted with cysticercoids only. Sera from H. microstoma infected mice resistant to H. nana caused precipitations on 4-day-old H. nana in vitro. A correlation exists between the presence of stage specific antibodies and resistance to the different stages.     

Antagonistic effects of Schistosoma mansoni on superimposed Hymenolepis diminuta and H. microstoma infections in mice

Patent, but not prepatent, Schistosoma mansoni infections in mice enhanced the expulsion of a superimposed infection with Hymenolepis diminuta. An antagonistic effect was also directed against a superimposed H. microstoma infection in mice harbouring patent S. mansoni infections.     

Blast cell activity in mice infected with Hymenolepis nana, H. diminuta and Trichinella spiralis: in vivo uptake of 125IUdR in lymphoid tissues and gut

The kinetics of the lymphoblast response in mice during the course of a primary infection with Hymenolepis nana was measured by the in vivo uptake of 125IUdR. The response was most marked in tissues local to the site of infection, involving the nodes draining the small intestine but not other areas, e.g., inguinal lymph nodes. A close correlation between these responses and the course of infection was observed. Uptake of 125IUdR was greatest in the mesenteric lymph node (MLN) but the peak reached in this organ was later than that in Peyer's patches (PP), small intestine (SI) and spleen (S). The increase in lymphoblast activity of the MLN was similar with Trichinella spiralis; no significant blast cell response to infection with H. diminuta was found till day 9 after injection, the results being similar to those obtained when H. nana infections were established using cysticercoids rather than eggs. It has been shown that the increase in lymphoblast activity was closely correlated with the presence of cells which are most effective in adoptive transfer immunity. A dose-dependent effect was detected in blast cell activity of MLN in different infection levels with T. spiralis and H. nana.     

Reinfection and recidive in Hymenolepis nana infections (author's transl)]

The excretion of Hymenolepis nana eggs begins in CF-1 mice between the 11th and 12th day irrespective of the wormload. In Swiss mice, however, the onset of egg excretion can be retarded up to the 15th day if the number of parasites is high. The re-appearance of eggs after treatment occurs between the 6th and 9th day using an exact diagnostic method. If the number of parasites is low, than re-appearance of eggs occurs later than if it is high. An infection with eggs protects mice for several months against a re-infection with eggs but not against one with cysticercoids. If cysticercoids are used to establish the primary infection no immune reaction against a re-infection develops. If eggs reappear in the faeces after treatment then the following conclusion can be drawn: Eggs reappear within a week after treatment then it must be a relapse. Eggs reappear during the second week then it can be either a relapse or a re-infection. Eggs reappear at three weeks or later then it can only be due to a re-infection.     

Hymenolepis citelli, H. diminuta and H. microstoma: immunoglobulin-containing cells in the lamina propria of the mouse gut during primary and secondary infections

The indirect immunofluorescent technique was used to determine the occurrence of IgA, IgM and IgG1 immunoglobulin-containing cells in local intestinal mucosal immune responses to Hymenolepis citelli, H. diminuta and H. microstoma infections in mice. In the intestinal lamina propria of H. citelli and H. diminuta infected mice there was no increase in the mean numbers of immunoglobulin-containing cells when compared with uninfected control mice, but there was in H. microstoma infected mice. The numbers of IgG1- positive cells in both infected and uninfected mice were very small relative to IgA and IgM immunocytes. The distribution of immunocytes in the lamina propria of infected and uninfected mice was essentially similar and the localization of isotypes in duodenal sections showed no immunoglobulins in the villous epithelial cells. There was also no marked difference between primary and secondary infections indicating that immunoglobulin-containing cells play no major role in functional immunity against hymenolepid infections in the mouse. The presence of IgA and IgM was also demonstrated on the tegument of the tapeworms, although the distribution was patchy and more abundant on H. microstoma than on H. diminuta or H. citelli. The time of appearance of both isotypes was latest on H. citelli.     

Secondary infections of Hymenolepis diminuta in mice: effects of varying worm burdens in primary and secondary infections.

In one (1 c) and six (6 c) cysticercoid primary infections of Hymenolepis diminuta in NIH (inbred) and CFLP (outbred) male mice 6 +/- 1 weeks old greater than 85% of the worms established but were rejected (destrobilated or expelled) subsequently. Rejection occurs more quickly in 6 c infections than in 1 c infections. Considerable worm growth occurs in 1 c and 6 c primary infections but worms from 6 c infections weighed less than worms from 1 c infections on all days studied. Expulsion of H. diminuta does not occur more rapidly in secondary infections than in primary infections; loss of 6 c secondary worms occurs at the same rate as 6 c primary worms but 1 c secondary worms survive longer than 1 c primary worms. Although worms are not lost more quickly in secondary than in primary infections, they are affected at an early age by the immune response which stunts their growth. Increasing the intensity of primary and secondary infections increases the severity of stunting of secondary worms. The results are discussed and it is suggested that immune responses to Hymenolepis spp. in rodents are common but that thresholds of worm numbers exist below which appreciable worm loss does not occur. Stunting due to crowding, which generally is attributed to inter-worm competition, may be in part immunologically mediated. For future immunological studies attempting to induce secondary responses to H. diminuta in mice, worm growth, not survival, is the criterion to evaluate.     

Concurrent infections of the trematode Echinostoma caproni and the tapeworms Hymenolepis diminuta and Hymenolepis microstoma in mice

Superimposing the intestinal tapeworm Hymenolepis diminuta on an established infection with the trematode Echinostoma caproni or simultaneous infection of mice with H. diminuta and Hymenolepis microstoma caused destrobilation and expulsion of H. diminuta, whereas establishment and growth of H. microstoma under the same infection regimes were not affected. In contrast, simultaneous superimposition of H. diminuta and H. microstoma on an established E. caproni infection caused destrobilation and expulsion of both H. diminuta and H. microstoma.     

Hymenolepis diminuta: the effect of cold temperature exposure on infections in mice

Hymenolepis diminuta grown in mice maintained at 5 degrees C were significantly larger and markedly more developed than those grown simultaneously in control mice maintained at 21 degrees C. In mice maintained at 5 degrees C, the incidence of infection and the number of worms recovered per host were higher than in the mice kept at 21 degrees C. Regardless of the temperature of the hosts' external environment, primary infections were always expelled before Day 13 postinfection and secondary (challenge) infections were invariably lost before Day 7.