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…

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.

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!

First person to post wins the fantastic prize.

Moving on y’all: a logic table was passed out for the grant proposal, which we went over. You may have more than one research question. We were told to think about why our specific aim is important. Do our questions match our aim? If our data doesn’t fit, than we may need to change our question or our method. Research questions can go under our specific aim section. We were told to stay calm and take our proposals in bite-sized chunks. Small chunks, lest we choke. The length of the paper should be: Aims 20%, Background 40%, Methods 40%. Grad student (you poor souls), remember we need 15 page proposals! EEE-oolay. Grads also need to do a budget. If we have questions, email or call Dr. Hartley. Everyone has to be there the last day to receive credit for their proposals.

I blacked out at this point dreaming of the semester’s end, but came to, only to discover:

Lecture had started. Game on.

We are currently in the midst of the: Effect of Pathogen Behavior on Pathogen Transmission lecture. We started today in the Grooming section, and discussed how grooming can be seen as a defensive or avoidance measure. There was some hub-bub on what constitutes the difference between the two measures, and from what I gathered with my teeny primate mind pulling off a parasite that is not infected with a pathogen is defensive, but pulling off a vector can be construed as avoidance. While grooming seems insignificant, it actually takes up a large portion of an animal’s time (30% in rats). Therefore, it has costs associated with it: an organism can’t use this time for other behaviors (foraging, mating, etc…) plus the saliva costs are ridiculous. Rats loss a third of their evaporative water loss from the saliva used while grooming! The plus though is grooming does reduce parasite load. There was one weird example where a researcher put metal ‘bits’ in the jaws of doves to prevent them from grooming and measured the increase in parasite load (Kind of falling into the: No Duh category of science. Also, a ‘bit’ sadistic if you ask me, pun painfully intended.). Another example featured house mice that were collared and their lice load increased more than ten-fold within a month. After being de-collared for a day, the number of lice went to its normal amount (and after eating 900 + lice in 24 hours the mice had indigestion no doubt). We finished off grooming talking about how some species each other and themselves, some use plants that are anti-insect or medicinal benefits to them, some species clean other species (one with the unfortunate name of oxpecker), and how some ectoparasites alter their behavior to get away from their groomers (ticks moving to armpits).

Moving on to the removal of parasites and self-medication: zoopharmacognosy (bless you). Some researchers examined the poo (dung) of apes and discovered there was a relationship between the presence of leaves of certain plants and worms. Leaves have trichosomes (fuzzy hair) and worms were folded into the leaves within the dung. It seems the leave’s physical properties than help expel the worms from the apes. A second example was given where chimps ate shoots of the plants Veronia amygadalina which cut down the number of those pesky heliminth ova in their feces. The chimps ate the plant in similar amounts to what humans in the same locality ate of the plant to treat themselves (pretty smart, if you ask me). It is interesting as this seems to happen from time to time. Nature provides a ‘cure’ or at least a salve for ailments in the vicinity they arise. We humans would be wise to take note and preserve places if for no other reason than self-preservation, although that is merely one benefit of doing so.

Here’s another example from the paper: Fur-Rubbing as a Form of Self-Medication in Pongo pygmaeus. Orangutans exhibit fur-rubbing possibly for medicinal use. I hypothesize that they use a species of Commelina, an uncommon herb in the peat-swamp forests of Central Kalimantan, Borneo, as either an antibacterial or anti-inflammatory agent. In Central Kalimantan, local indigenous people use the same species as an external medication to treat their arms after a stroke, for muscular pain, and for sore bones and swellings. Thus, the possible convergence of human and orangutan use of Commelina may indicate that orangutans are using it for a similar purpose.

 Speaking of humans, the last example covered a survey of ancient feces from Utah that found a correlation between Chenopodium seeds and a parasitic nematode. One of our classmates, Natasha, apparently found the occupation of archeoparasitology unappealing and downright disgusting! Posioned hemlock and spices also were noted as forms of self-medication versus parasites. In a semi-related note at a dinner-party last night a friend informed us that Steak Tartare came parasite and pathogen free when nomadic people, the Tarars, placed meat under their saddles and road all day. The meat would be tenderized by journey’s end, and the salt from the horses sweat would kill anything it carried (supposedly, but I’d say this is suspected, but not confirmed through research until I hear of any that studied nomad poop). Self-medication also can be used to alleviate discomfort. Classmates gave examples of behavioral modification: Aubrey- susceptibles may quarantine themselves, and (apologies here as I don’t know all of your names) Girl-Who-Often-Wins-the-Blog-Naming-Contest: infected individuals may want to infect others (aggression levels increasing in infected individuals with rabies).

Lastly in lecture, we discussed social partner choice and joining a group. Sociality promotes transmission, sometimes. Bunching and running demonstrate when sociality helps or hinders transmission. A meta-analysis of many studies showed mobile parasites benefit with smaller groups, yet contagious parasites benefit from larger groups. Back to us humans, agricultural practices spurred the growth of cities and travel, which increased populations and thus benefitted measles and smallpox. We finished the lecture by sticking to the notes with little tangents or detours, covering partner choice/sexual selection and also kin selection. It is interesting that the effects of pathogens on behavior haven’t been covered much so far in the scientific community. It is one of my favorite aspects to our class.

Finally, the Tas Group covered the Tasmanian Devil paper. They went over devil facial tumor disease- what it is, where it is found, how it has changed the population’s age structure and lifetime breeding events, the change in their reproductive strategy. There has been an increase in female precocial breeding. All five study sites showed infected devils by 2005. The devils were trapped, marked, weighted, measured, age estimated, and had their reproductive condition assessed. Before the disease occurred older Tas devils bred at age 2+ and had annual litters for 3 or so years.  After infections, females have one breeding opprotunity and may not even survive long enough to raise that litter! The devils are adapting from iteroparity to semelparity. It was really shocking to hear they could face extinction in twenty five years or so. Hopefully we can help the devils survive. Research to help them may also help stop cancer in us humans so that is just another incentive to help this species.

Okay, I hope this covers everything and everyone had a great weekend.

Lannie

We now get into the good stuff. We began a new section today: Behavior and Disease. The players are the usual suspects: pathogens, hosts, and vectors. The aim of every player is to survive and reproduce. Behaviors are categorized based on whether they promote or hinder survival and reproduction of the player. A behavior may benefit one player while at the same time hindering another player. We started by discussing behaviors that promote pathogen transmission. The first example given was when the effect of a pathogen changes the behavior of the host. Rabies attacks parts of the CNS causing aggressive behavior. Another interesting example is in a species of ant. A mermithid is an obligate parasite that attacks the ant host. The infected host will enter water and drown (ants can’t swim), and the mermithid will develop in the water. Several other examples were given where pathogens effect predators social behavior and secondary hosts. Next were the effects of pathogen on vector behavior. The pathogen can change the feeding or mating behavior of a vector. An example that we have seen before is plague. The pathogen Yersinia pestis affects fleas. The pathogen reproduces in the gut of the flea – the flea gets backed up – vomits – and keeps feeding. After that, it was how the effect of pathogen behavior on pathogen increases transmission. An interesting example in this case was the Rabbit flea which responds to cues in a pregnant rabbit. The flea stays on the prego rabbit and when the rabbit is ready to bear young, the flea relocates from the rabbit’s ears to the face and transfer the pathogen to the young… Pretty cool!

Now, let’s move on to behaviors that decrease pathogen transmission. Behavioral alterations can decrease Ro to below 1 by effectively removing susceptibles from the host population. This can be looked at simply as a cost v benefit analysis – Is it cost of the behavior greater than the cost of being infected? Hhhmmmmmm…. A formidable question indeed. We considered different ways transmission of a pathogen can be decreased. We talked about migration, latitudinal shifts, running away, submerging, microhabitat choice, posture changes, use of camouflage, and habitat & dietary influence. A hippo’s habitat choice is influenced by tabanids (a type of fly). In areas where the flies are abundant, the hippos stay in the water and avoid land. Sociality can also positively and negatively influence pathogen transmission. In the case of cattle, they congregate in groups and this benefits the parasite carried by the warble fly. The fly oviposits (lays eggs) on the cow and the fact that the cows group together allows the warble fly to oviposit on multiple hosts. Besides joining a group, we discussed how isolation, territoriality, and sexual selection also influences pathogen behavior. Sexual selection was an interesting topic. The Hamilton and Zuk hypothesis regarding sexual signaling states that animals should eschew (reject) parasitized mates to minimize the transmission of genetic susceptibility to offspring. This is cool because it bases animal behavior and sexual selection on secondary sexual characteristics. Basically, if an organism is healthy and not plagued by a parasite; it is not spending energy on immune response and can spend more time and energy on courtship displays. I mean, this is applicable to humans if you think about it – If you’re sick, you’re not going to want to go out to the bar and try to find a mate… And if you do, you’ve got bigger problems. Another applicable example was in the case of voles. Anogenital (new word) odors of male meadow voles that had recently and vigorously groomed themselves, were more attractive to females than the odors of males who groomed less. Now, this makes sense if you think about it in terms of humans – No girl is gonna be attracted to a guy that doesn’t spend much time on grooming, and the smell (maybe not anogenital) of a guy that has just had some good solid primp-time is gonna be much more appealing.

Almost done…

We moved on to defensive behaviors. This one seems pretty simple: As an alternative to running away from parasites, some hosts will stand and fight; doing things like batting, swatting, slapping etc. For instance, Howler monkeys have been observed to perform >1500 avoidance movements per 12 hours!!! That is tons of movement and it comes at a cost to the host. The monkey is expending a lot of energy with this defensive behavior; energy that could be spent mating or foraging for food. Different animals can differ in their defensive mechanisms and the size, age, and fitness of the host can also play a role.

Lastly, we talked about thermal preferences: Behavioral fever and behavioral chills. As we all know, fever can be important in fighting an infection and has been shown to enhance survival after an infection. But fever is also metabolically costly. An animal with a fever is spending valuable energy and this can have fitness consequences. Some animals will raise their body temperature intentionally when infected with a parasite. An example in our notes is of desert iguanas. When injected with killed gram-negative bacteria, they change their behavior which results in a 2 degrees C rise in body temperature. Chills can also harm a parasite. We discussed bumblebees. Bumblebee workers infected with a parasite remain outside the nest in colder temperatures. At lower temperatures, fewer parasites completed development. Although, Aubrey brought up an interesting alternative hypothesis: Perhaps the infected bee is staying away from the hive to not infect the other bees and having nothing to do with temperature… Hhhmmmmm.

There are several very good examples of everything we discussed on Tuesday, not all of which I included here, so be sure to refer to the lecture notes.

Some final IMPORTANT parting announcements – There has been a change in plans regarding presentations. Thursday will be the last day for primary literature presentations. Group 5 will be presenting the Tasmanian Devil paper and we will finish lecture. Group 6 is doing the Avian defense paper, but will likely not present until Tuesday. The last assignment will be an in class activity that is to be determined (refer to Dr. Hartley’s email).

That’s it!! For all of you that are still awake and made it thru my blog, this is John signing off. See you all in class!!!

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