The Metamorphosis of Giardia lamblia

By AK

Evolution is often cited as the core of biology but it has also been exhausted in various media outlets from television to newspapers and books. One very popular children’s television program, Pokémon, shows many of the organisms known as Pokémon “evolving” into different forms which acquire a wide array of new abilities that make them more successful than their previous forms. Understandably, much of the actual scientific meaning of evolution is lost in the show, but the concept of turning into a new form with new abilities often holds true in science. In this sense, the way the Pokémon “evolve” into another form is actually a metamorphosis rather than evolution as is known in the scientific context. One prime example, Giardia lamblia, also known as Giardia intestinallis or Giardia duodenalis, is a protozoan whose human infection life cycle revolves around the metamorphosis from the cyst form into the trophozoite form (Figure 1).

G. lamblia was first discovered in the seventeenth century and became relevant in the United States and Europe in the 1960s and 1970s (2). Transmission often occurs by ingesting food or water contaminated with G. lamblia cysts but can also spread directly through the fecal-oral pathway which is characteristic of poor hygiene practices (2). One very unique feature of giardiasis, or the infection with G. lamblia, is that the infectious G. lamblia trophozoites are confined strictly to the lumen of the small intestine which does not spread to the blood stream like many other protozoan infections (1). Due to the specific localization of this infection to the small intestine, the major symptoms associated with giardiasis include severe, watery diarrhea and stomach cramps. It is now cited as the leading cause for waterborne diarrhea in the United States (2). Approximately 5,000 people are hospitalized annually in the US and millions of cases are reported world-wide (2). One of the most effective medications against giardiasis is metronidazole, which is a nitroimidaozole antibiotic medication (2). One of the key elements of this drug and how it avoids harming human cells, is that it attacks the anaerobic pathways in G. lamblia which are essential for the protozoan’s survival. In giardiasis, this drug ultimately damages the DNA of the infectious trophozoite stage of infection and kills the protozoan before it completes its life cycle and damages the host.

Figure 1: G.lamblia life cycle.

The life cycle of G. lamblia can be split into two distinct phases; the dormant, cyst phase and the infectious, trophozoite phase. The cysts of G. lamblia have been shown to be extremely resilient to a wide variety of environmental conditions and also have a metabolic rate of just ten to twenty percent of the trophozoite form allowing them to survive for extended periods outside of their hosts. This begs the question as to how the cyst form of G. lamblia “evolves” into the trophozoite form so quickly in the human host intestine. The first step in human infection is ingesting the resilient cysts (only 10 required for infection) through contaminated water or food as stated above (2). Thereafter, the cysts have to travel through the digestive tract, avoiding degradation till they reach the small intestine. There have been several studies regarding the metamorphosis phenomenon which have found that the shift in pH from the acidic stomach to the slightly alkaline pH of the small intestine serves as a signal to alter the morphology and gene expression of the cyst which results in the formation of trophozoites (4). Hetsko et. al. found that it was likely that there was pre-made mRNA ready to be  translated when the cysts were exposed to the varying physiological pH transitions, which may encode for a variety of surface proteins such as adhesive molecules for localization in the small intestine (4). This “evolution” of the cyst form of G. lamblia to the trophozoite is termed excystation or encystation depending on the stage of infection (Figure 1).

After “evolving” into the infectious trophozoite form due to the various pH signals in the digestive tract, they start causing symptoms in individuals by localizing to the duodenum and the upper intestine (2). Symptoms such as watery diarrhea, excessive flatulence, greasy stools, stomach cramps, and bloating are some of the most common symptoms associated with giardiasis (1). However, it should be noted that giardiasis can be asymptomatic in people with strong immune systems and usually causes very severe symptoms only in immunocompromised individuals. It is hypothesized that the colonization of G. lamblia in the small intestine results in disease due to a variety of mechanisms such as: by the direct damage of the human intestinal mucosa, through the release of cytopathic substances from the trophozoites, and/or that an immune response that results in the  inflammation of the mucosa cells (2)(3). Finally the trophozoites’ extended stay in an alkaline pH in the small intestine also serves as a signal for the encystation process which triggers metamorphosis back into the dormant cyst form which are excreted through the large intestine and ultimately in the feces circling back to the first stage of the G. lamblia life cycle (2)(4).

Just as Pokémon “evolve” into different forms with different characteristics, Giardia lamblia metamorphoses from its dormant, cyst form to an infectious, trophozoite form by sensing sudden physiological pH changes seen in the digestive tract. This metamorphosis event is vital for the protozoa to cause disease in humans and ultimately complete its life cycle. Further understanding of this mechanism of metamorphosis can be vital in furthering treatment and prevention of this disease.

References

1)     Gardner, T., & Hill, D. (2001). Treatment of Giardiasis. Clinical Microbiology Review. 14 (1): 114-128.

2)     Adam, R. (2001). Biology of Giardia lamblia. Clinical Microbiology Review. 14 (3): 447-475.

3)     Faubert,G.(2000). Immune Response to Giardia duodenalis. Clinical Microbiology Review. 13 (1): 35-54.

4)     Hetsko, M., McCaffery, J., Svard, S., Meng, T., Que, X., and Gillian, F. (1998). Cellular and Transcriptional Changes During Excystation of Guard lamblia in vitro. 88 (3): 172-183.

Florida red tides (Karenia brevis): causes, effects and prevention techniques

By JK

Suppose you are on a summer vacation to Florida when you decide to visit the beautiful blue waters of the Atlantic Ocean. Upon your arrival you are alarmed to find the water is not blue at all but instead its bright red! For someone who has never witnessed a Florida red tide this phenomenon would undoubtedly cause some concerns and for good reason. Florida red tides are also known as a harmful algal blooms (HABs) and they are formed when concentrations of the phytoplankton, Karenia brevis, increase drastically (1). When these events occur, the ocean not only turns red but it becomes an extremely toxic environment for circumambient organisms such as dolphins, fish and humans. This blog post attempts to integrate some of the major studies on Florida red tides and their impacts on aquatic organisms as well as terrestrial animals such as humans.

Florida red tides occur primarily along the west coast of Florida and the Gulf of Mexico but have also been reported along the East coast of North Carolina (2). They are termed “harmful” algal blooms because K. brevis produces a suite of neurotoxins known as a brevetoxins (PbTx), which cause acute central nervous system damage in humans and other mammals (2). Some negative effects of HAB events include gross marine organism mortality rates, human neurotoxic shellfish poisoning and economical disruption of the fishing industry (2). There have been numerous studies of bottlenose dolphin mortality events coinciding with HABs. Fish communities were also studied during HAB events and the species richness and density were both found to be negatively affected by the events (3). A human impact of Florida red tides is the possibility of consuming shellfish highly concentrated with PbTx, causing neurotoxic shellfish poisoning. Although, the correlation between K. brevis blooms and brevetoxin poisoning may seem clear, only a small number of studies have been performed that actually test marine animals and their communities for this toxin after their death to determine if PbTx was indeed present.

K. brevis is a photoautotrophic dinoflagellate that occupies a planktonic and oceanic niche with optimal growth occurring in temperate to tropical waters (3). This microbe has two flagella, one wrapping around the cell and the other aiding in locomotion (1). The cells are pinkish/red in pigment, which is visible to the naked eye when their concentrations are high enough (1). They are ubiquitously found in low concentrations in the coastal waters of the Gulf of Mexico and Western Florida but concentrations drastically increase during HABs. This is when marine and terrestrial organisms are most threatened by the PbTxs (2). There are two types of brevetoxins, PbTx1 and PbTx2, each contributing a suite of derived compounds that form during HAB events and they differ in the number of carbon rings that each contains (2). These compounds contain a polycyclic ether ladder that binds to sodium pumps located on neurons, ultimately altering their function and inducing cell death (2). Brevetoxins are heat-stable as well as lipid soluble allowing for them to persist in high saline concentrations such as those of oceans. These factors are what make PbTxs so dangerous to the ecosystem and the surrounding life forms.

The frequency of HABs has notably increased over the last few decades and numerous fish kill events have been recorded in areas and times coinciding with these events (3). Occurrences of HABs are relatively sporadic but they are though to be primarily human induced (3). This is due to extra nutrition being added to the oceans that the phytoplankton can utilize and thrive on (3). Geographical location also is found to play a role in HAB occurrence (3). A study was conducted in order to determine if Florida red tide events were in fact affecting the surrounding fish communities, species diversity and population densities (4). They chose a system termed; catch per unit effort (CPUE), where they used a single large net and attempt to catch as many fishes as possible within designated areas during HABs and non-HABs. It was found that fish species richness and fish populations both decreased with the occurrence of HABs but replenished when there was no such event. This indicated that K. brevis blooms affect fish communities, their population densities and species richness in the surrounding coastal waters (4).

Numerous mortality events coinciding with HABs have been reported in bottlenose dolphins where hundreds of carcasses washed up onto the shores of Western Florida and the Gulf of Mexico (1). Samples were obtained from some of the dolphins found and high concentrations of brevetoxins were discovered (1). Some were also taken from dolphin prey species including different types of fish, which also contained high concentrations of brevetoxins (1). This suggested that the dolphins were getting sick from eating poisoned fish (1). In 1999/2000 152 bottlenose dolphins died followed a major HAB event and PbTxs were found in 52% of the samples tested. In 2004 105 bottlenose dolphins died without an apparent HAB event but all of the samples tested positive for brevetoxins in very high concentrations. It was concluded that there must have been a HAB effecting the bottlenose dolphin population that was not detectable with the current tools used to sense increases in K. brevis concentrations (1). Lastly, in 2005/2006 90 bottlenose dolphins died and 93% were positive for brevetoxins. These records indicate that HABs of K. brevis are responsible for the bottlenose dolphin mortality events that occurred along the west coast of Florida and the Gulf of Mexico from 1999 to 2006.

Filter feeders occupying a benthic niche, including mussels, clams and oysters are prone to high accumulations of PbTx (3). This is because they continuously feed on these toxic algae, which often settle in the benthic zone when dead (3). Neurotoxic shellfish poisoning in humans occurs through consumption of these contaminated shellfish (3). This directly leads to disruptions of the fishing industry and economy by contaminating their catches and limiting productivity (3). Brevetoxins excreted from K. brevis can also become aerosolized through regular oceanic currents and this can cause harm to humans and other mammals (3). Inhalation of PbTx is noted to cause burning of the nose and eyes, a choking cough and asthma attacks (3). Despite the clear negative effects that brevetoxins have on humans there has never been a reported death caused by brevetoxins (3).

Current preventative measures being taken to minimize casualties and other losses during Florida red tide events include satellite-imaging detection, which utilizes different mathematical algorithms to detect blooms (4). There are also multiple types of sensors that are used to sense color changes in the ocean and increases in K. brevis concentrations (4). It is well known that Florida red tides are harmful events, so it is comforting to know combative measures are being taken to prevent mass mortality events of aquatic organisms along with human and bird brevetoxin poisoning.

Literature Cited

1. Twiner, M. J., Flewelling, L. J., Fire, S. E., Bowen-Stevens, S. R., Gaydos, J. K., Johnson, C. K., … Rowles, T. K. (2012). Comparative analysis of three brevetoxin-associated bottlenose dolphin (Tursiops truncatus) mortality events in the Florida Panhandle region (USA). PloS One, 7(8), e42974. doi:10.1371/journal.pone.0042974

2. Pierce, R. H., & Henry, M. S. (2008). Harmful algal toxins of the Florida red tide (Karenia brevis): natural chemical stressors in South Florida coastal ecosystems. Ecotoxicology, 17(7), 623–631. doi:10.1007/s10646-008-0241-x.Harmful

3. Shen, L., Xu, H., & Guo, X. (2012). Satellite remote sensing of harmful algal blooms (HABs) and a potential synthesized framework. Sensors (Basel, Switzerland), 12(6), 7778–803. doi:10.3390/s120607778

4. Gannon, D., Berens McCabe, E., Camilleri, S., Gannon, J., Brueggen, M., Barleycorn, A., … Wells, R. (2009). Effects of Karenia brevis harmful algal blooms on nearshore fish communities in southwest Florida. Marine Ecology Progress Series, 378, 171–186. doi:10.3354/meps07853

5. Shen, L., Xu, H.,& Guo, X. (2012). Satellite remote sensing of harmful algal blooms (HABs) and a potential synthesized framework. Sensors (Basel, Switzerland), 12(6), 7778–803. doi:10.3390/s120607778

Collapsing Colonies and Crithidia bombi

By Matthew Lowe

Over the past decade there has been a growing concern over the phenomenon known as Colony Collapse Disorder (CCD) among commercially raised and wild bees. CCD was initially characterized in 2006 by David Hackenberg, a prolific apiarist with multiple hives in Florida and Pennsylvania¹. Upon investigation of lagging production, it was discovered that despite there being no adult worker bees in 20-30% of his hives the queens and brood appeared healthy¹. The loss of worker bees and production from the hive while still maintaining a seemingly healthy brood and queen has now become the definitive end result of CCD.

C. bombi

Since 2006, there have been numerous investigations into potential causes but so far no single cause has been definitively linked to CCD. Some of the more extreme claims include cell phone radiation and commercial use of insecticides, however there is no strong evidence to support that either is the cause of CCD¹.  Of the potential rational causes for CCD, the most likely is an increased prevalence of parasites and viruses within the bee population¹. Crithidia bombi, a recently implicated parasite, is one of the more interesting because of its ability to infect a large variety of different bee species, including those found within the pyrobombus, thoracobombus and bombus sensu stricto subgenera².  Of the North American species infected, Occidentalis and Pensylvanicus are currently undergoing massive population decline due to CCD². C. bombi infection is also 6 fold higher in CCD colonies as opposed to hives not experiencing CCD³.

Figure 1 from here

C. bombi is a pathogenic unicellular eukaryote with two distinct life phases; the flagellated choanomastigote and the anchored amastigote cells⁴. The amastigote cells upon ingestion will extend their flagella and swim as a choanomastigote until they can attach to the bee’s intestinal wall and once again become an amastigote⁴. Upon attachment the cell can siphon off nutrients that pass by and will divide into new amastigote cells⁴. Some of these cells will be excreted in feces and can be transmitted from bee to bee through the ingestion of infectious cells to begin the cycle anew^{2, 4, 5}. The amastigote cells can either be ingested within the hive, leading to a high level of infection amongst the workers and queen, or at flowers allowing for the parasitic colonization of new hives⁵. Once within a hive, infection spreads rapidly until about 80% of the colony is infected⁶. Due to C. bombi having a genotype-genotype model of infection, in which the unique genetic profile of the host and the parasite both play a role in infection success, the highly related individuals within a hive are much more frequently infected⁷. However, once a cross hive infection is established it will rapidly spread within the new colony⁷. While infection has not been linked to any significant lethality in otherwise healthy bees, an infected bee experiencing starvation has a 50% increase in mortality⁵. Upon infection the bee will have a harder time distinguishing between the flowers that are the most rewarding based on color, as shown in figure 1⁸. This suboptimal foraging will lead to less food collection for the hive as a whole and a potential minor starvation event that would cause increased mortality in the infected bees⁸. If a queen is infected she will have reduced ovarian capacity leading to a decreased worker population⁶. An infected queen also experiences a decrease in the ability to store energy as fat for the hibernation over winter greatly decreasing her chances of survival⁶. If the queen manages to survive the winter, she will produce fewer offspring that will also become infected⁶. This generational transmission pattern is particularly vexing for apiarists because an infected queen not show symptoms until the following year when she establishes a colony.  During the time between infection and diagnosis, C. bombi is also being spread to nearby flowers and potentially other hives which could account for the high infection rate in commercial colonies every year.

Figure 2 from here

This continual transmission and difficulty of removing C. bombi begs the question, why should we care if all of the bees die? The economic impact of the insect pollination industry is valued at over 150 billion euros⁹. As shown in figure 2, this is roughly equivalent to 10% the total value of global agricultural production⁹. The use of bees makes up over 70% of the insect pollination industry and the value of crops that are been pollinated is roughly 5 times higher than those that are not⁹. This is not even considering that the apiary industry as a whole, including all of the production facilities to manufacture bee related goods, employs millions of workers worldwide. A shrinking of the bee population will also lead to an increase in the cost of pollination services which will get passed on to the consumer as a wide variety of fruits, nuts and vegetables increase in price to compensate.

While the apiary industry is one of the main driving forces for CCD research, the disorder is not limited to just commercial hives. Commercial bees are commonly raised in greenhouses with a crop to pollinate and it has been shown that a few bees escape and carry infection into the wild¹⁰. The close confines of the greenhouse and the fact that the bees are likely more related due to being commercially raised, infection spreads rapidly between hives leading to a higher parasite load than in wild bees^{7, 10}. Any bee that escapes can spread infectious cells out of the greenhouse and to wild bees through the shared use of nearby flowers. Due to C. bombi’s ability to infect a wide range of bee species, this could lead to collapse of wild bee colonies throughout many different regions of the world. Even more worrisome, commercial colonies are commonly transferred across the globe for pollination purposes as well as to start up new colonies¹. Therefore any infection from a single colony has the potential to spread globally and infect numerous native colonies. While it has been shown that a single bee proof mesh placed over the air duct will greatly diminish the chances of escape, Commercial bee keeping still exists as a potential method of transferring infectious agents to native bee populations across the globe¹⁰. If the native population of bees were to die, thousands of native plant species would lose a prime pollinator which could lead to an inability to efficiently reproduce devastating animal populations that rely on them for food.

Though it is likely that there is no single cause to CCD, the research into it has turned up several interesting parasitic species that all are likely to play a role in colony collapse. Crithidia bombi is but one of the more interesting due to its ability to infect a wide range of bees beyond the commercial species and infection has been correlated with CCD^{2, 3}. This in no way means that C. bombi is the sole cause of CCD but that it likely contributes to the decline of affected hives. Further research into the topic is definitely needed to determine other contributory factors that when combined will lead to CCD. Until a large scale prevention method is identified there are a few things that an individual can do to help maintain local bee populations. Becoming an apiarist and setting up a hive or two in your backyard can help provide a home for local varieties of bees and provide a strong pollination source for nearby gardens¹¹. Planting a variety of species in gardens can also lead to more diverse food sources and increase a colony’s overall health¹¹. By supporting further research into CCD and following through on few basic prevention methods we can hopefully save the bee population as a whole!

1.     Watanabe M. 2008. The Xerces Society » Colony Collapse Disorder: Many Suspects, No Smoking Gun. http://www.xerces.org/2008/05/01/colony-collapse-disorder-many-suspects-no-smoking-gun/

2.     Cordes N, et al. 2012. Interspecific Geographic Distribution and Variation of the Pathogens Nosema bombi and Crithidia Species in United States Bumble Bee Populations

3.     Cornman RS, Tarpy DR, Chen Y, Jeffreys L, Lopez D, et al. (2012) Pathogen Webs in Collapsing Honey Bee Colonies. PLoS ONE 7(8): e43562. doi:10.1371/journal.pone.0043562

4.     Olsen OW. 1974. Animal Parasites: Their Life Cycles and Ecology. Courier Dover Publications.

5.     Deshwai S, Mallon EB. 2014. Antimicrobial Peptides Play a Functional Role in Bumblebee Anti-trypanosome Defense. BioRxiv

6.     Erler S, Popp M, Wolf S, Lattorff HMG. 2012. Sex, horizontal transmission, and multiple hosts prevent local adaptation of Crithidia bombi, a parasite of bumblebees (Bombus spp.). Ecol Evol 2:930–940.

7.     Riddell Carolyn, et al. 2014. Insect Immune Specificity in a Host-parasite model. BioRxiv

8.     Gegear RJ, Otterstatter MC, Thomson JD. 2006. Bumble-bee foragers infected by a gut parasite have an impaired ability to utilize floral information. Proc Biol Sci 273:1073–1078.

9.     Savrieno A. 2012. Colony Collapse Disorder As Part Of An Acquisition Strategy. Seeking Alpha. http://seekingalpha.com/article/590411-colony-collapse-disorder-as-part-of-an-acquisition-strategy

10.  Otterstatter MC, Thomson JD. 2008. Does Pathogen Spillover from Commercially Reared Bumble Bees Threaten Wild Pollinators? PLoS ONE 3:e2771.

11.  What you can do about Colony Collapse Disorder - Honeybees - Silence of the Bees | Nature | PBS. http://www.pbs.org/wnet/nature/episodes/silence-of-the-bees/how-can-you-help-the-bees/36/

Trypanosoma cruzi

By Noora Hussain

The human body has an army at the ready to attack and protect itself from invaders. This army is called the immune system. It is equipped with weapons that span the physical body, are effective against many different types of attacks, and are organized in such a way that allows for strategic interactions which amplifies the body’s defenses. When a parasite wages war on the body, the body’s army goes into battle with full force. Winning results in successful elimination of the parasite from the body, but may leave the immune system weakened. Losing the battle can result in disease. Parasites have their own arsenal of weapons, which allows them to defeat the immune system. Parasites have mechanisms that shield them from host’s defenses and have ways to attack specific target cells. One such parasite that wields its own sword and shield is Trypanosoma cruzi. This motile protozoan pathogen is the causative agent of Chagas disease.¹ Chagas disease affects the cardiac and digestive systems of the body and can cause acute or chronic infections².  The parasite T. cruzi uses offensive mechanisms to counterattack a host cell’s defenses.

Chagas disease affects eight million people in Latin America.² The disease was discovered in 1909 by the Brazilian physician Carlos Chagas, who named the parasite after his mentor Oswaldo Cruz.³ Chagas disease can cause acute or chronic infection that affects many different cells of the body.² Clinical manifestations of acute infections include myocarditis, pericardial effusion, or meningoencephalitis.³ After the initial acute stage subsides, the diseases enters the chronic stage.³ Most patients can survive with the chronic infection, but a small percentage of patients develop cardiomyopathies within a year.³ Infection by T. cruzi occurs in a cycle and involves blood sucking insect vectors belonging to the Reduviidae family. ⁴ From the insect, the parasite comes into contact with a human or a wild animal.² Then, it goes back to the insect when the insect feeds off the infected human.² When the blood sucking insect lands on skin to feed, it also defecates in that spot leaving behind T. cruzi infected feces.⁵ Fecal droplets can get passed inside of humans through mucosa or through breaks in the epithelial barrier.⁵ T. cruzi can also infect through oral transmission with infected foods.⁵ Another much less common transmission mechanism is from blood transfusion.⁵ Congenital transmission from infected mother to child is also possible, but like blood transfusions is not a very common mechanism.⁵

Trypomastigotes are the infectious forms of T. cruzi and they infect the endothelial and mucosal cells of humans and other mammals.⁶ They invade these cells in order to differentiate and replicate inside of the host cell lysosome and cytoplasm.⁶ The invasion mechanism of T. cruzi is unique because it uses the host cell machinery that would generally be used against a protozoan parasite. T. cruzi trypomastigotes are highly motile⁷. A flagellum is attached to the cell body of T. cruzi, which enables the parasite to move on its own.⁸ Active motility of T. cruzi is a mechanism that the parasite uses to penetrate through the host cell membrane.⁹ After it gains entry, the host cell is infected.⁹ Once the host cell is infected, the trypomastigotes undergo cytokinesis, but their nuclei do not divide.⁹ The division occurs towards the back end of the basal body where the flagellum is attached.⁹ Through this process, the unnecessary flagellum is discharged into the host cell cytoplasm where it is then degraded.⁹ 

The surface of T. cruzi provides a shield for the parasitic pathogen. This enables the parasite to travel throughout the body without being defenseless against the host’s immune system. The major surface components of T.cruzi provide the parasite with protection against the host’s cell defenses and enables the parasite to adhere to specific target cells for invasion.⁵ Mucin is a glycoprotein and one of the major surface components that plays a role in infection.¹ Mucin sticks out from the outer phospholipid layer of T. cruzi’s plasma membrane.⁵ They are anchored  to the plasma membrane by glycosylphosphatidylinositol (GPI).¹ These GPI-anchored glycoproteins cover the majority of the T. cruzi’s surface.⁵ Mucins recognize and target endothelial cells for invasion.⁵  They attach themselves onto the lipid bilayer of host cells.¹⁰ A signal is transduced that directs the glycoprotein into the cytoplasm and to the endoplasmic reticulum of the host cell.¹⁰ Once inside the host cell, T. cruzi can also interact with other organelles in the cytoplasm and use them to mediate infection.¹⁰

Host cells have lysosomes to remove unwanted material from inside of their cells. Normally, a lysosome would ingest, destroy, and secrete an invading pathogen. However, upon infection, T. cruzi’s plasma membrane fuses with the host cell lysosome, creating what is called a lysosome derived parasitophorous vacuole.⁶ The formation of the parasitophorous vacuole anchors the parasite to a structure of the host.⁶ The anchored parasite can undergo replication before disseminating into the host’s bloodstream and throughout the body.⁶ T. cruzi interacts with lysosomes of the  host cell because they have a low pH value.⁶  Having a highly acid organelle is a defense weapon of the host, but is used against the host when it facilitates trypomastigotes differentiation, replication, and dissemination.⁶ The parasitophorous vacuole membrane is disrupted and the acidic environment can have its full effect on the trypomastigotes.⁶  Disruption of the membrane is caused by the release of the pore forming molecule TcTox from trypomastigotes.⁶ Release of this molecule is triggered by the lysosome’s acid environment.⁶  Acidity also serves as a trigger to initiate differentiation of trypomastigotes into amastigotes.⁶ Amastigotes replicate, exit the lysosome, and disseminate into the blood stream.³ This spreads infection to other cells of the body.^3-6

            The outcome of a battle between a parasite and the human body is critically important. A human’s immune system is well equipped to defend against many infections. However, parasites have developed mechanisms that provide them with a good offense and can retaliate against the immune system. So, in a battle between the two, the immune system does not always defeat the invader and the parasite can conquer and win.  

References

1. Gonzalez MS, Souza MS, Garcia ES, Nogueira NFS, Mello CB, et al. (2013) Trypanosoma cruzi TcSMUG L-surface Mucins Promote Development and Infectivity in the Triatomine Vector Rhodnius prolixus. PLoS Negl Trop Dis 7(11): e2552. doi:10.1371/journal.pntd.0002552
2. Rassi Jr, A., Rassi, A., & Marin-Neto, J. A. (2010). Chagas disease. The Lancet, 375(9735), 17-23. doi:10.1016/S0140-6736(10)60061-X
3. Pereira Nunes, M. C., Dones, W., Morillo, C. A., Encina, J. J., & Ribeiro, A. L. (2013). Chagas Disease. Journal of the American College of Cardiology, 62(9), 767-776. Retrieved from https://www-clinicalkey-com.ezp2.lib.umn.edu/#!/content/playContent/1-s2.0-S073510971302250X
4. Prata, A. (2001). Clinical and epidemiological aspects of Chagas disease. Lancet Infectious Diseases, 1(2), 91-100. doi:10.1016/S1473-3099(01)00065-2
5. Campo, V. A., Frasch, A. C., Buscaglia, C. A., & Noia, J. M. (2006). Trypanosoma cruzi surface mucins: host-dependent coat diversity. Nature Reviews Microbiology, 4, 229-236. doi:10.1038/nrmicro1351
6. Burleigh, B. A. and Woolsey, A. M. (2002), Cell signalling and Trypanosoma cruzi invasion. Cellular Microbiology, 4: 701–711. doi: 10.1046/j.1462-5822.2002.00226.x
7. Andrade, L. O., & Andrews, N. W. (2005). The Trypanosoma cruzi–host-cell interplay: location, invasion, retention. Nature Reviews Microbiology, 3, 819-823. doi:10.1038/nrmicro1249
8. Sacks, D. (2014). Lost but Not Forgotten. Cell Host & Microbe, 16(4), 423-425. doi:10.1016/j.chom.2014.09.017
9. Kurup, S. P., & Tarleton, R. L. (2014). The Trypanosoma cruzi Flagellum Is Discarded via Asymmetric Cell Division following Invasion and Provides Early Targets for Protective CD8+ T Cells. Cell Host & Microbe, 16(4), 439-449. doi:10.1016/j.chom.2014.09.003
10. Canepa, G. E., Mesias, A. C., Yu, H., Chen, X., & Buscaglia, C. A. (2012). Structural Features Affecting Trafficking, Processing, and Secretion of Trypanosoma cruzi Mucins. The Journal of Biochemistry, 287, 26365-26376. doi: 10.1074/jbc.M112.354696