Competency of Anopheles stephensi mysorensis strain for Plasmodium vivax and the role of inhibitory carbohydrates to block its sporogonic cycle

<p>Abstract</p> <p>Background</p> <p>Despite the abundance of studies conducted on the role of mosquitoes in malaria transmission, the biology and interaction of <it>Plasmodium </it>with its insect host still holds many mysteries. This paper provides the first study to follow the sporogonic cycle of <it>Plasmodium vivax </it>in a wild insecticide-resistant mysorensis strain of <it>Anopheles stephensi</it>, a major vector of vivax malaria in south-eastern Iran. The study subsequently demonstrates that host-parasite sugar binding interactions are critical to the development of this parasite in the salivary glands of its mosquito host. The identity of the receptors or sugars involved was revealed by a receptor "pre-saturation" strategy in which sugars fed to the mosquitoes inhibited normal host-parasite interactions.</p> <p>Methods</p> <p><it>Anopheles stephensi </it>mysorensis mosquitoes were artificially infected with <it>P. vivax </it>by feeding on the blood of gametocytaemic volunteers reporting to local malaria clinics in the Sistan-Baluchistan province of south-eastern Iran. In order to determine the inhibitory effect of carbohydrates on sporogonic development, vector mosquitoes were allowed to ingest blood meals containing both gametocytes and added carbohydrates. The carbohydrates tested were GlcNAc, GalNAc, arabinose, fucose, mannose, lactose, glucose and galactose. Sporogonic development was assessed by survival of the parasite at both the oocyst and sporozoite stages.</p> <p>Results</p> <p>Oocyst development was observed among nearly 6% of the fed control mosquitoes but the overall number of mosquitoes exhibiting sporozoite invasion of the salivary glands was 47.5% lower than the number supporting oocysts in their midgut. Of the tested carbohydrates, only arabinose and fucose slightly perturbed the development of <it>P. vivax </it>oocysts at the basal side of the mosquito midgut, and the remaining sugars caused no reductions in oocyst development. Strikingly however, sporozoites were completely absent from the salivary glands of mosquitoes treated with mannose, GalNAc, and lactose.</p> <p>Conclusion</p> <p>The study indicates that <it>An. stephensi </it>in southern Iran has the potential to survive long enough to be re-infected and transmit vivax malaria several times, based on the average adult female longevity (about 30 days) and its gonotrophic cycle (2–3 days) during the malaria transmission season. Certain sugar binding interactions are important for the development of <it>P. vivax </it>sporozoites, and this information may be instrumental for the development of transmission blocking strategies.</p

Can Insects Develop Resistance to Insect Pathogenic Fungi?

This paper presents new, important information on the microevolution of insect resistance to the insect pathogenic fungus Beauveria bassiana which will have far-reaching implications for the development of insect pathogenic fungi as biological control agents. We placed successive generations of a melanic population of the Greater wax moth, Galleria mellonella, under constant selective pressure from the insect pathogenic fungus, Beauveria bassiana. Enhanced fungal resistance was observed and larvae from the 25th generation were studied in detail to uncover mechanisms underpinning resistance, and the possible cost of those survival strategies. There are 3 novel, core findings from the study:1.Antifungal resistance in these insects is pathogen species-specific, and probably arises through trans-generational immune priming. The resistance was less obvious in earlier generations, suggesting subtle cumulative changes that are only fully apparent in the 25th generation. 2.The insect’s fecundity is already pushed close to minimum by its melanic phenotype. Therefore, the additional drain on resources required to boost antifungal defence still more, comes not from further compromising life history traits but via a re-allocation of the insect’s immune defences. Specifically during B. bassiana infection, systemic (fat body and hemocoel) responses, particularly the expression of antimicrobial peptides, are damped down in favour of a tailored repertoire of enhanced responses in the integument (cuticle and epidermis) – the foremost and most important barrier to natural fungal infection. 3.A previously-overlooked range of putative stress-management factors are activated during the specific response of selected insects to B. bassiana. This too occurs primarily in the integument, and contributes to antifungal defense and/or helps ameliorate the damage inflicted by the fungus or the host’s own immune responses during the battle between host and pathogen.No other study to date has examined so many genes in this context. Indeed, we show that the epidermis has a great capacity to express defense and stress-management genes as well as the fat body (which is the main tissue producing antimicrobial peptides and has been the traditional focus of attention). We therefore propose a “be specific / fight locally / de-stress” model to explain resource allocation and defence priorities for insects selected for superior resistance to insect-pathogenic fungi. However, we also show that these insects are less fecund and probably at no evolutionary advantage in the wild, implying that the risk is small of biological control agents failing in the field

Competency of mysorensis strain for and the role of inhibitory carbohydrates to block its sporogonic cycle-1

as the mean of three independent experiments. For each of the three developmental stages, the number of insects containing parasites in each treatment group was statistically compared with the corresponding control using the Chi Squared test (* P < 0.05). Numbers in parentheses refer to the sample size (n), i.e. total number of engorged insects.<p><b>Copyright information:</b></p><p>Taken from "Competency of mysorensis strain for and the role of inhibitory carbohydrates to block its sporogonic cycle"</p><p>http://www.malariajournal.com/content/7/1/131</p><p>Malaria Journal 2008;7():131-131.</p><p>Published online 15 Jul 2008</p><p>PMCID:PMC2500038.</p><p></p

Competency of mysorensis strain for and the role of inhibitory carbohydrates to block its sporogonic cycle-0

Staining.<p><b>Copyright information:</b></p><p>Taken from "Competency of mysorensis strain for and the role of inhibitory carbohydrates to block its sporogonic cycle"</p><p>http://www.malariajournal.com/content/7/1/131</p><p>Malaria Journal 2008;7():131-131.</p><p>Published online 15 Jul 2008</p><p>PMCID:PMC2500038.</p><p></p