Wednesday, February 29, 2012

Trypanosoma cruzi: The Kiss of Death







[1]



Introduction:
Trypanosoma cruzi is a flagellar protozoan [2], which causes Chagas disease in humans. Humans are infected with T. cruzi when they come in physical contact with the carrier of the disease, the reduviid bug. Chagas disease is also known as American Trypanosomiasis and it infects about 16-18 million humans. Chagas disease causes the highest disease burden in Latin America [1].


Symbiont Description:
T. cruzi is from the phylum Sarcomastigophora; the class Zoomastigophora; the genus Trypansoma; and Species cruzi [3]. These flagellar organisms only have one nucleus and organelle. These asexual organisms reproduce by binary fission. T. cruzi lives one stage of their lives in the blood or tissues of vertebrate hosts and another stage in the intestines of their invertebrate vector [2]. T. cruzi are blood-dwelling protozoa, therefore they are considered trypanosomes. The trypomastigote form is an elongated cell (about 20 ┬Ám long) with flagella on the outer part of the membrane [1].


Host Description:
As stated above, T. cruzi chooses an invertebrate as its vector and a vertebrate for its definitive host. The reduviid bug, Panstrongylus megistus, also known as the kissing bug, is the main vector for T. cruzi to choose. Other insect types are used as its vectors, but 80% of Chagas disease cases are from the kissing bug. Other than these hosts, T. cruzi uses many different types of animals for reservoirs such as marsupials, rodents, primates, and several types of mammals  [1].

[1]



Life Cycle:
When the kissing bug feasts on human’s blood, infected metacyclic trypomastigotes are left on the human’s skin through the feces of the insect. When the human scratches around the puncture site from the insect, the human is exposed to the trypomastigotes from the feces. When human cells are invaded, the trypomastigotes become amastigotes then they are released into the blood. Here, they develop back into trypomastigotes where the insect vector obtains them through the human skin in a blood meal. In the insect’s intestines, T. cruzi undergoes binary fission and migrates towards the rectum. This is so the parasite can be released through the insect’s feces onto the skin of the next human during the insect’s blood meal [4].


[4]

Ecology:
            Chagas disease is endemic in Mexico, Central, and South America. Thriving in poor housing conditions, the vector of T. cruzi, the kissing bug, will pose a higher threat of infecting humans in those conditions. Therefore humans with poor living conditions in endemic countries have a greater risk of becoming infected with the T. cruzi parasite [4]. Symptoms of having Chagas disease range in three different stages: acute, indeterminate, and chronic stages. Rashes, fatigue, fever are just a few of the possible symptoms seen in the acute stage. The indeterminate stage is asymptomatic, occurs about 10 week after infection, and may last for several years. The chronic stage occurs 10-40 years post-infection and its symptoms include heart and intestinal problems that very likely lead to death [1].




[1]



An example of:
           T. cruzi is an example of the direct correlation between social status and parasitic infestations. The lower the social status of a person, the more exposure there is to these parasites due to poor hygiene, nutrient sources, and housing or living conditions. The vector of T. cruzi, the kissing bug, is found in the walls and roofs of poorer built houses such as ones with mud walls or thatched roofs. Where these housing conditions are present, the vector of the parasite can survive, therefore allowing the parasite to continue to thrive. Eradication of these types of houses in poorer countries would lower the number of thriving kissing bugs and overall lowering the number of parasitic infestations of T. Cruzi [5].



Sources
[1] Schneider, Jeremy, and Claire Nordeen. "Trypanosoma cruzi." Parasites & Pestilence: Infectious Public Health Challenges. Stanford University, 2007. Web. 28 Feb 2012. <http://www.stanford.edu/class/humbio103/ParaSites2006/T_cruzi/index.htm>.

[2] "Trypanosoma cruzi." The Kiss of Death: Chagas' Disease in the Americas. University of Texas at Arlington, 2012. Web. 28 Feb 2012.<http://www.uta.edu/chagas/html/biolTcru.html>

[3]"Taxonomic Classification." Explore and Learn: Parasites. Brian E. Keas, 1999. Web. 28 Feb 2012. < https://www.msu.edu/course/zol/316/tcrutax.htm>

[4] "Parasites-American Trypanosomiasis." Centers for Disease Control and Prevention. USA.gov, 02 Nov 2010. Web. 28 Feb 2012. <http://www.cdc.gov/parasites/chagas/biology.html>.

 [5] Combes, Claude. Parasitism: The Ecology and Evolution of Intimate Interactions. Chicago: The Univeristy of Chicago Press, 2001. 290. Print.

Tuesday, February 28, 2012

S. japonicum


Schistosoma japonicum, the Blood Fluke



Introduction: S. jasponicum is mostly found in the Far East [1]. It is also found in various parts of Southeast Asia and the Western Pacific countries. They are consisted digenic trematodes due to that fact that they have two host involved in their life cycle [2]. They can infect human with a disease called Katayama Fever. This is a disease that has lots of side effects but is something that is treatable.

Symbiont Description: S. japonicum cercaria look like flatworms with fishtails. They are approximately 200 by 70 micrometers. It grows to be about 15mm in length. Males are consisted shorter compared to the females. They consist of strong suckers around the mouth to attach to the host easily. S. japonicum also have sensory organs that help in resisting and avoiding the vertebrate immune system. [3]

Host Description: There are two hosts that are needed in the life cycle of S. japonicum. It consists of intermediate host, which is an aquatic snail. The snail that they use is Onchomelania hupensis. The definitive hosts are humans. It could also be any vertebrate that is wild, such as cattle, dogs, pigs, rodents. [2]


Life Cycle: Eggs are released in feces. The eggs are hatched and release miracidia under correct conditions. The miracidias swim and penetrate through snail intermediate hosts. S. japonicum produces two generations of sporocysts and produce cercariea in the snail. The cerariaes are released from the snail, which they are free swimming in the water. Humans come into contact and cerariae goes through the human skin. They are found in the superior mesenteric veins that are draining to the small intestine. Eggs move towards the lumen of the intestine, which eventually leads to leaving the human body through the feces. [1]

Ecology: A number of disease have infected host because of the large number of eggs that are produced inside of the vertebrate. S. japonicum can lead to Katayama fever, which is an acute schistosomiasis. This disease causes fever, cough, abdominal pain, diarrhea, hepatosplenomegaly, and eosinophilia. Cerebral granulomatous disease may be caused by ectopic S. japonicum eggs in the brain. There are treatments to help with the diseases that are transferred from S. japonicum. [1]

Example of Water-Born Transmission: It can be seen that the transmission of the S. japonicum is through the water. To move from one host to the next, the parasite swims through the water and infects each host.

Reference:
[1] "Schistosomiasis." DPDX. CDC, 23 Feb. 2010. Web. 27 Feb. 2012. <http://dpd.cdc.gov/dpdx/html/Schistosomiasis.htm>.

[2] "Schistosoma Japonicum." Schistosoma Japonicum, Blood Fluke: Taxonomy, Facts, Life Cycle at MetaPathogen. 22 Apr. 2011. Web. 27 Feb. 2012. <http://www.metapathogen.com/schistosoma/schistosoma-japonicum.html>.

 [3] Green, S. 2001. "Schistosoma japonicum" (On-line), Animal Diversity Web. Accessed February 27, 2012 at http://animaldiversity.ummz.umich.edu/site/accounts/information/Schistosoma_japonicum.html

Monday, February 27, 2012

Immigrants from Afar: Clonorchis sinensis


Introduction:
Which trematode may cause serious disease, with loads of over 25,000 parasites per patient? If you answered the Clonorchis sinensis, you are correct! Clonorchis sinensis, also known as the Chinese liver fluke, lives in the liver of humans and is commonly found in the bile ducts and gall bladder [1]. The geographic distribution of this parasite is in endemic areas in Asia including China, Japan, Korea, Taiwan, and Vietnam [1]. It is found mainly in Asian immigrants, or following ingestion of imported, undercooked, or pickled freshwater fish. C. sinensis has also been reported in non-endemic areas including the United States.

Figure 1. Clonorchis sinensis: Chinese liver fluke
http://www.suite101.com/view_image.cfm/2299692

Do Hyun Park, M. D., Ph. D. and Hyun-Young Son, M. D. from the New England Journal of Medicine presented a clinical case dealing with the disease associated with C. sinensis. Briefly, an elderly man reported fatigue, fever, and abdominal pain for a week along with the consumption of raw pond smelt [2]. A duodenoscopy was performed and after the cannulation of the common bile duct, numerous leaf-shaped worms popped out (see video below)—subsequently identified as C. sinensis [2]. The worm burden and the duration of infection tend to reflect the clinical manifestations of the disease clonorchiasis [2]. 
 
 
Video 1. Cannulation of the common bile duct displaying numerous trematode parasite C. sinensis being popped out of a patient with the disease clonorchiasis.
http://www.nejm.org/doi/full/10.1056/NEJMicm054461#t=article

Symbiont Description:
Clonorchis sinensis is a trematode in the phylum Platyhelminthes [3]. Because this parasite exhibits a three-host sequence, part of its life cycle takes place in aquatic habitats while the other part takes place in terrestrial habitats. The physical appearance of C. sinensis includes many forms: egg, miracidium, sporocyst, redia, cercaria, metacercaria, and adult [3]. C. sinensis is classified as hermaphroditic; as a result, every single sexually mature form will produce eggs [3]. Interestingly, each adult yields a daily production of 4000 eggs for at least six months [3]! C. sinensis is currently infecting an estimated 30,000,000 humans and is believed to be the third most prevalent trematode parasite in the world [3].
 
Host Description:
C. sinensis includes three species of hosts: the mollusk, the fish, and the mammal. Eggs are evacuated with feces and ingested by a freshwater gastropod mollusk. A dozen species have been reported as vectors, but the most frequent one is Parafossarulus manchouricus [4]. Numerous swimming larvae, also known as cercariae, are produced by asexual multiplication and then leave the mollusk [4]. The cercariae penetrate a variety of fish species—almost a hundred—where they then encyst in the muscle as metacercariae [4]. Once the metacercariae are eaten by the fish, they excyst in the mammal’s stomach and mature in the bile ducts of the liver [4].

Life Cycle:
DPDx—a website developed and maintained by CDC’s Division of Parasitic Disease and Malaria—provided an outstanding photo depicting the life cycle of C. sinensis. First, embryonated eggs are discharged in the biliary ducts of humans [1]. Second, eggs are ingested by a suitable snail intermediate host [1]. Each egg releases a miracidia, which go through four developmental stages: miracidia, sporocysts, rediae, cercariae [1]. The cercariae are then released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metaceriae [1]. After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract via the ampulla of Vater [1]. The cycle repeats over and over again from this point on.



Figure 2. The three-host sequence life cycle of C. sinensis.
http://dpd.cdc.gov/dpdx/html/Clonorchiasis.htm
 
Ecology:
C. sinensis has had large detrimental effects on humans, specifically those in areas such as Asia, where eating raw or undercooked fish is a part of their cultural upbringing. A human host with an average of infection will have or three dozen worms, and heavily infected individuals have been found with as many as 20,000 worms [3]. These parasites reside in the biliary system of the liver and occasionally in the pancreas. Although the liver or pancreas is not attacked, they are greatly damaged due to the parasites’ migration through the biliary system [3]. Damages include erosion of the epithelial lining of bile ducts, which leads to the development of blockage in the ducts due to the thickening of scar tissue [3]. This erosion, along with the effects of C. sinensis’ perforation into the parenchyma of the liver leads to possible disturbance of normal hepatic functions [3].
 
An Example of the Three-Host Sequence:
Several unrelated species of hosts may be successively exploited as the parasite develops over its life cycle. The sequence of hosts consists of the series of hosts utilized during the life cycle and is often referred to as the longitudinal component of the cycle [4]. This sequence involves two dimensions: ecological (the succession of environments) and ontogenetic (the various developmental states of the parasites) [4]. The parasite undergoes a metamorphosis at each change of host because each time that the parasite changes host, some genes are turned off while others are activated, resulting in a morphologically, anatomically, physiologically, and ethologically distinct organism [4]. Adults of C. sinensis demonstrate an example of the three-host sequence: the mollusk, the fish, and the mammal.

References:
[1] Laboratory Identification of Parasites of Public Health Concern. “Clonorchiasis.” Centers for Disease Control and Prevention. Online. Accessed 24 Feb. 2012. <http://dpd.cdc.gov/dpdx/html/Clonorchiasis.htm>.

 [2] Park, D. H. and H. Y. Son. “Images in Clinical Medicine: Clonorchis sinensis.” The New England Journal of Medicine. (2008); 358: e18.

[3] Eckroad, E. and H. Lee. 2001. "Clonorchis sinensis." Animal Diversity Web. Online. Accessed 24 Feb. 2012. <http://animaldiversity.ummz.umich.edu/site/accounts/information/Clonorchis_sinensis.html>.

[4] Combes C. 2001. Parasitism: The Ecology and Evolution of Intimate Interactions. Chicago: University of Chicago Press. 36-38 p.