Haemolymph from female beetles infected with Hymenolepis diminuta metacestodes retards the development of ovarian follicles in recipient Tenebrio molitor (Coleoptera)

Parasitology ◽  
1997 ◽  
Vol 114 (2) ◽  
pp. 175-179 ◽  
Author(s):  
M. MAJOR ◽  
T. J. WEBB ◽  
H. HURD

Infection with developing metacestodes of the rat tapeworm, Hymenolepis diminuta, is known to retard the accumulation of the yolk protein, vitellin, in the terminal ovarian follicles of the intermediate host, Tenebrio molitor. It is probable that this is the result of competitive inhibition of juvenile hormone binding at a microsomal binding site in the beetle follicular epithelium. Experiments were designed to test the hypothesis that inhibitor molecules were circulating in the haemolymph of infected beetles. Whole haemolymph, collected from male or female beetles at various stages post-infection, was injected into non-infected female recipients 2 days post-emergence. Ovaries were removed 3 days later and the vitellin content of the same sized follicles measured using an ELISA. The vitellin content of follicles from recipients of haemolymph from females infected with metacestodes at stage 1 and stage 3–4 was significantly reduced (24 and 27·9%) compared to sham-infected females. However, haemolymph from females infected with mature metacestodes did not affect the vitellin content. Results were thus comparable to those obtained by monitoring ovarian vitellin levels in female T. molitor with bona fide infections. Haemolymph from infected males did not affect ovarian vitellin content. These results indicate that molecules that can modulate vitellogenesis may be present in the haemolymph of females infected with developing metacestodes but that these factors disappear later in infection.

Parasitology ◽  
1995 ◽  
Vol 110 (5) ◽  
pp. 565-571 ◽  
Author(s):  
T. J. Webb ◽  
H. Hurd

SUMMARYAspects of vitellogenesis, known to be controlled by juvenile hormone, are adversely affected by Hymenolepis diminuta infection of Tenebrio molitor, in spite of circulating titres of the hormone remaining unchanged. It has therefore been proposed that juvenile hormone binding is disrupted at the tissue site level. Juvenile hormone III binding sites were located in the nuclear, microsomal and post-microsomal supernatant fractions of the follicle cells of Tenebrio molitor. When JH-III binding was quantified for both control and Hymenolepis diminuta-infected beetles, binding in the nucleus and cytosol were found to be largely unaffected. However, microsomal binding was severely disrupted; on days 3 and 6 post-infection, binding was greatly diminished, on day 9 post-infection, binding was slightly reduced and, by day 15, binding was ‘restored’ to that of control insects. Using follicle cell microsomes at day 3 post-infection, previous Scatchard analysis revealed the presence of at least two JH-III binding sites. The first is of higher affinity, Kd = 5·3 x 10·5 x 10−11 mol/mg protein and the second of lower affinity Kd = 7·7 x 10−7 M, Bmax = 9·75 x 10−11 mol/mg protein. A comparison with microsomal binding parameters of follicle cells from non-infected Tenebrio indicated that although the Bmax values were unchanged, the Kd value of the higher affinity site was increased by approximately 5-fold. These data are indicative of a parasite-induced competitive binding inhibitor.


Parasitology ◽  
1996 ◽  
Vol 112 (4) ◽  
pp. 429-436 ◽  
Author(s):  
T. J. Webb ◽  
H. Hurd

SUMMARYVitellogenin synthesis by the fat body has been monitored using in vitro culture and immunoprecipitation. This system was found to be efficient for measuring vitellogenin production in both non-infected Tenebrio molitor and those infected with Hymenolepis diminuta. In fat bodies from infected beetles, vitellogenin production was decreased by up to 75% (day 24 post-infection) and, at all times investigated, vitellogenin synthesis was significantly below control levels (days 3–30 post-infection). Incubating fat bodies from control insects with isolated metacestodes indicated that this may be a direct effect by the parasite which is developmental stage-specific. Stage II, but not stage III–IV, nor heat-killed parasites could bring about this decrease in vitellogenin. In addition, these effects may be density dependent within the range of 2–20 parasites per fat body; only 2 metacestodes were necessary to cause a significant decrease. Since metacestodes do not take up vitellogenin, nor limit the amount of [14C] leucine available to the fat body for vitellogenin production, it is conceivable that the parasite produces a potent inhibitor of vitellogenin synthesis, or a molecule which induces cells within the fat body to do so.


Parasitology ◽  
1986 ◽  
Vol 93 (1) ◽  
pp. 111-120 ◽  
Author(s):  
Hilary Hurd ◽  
C. Arme

SUMMARYFemale Tenebrio molitor infected with metacestodes of Hymenolepis diminuta exhibit elevated concentrations of female-specific proteins in their haemolymph and the origin of these has been investigated. Following a 4 h in vitro incubation with [14C]leucine, fat bodies from non-infected females secreted 13 times more protein than those from females 12 days post-infection. A comparison of the uptake in vivo of radio-isotope labelled amino acids by ovaries from non-infected and infected beetles of various ages revealed no differences; however, a 51·5% decrease in protein sequestration was detected in females 12 days post-infection. Electrophoresis of homogenates of radio-isotope labelled ovaries demonstrated that the majority of label was associated with vitellin sub-units. It is suggested that the decrease in vitellogenin sequestration associated with infection results in an increase in the haemolymph concentration of these proteins despite a concomitant reduction in their secretion by fat bodies. Both fat body synthesis and ovarian sequestration are under juvenile hormone control and it is proposed that metacestodes of H. diminuta may cause a reduction in the concentration of this hormone in the intermediate host.


Parasitology ◽  
1990 ◽  
Vol 100 (3) ◽  
pp. 445-452 ◽  
Author(s):  
H. Hurd ◽  
C. Strambi ◽  
N. E. Beckage

SUMMARYMetacestodes of Hymenolepis diminuta cause a perturbance of vitellogenesis in the intermediate host Tenebrio molitor. The reduction in host reproductive output associated with infection may be due to this pathophysiology. Many of these events are regulated by host juvenile hormone (JH). A comparison of the titre of JH and its rate of degradation in female control and parasitized 15-day-old insects has been made. Haemolymph from female beetles contained 1·27 pMol JH equivalents/100 µl. No significant difference was associated with infection. However, topical application of a JH analogue, methoprene, at the time of infecion or 8 days post-infection reduced the significant accumulation of vitellogenin usually found in the haemolymph of females 12 days or more post-infection. These findings indicate that parasite-induced alteration of host vitellogenesis is not mediated via alteration in JH titres, although observations made after hormone supplementation suggest some form of interaction between the parasite and the host endocrine system.


Parasitology ◽  
1994 ◽  
Vol 108 (4) ◽  
pp. 473-478 ◽  
Author(s):  
J. Y. Kearns ◽  
H. Hurd ◽  
A. S. Pullin

SUMMARYThe metamorphosis of oncospheres of the rat tapeworm, Hymenolepis diminuta, to mature metacestodes induces several pathophysiological effects in the intermediate host, Tenebrio molitor (Coleoptera). Previous investigations have failed to elucidate the mechanism responsible for changes in the host reproductive physiology and behaviour. This work forms part of an assessment of the degree to which nutrient resource management may be involved in these interactions. We report that developing metacestodes exert a pronounced effect upon host carbohydrate reserves and also alter circulating carbohydrate titres at some stages post-infection. Biochemical studies of fat body glycogen demonstrated a significant depletion of reserves as early as 3 days post-infection in males and 5 days post-infection in females. Gas chromatography revealed trehalose to be the predominant haemolymph carbohydrate, titres being significantly elevated in male beetles 5 and 9 days post-infection and in females 12 days post-infection. Metacestodes had no effect on glucose concentrations in male or female beetles.


1996 ◽  
Vol 74 (7) ◽  
pp. 1268-1274 ◽  
Author(s):  
Tonia Robb ◽  
Mary L. Reid

Although the cause is often unclear, many parasites alter the behaviour of their intermediate hosts. The larval form of the rat tapeworm, Hymenolepis diminuta, has previously been shown to modify the behaviour of its intermediate host, the flour beetle, Tribolium confusum, in a manner that may be adaptive to the parasite. To test this explanation we observed host behaviours including activity, concealment, and the response to and production of pheromones. Infected female beetles examined both 4–5 and 11–12 days post infection were slower moving and slower to conceal themselves than uninfected conspecifics; however, they did not differ from uninfected individuals in staying concealed. Infection of T. confusum did not affect the production of pheromones by mated and virgin females or the response of females to male pheromones. A second hypothesis for altered behaviours may be that modified behaviours result from pathology. The survivorship of mated infected female beetles was significantly lower than that of infected virgin beetles and uninfected beetles. Thus, both mated status and infection were important factors in survivorship, but only infection had significant effects on the altered behaviours. In this system, therefore, the hypothesis that behavioural changes are due to adaptive manipulation of the host by the parasite is supported.


1993 ◽  
Vol 128 (1) ◽  
pp. 88-94 ◽  
Author(s):  
Nobuyoshi Kokawa ◽  
Mareo Yamoto ◽  
Kenichi Furukawa ◽  
Ryosuke Nakano

We performed partial purification of low molecular weight luteinizing hormone binding inhibitor from porcine follicular fluids and examined its biological activities. Following ultrafiltration, gel filtration and anion exchange of the pooled porcine follicular fluids, low molecular weight fractions (500–10,000 MW) inhibited [125I]hLH binding to porcine granulosa cells in a dose-dependent manner. The binding inhibition kinetics study revealed that the luteinizing hormone binding inhibitor may indicate a non-competitive inhibition with [125I]hLH binding. In vitro bioassay using adult mouse testicular interstitial cells revealed that the partially purified luteinizing hormone binding inhibitor reduced ovine LH-stimulated testosterone and cAMP production in a dose-dependent manner, whereas the luteinizing hormone binding inhibitor did not affect basal production of testosterone and cAMP. The inhibitory activity was heat stable and did not disappear with activated charcoal adsorption. The results of the present study suggest that the luteinizing hormone binding inhibitor may play an important role as an ovarian non-steroidal regulator modulating the receptor binding of LH and LH-mediated steroidogenesis.


1978 ◽  
Vol 56 (4) ◽  
pp. 604-607 ◽  
Author(s):  
Marie Novak ◽  
W. S. Evans

Tribolium confusum beetles infected with Hymenolepis diminuta were fed continuously from day 1, 3, 5, 6, or 7 to day 10 post infection (p.i.) on a mixture composed of two parts Telmin (containing 16.67% of mebendazole) and one part flour. The drug inhibited the worm development and this effect decreased as the age of larvae at the time of the first exposure increased. Lowered incidence of infection, decreased population size, and retarded development were apparent when the beetles were given drug from day 3 p.i. or earlier. Retarded development was also observed in cysticercoids from beetles given drug from day 5 p.i. When given from day 6 or later, it had no effect on worm development. However, when compared with larvae from beetles fed only flour, cysticercoids exposed to the drug from day 6 or later showed reduced infectivity and a decrease in their ability to excyst in vitro. Fully developed infective cysticercoids exposed to the drug from day 10 p.i. or later were not affected by it.


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