Symbiosis: Relationship Status

Defining Symbiosis 

When it comes to relationships, nobody wants to feel used. Figuring out the perfect balance of give-and-take is quite tricky. For parasites and other organisms, “relationship statuses” are quite complex. The term symbiosis refers to an association that is both close and prolonged between at least two organisms of different species [1]. This association can be further categorized into three forms: mutualism, commensalism, and parasitism [6]. Furthermore, these broad categories also contain subcategories. For example, mutualism can be trophic, dispersive, or defensive [6]. This means two organisms are either equally sharing resources, one is providing resources and the other services, or both are providing services to each other respectively [6]. Given these details, it is evident that deciphering between these three forms can be a bit problematic. 

So, Which Relationship Is It?

When examining symbiotic relationships, one must take into account both costs and benefits of the species involved. In the case of the hermit crab and its sea anemone(s), the advantages that the species gain are difficult to categorize.

Hermit Crabs and Sea Anemones

http://animals.pawnation.com/relationship-between-hermit-crabs-sea-anemones-1857.html [3]

In “The Art of Being a Parasite”, Claude Combes claims that the hermit crab and its sea anemone(s) have a mutual relationship [2]. The anemone, which is attached to the shell of the crab, provides protection for the crab, while in turn becoming more mobile as a result of its attachment [2]. However, is this trade-off significant enough to label as an example of mutualism? This is where things become complex. Sandy Vigil, author for Demand Media, says these two species actually display commensalism [3]. Why is this important? Well, mutualism refers to two organisms sharing equal benefit in a relationship. On the contrary, when one organism benefits and the other remains unharmed one considers the relationship to be commensalism [3]. Vigil acknowledges the same advantages that Combes presents: protection for the hermit crabs and increased mobility and a subsequent steady food supply for the sea anemones. So, why do they view the interaction differently? It seems that Vigil believes that due to the symbiotic relationship being necessary for the survival of the hermit crab and not the anemone, the two are not equally benefiting. Therefore, the interaction exhibits characteristics of commensalism [6]. If these organisms could talk, the crab would most likely side with Combes and the anemones with Vigil. The type of relationship shared by these organisms all comes down to perception. Thankfully, there are cases where organisms do share a clearly defined symbiotic relationship and the perspective towards their relationship is consistent among observers.

Honey Bees and Flowering Plants

http://sciencewithme.com/learn-about-pollination/pollination_1/ [7] 

The relationship between Apis mellifera, commonly known as the honey bee, and angiosperms (flowering plants) is a great example; these two species share an undeniably mutualistic relationship [5]. Both the honey bee and the flowering plant rely on each other for survival. There are three different groupings of honey bees which include: the queens, drones (males), and the workers. The worker bees are the pollinators [5]. Pollination is not an active process; instead, it occurs passively as the workers search for food. During this search, the bees fly from one flower to another collecting pollen and nectar. As the bees acquire these necessities, they transfer pollen among the plants which fertilizes them [4]. In this case, it is obvious that both species need each other to survive and working together is in the best interest of them both.

Is There Ever a Right Answer?

Ultimately, when examining the interactions between organisms it is up to the individual to decide which symbiotic relationship is being displayed. In some cases, like the honey bees and flowering plants one will find it easy to decipher between the choices. On the other hand, in cases like the crab and its anemone(s), it will take more effort for one to come to a conclusion. The complex nature of symbiotic relationships is not in the interactions themselves, but in the details of the interaction. Are the organisms equally benefiting by sharing resources, only using another species for transportation, or simply providing shelter [6]? It is up to the spectator to decide.

References

[1] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1317043/

[2] http://books.google.com/books?id=bEtEL2z3hXcC&printsec=frontcover&source=gbs_ge_summary_r&cad=0#v=snippet&q=anemone&f=false

[3] http://animals.pawnation.com/relationship-between-hermit-crabs-sea-anemones-1857.html

[4] http://www.orkin.com/stinging-pests/bees/honeybee-pollination/

[5] http://www.gpnc.org/honeybee.htm

[6] http://www.buzzle.com/articles/types-of-symbiotic-relationships.html

[7] http://sciencewithme.com/learn-about-pollination/pollination_1/

Parasites Defy Koch’s Postulates

Parasites are organisms that inhabit and get food from a host and often cause diseases.  Once a parasite gets into a host, it can go unnoticed, or it can cause severe infections.[1] Usually when a microorganism is in a host, it can be found, isolated, and associated with a particular disease to then be treated. That is not always the case for parasites, which go against the criteria for identifying the relation between disease and microorganism.

Koch and His Postulates 

 

Before a bacteriologist named Robert Koch, scientists were baffled about the idea of how a specific microorganism caused a particular disease[3]. After a series of scientific experiments, Koch and his colleagues came up with the Koch’s postulates in the 1800’s to help identify the relationship of the pathogen or microorganism and the disease it causes.[3,5]  He and his colleagues used mice as the hosts in experiments to study the connection between microbes and diseases. Koch’s four postulates are:

[7]

   
1)  The organism/pathogen must be present with every case of the disease and absent in healthy individuals

2) The pathogen must be grown in a pure culture when isolated from the diseased host

3) Then, that isolated pathogen should cause the same disease when re inoculated into a healthy test subject/host.

4) The pathogen must then be re isolated from the new host and cause the same disease in a pure culture as the initial one.[5] 

                                                                         

Parasites Disregard the Postulates 

                  

When the postulates were first introduced, they helped clarify questions in the scientific community about diseases related to pathogens. . The postulates could not be used for studying diseases caused by things such as parasites. Parasites are not the only ones that do not follow the postulates though; there were limitations to Koch’s findings when diseases such as Cholera and some viruses were studied. For example, Vibrio cholerae, the bacterium that causes cholera, can also be found in healthy hosts, invalidating the first postulate.[4]

An example for a parasite that does not follow the postulates is the plasmodium that causes malaria.

[9]

The problems found in the postulates for studying parasites were:

1) Many parasites are asymptomatic and so we cannot tell when the parasite is present or not present. Also, the parasite could be hidden or dormant for its own benefit. A female mosquito carries and transfers the plasmodium but it could be present in a healthy host in low levels and therefore go unnoticed, voiding the first postulate. [4,2]

2) The second postulate states that the microorganism must be grown in a pure culture and parasites are not easily grown in pure cultures. Parasites need adequate conditions to grow in and so the second postulate was not useful in finding a parasite causing a disease. The plasmodium of malaria cannot be grown in a pure culture outside of a host, defying the second postulate.  [4,2]

[6]

3) The third postulate states that the pathogen must infect another animal host and produce the same outcome. This cannot be tested because there may not be adequate animal hosts that would cause the same outcome as in humans. For malaria, humans cannot be tested on due to ethical issues. It would not be ethical to use humans as test subjects and perform experiments on. Some parasites only cause the disease when in humans and not in other animals. Also, some animals may not carry the parasite in the same way as humans. For another example, Kuchenmeister, a scientist, studied parasites that were seen as bladder worms in pigs but tapeworms causing Taeniasis in humans.[1] This showed that there are different stages of a parasite’s life cycle expressed in different hosts making it difficult to say that the same parasite causes the same disease. There can be many intermediate hosts of parasites before reaching a definitive or final host.[4]

[8]

  

4) The dilemma with the fourth postulate is that since the life stages of the parasites could be different in different hosts, it would be difficult to re-isolate the microorganism and grow it in a pure culture to produce identical results. Again, the plasmodium cannot be isolated and re-grown in a pure culture due to the nature of the parasite and the environment it needs to grow. [4,2] 

The Postulates Now 

          

 Today, Koch’s postulates are still used in determining the links between microbes and the disease they cause but are not very useful in finding the relationship between certain microorganisms such as viruses and parasites and diseases they cause.

Works Cited 

1)  http://www.cdc.gov/parasites/

2) http://www.microbemagazine.org/index.php?option=com_content&view=article&id=3664:kochs-postulatesthen-and-now&catid=812&Itemid=1095

3) http://www.historyofvaccines.org/content/koch%E2%80%99s-postulates

4)  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3158372/ 

5)  http://www.princeton.edu/~achaney/tmve/wiki100k/docs/Koch_s_postulates.html   

6) http://wordpress.as.edu.au/tlane/2013/02/20/clonorchis-sinesis-pork-tape-worm/  

7)  http://www.youtube.com/watch?v=Ffrq1lIfE1o

8) http://www.youtube.com/watch?v=bb32g02IIs8

9) http://www.cdc.gov/malaria/about/biology/

 

Hygiene Hypothesis and Helminthic Therapy

Hygiene Hypothesis and Helminthic Therapy

The parasites are usually recognized as notorious creatures which infect and damage hosts’ bodies, even though they do not mean to harm the hosts—they are merely trying to survive and continue their generations. However, this is not always true. Recent studies suggest that some parasitic worms may be useful in treating autoimmune diseases such as Crohn’s disease or allergies.

Hygiene Hypothesis

Autoimmune disease refers to the abnormal functioning of one’s immune system that cannot differentiate self-tissues and other tissues. This leads to one’s antibody attacking one’s own body. One possible cause of this disease can be explained with the hygiene hypothesis, which states that early life exposures to germs decide the sensitivity to allergic and autoimmune diseases. In fact, the more advanced countries with better hygiene systems with less exposure to germs have an increasing rate of autoimmune diseases.

So, what effect do germs, including parasites, have on the immune system? They trigger the Type 2 helper T cells by tickling proteins called cytokines, which initiate a healing process. However, if there are not enough germs in the body, then the immune system would attack its own body instead of the germs, and this leads to inflammation and diseases.

Trichuris trichiura—great for Helminthic Therapy

Trichuris trichiura

http://www.isciencetimes.com/articles/4998/20130423/worm-therapy-swallowing-live-parasites-help-treat.htm

One of the best parasites that were found so far would be Trichuris trichiura, also known as whipworms. This is usually found in humans or pigs and is known as a great treatment for Crohn’s disease. This disease affects any part of the gastrointestinal tract and causes inflammation. This creates symptoms such as diarrhea, rectal bleeding, fever, etc. Whipworms are great to be used since they do not cause any serious damages in human body even though they are still parasites. Also, they are big enough to be recognized by immune system, and the antibodies would attack the whipworms instead of its own body tissues. This in fact results in 75% of cure of Crohn’s disease.

Controversy

Even though the use of helminthes significantly increased of cure of autoimmune diseases, some scientists still doubt about the safety.  They argue that parasites are parasites and they may cure some diseases, but they also may cause other problems, so it has to be studied a lot further. It also needs to be very carefully used.

References:

http://www.sciencedirect.com/science/article/pii/S1201971213000982

http://gut.bmj.com/content/54/1/87.full

http://www.livescience.com/17923-parasitic-worms-wound-healing.html

http://nutritionwonderland.com/2009/02/parasitic-worms/

http://www.cdc.gov/parasites/whipworm/biology.html

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828/

http://www.sciencedaily.com/releases/2012/03/120322142157.htm

Defense Evasion: Molecular Mimicry

Parasites, like ninjas, need to come up with intuitive ways to evade their targets defenses.  Parasites are organisms that rely on a host in order to reproduce and survive. The ability of a parasite to withstand the onslaught of their host’s defenses, such as the immune system, is a critical factor in determining life or death.  Natural selection has given parasites multiple ways of avoiding the host defense.  Some of the survival mechanisms  parasites utilize include hiding in areas of the host where the immune response is overlooked, suppressing the immune system in order for easier invasion, and forming a protective cyst. [1] In addition to these avoidance mechanisms, parasites have clever method  to cloak themselves from  phagocytic cells of the host. These parasites can produce compounds in order to disguise itself as part of the host. This sneaky tactic, molecular mimicry is an ingenious method of protection from a hosts immune system. [1]

Hide and Seek

 Parasites rely on molecular mimicry in order to stay hidden from dangerous phagocytes of the immune system. The basic premise of this mechanism  is for the parasite to produce a cellular component that can be identified by the host immune system as its own.[1] This stealthily enables the parasite to hide its antigen characteristics, and this lowers the risk of recognition by phagocytes. [1] This molecular deception is used by various parasites to enhance their chance of survival in hosts.  For example, the intracellular parasite, Neisseria meningitids, which causes meningitis, uses molecular mimicry to protect itself from the hosts immune system. [5] Neisseria is able to avoid the antibody mediated immune system response by producing a protein that binds to factor H of the immune system. [5] Factor H  binds to normal cells for autoimmune protection. [5] This prevents the healthy cell of the host from being attacked by its own immune system. [5] By being able to produce a protein that binds to factor H, Neisseria, is able to hide and gain similar protection just like normal cells.[5]  As a result, Neisseria, is able to hide among the cells without facing destruction.

We Are Cloaked!

The blood fluke, Schistosoma mansoni, is a small worm that infects millions of people with the chronic illness known as intestinal schistosomiasis. [4] The fluke goes through different stages of development in order to reach full maturity. [4] Before mansoni can infect humans, it uses snails as an intermediate host. [4] The snail provides a place for the fluke to mature on its journey to reach its definite host. [4] The problem that arises during this period of growth is the snail's immune system, and in order to survive, mansoni must use the power of molecular mimicry.[4] The immune system of a snail is comprised of molecules called lectins, and these function  in the recognition of various molecule such as carbohydrates and sugars. [4] The lectins help seek out foreign particles in the snails immune system and stimulate an immune response. [4]  In order to counteract this detection system, the  fluke possess sugars that are already present in snails, and this makes it very difficult for the lectins to recognize the flukes’ presence as foreign.[4] By using molecular mimicry the blood fluke is to cloak itself while developing in the intermediate host without any interruption. Molecular mimicry makes it possible for parasites to sustain themselves in the unforgiving environment of the host. 
As a result, molecular mimicry gives parasites a fighting chance against the deadly defenses found in many host organisms. Out of all the methods that  parasites can utilize to stay alive in the host, molecular mimicry is a devious approach to achieving a higher chance of survival. 

References: 

1)  http://textbookofbacteriology.net/antiphago.html
2) http://www.ppdictionary.com/parasites/mansoni.htm
3) http://textbookofbacteriology.net/themicrobialworld/meningitis.html
4) http://www.news.wisc.edu/21575
5) http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/G/Games.html#Phagosome_Lysosome

Adaptations of Organisms Upon Encounter

Death or Survival?

For a parasite to survive, it must be able to do two things, encounter the host, and be compatible with the host. To encounter the host, the parasite evolves special phenotypes which allow for a greater rate of encounter, or it simply lives in areas where the host must meet the parasite at some point. Unfortunately for the parasite, hosts also evolve to be able to either fight the parasite or avoid it. If the parasite has been able to latch onto or enter the host, it must now survive while draining nutrients from its victim. This is where being compatible with the host is essential. If the host is able to detect the parasite and remove it, the parasite dies and the host is able to keep its resources to itself. This is where either closing the encounter filter or the compatibility filter is important in the destruction of the parasite.[1]

Fleas Fleas Everywhere!

When a host is able to detect a parasite, it must decide whether to avoid it entirely or kill it off. Two similar hosts, the great tit and the blue tit, must make the decision whether to live in a nest with fleas or without. Normally, both tits prefer to live without fleas so that they my keep their resources and not share them with the fleas, but this is not always possible.[1] For multiple reasons, a tit may decide it is easier to contend with the fleas and must now compensate in a variety of ways for the resources the fleas are taking from both parents and nestlings. For both species of tits, the nestlings are greatly affected from the presence of fleas. They are smaller in size and weight which makes it harder for them to survive and mature. There begging rate also increases because they lack resources sufficient resources to allow development into a mature adult. This increased begging rate causes stresses on the father because he is focused on providing for the current generation of nestlings. To do this, he will leave the nest more frequently to find food which tires him and makes him more susceptible to disease like malaria.[1] While the father puts in effort to acquire more food, the mother tit usually bears a larger brood because she focuses on the future generations she will lay.[2,3] These behavioral changes were all the result of not closing the encounter and compatibility filters and resulted in a lifestyle which greatly reduced the health of both parent and nestling tit.

Changing Your Skin to Avoid Detection

When a parasite enters its host, it must either avoid detection or be able to withstand the persecution of the hosts’ immune response. Trypanosoma Brucei is a protozoan which causes African sleeping sickness.

http://www.cdc.gov/parasites/sleepingsickness/biology.html [7] 

 To be able to survive in mammals, it has developed the ability to change properties of antigens upon its membrane surface.[4] An antigen is a foreign substance which triggers an immune response which ultimately results in antibody development for that specific foreign substance.[5] The antigens of T. Brucei are concentrated on the surface of the protozoan in a thick glycoprotein known as the variable surface glycoprotein (VSG). What distinguishes T. Brucei from other microorganisms is that its VSG has over 1000 genes which allow it to adapt to immune responses.[6] When the immune system is able to detect the antigens expressed by the VSG and mount a response to kill T. Brucei, it mutates its VSG using a different gene which expresses another antigen the hosts immune system has not yet identified and formed antibodies for.

http://www.nature.com/nrmicro/journal/v4/n6/fig_tab/nrmicro1428_F2.html [8]

By mutating the VSG T. Brucei, it is able to thrive within its mammalian host for extended periods of time. This lengthy survival is possible because of the roughly one week period of time the body takes for an adapted immune response to target and kill T. Brucei. With over 1000 different genes in the VSG, it can avoid detection of the mammalian adaptive immune system for a minimum of 1000 weeks (19.23 years) which allows an ample amount of time for it to be able to reproduce and pass its genes to the next generation.

References:

1) The Art of Being A Parasite by Claude Combes http://books.google.com/books?id=bEtEL2z3hXcC&pg=PA44&lpg=PA44&dq=bothriocephalus+gregarius&source=bl&ots=zEQ9I30Ou0&sig=IGbgHPXOnso-3mDBKJSu2nwbtMo&hl=en&sa=X&ei=khPvUsryCubXyAGP1oCoBA&sqi=2&ved=0CEQQ6AEwAw%23v=onepage&q=bothriocephalus%20gregarius&f=false#v=snippet&q=compatibility%20filter&f=false

2) http://www.jstor.org/stable/5390

3) http://beheco.oxfordjournals.org/content/7/2/127.short

4) http://www.sciencedirect.com/science/article/pii/0166685192900044

5) http://www.biology-online.org/dictionary/Antigen

6) http://apps.webofknowledge.com/full_record.do?product=WOS&search_mode=GeneralSearch&qid=13&SID=1FW128QdnJBfbUMaBwq&page=1&doc=4

7) http://www.cdc.gov/parasites/sleepingsickness/biology.html

8) http://www.nature.com/nrmicro/journal/v4/n6/fig_tab/nrmicro1428_F2.html

Fight or Flight?

Two lines of defense

The evolution of parasite and host interactions is a never-ending arms race: the parasite tries to get ahead of the host while the host tries to get ahead of the parasite. According to Claude Combes, two filters can represent the arms race between hosts and parasites: encounter and compatibility.  The parasite wants to open the filters where as the host wants to close them¹. Going along with this idea, there are two lines of defense that can help a host evade parasitism. The first line of defense is to avoid the parasite all together, which in turn closes the encounter filter. The second line of defense is, in the event that the encounter does occur, to fight off the infection, which closes the compatibility filter¹. Idealistically, both of these lines of defense work; however, which one do hosts utilize more frequently: flight or fight?

Flight

                 

       

Lifecycle of Paragonimus westermani

 Have you ever gotten a small scratch or bug bite that you did not notice until it started burning or itching? Most of the time we do not realize when we got the scratch or bug bite because they are so minute. The same can be applied to a host/parasite relationship. Parasites are incredibly small to the point where they are not visible to the naked eye. Hosts need to be able to detect a parasite in order to avoid it. Because they are so small, even though they give off signals for detection, the amount of signals given off by a parasite is not detectable by a host¹. Just like how we don’t realized the cut until it burns, in the same way, the host doesn’t detect the parasite until its immune system has.

Lifecycle of Dracunculus medinensis

Another reason why parasites are hard to avoid is because they are found in places that cannot be avoided, such as the water and prey². All of the parasitic helminthes (which include the roundworms, flatworms, and flukes) have a period of their life cycle in which they spend in an aquatic environment³. For example, the female Dracunculus medinensis, otherwise known as the guinea worm, causes a blister to form in the human host. The blister causes severe pain and discomfort, which can bee soothed by the water. This is when the guinea worm emerges from the skin so that it can release its eggs into the water⁴. The cycle repeats when humans ingest contaminated water. This is why avoiding parasites is not the preferred line of defense for hosts.

Fight

                  Generally, hosts tend to use the second line of defense more frequently which occurs after an encounter has been made. A host’s immune system is programmed to recognize “self” and “non-self” molecules. Every “self” molecule has a specific set of protein on the surf of the cell that allows lymphocytes to recognize them. Parasites have different proteins on their surface that alert the lymphocytes that a foreign body, or antigen, is present. The immune system goes on to produce antibodies to fight off the infection⁵. This is one way the host can fight off an infection. Another way hosts can deal with an infection is to reallocate resources¹. A host may compensate for an infection by shifting their life cycle to reproduce earlier in life. This is what the crustacean Daphnia magna tends to do when parasitized by Glugoides intestinalis6,7.  Studies show that infected Daphnia tend to produce up more offspring in their first clutch than those that were not infected^6,7. This may be due to a trade off that lowers reproduction later on in life due to the infection.

Infected Daphni vs uninfected Daphnia 8

References

  1.http://books.google.com/books?id=bEtEL2z3hXcC&printsec=frontcover&source=gbs_ge_summary_r&cad=0#v=snippet&q=line%20of%20defense&f=false

 2. http://www.cdc.gov/parasites/water.html

 3.http://parasite.org.au/para-site/contents/helminth-intoduction.html

4. http://www.cdc.gov/parasites/guineaworm/biology.html

5. http://www.cancer.gov/cancertopics/understandingcancer/immunesystem/AllPages

6. http://rspb.royalsocietypublishing.org/content/272/1562/505.full

7. http://www.ncbi.nlm.nih.gov/books/NBK2046/

8. http://evolution.unibas.ch/people/dita/old_res/organis.html

Pathogenicity and Virulence

A Reoccurring Concern

Spanish Flu, Bird Flu, Pig Flu, Ebola(diseases). Every so often it seems as if a new disease is going to be the next pandemic, with the exception of the Spanish flu that proved to be a pandemic. Somehow many of us survive to face the next one. Conspiracy theorists say the government is behind it. Though there is possibility that they are right, the correct answer lies within a deeper understanding of how pathogens function. The pathogen’s ability to infect and the magnitude of the infection play a significant role in its success. When a pathogen finds the perfect balance, it will be very successful.

http://www.invmed.info/historyofinfluenza/images/img_spanish_map.jpg [5] 

The Difference 

A pathogen is defined as a microorganism that causes disease. The pathogen has two important characteristics. The first is pathogenic character, which is defined as the pathogen’s ability to cause disease in its host. The second characteristic is virulence, which is defined as the magnitude at which the disease occurs. Pathogenicity is a quality that is either on or off. The virulence factor measures the level of pathogenicity. There are multiple virulence factors, such as attachment, destructive enzymes and toxins. Virulence factors allow for the pathogen to be more successful within a limit. To explain, if a pathogen has zero virulence then it is no longer actually a pathogen by definition because it is not causing disease. On the other hand, if the virulence factors are too high then the pathogen will be so efficient at killing its host that it may deplete its reservoir, the host it infects, and no longer reproduce.

Chestnuts No More

Chestnut trees(host) were one of the most utilized trees in America. It was used for the durability of its bark and the tastiness of its chestnuts. However, this only lasted up until the 1900.This is when the Chestnut blight took place. A fungus, Cryphonectria parasitica that originated in China and only infected dying twigs and pieces of bark, was introduced to America around 1893. In the fungus' native region there existed a different kind of chestnut tree which was resistant to the fungus. Once introduced t the American chestnut tree it only took 40 years to wipe out all the chestnut trees in America. Cryphonectria parasitica spread up to 50 miles of chestnut forestry a year. Once the chestnut trees were decimated the fungus' reproduction rate plummeted, without a host to provide the nutrients and a habitat it's reproduction was halted. ^[2]

http://www.youtube.com/watch?v=oVrGgW-bBz4 [3]