Evolution Assessment

Hello!
Apparently I do not have the grasp on the Trade-off Model I thought I had and I found myself trying to define it without much success. Anyone have a better definition than “the virulence of the pathogen promote an increase in the secondary infections brought on by the primary infection”? Is that it or am I completely missing it? Thanks for any help.

December 1st Class

Sorry for blogging so late. First on the list is due dates. Dr Hartley indicated that the Evolution homework is due on or before December 8th by email or digital box. The grant proposal is due tomorrow December 3rd in class. Please bring 3 copies of your proposal to class, two of which cannot have names. On final day (12/8/2009) bring your grant reviews. Also on tomorrow Dr. Hartley will bring a list indicating the number of blogs each person has done so far…. REMEMBER: YOU HAVE UNTIL DECEMBER 8TH (Finals day) TO GET YOUR 8 BLOGS IN!!!

This coming up class we will have a group assignment. Please bring all of your notes from class. The assignment will be a way to recap the different concepts we have learned. DO NOT MISS CLASS THE ASSIGNMENT WILL COUNT FOR A GRADE!!!

We started lecture by reviewing a few terms and concepts. They are listed below:

- Evolution - Evolution in simple terms is change in gene frequency over time. In order for it to occur there has to be mutation, selection (natural and artificial), gene Flow/migration, and genetic drift.

We also talked about what needs to happen in order for natural selection to occur. We need variation, heritability, selection, and time.

- Evolution of virulence-  under this topic we talked discussed the definition of virulence which is, a parasite mediated morbidity and mortality. Virulence can either be avirulent where the symptoms of the host does not directly affect the parasite. Asymptomatic the symptoms do directly affect the parasite. Asymptomatic is usually fast killing.

One model for evolution of virulence we talked about was the Trade-Off model. Ying explained, if pathogen is more virulent it would kill the host to quickly. So the pathogen cannot be too virulent, but it has to be virulent enough to continue to the chain of infection. It is not in the best interest of a pathogen to be too virulent.

Effects of vaccines on pathogen evolution- In regards to this topic we talked about how even if a pathogen vaccines can alter the immune pressures experienced by the pathogen.  Sometimes the pathogen can evolve a new way to be virulent. Dr. Hartley clarified the definition of vaccine breakthrough. It is when a person has received a vaccine but still becomes sick with the disease the vaccine was to prevent.

After review we continued began talking about evolution of antimicrobial resistance. She discussed nosocomial infections, which are hospital- acquired infections that are a major public health problem. Out of about 200,000 people many people are dying of these kind of infections. The numbers estimated are 17,000 AIDS/HIV, 37,000 flu, and 40,000 breast cancer. WHO (World Health Organization) estimated that 8.7% of hospital visits will result in these types of infections. This is because there are many anti-viral resistent strains of bacteria in hospitals.  Because evolution pressure is different in hospitals it is important that people should get antibiotics unless needed because it will increase the evolution of infection causing more resistant strains.

On the slide listed history of antibiotic resistance with the list of antibiotics, Dr. Hartley indicated that the first   Vancomycin listed is the correct one. This particular drug we discussed is usually for the last resort. It has to be administered intravenously because it cannot be absorbed orally. It is used when all other antibiotics have failed. Looking up more research on the drug some of the side effects are hearing lost and kidney damaged when tested in the 1950′s. Recent studies have shown that vancomycin can induce platelet-reactive antibodies which leads to severe thrombocytopenia ( platelets in the blood) and bleeding with florid petechial hemorrhages (small spots on the body), ecchymoses ( bruises), and wet purpura. http://en.wikipedia.org/wiki/Vancomycin

Dr. Hartley also explained how pathogens become antibiotic- resistant. What she is explained is that after the antibiotic is administered the first time the pathogen dies off leaving only a few that were able to resist drug. Over time more of the pathogens become antiobiotic-resistant. We discussed what mechanisms there are that cause antibiotic resistant phenotypes. The mechanisms are: Point mutations, homologous recombination, and heterologous recombination. These phenotypes arise from natural soils, agriculture use, and hospital use. In regards to agricultural use, the slide indicates that the phenotypes are passed on  because the farmer works in the farm and gets sick and goes to the hospital passing it on to whoever he comes in contact with there. If he gives it to people within hospital when those people leave they are then passing it on to whoever they come in contact with too.  Then food from the farm makes it to grocery stores and restaurants. People then get the food from stores and food places getting them sick…

Dr. Hartley wanted me to look up what patients with MRSA are treated with. I checked the blog and it looked like that was answered for me. We did learn that subtherapeutic are lower doses of a vaccine that does no kill bacteria, and therapeutic are doses of a vaccine that are used to kill bacteria.  There are higher selection pressure in hospitals because they have weaker immune systems and can get infected easily. When the staff get infected because of high turnover rate it is passed on to the neighborhood easily.

Lastly, we talked about the different ways to prevent or treat resistance. Mixing and cycling are two different ways it can be treated or prevented. Mixing is when different antibiotics are administered to each person so that they are never introduced to the patients near them. Mixing is within space. Coupling is when a hospital administered a specific antibiotic to all the patients and then over time switch the antibiotic. The only problem is the lobster trap could keep cycling from working. The lobster trap is  a genotype easy to reach by selection in one direction, but difficult to leave when selection goes in the other direction ( Hartley 2009). Strategies that c an be used are: 1)Predicting resistance evolution 2) narrowing spectrum antibiotics 3) Bacteriocins 4) Ecological modeling

And class is over…. remember to be in class thursday…

MRSA treatment

I called one of the pharmacists that I work with and there are still antibiotic treatment options for MRSA. If the infection is intranasal then this ointment Bactroban is used. Depending on the strain and susceptibility of MRSA then other antibiotics are used which include; clindamycin, Bactrim, vancomycin and/or Zyvox. Zyvox was approved for use in the market in 2000, so it is a very new antibiotic, it is also very powerful and a last resort (we almost never see this drug prescribed even though our patients are about 99% nursing home residents).

New Blog Header

Hello Class, 

The first person to guess what this disease is will win a fabulous prize.  The pathogen affects humans and dolphins.  The pathogen is in Kingdom Fungi.

November 19th Class Lecture

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!

New Blog Header

On the blog header is an animal infected with an insect-borne viral disease that affects ruminants.  One of the symptoms is cyanosis of the tongue.  The disease is also called Catarrhal fever.  What is the name of the disease and the pathogen that causes it? 

First person to post wins the fantastic prize.

New Blog Header

The first person to post a comment with the scientific name of this vector and the name of an emerging disease that it transmits will win a fantastic prize.  Hint – The vector currently spreading a virus in India and that virus was recently found in Italy and other parts of the world.

November 12th class lecture

Class today began with Dr. Hartley talking about our Disturbance Assignment and commented that she was, quite frankly: DISTURBED. <this despite my giving her a coupon promising 1 gram of medical marijuana for free at a local dispensary which I got as proof I went to the Sustainability Fair>. Why then was she disturbed? Because many people had neglected to cite their sources. She wants us to cite (author’s name, year published) with in the paper and will also accept if you note it with a number and the number is listed in the literature cited section at the end of your assignment. For class notes: (Mooore 2002 in Hartley 2009). A lecture citation in the literature cited section should read: Hartley, L.M. 2009. Effects of Disturbance on Disease lecture, Disease Ecology, University of Colorado at Denver. She wants us to get comfortable citing sources and said she will take hypothetical examples  noted as, “suspected, but not confirmed through research.” She also gave us a new deadline to turn in this assignment: Monday by mid-night.

November 10 Lecture

Ok, here we go. We began class today (as usual) with some announcements. First off, Dr. Hartley changed the disease picture on the blog and Alyse won a fantabulous prize… FAKE SNOW!!!! Damn, I wish I would have won… Oh well, maybe next time. Then Sarah gave a public service announcement regarding an upcoming event that COPIRG is hosting. On Thursday the 12th (yes, thats this Thursday) from 10:00 am to 3:00 pm in the P.E. Event Center Lobby, it will be the Campus Sustainability Fair. Attendees will learn about sustainability initiatives on our campus and around Denver. Also, Dr. Hartley will give one extra credit point on any assignment to anyone who attends provided that you bring back some sort of evidence that you went. For more info, click here <http://www.cudenver.edu/Academics/Colleges/SPA/About/Pages/ViewOurSpecialEvents.aspx>. We then talked about blogging and Dr. Hartley pointed out how “the chain of infection” has been broken!! (a.k.a noone has blogged in a while). Lannie and I are the only two who have not blogged yet… So, here I am and Lannie has taken Thursday’s blog. Don’t forget, we all have to comment on the blog at least 8 times in the semester, and the semester is quickly coming to an end. So for all of you that don’t have Disease Ecology Blog as your homepage (like I do) get with it and start posting. I’m sure my post will give you PLENTY to comment on. One more thing before we get into the meat and potatoes of todays lecture – The disturbance assignment is due on Thursday!!

DISTURBANCE ASSIGMENT

Hi everyone,

I made this short blog, because I have been having difficulty with the disturbance assignment.  I also thought that it could help others who are also having difficulty with the assignment. If anyone is having difficulty finding a specific disease that decreases with the help of non-native species, there is an article called, Release of invasive plants from fungal and viral pathogens, by Charles E. Mitchell and Alison G. Power that can help. If anyone found anything for how pollution can decrease a disease, please let me know.

Marie