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Some of my colleagues and I are aiming to identify open questions in disease ecology within the context of animal behavior that, if answered, will make a considerable difference to the fundamentals of the field of disease ecology. Therefore, we are interested in engaging with researchers worldwide who are involved in the fields of disease ecology and/or behavioral ecology. It is important to note that these should be questions that are unanswered but could be answered by a research program. In your opinion, what are some questions that meet these criteria and could set the agenda for future research in the field of disease ecology in the context of animal behavior?
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Depending on the species and their habitat, a co-evolution of the animal and what it eats occurs over generations of time. I would try to figure out what positive or negative feed backs have occurred or are occurring between the animal and what it eats. Especially important would be identifying any positive selections occurring in morphology/physiology.
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nematodes parasites 
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Dear colleagues
One small note: if humans become infected after ingestion, as some pet animals do, the infective stage should be an L3, because eggs are morulated when shed in faeces and are not infective. These eggs will develop till they have an L1 inside, after some hours in the environment. Then L1 hatch and must go through two molts before reaching the L3 stage, the real infective stage.
These L3 can be easily ingested by children/adults eating raw vegetables in salads, or while doing geophagia, when playing on the ground without washing their hands or while doing gardening without gloves.
There are some eosinophilic enteritis reported in Australia since the 1990s, whose nematodes were collected and identified after colonoscopy, and after this report, parasitologists also began to consider both cutaneous and enteric syndromes caused by this agent in humans.
Best regards
Luís Carvalho
Parasitology and Parasitic Diseases
Faculty of Veterinary Medicine
Lisbon University
Portugal
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interactions between hosts and parasites.
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 thans for all
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what do you know about wandering parasites.
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Hello,
Mostly a parasite, on gaining entry into the body of the host, migrates within the host body in search of a suitable site and finally becomes established in that region of the host body where it lives and reproduces. However, sometimes the parasite happens to reach a place which is not its usual site of localization. Such parasite which fails to reach its normal destination is termed as aberrant.
The parasites are also categorized into two different types on the basis of the number of hosts required for the completion of their life history. The parasites that complete their life cycle in one host only are called as monogenetic. Some parasites display alternation of the host as well as alternation of generation. These parasites which require two different hosts for the completion of their life cycle are called as digenetic. Generally, out of the two hosts one is a vertebrate host which is referred as definitive or final or primary host and the other is invertebrate host, commonly known as secondary or intermediate host.
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There has been a greater emphasis lately on abortive infections when characterising host range of avian haemosporidians (see recent articles by Valkiunas and Palinauskas). I was under the impression that abortive infections generally never reach the tissue stage of development. However I read in the recent paper by Valkiunas et al. that abortive infections can still develop to the tissue stage, but of course gametocytes will not develop in the blood. This could lead to a very similar parasite DNA distribution within the host to latent infections.
So I am wondering if there is any particular way to accurately tell the difference between an abortive infection and a latent infection where (1) parasite DNA exists in muscle and organ tissues and (2) gametocytes are absent from the blood. What do you think about this issue? Would you basically have to identify abortive stages in the blood to confirm (could be very difficult I imagine). Thanks again, I appreciate the help.
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You mention liver, so if you are referring to histological detection of hypnozoites in primates (rather than to avian haemosporidian infections), the answer is "No". It would be like looking for a needle in a haystack. Hypnozoites are directly sporozoite-derived and relatively few sporozoites are inoculated by mosquitoes. It is difficult enough to find hypnozoites in the liver (a primate liver is large) after injection of massive numbers of sporozoites experimentally. As for avian infections, finding schizonts in whatever tissue(s) histologically would not reveal for certain whether or not an abortive infection is involved (see the original question).
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Dear Claude
We work on parasite effectors and various other aspects for better understanding of parsitism and genetics of parasitism. would you be interested in any collaboration with our group. we can initially have some technical collaboration and depending on some promising leads, we can explore funding opportunities. Presently EU-dept of Biotechnology (DBT) funding is open. There will be an advantage working with India since one can have access to many parasites of animal, human and plant which is highly advantageous to prove any concept across different systems
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Dear Uma,
If you are interested in spatial processes (cartography, patterns, distributions...) or the interaction of the parasitism process with social or ambiental factors, for example; then may a collaboration between us could be productive.
Yours sincerely,
Daniel.
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More specifically, will a plant virus achieve greater inoculation success if the vector feeds on a growing plant part vs. a senescent part?
I've heard that fast growing parts of a plant may be more susceptible to infection from viruses, but haven't been able to find anything empirical backing this up.
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Dear Paul Chisholm
Usually we Called it age resistance, its not only for transmission by vectors, also affected by interference , signals and pathways, movement protein, plant hormone (http://www.springer.com/us/book/9789401792844)...
Pls. find the attached files
page 287 in: IRRI, 1969 The Virus Diseases of the Rice Plant: Proceedings of a Symposium at the International Rice Research Institute, April, 1967 International Rice Research Institute
Hoping this will be helpful
Regards
Prof. Houda Kawas
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I teach parasitology and have been frustrated at the dearth of exercises involving living systems (as opposed to viewing prepared slides).  Collecting hosts that are already parasitized has been hit or miss.  Ideally, if both host and parasite could be maintained in the lab this would open up lots of possibilities.  Can anyone recommend such a system?  I’m open to all ideas, although I’d rather avoid maintaining mammals.  Thanks in advance.
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I like the old stand by Hymenolepis diminuta in Rattus. Also, easily useable are gregarines in Tenebrio. Scott
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I am looking for PCR primers that will amplify in the presence of any avian haemosporidian infection and indicate presence/absence of infection in a North American passerine. Ideally, the primers would amplify in the presence of plasmodium, haemoproteus, and/or leucocytozoon. I am interested in using the PCR to identify all infected individuals, including low intensity infections that may be missed when reviewing blood smears. There is a large variety in available primers and I would appreciate any recommendations on which primers you have used successfully and any suggestions for modifications on published protocols.
Thank you!
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We are working almost 10 years with Hellgren's et al. (2004) and Waldenstrom et al. (2004) protocols for screening avian blood samples . We also do a lot of microscopy for comparison of sensitiveness with PCR protocols (Valkiunas et al. 2008, J Parasitology). For detection of haemosporidian parasites with light parasitemia, these nested PCR protocols are very good. The biggest issue is co-infections. As Javier said, if there is co-infection in the sample, it should be seen on electropherogram as double peaks in particular places. However, after comparison with microscopy results we see that its not the case in many samples. We tried different primers and it seems that this selective amplification exist with other primers as well. In most of the studies based on PCR screening the data shows that single infections are predominant and that co-infections exist but are not that prevalent. By microscopy co-infections are detected significantly more often (Valkiunas et al. 2008, J Parasitology). 
We should also remember that PCR's detect DNA of parasite, but does not show if that DNA is from infective stage (gametocyte) or other stage which can be dad end for further development (Valkiunas et al. 2009, J Parasitology, 95). In this case the bird should not be assigned as the host.      
To conclude, at present we have good, sensitive primers (mentioned above) for light infections for parasites of Plasmodium, Haemoproteus and Leucocytozoon, but co-infections (Haemoproteus/Haemoproteus,  Plasmodium/Haemoproteus or Plasmodium/Plasmodium) is still big problem when you do only PCR's. The best is combination of PCR and microscopy so far.
   
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I am looking to read comprehensive texts in Physical Oceanography and in the Evolution and Ecology of Infectious Diseases and am looking for direction into which texts may be the best to acquire.
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Regarding the "evolution of infectious diseases" there are quite numerous papers in the field of palaeoparasitology, but nearly exclusively on material from archaeological and Quaternary contexts. Some recent review papers are:
Araújo, A., Reinhard, K., Leles, D., Sianto, L., Iñiguez, A., Fugassa, M., Arriaza, B., Orellana, N., Ferreira, L.F. 2011. Paleoepidemiology of intestinal parasites and lice in pre-Columbian South America. Chungara, Revista de Antropología Chilena: 43(2): 303-313.
Beltrame, M.O., Souza, M.V., Araújo, A., Sardella, N.H. 2014, in press. Review of the rodent paleoparasitological knowledge from South America. Quaternary International.
Bryant, V.M., Reinhard, K.J. 2012. Coprolites and archaeology: the missing links in understanding human health. New Mexico Museum of Natural History and Science Bulletin 57: 379-387.
Frías, L., Leles, D., Araújo, A. 2013. Studies on protozoa in ancient remains - A Review. Mem Inst Oswaldo Cruz 108(1): 1-12.
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In case you are interested in pre-Quaternary parasites, this is the reference list (not textbook or review-type papers):
da Silva, P.A., Borba, V.H., Dutra, J.M.F., Leles, D., da-Rosa, A.A.S., Ferreira, L.F., Araujo, A. 2014. A new ascarid species in cynodont coprolite dated of 240 million years. Anais da Academia Brasileira de Ciências 86(1): 265–269.
Dentzien-Dias, P.C., Poinar, G.Jr., de Figueiredo, A.E.Q., Pacheco, A.C.L., Horn, B.L.D., Schultz, C.L. 2013. Tapeworm Eggs in a 270 Million-Year-Old Shark Coprolite. PLoS ONE 8(1): e55007. http://dx.doi.org/10.1371/journal.pone.0055007
Hugot, J.P., Gardner, S.L., Borba, V., Araujo, P., Leles, D., Da-Rosa, Á., Dutra, J., Ferreira, L.F., Araújo, A. 2014. Did the dinosaurs have pinworms? Discovery of a 240 million year old nematode parasite egg in a cynodont coprolite sheds light on the early origin of nematode parasites in vertebrates. Parasites & Vectors 11-2014.
Poinar, G., Boucot, A.J. 2006. Evidence of intestinal parasites of dinosaurs. Parasitology. http://dx.doi.org/ 10.1017/S0031182006000138
Tweet, Chin, K., Murphy, N. 2006. Paleobiological implications of diminutive invertebrate burrows within probable gut contents of a hadrosaurid dinosaur from the Upper Cretaceous (Middle Campanian) Judith River Formation of Montana. Geological Society of America, Abstracts with Programs 38(7), p. 476. https://gsa.confex.com/gsa/2006AM/finalprogram/abstract_112739.htm
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Some recent review papers on palaeovirology:
Aswad, A., Katzourakis, A. 2012. Paleovirology and virally derived immunity. Trends in Ecology and Evolution 27(11): 627-636.
Feschotte, C., Gilbert, C. 2012. Endogenous viruses: insights into viral evolution and impact on host biology. Nature Reviews / Genetics 13, April 2012: 283-296.
Katzourakis, A. 2013. Paleovirology: inferring viral evolution from host genome sequence data. Phil Trans R Soc B 368: 20120493. http://dx.doi.org/10.1098/rstb.2012.0493
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What would be better? Isolation from cloacal swab or from fecal samples? I want to use agar or API test. What's your experience?
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Don't use the API system-waste of money for Salmonella. The comment from M. Musgrove is by and large accurate, apart from the fact that reptiles are cold-blooded and may carry both serovars of S. enterica and also Salmonella bongori. As such culture is still arguably the better method. Selenite enrichment followed by a selective media- Brilliant Green, XLD, RV or one of the newer commercial agar should work relatively well. If you wish PCR is a reasonable confirmatory test for S. enterica with genes such as invA and the aforementioned hilA found in visually all isolates. If you want to type the isolates then MLST should also tell you the serotype and is cheaper unless you already have the full set of typing sera.
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I need peer-reviewed papers on or what limits exist in terms of engineering and breeding plants for disease and drought resistance (for example). Papers with an evolutionary query - if generalized disease resistance is expressed in plant populations with reduced genetic variation. Is this a selective force for increased disease virulence? Are these strategies temporally limited or due new techniques employing gene cassettes address such issues?
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Published online 17 February 2011 | Nature | doi:10.1038/news.2011.102
Wu D, Cai S, Chen M, Ye L, Chen Z, et al. (2013) Tissue Metabolic Responses to Salt Stress in Wild and Cultivated Barley. PLoS ONE 8(1): e55431. doi:10.1371/journal.pone.0055431
Araus, José Luis , Slafer, Gustavo A. , Royo, Conxita and Serret, M. Dolores(2008) 'Breeding for Yield
Potential and Stress Adaptation in Cereals', Critical Reviews in Plant Sciences, 27: 6, 377 — 412
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Would spiders impact disease dynamics, or productivity in some way? How do spiders effect their ecosystems?
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Spiders and mygalomorphs display an important role as predators in many ecosystems. This contributes to the regulatory function of their prey populations which may limit demographic explosions that may include disease vectors, and/or herbivores. In this sense they represent potential allies for disease regulation and plant productivity. On the other hand, and as Dr Mario Ruiz-Gonzalez explained, they present several adaptations to predate at different ecosystem levels (soil surface, subsoil, understory, trees), and on different prey types depending on the species (even if the most of Arachnids are rather generalists within their preying strategy). Each of these strategies and strata can be considered as predation traits. The diversity of traits is a good indicator of a complex trophic web, while the abundance of a given trait is an indicator of abundance of a particular resource (prey type). Therefore even if their diversity and abundance is potentially beneficial, I think they might also constitute indicators of prey abundance.
But as suggested, if the ecosystem features remain constant, varying only an increased abundance and/or diversity of spiders, I think that both disease control and productivity might be enhanced.