The effect of mebendazole on the development of Hymenolepis diminuta in Tribolium confusum

1976 ◽  
Vol 54 (7) ◽  
pp. 1079-1083 ◽  
Author(s):  
W. S. Evans ◽  
Marie Novak

Tribolium confusum parasitized by Hymenolepis diminuta were allowed to feed on mixtures composed of 0.005 to 20 g of mebendazole (Telmin: methyl-5-benzoyl benzimidazole-2-carbamate) in 10 g of flour from day 1 (24 h) to day 9 post infection. Retarded cysticercoid development, lowered incidence of infection, and reductions in the number of cysticercoids recovered per beetle were produced by drug levels of 0.1, 1.0, and 10 g respectively. None of the drug concentrations tested produced 100% mortality, and developing cysticercoids varied considerably in their tolerance of mebendazole.

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.


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.


Parasitology ◽  
1986 ◽  
Vol 92 (2) ◽  
pp. 405-412 ◽  
Author(s):  
Malefane Maema

SUMMARYSome effects ofHymenolepis diminutaon the fecundity ofTribolium confusumare described. Host fecundity is observed to be reduced exponentially with increasing parasite burden/host, although there are differences in the ability of individual hosts to respond to parasitism. Of particular interest is the finding that host fecundity is greatly reduced in young beetles on or by day 14 post-infection (p.i.). This age-related reduction in host fecundity is discussed in relation to the population dynamics of this hostr-parasite relationship.


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.


2020 ◽  
Vol 38 (15_suppl) ◽  
pp. 2568-2568
Author(s):  
Carlos G Romo ◽  
Brian Michael Alexander ◽  
Nathalie Agar ◽  
Manmeet Singh Ahluwalia ◽  
Arati Suvas Desai ◽  
...  

2568 Background: Wee1 is a key regulator of the G2/M checkpoint and is frequently overexpressed in glioblastoma (GB). Adavosertib is a first-in-class oral, small molecule inhibitor of Wee1 that acts primarily as a DNA damage sensitizer. A phase I clinical trial was conducted to evaluate its safety and establish the recommended phase II dosing. Studies were undertaken to evaluate whether potentially therapeutic concentrations of the drug are achieved in recurrent tumor and adjacent non-enhancing brain regions with presumed intact blood-brain barrier (BBB). Methods: Twelve patients received five daily doses of adavosertib pre-operatively at either the maximum tolerated dose (MTD) for concurrent radiation or adjuvant temozolomide. Tissue from contrast enhancing (CE) and non-enhancing (NE) brain regions was obtained for analysis during surgical resection. A second stage is being conducted using microdialysis (MD) to facilitate continuous sampling of extracellular fluid (ECF) and measuring free drug concentrations in: normal-appearing brain, contrast enhancing tumor, and a peritumoral T2 hyperintense area. The concentration of total adavosertib in plasma and tissue homogenates and free drug in ECF were determined by validated LC/MS/MS methods. Results: Geometric mean concentrations of adavosertib after a 200 mg dose were 644 ng/mL and 119 ng/mL in CE and NE tissue specimens, respectively (6 patients). At the 425 mg dose, the mean concentrations were 3,576 ng/mL in CE tissue and 885 ng/mL in NE tissue (6 patients). MD was performed in 2 patients. Samples from functional MD catheters were collected from NE brain in patient no. 1 and from two NE areas and a FLAIR hyperintense region in patient no. 2, with the following results in the table. Conclusions: The total drug concentration in tissue samples was notably lower in regions of the brain with a relatively intact BBB as compared to contrast enhancing tissue. Concentrations of adavosertib measured by MD vary markedly depending on catheter location. Free drug levels in ECF within brain with a functional BBB, although considerably lower than total drug levels in tissue, were 2-10 times below the previously reported IC50 for antiproliferative activity against sensitive GB cell lines (127 ng/mL). Whether or not the target of the drug is effectively inhibited at these concentrations remains to be demonstrated. Clinical trial information: NCT01849146 . [Table: see text]


1992 ◽  
Vol 70 (12) ◽  
pp. 2311-2314 ◽  
Author(s):  
W. S. Evans ◽  
M. C. Hardy ◽  
Renate Singh ◽  
G. E. Moodie ◽  
J. J. Cote

Populations of Tribolium confusum that had been fed continuously (satiated) or starved for 48 h were separated into groups of 10 beetles each. Each group was placed in a test arena (diameter 90 mm) that contained two infective baits (feces from rats infected with patent Hymenolepis diminuta) and two baits from uninfected rats and allowed to forage for 120 or 240 min. The number of beetles aggregated in the immediate region of each bait was recorded every 20 min until the experiment was terminated. During the first 180 min the distribution of the beetles in the starved populations invariably favoured (P < 0.025) the infective baits. A similar trend was observed with satiated beetles but the difference in beetle distribution was significant (P < 0.001) only at the 100-min observation time. With both starved and satiated populations the differences in distribution between bait types were not significant after 180 min.


Parasitology ◽  
1981 ◽  
Vol 83 (3) ◽  
pp. 489-496 ◽  
Author(s):  
Erling Bindseil ◽  
Jørn Andreassen

SUMMARYMice inoculated with 2000 Ascaris suum eggs 7 days before an infection with 2 cysticercoids of Hymenolepis diminuta harboured significantly fewer and/or smaller tapeworms than control mice by day 7 post-infection. When the interval between the infections was increased, the effect on H. diminuta decreased and no effect was found 21 days after the A. suum infection or if the infections were given simultaneously in ńaive or in mice immune to A. suum. Two possible explanations for the rejection and/or stunting of H. diminuta in mice infected 7 days earlier with A. suum are suggested; either a host reaction in the small intestine stimulated by the returning larvae of A. suum after their hepato–pulmonary migration or an indirect effect of decreased food intake of the host caused by this migration. It is concluded that experiments on possible immunodepressive or immunostimulating effects of parasites ought to include studies on living agents and that they should not rely on measurements of immune responses only.


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