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H Hurd

Publications and source records attributed to H Hurd.

At least 37 records · Page 2Linked to original sources

The effect of metacestodes of Hymenolepis diminuta on the bean-shaped accessory glands in male Tenebrio molitor.

Metacestodes of Hymenolepis diminuta affect several aspects of female reproductive physiology in Tenebrio molitor and such effects are mediated via the endocrine system. The effects on male reproduction are less well known and were studied with respect to the Bean-Shaped Accessory Glands (BAGs). The size and wet and dry weight of BAGs from infected and uninfected beetles were compared and rose to a plateau from 0-6 days post-emergence in uninfected beetles but in infected individuals continued to increase in both size and weight. These effects were density independent. Glands from both infected and uninfected beetles were assayed for trehalase activity measured by its ability to convert the sugar trehalose to glucose. The activity of this enzyme, per mg wet weight, was not affected by the parasite. However, total activity per gland increased in infected males. Total protein content and electrophoretic profiles of BAGs from infected and uninfected individuals showed no change in profile but showed an increase in all protein subunits per gland over a broad molecular weight range.

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Effect of Plasmodium yoelii nigeriensis (Haemosporidia: Plasmodiidae) on Anopheles stephensi (Diptera: Culicidae) vitellogenesis.

Our previous studies demonstrated a significant reduction in the egg production and survival of Anopeles stephensi Liston infected with Plasmodium yoelii nigeriensis Killick-Kendrick. We investigated the physiological mechanism underlying the malaria-induced curtailment of reproductive fitness. Polyclonal antibodies were raised against An. stephensi vitellin (Vn) and used in an enzyme immunoassay to quantify ovarian Vn and hemolymph vitellogenin (Vg) at 8, 12, 16, 20, 24, and 48 h postblood feeding in infected and noninfected mosquitoes. Initially, the concentration of Vg in the hemolymph and the accumulation of Vn in the ovaries of infected females were identical to females fed on noninfected mice, indicating that the synthesis of yolk protein by the fat bodies was initiated normally. However, there was a significant reduction in ovarian Vn at 24 and 48 h postblood feeding and a significant accumulation of Vg at 20 and 24 h postblood feeding in the hemolymph of infected mosquitoes. This increase in concentration of Vg in the hemolymph just before Vn reduction in the ovaries of infected mosquitoes indicated that synthesis at the fat body level may not be affected, but that sequestration of Vg by ovarian follicles of malaria-infected mosquitoes may be affected before resorbing follicles lose protein.

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The effect of Plasmodium yoelii nigeriensis infection on ovarian protein accumulation by Anopheles stephensi.

Both anopheline and culicine mosquitoes have been shown to incur a reduction in reproductive fitness when infected with malaria parasites. The agent of rodent malaria, Plasmodium yoelii nigeriensis, was used as a laboratory model to investigate changes in the accumulation of protein in the ovaries of Anopheles stephensi when infected with oocysts or when feeding on mice with heavy asexual parasitaemia but no mature gametocytes. Herein we report that during the early phases of the gonotrophic cycle the ovarian protein content increased normally; however, after 16 h post-blood-feeding there was a significant reduction in the total protein content in ovaries from infected mosquitoes. The development of ovaries from mosquitoes undergoing a second gonotrophic cycle and containing maturing oocysts was similarly affected. Ovarian protein profiles produced by sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed a depletion of the yolk protein vitellin. Ovaries from mosquitoes feeding on a mouse with 31% parasitaemia, no detectable gametocytes and a low haematocrit (29% packed cell volume) also exhibited a reduction in protein content, although this did not occur until much later in the gonotrophic cycle. The role of blood-meal quality and malaria infection in the reduction in egg production is discussed.

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

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.

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The effects of natural Plasmodium falciparum infection on the fecundity and mortality of Anopheles gambiae s. l. in north east Tanzania.

Rodent and avian malaria parasites have been reported to have an adverse affect upon the reproductive fitness of mosquitoes. In order to determine whether fecundity reduction occurs in Anopheles gambiae s. l. infected with human malaria a study of wild-caught mosquitoes was undertaken in the Muheza district of north east Tanzania. Fully engorged, indoor resting females were collected daily for 4 months and maintained for 5 days. A sporozoite rate of 11.5% was detected for the whole collection and of those females alive on day 6 an additional 17.5% were infected with oocysts alone. Oocyst, but not sporozoite, infection resulted in a 17.5% reduction in egg production. Fecundity reduction was not caused by a reduction in bloodmeal size in infected females and no size difference was detected between oocyst-infected and uninfected females although sporozoite-positive females were significantly larger. Comparisons in parity between uninfected and infected groups indicate that infection does not affect survival beyond the first gonotrophic cycle as no changes in survivorship occurred as a result of sporozoite infection.

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The effects of infection with Plasmodium yoelii nigeriensis on the reproductive fitness of Anopheles stephensi.

Infection with the rodent malarial parasite Plasmodium yoelii nigeriensis caused a significant reduction in the reproductive fitness (number of eggs produced and proportion of eggs hatched) of two different generations of Anopheles stephensi. Overall fertility (number of larvae produced) was reduced by 38.3% in the generation containing smaller mosquitoes (with a wing length of 3.2 +/- 0.1 mm) with relatively larger parasite burdens, and by 48.81% in the generation containing larger mosquitoes (with a wing length of 3.4 +/- 0.1 mm). The contribution that reduction in egg production and egg hatching made to overall reduction in reproductive fitness differed in each experiment. No significant difference was observed in the egg size (length from tip to tip and breadth at the centre) of control and infected mosquitoes in another generation of infected An. stephensi.

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Effects of Plasmodium yoelii nigeriensis infection on Anopheles stephensi egg development and resorption.

It has been shown previously that infection with Plasmodium yoelii nigeriensis reduces the number of eggs produced by female Anopheles stephensi. Here we examine the mechanism underlying fecundity reduction. Ovaries from infected and uninfected (control) female mosquitoes were examined 12, 24 or 36 h after blood-feeding during the first gonotrophic cycle (replicated) or the second gonotrophic cycle (unreplicated). Follicular development was assessed according to Christophers' stages and the proportions of developing and resorbing follicles per ovary were determined. Resorption of some follicles commenced within 12 h of blood-feeding, affecting significantly more follicles in the infected females: 1.1% v. 3.2%. The difference was greatest 36 h after blood-feeding: 25% reduction (10 v. 35%) in the first cycle; 16% reduction (9 v. 25%) in the second gonotrophic cycle. The mean speed of oogenesis was also found to be significantly retarded in infected mosquitoes. During the second gonotrophic cycle, for example, only 92-94% of follicles reached stage III by 24 h and stage IV by 36 h in infected females, whereas all the developing follicles of uninfected females reached these stages more or less synchronously in the time specified.

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Hymenolepis diminuta: metacestode-induced reduction in the synthesis of the yolk protein, vitellogenin, in the fat body of Tenebrio molitor.

Vitellogenin 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, not 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.

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Comparative fecundity and associated factors for two sibling species of the Anopheles gambiae complex occurring sympatrically in The Gambia.

For two sibling species of mosquitoes belonging to the Anopheles gambiae complex of malaria vectors, the effects of body size (wing length) and bloodmeal size (haematin excretion) on fecundity of wild females were investigated in The Gambia, West Africa. Freshly blood-fed individuals from sympatric populations of An.arabiensis and An.gambiae sensu stricto were sampled by collection at 07.00-09.00 hours from within bednets during July/August 1993, at the beginning of the rainy season. The possible confounding effect of infection with Plasmodium parasites was removed by eliminating infected mosquitoes from the study samples. An.arabiensis females comprised 75% of the An.gambiae sensu lato population and were significantly larger (greater mean wing length) than those of An.gambiae s.s. mosquitoes. Mean egg production per female (for the subsequent gonotrophic cycle, excluding pre-gravids) for the two species was not significantly different, though the relationship between wing length and egg production showed An.gambiae s.s. to be more fecund than the An.arabiensis of the same size. Pre-gravid An.gambiae s.s had consumed significantly smaller bloodmeals than gravid females but the mean wing length of these two gonotrophic categories was not significantly different. In contrast, An.arabiensis pre-gravids were smaller and had consumed smaller bloodmeals than the gravids.

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Steroid elution improves the stimulation threshold in an active-fixation atrial permanent pacing lead. A randomized, controlled study. Model 4068 Investigators.

BACKGROUND: Prior work suggests that the addition of a steroid-eluting reservoir to a passive-fixation permanent pacemaker lead improves the stimulation threshold; however, no large randomized study has addressed this tissue. Over the last several years, there has been an increase in enthusiasm for the use of active-fixation permanent pacemaker leads for various reasons in spite of the generally accepted notion that active-fixation leads have higher stimulation thresholds. METHODS AND RESULTS: This multicenter, randomized, controlled study examined the difference in performance between a standard active-fixation atrial lead (Medtronic model 4058) and a steroid-eluting lead (Medtronic model 4068). Stimulation thresholds were obtained in a four-point strength-duration fashion. Evaluations of sensing and impedance were performed as well. These evaluations were performed at implantation, at weeks 1 through 4, and at weeks 6, 12, 24, and 52. Stimulation thresholds were significantly better in the steroid lead than in the nonsteroid lead at each measurement point from 1 week to 12 months. The mean 1.6-V stimulation threshold at 12 months was 0.19 +/- 0.2 ms in the steroid lead and 0.41 +/- 0.30 ms in the control lead. No acute peaking was observed with the steroid lead, whereas significant peaking was observed with the control lead. There was no difference in long-term sensing or impedance. CONCLUSIONS: Inclusion of a steroid-eluting reservoir in an active-fixation permanent pacing lead improved stimulation thresholds in both the subacute and chronic periods and therefore should extend pulse-generator longevity.

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Microsomal juvenile hormone binding proteins in the follicle cells of Tenebrio molitor.

The microsomal fraction of Tenebrio molitor follicle cells has been found to contain both high and low affinity binding sites for juvenile hormone (JH) III. Using Scatchard analysis, the equilibrium dissociation constants, Kd, were calculated as 1.0 x 10(-8) and 4.3 x 10(-7) M respectively. Kinetic data support a rapid binding of the hormone to the site(s), with rate constants of ka = 3.77 x 10(8) M-1 min-1 and kd = 0.0075 min-1. Affinity of the binding site(s) for JH III was higher than for either JH I or methoprene. The significance and possible function of such microsomal binding proteins are discussed, with reference to the perturbance of vitellogenesis found in beetles parasitized by Hymenolepis diminuta.

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Hymenolepis diminuta-induced fecundity reduction may be caused by changes in hormone binding to Tenebrio molitor ovaries.

Aspects 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(-8) M, Bmax = 1.5 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.

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Plasmodium yoelii nigeriensis: the effect of high and low intensity of infection upon the egg production and bloodmeal size of Anopheles stephensi during three gonotrophic cycles.

Anopheles stephensi mosquitoes showed a reduction in fecundity over 3 successive gonotrophic cycles, after becoming infected with Plasmodium yoelii nigeriensis. This effect could be observed at high oocyst burdens (> 75) or at low oocyst burdens (mean of 4.36). Mean bloodmeal size of the infected mosquitoes was significantly reduced only when feeding upon a mouse with a high gametocytaemia and the conversion of the bloodmeal into eggs by the infected mosquitoes was disrupted. Patterns of infected mosquito mortality, over the 3 gonotrophic cycles, varied with severity of infection. Although in 1 case increased mortality and decreased bloodmeal size may have affected fecundity, this could not have accounted for all of the observed fecundity reduction. We propose that other, unknown parasite related factors, are involved.

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Malaria-induced reduction of fecundity during the first gonotrophic cycle of Anopheles stephensi mosquitoes.

Anopheles stephensi mosquitoes which had fed upon mice infected with Plasmodium yoelii nigeriensis malaria parasites produced significantly fewer eggs than mosquitoes fed on an uninfected mouse. Fecundity reduction was more pronounced when the bloodmeal contained malaria gametocytes and the mosquitoes developed oocysts. Egg production and haematin excretion were correlated for uninfected bloodfed mosquitoes; the presence of P.y.nigeriensis in the blood affected this relationship. Reduced fecundity was associated with a significant reduction of bloodmeal size (measured by haematin excretion) in mosquitoes which ingested gametocytaemic blood. The bloodmeal size in mosquitoes fed on parasitaemic blood without gametocytes was not significantly reduced. The use of haematin assays for determination of bloodmeal size in mosquitoes is discussed.

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Effect of metacestodes of Hymenolepis diminuta on storage and circulating carbohydrates in the intermediate host, Tenebrio molitor.

The 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.

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The effects of Onchocerca lienalis infection on vitellogenesis in the British blackfly, Simulium ornatum.

We have previously described the major yolk protein, vitellin, in the British blackfly Simulium ornatum Meigen. Here we demonstrate that vitellogenin, synthesized in the fat body and secreted into the haemolymph, is composed of subunits with the same approximate molecular weight as vitellin, namely 200 and 68 kDa. Simulium ornatum is the natural vector for the cattle filarial nematode Onchocerca lienalis Stiles, which induces host fecundity depletion. A significant reduction in ovarian vitellin content was associated with infection by intrathoracic injection of 20 O. lienalis microfilariae immediately after blood-feeding. Fat body synthesis of vitellogenin was significantly reduced as early as 8 h post-infection in comparison with sham-injected flies. When total haemolymph protein from infected and sham injected flies was compared, titres were significantly depressed 6 h post-infection. However, later in the infection, titres were elevated by 30%, the major component being vitellogenin. The injection of dead microfilariae had no effect. An infection burden of a single parasite caused a significant reduction in ovarian protein content in comparison with shams, but no further significant decrease was observed as the parasite burden was increased from 5 to 20. Possible mechanisms underlying the disturbance of Simulium reproductive physiology are proposed.

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Interactions between parasites and insects vectors.

This review stresses the importance of studies that will provide a basic understanding of the pathology of parasite-infected vector insects. This knowledge should be a vital component of the very focussed initiatives currently being funded in the areas of vector control. Vector fecundity reduction is discussed as an example of such pathology. Underlying mechanisms are being investigated in a model system, Hymenolepis diminuta-infected Tenebrio molitor and in Onchocerca-infected blackflies and Plasmodium-infected Anopheles stephensi. In all cases, host vitellogenesis is disrupted by the parasite and, in the tapeworm/beetle model, interaction between the parasite and the endocrine control of the insect's reproductive physiology has been demonstrated.

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Anthelmintic effects of cyclosporin A on protoscoleces and secondary hydatid cysts of Echinococcus granulosus in the mouse.

Cyclosporin A (CsA), employed primarily as an immunosuppressant during the management of organ and graft transplants, exhibits anthelmintic properties. However, its efficacy against tapeworm infections in laboratory models is variable. A preliminary investigation has been undertaken to assess the action of CsA on the establishment and growth of protoscoleces and secondary hydatid cysts of ovine Echinococcus granulosus in mice. Administration of CsA in five consecutive daily doses, beginning 2 days prior to infection, resulted in significant reduction in cyst establishment (measured in terms of cyst masses, cyst numbers and cyst wet weights), when mice were autopsied 20 weeks post-infection. None of these parameters were significantly reduced when the drug was administered 18 weeks post-infection, although wet weight decreased by 42%. Ultrastructural examination of the germinal membrane and laminated layer of late-treated E. granulosus revealed abnormalities in all cysts studied whereas control and early-treated hydatids were normal. A case is made for the consideration of a clinical use for CsA for post-operative control of secondary hydatidosis and its efficacy against hydatid cysts is discussed.

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