Thursday November 19, 2009…
We started off with a few new announcements: John was the winner of the new blog header however Lannie did come in a close second! I must admit the conversation between the two was quite entertaining and it certainly made for a fun read! In the end John walked away with a fabulous prize: an inflatable globe! Now he is able to track the movement of disease! YAY!
Moving forward…
As of Thursday the 19th Dr. Hartley has returned all of our assignments EXCLUDING the Disturbance paper, she has also updated all of our grades on blackboard. Therefore, if you are missing any assignments (minus the disturbance paper) or if you are showing a zero for anything you have turned in it is probably wise that you bring it to Dr. Hartley’s attention. Another IMPORTANT notice: Dr. Hartley will be gone next Wednesday through Saturday and will not be having office hours, however she will be available by email or phone (preferably) and is willing to meet on campus for anyone who to would like to meet concerning the grant proposal. On another note, Natashia had some useful information, if you are not sure how many times you have commented on the other blogs you can log on to your account and find this information under “My Comments” which is located under “Dashboard.” However, if you’re like me and do not log on every time you leave a comment then you will have to go back to each blog and manually count the number of times you left an entry. (*SIGH) Also, Dr. Hartley is giving us until the day of the final to comment on other blogs.
Now on to the lecture…
We started off the lecture in groups of four and discussed the philosophical predictions from the Trade-off model. After spending a few minutes wrapping our brains around these “answer-less” questions we had a discussion on our thoughts. Here were the final conclusions: For the first question we (as a class) decided that hosts with a short life span will favor higher parasite virulence. If a host has a short amount of time to live it needs to be a very affective at transmitting the disease. As for the second argument we decided that lower host densities will lead to higher parasite virulence in the epidemic phase, because each encounter has to be just as effective as the last. In regards to the third “answer-less” question it was determined that generalist parasite species are less virulent then the specialist species. This is because the parasite has more opportunities therefore it doesn’t have to be as virulent. In the absence of parasite evolution, the virulence will decrease as a result of host selection for reduced costs of parasitism. Since the host evolves to defend itself from the parasite then it too has to evolve to survive the defenses. Here is where it got a bit tricky! The fifth question asked “Will within host competition between two parasites favor higher or lower parasite virulence?” Although there were compelling arguments for why it would be higher Dr. Hartley intended the question to be answered differently. She explained that the effect of two parasites living in the same host will result in premature host death which will decrease disease transmission. It then becomes an issue of how fast and how long. The class had concluded that yet again there was no correct or incorrect answer to the last question. These questions were good examples of the many questions that arise in the ecology of disease. Many times because these questions have not been tested they are un-answerable.
The next topic discussed the limitations of the trade-off model. In summary it is hard to apply the trade-off model to pathogens that do not kill their hosts. This model is also limited because behavior is not only controlled by genes but it is also controlled by the environment, (an issue of nature vs. nurture). In conclusion when discussing the evolution of virulence, virulence is a complex trait. Its expression depends on the host and parasite genotypes, and the evolutionary history of the association and the current conditions. Evolution of virulence by natural selection can be partitioned into phase 1, 2 and 3. The most common model of virulence is the trade-off model which is a good starting point for thinking but has its flaws.
On to the next topic that rose SO many lovely questions that I now have the privilege of answering!!!! Pathogen Evolution in a Vaccinated World
We started off with a few definitions and I learned that drugs are different from vaccines because they illicit an immune response. We also learned that pathogens can evolve to have a resistance to vaccines. In the example of the Diphtheria vaccine we learned that since the vaccine has been introduced, the toxin producing strain has declined from 80% of the C. diptheriae population to less than 5%. So in this instance the vaccine is working. We also learned that the vaccine for Hepatitis B only covers the mutant form that is found in the greater proportion of the vaccinated individuals. In the in case of Streptococcus pneumonia it has been speculated that evolution could be the result of a rise in frequency of strains with non-vaccine serotypes filling the niche vacated by the strains of the targeted by the disease. Indicating that the vaccine becomes useless and prevalence increases. In Avian Influenza the antigenic variants that existed prior to vaccination were well-controlled by vaccine-induced immunity, but new lineages arose after vaccination that replaced the originals. This was a prime example of the Red Queens hypothesis in action. Sarah asked an interesting question… “What is the point of getting the H1N1 flu shot if you can get the swine flu more than once?” (So she heard) Dr. Hartley thought it could be because there are different strains for the swine flu but she said that she would look into it and get back to us. Even though evolution occurs, vaccines still continue to fight against disease. Smallpox, polio, measles, pertussis, diphtheria, mumps and rubella all have effects that are controlled by vaccines. However, even though vaccines are protecting us they may hurt the population in the long run. In order to be sure of this we can use the Red Queen hypothesis to verify, the only downfall is that this requires a lot of time.
Alyse also asked an interesting question, “How do anti-malarial drugs work?” Believe it or not this question does not have a simple answer, so I have provided a link that explains how they work. I like this website because it also has a link that explains how the malaria disease works. Hope this answers your question!
http://health.howstuffworks.com/healthillness/treatment/medicine/medications/malaria-drug.htm
Another question that arose was, “do antibodies go away?” and according to the American Association of Clinical Chemistry, No they do not go away. They may drop to low levels in the blood but once you have them, your body will keep a “library” of them so that they can be produced as needed. This answer was a little different from the one we had hypothesized in class but it appeared to be an accredited website. I actually thought that the idead of having a “library of antibodies” was pretty cool. It makes you think about the things we ingest and how it too could be collecting in a “library” of its self! I personally enjoyed this class because it relates to some of the things I have recently learned in Physiology.
I hope I covered everything from lecture acurately, we will finish the evolution discussion on Tuesday after break.
Closing announcements:
Before Dr. Hartley handed over the power of evaluations she did have some concluding announcements. The final for our class will be on THURSDAY of finals week and NOT on Tuesday. Even though we do not have a final we are required to attend or else our grant proposals will not be graded. Good luck to the grad students for they have to present their proposals! Secondly, the evolution assignment is NO longer due on Tuesday after break, from what I gathered it will be due on Thursday. However, there was talk of it being due the day of the final since our grant proposals are due that Thursday, so I am cOnFuSeD!!! Just note that it is no longer dues on the Tuesday after break! (If anyone has any insight please feel free to shed some light!)
And finally…
Dr. Hartley announced that for our final assignment we are taking a trip back to the third grade with “Cootie Catchers!” Haha! The goal is to randomly choose 2 topics (related to disease ecology and NOT the boy/girl you have a crush on!) and discuss how they are related. This actually sounds like fun because we finally get to put it all together and discuss disease ecology from a whole new perspective.
That’s all for now Folks! I wish you all a very Happy Thanksgiving!
Enjoyed your blogging and the asides.
Think I got a nasty little flu for my fall break present. Can’t say if it was a generation of swine (nods to H. Thompson). Whatever it was ran me over like a truck and left me with a sore throat, body aches, enough mucous to call a plumber, and general feelings of…blah. Wuz sleeping about 20 hours each of the last two days (to think this is the norm for most cats).
Maybe I can get extra credit.
Hope everyone has a fantastic break and y’all dodge them flutrucks on the road.
Hey everyone.
I wanted to clarify a fact that was brought up during my groups last paper presentation. The presentation was about Tasmanian Devil Facial Tumor Disease. It was said that female devils stop reproducing at age 2. This is not entirely accurate. Normaly, lifespan is on average 6 years and females reach sexual maturity at age 2, but are able to produce (usually) until age 5. I think there was a little confusion because the paper that we presented was suggesting that selection (thanks to the disease) has favored females who reproduce early and have more offspring in their first litter, as it is unlikely she will survive to the next breeding season.
The research showed that the impact of the disease seemed to alter the reproductive stategy of the individuals in the devil population.
Sorry for the confusion, but I wanted to make sure that we got this point accurate, as it was relevant to the main idea of the paper.
Have a GREAT Thanksgiving!
I had a question that occurred to me during your group’s presentation. For four of the five study sites, there was a sufficient number of years between the ‘before’ and ‘after’ data collections so that the animals used in the Before data must have been different animals from those used in the After group, because the Before animals would have died from old age (if not from the disease). The authors are suggesting that the shift from iteroparous to semelparous reproduction is the result of “phenotypic plasticity”, or behavioral changes resulting from direct experience with the cancer. But there seems to be some contradiction because a Devil wouldn’t develop the Facial Tumor until it reached breeding age and tried to reproduce, which (pre-DFTD arrival) was 2 years old. So what would induce a Devil to mature at an earlier age if it doesn’t become infected until it tries to mate? (I must be forgetting something basic.)
Another question I had concerned the prevalence of the biting behavior that spreads the tumor. I know it’s supposed to be a “common” behavior, but how frequent is that? I assume it’s probably somewhere in the 80-90% range, but that still leaves 10-20% of the population that doesn’t practice the behavior. So wouldn’t the high mortality rate actually be selecting for those few animals who didn’t bite as part of their mating behavior? Even if biting is part of everyday social behavior, my question is still there: wouldn’t there be an initial, small minority of animals who would escape being infected because they didn’t engage in the behavior that spread the cancer and then, over just a few years, become a larger and larger proportion of the population?
About your query concerning the biting behavior of Tasmanian Devils, I wonder why you assume biting prevalence to be limited to only certain individuals in the population? It seems to me that this behavior is necessary for survival and reproduction and therefore would eventually cause extinction.
I just think that all Devils have biting behavior.
I like the idea of “library of antibodies”; antibodies are like books that are stored on the shelves until someone needs them. Then they go to the library and get what they need, not all books will be present but a person will still find what they are looking for. Antibodies are like books, they are present until needed, not in the same amount all the time but enough for the body to fight off the infection.
Hey everyone.
I figured out a really easy way to see your comments. Go to the Disease Ecology Dashboard under “my dashboards.” Press where it says “comments” on the left side (not “my comments”). On the upper right corner, type your username in the search comments box and press search. This will bring up all of your comments.
Thanks, that is really helpful!
I thought the group exercise we did really emphasized the “new paradigm” which states that whether the parasite will be more or less virulent really depends on a number of factors. There may not be enough information provided for us to come to a definite conclusion, though we may be able to speculate. Great blog by the way..
A quick question when it comes to the vaccination and pathogen evolution. In the blog it says that the vaccine covers the mutant form of HepB. What covers the original form? I may be misinformed about this, but it is the only question that arose when i read this blog. Great blog though!
One thing that goes back to the “library of antibodies”, after learning about HIV extensively in virology, one of the reasons in which it is so detrimental to its victims is because it attacks your memory T cells, and therefore erases your “antibody library”. So in other words, you can get chicken pox as a child, and if you were to become HIV positive as an adult, you are at risk for contracting chicken pox again, due to lack of memory T cells……scary!