Tropical Diseases - Science topic

This is an interesting question, However Age alone may not affect the integrity of the blood or increase the the risky of transmitting a disease unless coupled with Social factors. Social factors such as sexual activity of the individual( may increase chances of acquiring and transmitting sexually acquired infections that can be transmitted through transfusion such as hepatitis, HIV, Syphylis etc.), travelling to disease endemic areas, drug use and many other factors that may increase risk of acquiring blood transmissible infections. it would be nice to conduct a case control study to look at the donated blood screening outcomes vs age as one model and a model comprising Screening outcomes vs age, and adding components of social behavior, then compare to see which model gives significant correlation.

schistosomiasis is considered as a major parasite and prevalent parasitic infections, affecting an estimated 200 million people infected, mostly in Africa. Equatorial guinea is a country located on the west coast of central africa, where schistosoma spp. is endemic. Human schistosomiasiscin equatorial guinea is caused by Schistosoma intercalatum. In studies conducted in Bata, mollusc species could serve as a potential host for schistosomiasis was found in Bulinus forskalii. The prevalence of the disease is higher in the city of Bata than in rural areas.

How the malaria parasite increases the risk of blood cancer

in this link;

Thanks for all the tips! This was extremely helpful

Thanks for all the tips! This was extremely helpful

For usutuvirus there is a greater risk in North America by the vectors, however the spread could happen from North America to South America (in the opposite way that Chik and Zika)

following

Check the following reference Please.. it might's assist you in your question …

The resistance mechanism for imidocarb and diminazene are unknown.

You can find here an example of a FDA-approved compound (novobiocin) that our group has repurposed as potent in-vitro and in-vivo Zika virus inhibitor:

Also, our web server for blind docking calculations can be of help in this context:

Thanks Noor, let me give it a try

you can read this links

 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC120052/

Thanks a lot Jana. I ve been looking for the paper for long. many many thanks.

regards,

SD

Though the negative test may not exclude typhoid, the positive test (titre of >1/160) will be useful in culture negative, or when blood or stool cultures are not practical, or in out-patient settings. In Sri Lanka, the country is considered endemic and often the disease is diagnosed with the suggestive clinical presentation. The disease is more prevalent in urban areas where culture facilities are usually available in tertiary care centers but the prior antibiotics render the cultures negative. I, though not often, still use widal to get a clue in difficult cases. Please read the following research as well; 

Trop Geogr Med. 1981 Dec;33(4):329-33, Diagnostic value of the Widal test, Abraham G, Teklu B, Gedebu M, Selassie GH, Azene G.

Clin Diagn Lab Immunol. 2002 Jul; 9(4): 938–941, Widal Test in Diagnosis of Typhoid Fever in Turkey, Ayse Willke,,* Onder Ergonu, and Banu Bayar

Asymptomatic parasitemia will test positive. A completely treated patient of p.falciparum malaria will also be positive for hrp2 for next few weeks and thus causing confusion for the treatment. However ldh based kits maybe more useful.

Dear Miles,

We have worked extensively on engineering aspects of malaria control and they play a crucial role in mosquito control. For e.g. water stagnating around a community tape water supply can be directly channelized through a plastered covered drain to a pond and that will stop water stagnation and mosquito breeding. Similarly in rural areas lot of waste water gets collected in front of the houses and this can be avoided by constructing  a soakage pit through applying best engineering methods. Leveling of ditches through earth work on wasteland and thereafter tree plantation on such ground control mosquito breeding and proves to be eco-friendly method of malaria control.  Flushing of irrigation canals, lining of canals to stop water seepage and intermittent irrigation are all engineering methods of malaria control and we have successfully demonstrated it in Kheda district of central Gujarat in India.    

Perhaps this a a good source.

Good luck.

Yes, we can develop certain primers for the sporozoites or the structures of the erythrocytic cycle

Thank you so much Kathryn, but I can not take the article would you please mail me it?

Tracey Lamb at Emory University (Atlanta GA USA) does some work on this. 

Or I might need to try to contact directly the authors...

I think you can take the age of kindergarten and primary school kids,continuous itching, the use of cellophane tape

"A volunteer team of Google engineers, designers, and data scientists is helping UNICEF build a platform to process data from different sources (i.e., weather and travel patterns) in order to visualize potential outbreaks. Ultimately, the goal of this open source platform is to identify the risk of Zika transmission for different regions and help UNICEF, governments and NGO’s decide how and where to focus their time and resources. This set of tools is being prototyped for the Zika response, but will also be applicable to future emergencies..."

I hope that following paper be useful.

Regards

Ron P. Marchand et al (2011)Co-infections of Plasmodium knowlesi, P. falciparum, and P. vivax among Humans and Anopheles dirus Mosquitoes, Southern Vietnam

Thanks Bruce,

 Much appreciated.

Ernest

My dear friends. I think that high commited blood transfusion specialists like ourselves are actually paying attention very carefully and closely about the insurgence of this quite unknown virus. There is no doubt that it is very important, particularly for pregnant women, and for them, all attention must be driven from authorities in order to avoid new cases. But most importantly, if we do not fight the real culprit, the mosquito, we will certainly lose not only this battle, but the whole war. Unfortunately, this I haven´t seen not only in my country, but in several places.  This is a great forum for discussion. Regards

I don't have expertise in this area, but you could contact this researcher, he is an expert in Measles and interested in using it as oncolytic therapy, so he would probably have the answer:

I think it needs to be noted that o'nyong-nyong virus is the one medically important  arbovirus that can be transmitted by anophelines and culicines. In practically all other instances, culicines are the exclusive or nearly exclusive vectors. In general, the main genera involved are Aedes and Culex. An arbovirus may have been isolated from numerous species but may reflect the presence of an undigested infected blood in the midgut or a salivary gland infection barrier, for example. Susceptibility must not be confused with the ability to transmit.

Hi! Sumodan,

If you are interested check the following link

"Wanted: Zika virus researchers 

What are the MRC looking for? The organisation seeks twelve to eighteen month proposals that will provide novel, critical and timely insights into the nature of the risk posed by the Zika virus and/or potential avenues for its management or prevention. The MRC says that robust evidence is needed for the risks associated with Zika transmission and infection and is obtained as soon as possible. 

The MRC says that the studies should build on existing relationships, either with researchers in affected countries and/or with relevant data/resource holders. Interdisciplinary proposals are welcomed, where appropriate. 

It adds that possible avenues of research to be funded by this initiative could include:........." 

It is very difficult to commenet at this point about the potential of Zika virus epidemic in India. Theoretically India is prone to the invasion of Zika virus, as and when it occurres. Vector mosquitoes are  abundantly available , breeding sites are innumerable, susceptible population is there...it is a question of entry of the Zika virus in the Country and theoretically yes recipe is ready for the epidemic. On the other hand the example of Yellow fever virus is in contrast. In spite availability of hosts, vectors and all favourable conditions of transmission yet  we do not have the problem of Yellow Fever in India. The same might happen with Zika virus as well w- who knows

As far as I'm aware, the recent detection of Zika virus within saliva is the first reporting of its kind - very little is known at this stage as to if ZKV infection can be transmitted from human to human through saliva itself, and further testing would be required to determine this.

Relating back to your question, I imagine that it would depend on what the viral load is within saliva compared to serum/traditional sample techniques, and if this is a high enough titre to be detected consistently. 

Another thing to bear in mind is that viral RNA tends to be easier to detect in serum during the first 7 days of illness; viremia decreases over time. We would need to determine at what stage of zika infection viremia is detectable in saliva. It would indeed be interesting to see if testing of saliva samples result in a higher sensitivity/detection rate compared to traditional serum testing by RT-PCR. 

Very interesting question!

We need to remember that sika is a vector borne disease, which means that the way to stop or at least slow down transmission is to control de mosquito Aedes aegypti from passing the virus from infected hosts to healthy ones. The classical concept of quarantine is probably not as effective when transmission person to person is not the main mean of transmission (it is mentioned as a possibility). People infected by sika requires too a level of protection from mosquitoes to avoid to become a reservoir for the mosquitoes.

There is  limited knowledge on the EIP (extrinsic incubation period) in the field, which would be needed to assess whether  regions and periods with the risk for transmission will evolve. Are there any hard facts, data, experiments that can be used or applied to this virus. The two papers that might gives a first answer under fixed lab conditions are  (see graphics)

Li MI, Wong PS, Ng LC, Tan CH. Oral susceptibility of Singapore Aedes (Stegomyia) aegypti (Linnaeus) to Zika virus. PLoS Negl Trop Dis. 2012;6(8):e1792.

Wong PS, Li MZ, Chong CS, Ng LC, Tan CH. Aedes (Stegomyia) albopictus (Skuse): a potential vector of Zika virus in Singapore. PLoS Negl Trop Dis. 2013 Aug;7(8):e2348.

Friendly greetings from Stockholm. B.

Hi Monika, you could try the protocol in this paper first:

Hi Corrado,

Here is a publication for the preservation of insects to be used in spectroscopy. This publication resulted from experience on field trips in Nigeria and Cameroon for insects that would be analyzed in Bamako, Mali. And Dr Floyd Dowell's experience in Tanzania. It is good you are not involving cryo-preservation at any point in the tropics.

I may suggest SILICA GEL for a short period. I had serious degradation of materials preserved in ethanol on one hand and on the other hand, methanol fixes molecules and may not yield very good results during DNA/RNA extraction.

I hope this helps

good luck

"Immunization by means of vaccines seems to provide a certain degree of protection. Vaccines are, in principle, suspensions of killed leptospires. Protection is largely serovar-specific. In areas where many serovars are causing leptospirosis, a vaccine must consist of different serovars matching those circulating locally. In some countries,  where many serovars occur, vaccines consist of a mixture of a few of the most prevalent. Protective antibodies are produced only against the serovars present in the particular vaccine used.

Commercial human vaccines have been produced in France and Cuba. However, these vaccines do not induce long-term protection against infection and do not provide cross-protective immunity against heterogenous leptospiral serovars."

From WHO fact sheet

I don't think anybody can identify them on the basis of these pictures, certainly not as long as no multiplying forms are shown. And even then, one would need molecular tools.

Dear ,referring to added link.Thanks

Thank you. Please give your email ID

Apart from awareness creation about basic symptoms of disease, a lot needs to be done in the area of stigmatization. Infected persons especially females may be reluctant to seek medical help because of stigmatization, and this will hinder control efforts. So emphasis of the social mobilization should rest more on sustained, simple and repetitive information to discourage discrimination against infected and affected persons. This is very vital. Advocacy visits to political leaders and government should engender the desired shift in priority from curative to preventive programs such as community mobilization for adequate participation. In other words, advocacy can lead to political will and commitment by Government in favour of leprosy control and eradication.

also be carried

There are no current classical antibodies to neutralize DENV, but there is a new development that shows promising results (antibodies against the E dimer conformation region, please refer to Galvin Screaton 2015), also there has been extensive research showing that the permissive cells in vivo are of stem cell which bear megakaryocyte phenotypes, this could also help understand dengue and develop strategies against it

 I'm semi-retired so have the luxury of ignoring impact factors, but my younger colleagues don't have that choice because university administrators and other gatekeepers have become obsessed with supposedly "objective" indicators of "quality." It's perverse, unfair, and stupid, but it's reality.

Because we have ruled out bacterial infections with appropriate tests and left with a huge chunk of patients with clinical picture similar to Dengue fever

I have never been able to get a plaque assay working for dengue virus. I have found that an immunoperoxidase staining assay is a good way to determine titers. Here is the method that I use from Durbin et al. 2001. ATTENUATION AND IMMUNOGENICITY IN HUMANS OF A LIVE DENGUE VIRUS

TYPE-4 VACCINE CANDIDATE WITH A 30 NUCLEOTIDE DELETION

IN ITS 3-UNTRANSLATED REGION

Vero cell monolayer cultures in 24-well plates. After a 1-hr incubation at room temperature, the monolayers were overlaid with 0.8% methylcellulose

in OptiMEM (Life Technologies) supplemented with 5% FBS. Following incubation at 37C for four days, virus plaques were visualized by immunoperoxidase staining.

Briefly, cell monolayers were fixed in 80% methanol for 30 min and rinsed with antibody buffer (5% nonfat milk in phosphate-buffered saline). Rabbit polyclonal DEN-4 antibodies were diluted 1:1,000 in antibody buffer and added to

each well followed by a 1-hr incubation at 37C. Primary antibody was removed and the cell monolayers were washed twice with antibody buffer. Peroxidase-labeled goat-anti-rabbit IgG (Kirkegaard and Perry Laboratories, Gaithersburg,

MD) was diluted 1:500 in antibody buffer and added to each well, followed by a 1-hr incubation at 37C. Secondary antibody was removed and the wells were washed twice with phosphate-buffered saline. Peroxidase substrate (4-chloro-1-

naphthol in H2O2) was added to each well and visible plaques were counted.

Dear Alfonso,

what I learned from Nikos Vasilakis presentations during several arbovirus conferences/meetings held in Germany last year and this year was that the classical definition of dengue "serotypes" needs to be revised because it do not fit with the genetic characterization of the "novel" strain. Beside this, it is more likely to be a new genotype of serotype 4. However, the discussions are ongoing and I believe Nikos is trying to convince the reviewers with additional experimental data...

Dear Terri and Alfonso,

although CHIKV can invade endothelial cells, these are clearly not its elective target cells to cause, Th1 cytokine-driven plasma leakage and related organ dysfunctions leading to hemorrhagic fever syndrome (as for Dengue). As Alfonso wrote, to date there have been to few co-infections documented so that from a public health point of view, it may seem impossible to answer. However, the introduction of CHIKV in areas where DENV is prominent (Americas, Pacific, SE Asia) offers a good opportunity to answer your question in a larger extent and the potential interactions between the two viruses is an exciting issue to be solved. From my experience, in La Réunion island (266,000 cases of CHIKV in 2005-2006), mild bleeding manifestations in the setting of CHIKV infection were not so infrequent, while clearly severe hemorrhages were scarce and decreased with age (neonates >> infants > children > adults) or occur in adults with severe comorbidity (diabetes, alcohol-related hepatic dysfunctions, etc...). As a pediatrician involved in the first description of mother-to-child transmission of CHIKV, we documented hemorrhagic syndromes in neonates in the absence of bacterial, fungic or viral co-infections. Finally, even it may also depend on host factors, the interaction between the two pathogens remains to be explored (keeping in mind alphaviruses and flaviviruses are very different pathogens). I fully agree with Alfonso, many things with chikungunya are to be studied. Best wishes

pg

Take a look at this review

 

 

The following is an extract from Wyllie and Fairlamb Acta Tropica 97 (2006) 364–369:

"The spleens of infected animals were aseptically removed, weighed and homogenized in Dulbecco’s modified essential medium (D-MEM, Sigma) containing 10% (v/v) foetal calf serum, 20mM l-glutamine and 10mMsodium pyruvate. The homogenate was then centrifuged at 100×g for 5 min at 4 ◦C to remove large cell debris, supernatant collected and centrifuged at 2000×g for a further 10 min at 4 ◦C. The resulting pellet was resuspended in culture medium containing 0.05% (w/v)

saponin and incubated at room temperature for 5 min. Following centrifugation (2000×g, 10 min, 4 ◦C), the amastigote-enriched pellet was washed twice in fresh

culture medium before being resuspended in a final volume of 2 ml. The amastigote suspension was passed through a 23-G needle several times to disperse clumps

prior to counting."

Cells are counted microscopically using a Neubauer counting chamber. A Percoll gradient could be used for additional clean up as suggested above.

Best wishes

Alan Fairlamb

As mentioned by Mahmoud Elsibaei, usually S. haematobium eggs does not appear in rectal biopsies, but it's not impossible. Although I have not much experience with histological preparations, I can tell that normally, with a Ziehl-Neelsen stain, S. haematobium is the only Schistosoma egg that is NOT acid-fast and thus will not stain red. All the other Schistosoma species eggs would stain acid-fast (red). Easiest would be to use the morphology off the egg, but as Unu Airauhi said, the spine, used in this case, is not always visible. Much will depend on where the egg has been cut.

yes, that is correct, just read the ECDC statements on Dengue:

Potential vectors are not as likely to carry diseases-competent virus' as they might be in Brazil and/or other countries with mediterranean climates. But in European countries with suitable climate (e.g. mediterranean), the issue is currently discussed.

Hi Sibylle

Sorry I missed the notification of your response to my comments in October and have just picked it up.

When I refer to the "claimed repellent effects of neem limonoids" I was thinking of the claims made by those people using neem and its extracts for deterrence of blood feeding insects such as mosquitoes, fleas, and lice.  As far as I can see these are just claims with no real substantive evidence in support of those claims.

 If neem extracts do repel in the true sense it would have the opposite effect from that which is required for the anti-feedant effect, i.e. phytophagous insects should be repelled from treated plants, which we can reasonably assume not to be the case because those insects do feed off neem treated plants and suffer the anti-feedant effect as a consequence.  

My suggestion is that products containing neem that are sold for repelling mosquitoes etc may derive their activity from some other component of the formulation or perhaps, at the most basic level, the insects are deterred from biting either by the sticky nature of the neem oil component or else the unpleasant allium-like odour of the neem.

With regard to the comment "....we have looked for effects of mixed limonoids in other ways and to be honest we have never been able to identify any activity of any kind against the insects we deal with....." I was referring to the claimed effects of neem to kill blood feeding insects, such as lice, when applied topically to the insects.  There are numerous products on sale around the world that are claiming efficacy from azadirachtin and the other large limonoids against insects that could not possibly ingest the compounds due to their blood feeding habits and these compounds could also not possibly enter the insects via the cuticle.  Hitherto none of these products has a defined mode of action but the makers imply that as neem is considered a "wonder" insecticide the products work in a similar way to how neem controls phytophagous insects.  Largely a matter of BS baffles brains, as most of the purchasers have no idea how the material works against any insect - they just like the idea of a natural "wonder drug".

Ian

I'm not a chemist but you may want to have a look at Benier and others (2000 and 2001) analyzing skin emanations. They were able to detect Lactic acid through conventional GC-MS in spite of the difficulty.Picking from the work of Benier, the Takken lab at Wagenigen university, Netherlands have evaluated Lactic acid as a synergistic attractant of Anopheles gambiae s.l.. The compound is now considered an active part of synthetic blends for trapping malaria mosquitoes (Kline et al 2007; Okumu et al 2010; Olanga et al 2010; Mukabana 2012). The effectiveness of these blends is currently being evaluated in relatively large field trial in Rusinga Island under the umbrella of Solarmal - a malaria project that seeks to reduce malaria transmission using odour-baited mosquito traps. This might be totally irrelevant. I just though I might add it here :)

Dear Dr Conn,

The thiarid snail Melanoides tuberculata is a good example of invasive species involved in transmission of parasites worldwide. Please see the attached checklist .

Best regards

Hudson

The first step is DNA extraction , then  universal primers could be selected for fungi identification, according to different manuscript written in the field. then you can narrow your research and go ahead.

Regards

Dr. Abdigoudarzi

Thanks for the checklist

Cheers

Rodents indeed serve as reservoirs for many zoonotic diseases.  Many of these diseases are transmitted via parasitic arthropods, but others are transmitted simply by contamination of the environment by rodent feces or urine.  Also, many arthropod parasites of rodents do not survive long away from the host, and many do not prefer humans as hosts.  Thus, rodent-associated zoonotic diseases that involve synanthropic arthropod transmission actually circulate most effectively in the presence of healthy rodent populations close to human habitation or activity.  Thus, I would start with control of the rodents, then move to comprehensive sanitation of human activity areas that would eliminate both arthropods and other infectious contaminants.

Thanks!! Do you think that primers designed to amplify Alu do not cross-react with other vertebrate or insect DNA?

Dear Paul

I will check on that. However my question if exist or not. Thanks, Alfonso.

It is possible that it was happened. There are processes which indicate re assortment, as genes of body color are expressed due to change in the environment, they appear only due to switch on gene activity. when temperature and ecological factors they again become normal a silent copy of gene which can not be traced by molecular methods appear. As use of drug making the insects and micro-organisms resistant only due to exposure. If exposure is not provided then they come back to their normal position. Alienation and de-alienation always happen with the chance and frequency of mutations in important genes which are highly susceptible to  environmental changes.  

Dear Olufunmilola,

I guess that you are working with Schistosoma mansoni or S. japonicum because these species are usually associated with placental schistosomiasis. In designing experimental or quasi-experimental studies on schistosomiasis, one has to pay attention to the type of animal host that serves as the most permissive one for infection. Mice are the best choice for S. mansoni while guinea pigs are best for S. japonicum. These two types of hosts are quite refractory to infection with S. haematobium, which is rarely associated with placental infection.

Hope this helps.

Kind regards,

Rashad

Sorry Javier,

I do not have data about amount of DNA in the Schistosoma egg. But, was related by Ana Liza Gomes et al. 2006 that the genome of the S. mansoni worm weighs 580fg.

The best,

Edward Oliveira

If you are looking for a purely online program I prefer ClustalW over MAFFT. I find that my alignments are a little better as it gives me the option to input a few more parameters. That being said, there are much better programs out there if you have the CPU to handle as Jainder Chhillar suggested.

Hi, multiplicity of infection (MOI) is calculated by dividing the total number of alleles (fragments of all alleles or genotypes in a gene) by the number of samples positive for the same marker (eg: MSP1). below is the detail that i have found for the MOI calculation, the way that the author did:

family family pos. allele freq. msp1 pos MOI/family

k1 19 56 36 1.6

mad20 25 67 44 1.5

ro33 20 52 34 1.5

total 64 175 114 --

MOI/total 2.7 1.5 -- --

hope the table reach you in a good format. any way , MOI was calculated two times; 2.7 as an MOI of the whole msp1 gene and 1.5 -1.6 for each family (k1, mad20 and ro33). my opinion is to calculate MOI for the msp1 by dividing 175 (total genotypes) by 114 (36+44+34) but not (19+25+20), and it will be very closer to the allelic MOI (1.5).

hope this details being useful for u.

Below is a link to my own publication regarding msp1 and msp2 genetic diversity.

all the best

Clive, Thank you for your reply. This 2012 IAMAT document on shistosomiasis risk throughout the world (http://www.iamat.org/pdf/World_Schistosomiasis_Risk_Chart.pdf) makes it appear as though there are still infections taking place in Puerto Rico (apparently they haven't updated the status for Puerto Rico in a while). Thanks for the information.

There is at least one established B. glabrata population in Mississippi as I noted in an earlier post. It was only recently reported at a regional invasive species meeting (GSARP) . People had concerns that this new snail introduction could eventually lead to shistosomiasis disease in the area, so your comments help to put that risk into perspective.

It depends if you want the live leishmania on the promastigote or amastigote form. Just plating the cells at 28 °C for a week in leishmania M199 medium (or even RPMI with serum) is enough to free up the promastigote parasites.

I agree with Dr Manuja (above); the 50bp product is almost certainly a primer dimer. To help you, you'll need to describe the reactions in question, in detail...

I'd always encourage you to design your own primers rather than take those from a paper, especially if it's more than a couple of years old. The reason is that PCR has advanced technically so far in such a short space of time. Also so many things can affect a reaction that you really need to work it up using your own tubes, reagents, machine... Basically it's easier working it from scratch than trying to troubleshoot someone else's.

You have 6 qRT-PCR reactions, I assume (TNF, IL-1b, IL23p19, IL-10 and IL-6). First, decide on the annealing temperature of the primers that you want for all the reactions, the product length range and the reaction efficiency acceptable to you. It's perfectly possible to design 6 (or sixty) qRT-PCRs with the same conditions; unless they have the same reaction efficiencies, you can't cleanly compare their relative levels. Then, make sure your primers are bedded in different exons. Have one primer wholly within an exon and the other overlapping an exon-exon junction by three or four nucleotides (not more). Be SURE that those 3 or 4 nucleotides do not match the intronic sequence adjacent to the exon where the bulk of the primer is located otherwise you may get DNA amplification. Now, prepare a standard source or cDNA that contains all your targets - splenocytes activated with poly-IC and LPS (together) will be good for the cytokines you're suggesting. Lastly, you're now able to begin testing primer sets and working out the reaction efficiencies in order that you can begin your experiment. Of course, your housekeeping genes (two is preferable) have to be designed the same way. Avoid intronless genes as housekeepers. Good luck!!

G

ps - my answer assumes you have access to a real-time apparatus. If you do not, then it is very difficult to get reliable quantitative data, even relative quantitative data.

Dear Ravi,

To my knowledge there is not any such first or second line treatment for malaria as such. However there is treatment guideline with respect to the type of parasite found to be present in malaria fever patient as well as according to the complication/severity status.

You may like to refer the recent treatmment guideline issued by NVBDCP in 2013

http://www.nvbdcp.gov.in/Doc/National-Drug-Policy-2013.pdf

The Aedes mosquito can be controlled through fishes (Poecilia), small crustaceans, in small artificial deposits like water tanks baby turtles has been used (Trachemys scripta) to predate on Aedes larvae https://www.researchgate.net/profile/Gerardo_Borjas/publications.

Some products with biological spores have been used in some countries: Bacillus sphericus and Bacillus turingiensis var israelensis (Bti) but there is controversy about if this a chemical or biological product.

About the vaccine, there is an expectation that in less than five years we'll have one, since several pharmaceutical companies are working in its development with a very strong support from Universities and International Organizations. The information has been summarized in previous entries

Field study and useful description of reliable mosquito traps to combine with oviposition candidates....

Comparison of CDC and EVS Light Traps Baited with Carbon Dioxide and Octenol for Trapping Mosquitoes in Brisbane, Queensland (Diptera: Culicidae)

SCOTT A. RITCHIE, DANIEL L. KLINE

Australian Journal of Entomology (Impact Factor: 0.88). 03/2007; 34(3):215 - 218. DOI:10.1111/j.1440-6055.1995.tb01322.x

ABSTRACT Studies were conducted in Brisbane, Australia to test the efficacy of encephalitis virus surveillance (EVS) and Centers for Disease Control (CDC) mosquito light traps. Additionally, the relative attractiveness of different combinations of light, carbon dioxide (dry ice) and l-octen-3-ol (octenol) was assessed. the CDC light trap consistently collected more mosquitoes than the comparably baited EVS trap. Octenol, supplemented with dry ice, significantly increased collections of Aedes vigilax, Aedes procax and Culex annulirostris but not Aedes notoscriptus.

I believe the question is very hard to answer. In addition to all the human vector borne pathogens you have the pathogens that are spread between animals and between animals and humans. Most of the emerging diseases are vector borne and many of them are mosquito borne. There are probably several vector borne pathogens that are yet undetected. If you are looking into a future career I can assure you that medical and veterinary entomology is a fulfilling way to go with never ending challenges and rewards!

I think u need specific monoclonal antibody during the processing of the sample,,, this will be followed by coating with a dye either fluorescent or not..I am not sure what is available but u can ask pathologists

If you have access to unfrozen European herrings, these will be heavily infected, since they're the intermediate and/or paratenic hosts for both Anisakis and Contracaecum (and probably the other two species, as well). Get the raw herring, grind them up in a blender and digest them with artificial digestive fluid (HCl-pepsin) at 37 C (follow Trichinella protocols) and then isolate the larvae using the Baerman technique.

We use diluted heparin in hemimetabolous insects, and it works

In 18 year olds even in low transmission regions I would expect antibody to at least one of the antigens, though which one comes up more prominantly is hotly debated and possibly region dependent. The below literature should help. I have looked at both of these antigens following controlled human malaria infection (equivalent to a low dose, single exposure) and I see antibodies only to MSP1 not AMA1. You can find out more from my most recent paper, though I focus more on b cells that antibody.

Wipasa J, Suphavilai C, Okell LC, et al. Long-lived antibody and B Cell memory responses to the human malaria parasites, Plasmodium falciparum and Plasmodium vivax. PLoS Pathog 2010;6(2):e1000770.

Clark EH, Silva CJ, Weiss GE, Li S, Padilla C, Crompton PD, Hernandez JN, Branch OH. Plasmodium falciparum malaria in the Peruvian Amazon, a region of low transmission, is associated with immunologic memory. Infect Immun 2012;80(4):1583-92.

Nogaro SI, Hafalla JC, Walther B, Remarque EJ, Tetteh KK, Conway DJ, Riley EM, Walther M. The breadth, but not the magnitude, of circulating memory B cell responses to P. falciparum increases with age/exposure in an area of low transmission. PLoS One 2011;6(10):e25582.

Dorfman JR, Bejon P, Ndungu FM, et al. B cell memory to 3 Plasmodium falciparum blood-stage antigens in a malaria-endemic area. J Infect Dis 2005;191(10):1623-30.

Kinyanjui SM, Conway DJ, Lanar DE, Marsh K. IgG antibody responses to Plasmodium falciparum merozoite antigens in Kenyan children have a short half-life. Malar J 2007;6:82.

Thank you very much. Also I have another question: do you know which method is most appropriate to concentrate S. haematobium eggs before DNA extraction? and, What protocol should I use for extraction?