Déjà-vu is a feeling of having been somewhere before though (to one’s knowledge) they have never.
The prefrontal cortex is responsible for most high-level processes in the brain, and is generally thought to contain such subjective things as, morality, self control, self awareness, and many others. Evolutionarily the purpose of such a highly advanced neuro-network is theorized to be event prediction. For example, in order to accurately spear an animal well it is running, one must predict where it will be in relation to how long it will take for the spear to travel from ones self to the animal. If we did not process that the animal is moving at such a speed, and compensated for it, our ancestors would most likely have died quite a long time ago. As anyone who has played sports can tell you, hand eye coordination becomes subconscious at times, and the player is able to catch a ball or throw without any conscious processing.
I believe déjà-vu to be a link between our subconscious continual predictions on every day circumstances, and our conscious experience of these things. Though we cannot tap into our subconscious mind, it is not a far leap to conclude its role in attempting to predict future circumstances so as to protect ourselves from lack of water, food, or social persecution. Thus our unconscious must also attempt to predict our environments through which we must acquire our necessities.
Though I am presenting a lack of scientific evidence, and knowledge of research put into such a phenomena, I feel it is a simple explanation for something that is often misconstrued as proof of the paranormal or metaphysical realms.
Monday, August 2, 2010
Thursday, July 29, 2010
An Exploration of Toxoplasmosis
Toxoplasmosis is a widely prevalent parasitic infection, that if the symptoms are not treated, can lead to abortions (miscarriage), mental retardation, encephalitis, blindness, and death (Klaren, 2002). Recently there has been a positive correlation of toxoplasmosis infection and schizophrenia (Torrey, 2003). The parasite that causes toxoplasmosis is named as toxoplasma gondii. In order for toxoplansma gondii to reproduce, it must be in the definitive host, which is a feline (Dubey, 2005). Though it must reproduce only in felines, the infection can spread to any form of animal, and these animals can spread the parasite to a fetus; thus making the new born a carrier of the disease/parasite as well (Dubey, 2005). Toxoplasma gondii can also spread through contaminated meat and water (Dubey, 2005). But the truly astounding aspect of toxoplasma gondii, is how it rewires the brains of rats and mice to become attracted to cat pheromones (Sapolsky, 2007). This neurological phenomenon makes toxoplasma gondii’s complicated reproduction process astounding simple.
Toxoplasma gondii is classified as a coccidian. Coccidia are single celled, spore forming parasites, which infect the intestines of their animal host. To get even further into the specific taxonomy of toxoplasma gondii, their order is Eimeriorina (Dubey, 2005). According to J.P. Dubey the life cycle that most every Eimeria follows is, “The host becomes infected by ingesting sporulated oocysts of Eimeria. After excystation, the sporozoites penetrte intestinal epithelial cells and multiply asexually before forming male and female gamonts. Oocysts are produced after fertilization, and are passed in feces in unsporulated stage. Sporulation occurs outside of the host. (Dubey, 2005)” An oocyst, as defined by the Australian HSC is, “A thick walled structure in which sporozoan zygotes develop. It serves to transfer them to new hosts.” Sporulation of the oocyst occurs between 1-21 days after the host excretes the oocysts. It is important to note that the only animal in which toxoplasma gondii can reproduce in members of the Felidae family (i.e. domestic and wild cats). But toxoplasma gondii can spread through other means as well. When an infected animal that is not of the Felidec famly becomes pregnant, they can spread the infection by what is known as congenital infection of the fetus.
Toxoplasma Gondii has three infectious stages: the tachyzoites, the bradyzoites, and the sporozoites (Dubey, 2005).
Tachyzoites acquired their name from the rapid multiplication within any cell of the immediate host, and in the non-intestinal epithelial cells of the definitive host (Dubey, 2005). It is in this stage that the parasite multiplies, and can kill virtually all the host cells of a warm-blooded animal (Dubey, 2005). Also within this stage congenial infection can occur when the tachzoites from maternal blood are carried to fetal tissue (Dubey, 2005). The tachzoites enter a host cell either by “penetraiting through the host call plasmalemma,” or through phagocytosis (phagocytosis is a process in which phagocytes engulf and digest microorganisms and cellular debris; an important defense against infection [wordnetweb.princeton.edu/perl/webwn]) (Dubey, 2005). Once inside the cell, the tachyzoites become surrounded by a parasitophorous vacuole (Dubey, 2005). The next step is asexual reproduction through repeated endodyogeny, which is a “specialized form of reprodiction in which two progeny form within the parent parasite, consuming it,” (Dubey, 2005). Within hosts the toxoplasma gondii cells grow faster or slower, depending on the type of host cells (Dubey, 2005).
Bradyzoites and tissue cysts take only three days post infection to form (Dubey, 2005). The host of the tissue cyst might not realize their existence, because they do not cause inflammation, or any pain to them (Dubey, 2005). The tissue cysts develop within the host cells cytoplasm, and can contain hundreds of bradyzoites within its body. Another important difference to note between bradzoites and tachzoites is that bradyzoites are not as easily destroyed by proteolytic enzymes as tachzoites are.
Oocysts are the outer feline host for the sporont (the unsporilated version of a sporocyst), (Dubey, 2005). Sporulation occurs when the oocyst is outside of the feline host for one to five days, depending on factors like temperature (Dubey, 2005). The oocyst is the transport vessel of toxoplasma gondii from the definitive host, to the intermediate hosts or other animals.
Now that we have established the different stages of toxoplasma gondii, we will examine the definitive host of the parisite. The host must be any form of feline, for toxoplasma gondii to reproduce. Felines can become infected through ingestion of food or water that is contaminated with oocysts, or through parasitemia, which is the spreading the parasite from the mother to the fetus; if she becomes infected during pregnancy (Dubey, 2005). After the parasite sexually reproduction in the felines intestinal tract, it takes a minimum of 18 days for the oocysts to be excreted in their stool (Dubey, 2005). Over a period of only a few days, cats can shed millions of oocysts (Dubey, 2005). Sporulated oocysts can survive in a moderate climate for long periods of time (Dubey, 2005). In moist soil an oocyst can survive for months to years. With the colossal amount of oocysts produced in only a few days, even though only <1% of cats carry toxoplasma gondii, it is extremely easy for the oocysts to infect other animals. It can be spread on animals that have rolled over in infected cat feces, or on fruits and vegetables that are contaminated (Dubey, 2005).
The transfer of toxoplasma gondii to humans does not have a definitive origin, because of the numerous ways that it can be transferred from felines to humans, but the forms in which it is most likely to infect humans is through ingestion or handling of undercooked meat (generally pork) infected with tissue cysts, unfiltered water containing oocysts, and organ transplants (Montoya, 2004). Toxoplasma gondii infection can also be spread congenially, but only when the mother becomes infected during the pregnancy, or a maximum of three months before.
Toxoplasmosis in humans is generally asymptomatic, depending on the immune system of the infected person (Montoya, 2004). In a person with a normal immune system, the symptoms may be as small as swollen lymph nodes for a few weeks (Montoya, 2004). In Immunocompromised patients, toxoplasmosis can be life threatening, as the symptoms include “CNS lymphoma, progressive multifocal leukoencephalopathy, cytomegalovirus ventriculitis and encephalitis, focal lesions caused by other organisms including Cryptococcus neoformans, Aspergillus spp, Mycobacterium tuberculosis, and Nocardia spp, or bacterial brain abscess,” (Montoya, 2004).
Recently there has been a flux of information citing the abnormal behaviors of rats that are infected with toxoplasmosis. When put into a circler arena where bobcat urine was placed in an opposing quadrant to rabbit urine, non-infected rats had a fear response to the bobcat urine, and almost all of them went to the side that contained the rabbit urine (Sapolsky, 2007). These rats reacted quite normally, and showed a normal predatorily fear response (Sapolsky, 2007). But when the toxoplasmosis-infected rats were put into the same situation, more of them went into the corner with the bobcat urine than the rabbit (Sapolsky, 2007). Completely going against what seems to be an important fear for the rat’s survival. Obviously there is a large change in rat behavior from the infection of toxoplasmosis, and it would be easy to think that the rats would behave with no fear or anxiety in other situations. This is not the case, and the toxoplasmosis-infected rats show the same fear of open spaces, bright lights, and other learned fears (Sapolsky, 2007). There were no other noticeable changes within the rats behavior, they ate and weighted the same amount as the non-infected, but showed no fear to cat pheromones (Sapolsky, 2007). All of this data has made a team of researchers from Stanford University hypothesize something they termed “behavioral manipulation hypothesis.” The main theory of which is that parasites can specifically alter its host’s behavior to increase its own transfer efficiency. Thus providing a case for why these rats would only lose their fear for cat pheromones. The main concentration of parasitic cysts in the rats brain were in the amygdalar structures, which is the main brain region that deals with learned fear, anxiety-like behaviors, olfaction, and nonaversive learning (Sapolsky, 2007). The infection did not influence their fear conditioning or the extinction of fears, in the rats (Sapolsky, 2007). The infection did not affect the hippocampal-dependent learning, which are generally spatial learning skills (Sapolsky, 2007). Infection did not affect the social behaviors of the rats (Sapolsky, 2007). Yet the parasite seems able to rewire the brains of the rats, from a learned fear, into a sexual attraction (Sapolsky, 2007).
The implications of a rat’s behavior being manipulated by toxoplasmosis to such a degree that they become sexually attracted to something that will kill them are astounding, but if such mind control can be done on rats, what happens to humans infected by the same parasite? What change really happens in the human brain is not completely known, but there are some implications from a few different studies that span from, toxoplasmosis infection linking to schizophrenia, some behavioral changes from becoming infected with toxoplasmosis, and a major increase in car accident among infected individuals.
The findings of automobile accidents correlating with toxoplasmosis infection were very high, when a team from Prague studied a cohort group and a control comparing the rate of accidents between the two (Flegr, 2009). There are some flaws with the as they only studied men, and as implied by a different study on the behavior affects of toxoplasmosis on humans showed, there is a large difference between the affect on male and female subjects (Flegr, 2007). So the real measurement is on male subjects who are infected, and seeing if the rate of automobile accidents increase. When compared the infected men have a 2.6 times higher risk of being in an accident, than those who are not infected (Flegr, 2009). The explanation proposed was relating to a slower reaction time found from testing infected individuals (Flegr, 2009). Even though humans are “dead-end hosts” for the toxoplasma gondii, the infection could be similar to the findings within rats, but having a more general lack of anxiety (Flegr, 2009). They also proposed the alternative answer, that people who lead a general lifestyle are more likely to become infected, as well as having a higher risk of getting into car accidents, and the two being merely a correlation (Flegr, 2009).
The link between toxoplasmosis and schizophrenia has been observed since 1953 (Torrey, 2003). The majority of conclusions have been of a correlative nature (Torrey, 2003). In one study a substantial amount of patients diagnosed with toxoplasmosis, reported having psychiatric disturbances quite like symptoms of schizophrenia, and ranged from jumbled words to visual hallucinations. A study comparing the average toxoplasmosis infection rate in schizophrenic patients, whom resided in a clinic, to people that were not schizophrenic, showed a positive correlation between schizophrenia and toxoplasmosis infection (Torrey, 2003). Toxoplasma gondii has also been shown to affect levels of the neurotransmitters dopamine, norepinephrine and other neurotransmitters generally associated with schizophrenia (Torrey, 2003). There is no proof of causation between the two, but the importance of the symptoms associated with both, means that researching one will help solve the puzzle of the other. As shown by a different study, which found, “loss of fear to predator odor in infected rats can be reversed by treatment with the antipsychotic drugs haloperidol and valproic acid. This study provides one example of the value of integrating behavioral effects of Toxoplasma in models of emotional and psychiatric conditions, “(Sapolsky, 2007).
Toxoplasmosis is a globally prevalent disease, which previously has been thought of as asymptomatic, but now can be seen as having behavioral changes in humans. Toxoplasma gondii is an extremely evolved parasite, and is able to replicate itself, even though it is only to sexually reproduce in one form of definitive host. It can rewire the brains of its rat hosts, to easily find its way back into the stomach of a cat. With the current information about neurology, we cannot fully understand what happens within the human brain affected by toxoplasmosis, but the implications of what might be happening can lead to amazing knowledge about just how our brains work. This parasite can somehow lead itself to a specific neuropathway within the rat’s brain, and hijack it to produce a sexual response instead of fear.
If interested in Toxoplasmosis, please take a look at this interview given by Robert Sopolsky,
http://www.edge.org/3rd_culture/sapolsky09/sapolsky09_index.html
Papers cited in this post,
Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. Ajai Vyas, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky, 2007
http://hsc.sca.nsw.gov.au/biology/terms-and-definitions
Increased incidence of traffic accidents in Toxoplasma-infected military drivers and protective effect RhD molecule revealed by a large-scale prospective cohort study Jaroslav Flegr, Jiří Klose, Martina Novotná, Miroslava Berenreitterová, and Jan Havlíček
BMC Infect Dis. 2009; 9: 72. Published online 2009 May 26. doi: 10.1186/1471-2334-9-72.
PMCID: PMC2692860
Effects of Toxoplasma on Human Behavior
Jaroslav Flegr
Schizophr Bull. 2007 May; 33(3): 757–760.
Published online 2007 January 11. doi: 10.1093/schbul/sbl074.
Toxoplasmosis
J G Montoya, O Liesenfeld
THE LANCET • Vol 363 • June 12, 2004
Torrey EF, Yolken RH. Toxoplasma gondii and schizophrenia. Emerg Infect Dis Nov 2003 Available from: URL: http://www.cdc.gov/ncidod/EID/vol9no11/03-0143.htm
The Life Cycle of Toxoplasma gondii
J.P. Dubey, 2005
Toxoplasma gondii is classified as a coccidian. Coccidia are single celled, spore forming parasites, which infect the intestines of their animal host. To get even further into the specific taxonomy of toxoplasma gondii, their order is Eimeriorina (Dubey, 2005). According to J.P. Dubey the life cycle that most every Eimeria follows is, “The host becomes infected by ingesting sporulated oocysts of Eimeria. After excystation, the sporozoites penetrte intestinal epithelial cells and multiply asexually before forming male and female gamonts. Oocysts are produced after fertilization, and are passed in feces in unsporulated stage. Sporulation occurs outside of the host. (Dubey, 2005)” An oocyst, as defined by the Australian HSC is, “A thick walled structure in which sporozoan zygotes develop. It serves to transfer them to new hosts.” Sporulation of the oocyst occurs between 1-21 days after the host excretes the oocysts. It is important to note that the only animal in which toxoplasma gondii can reproduce in members of the Felidae family (i.e. domestic and wild cats). But toxoplasma gondii can spread through other means as well. When an infected animal that is not of the Felidec famly becomes pregnant, they can spread the infection by what is known as congenital infection of the fetus.
Toxoplasma Gondii has three infectious stages: the tachyzoites, the bradyzoites, and the sporozoites (Dubey, 2005).
Tachyzoites acquired their name from the rapid multiplication within any cell of the immediate host, and in the non-intestinal epithelial cells of the definitive host (Dubey, 2005). It is in this stage that the parasite multiplies, and can kill virtually all the host cells of a warm-blooded animal (Dubey, 2005). Also within this stage congenial infection can occur when the tachzoites from maternal blood are carried to fetal tissue (Dubey, 2005). The tachzoites enter a host cell either by “penetraiting through the host call plasmalemma,” or through phagocytosis (phagocytosis is a process in which phagocytes engulf and digest microorganisms and cellular debris; an important defense against infection [wordnetweb.princeton.edu/perl/webwn]) (Dubey, 2005). Once inside the cell, the tachyzoites become surrounded by a parasitophorous vacuole (Dubey, 2005). The next step is asexual reproduction through repeated endodyogeny, which is a “specialized form of reprodiction in which two progeny form within the parent parasite, consuming it,” (Dubey, 2005). Within hosts the toxoplasma gondii cells grow faster or slower, depending on the type of host cells (Dubey, 2005).
Bradyzoites and tissue cysts take only three days post infection to form (Dubey, 2005). The host of the tissue cyst might not realize their existence, because they do not cause inflammation, or any pain to them (Dubey, 2005). The tissue cysts develop within the host cells cytoplasm, and can contain hundreds of bradyzoites within its body. Another important difference to note between bradzoites and tachzoites is that bradyzoites are not as easily destroyed by proteolytic enzymes as tachzoites are.
Oocysts are the outer feline host for the sporont (the unsporilated version of a sporocyst), (Dubey, 2005). Sporulation occurs when the oocyst is outside of the feline host for one to five days, depending on factors like temperature (Dubey, 2005). The oocyst is the transport vessel of toxoplasma gondii from the definitive host, to the intermediate hosts or other animals.
Now that we have established the different stages of toxoplasma gondii, we will examine the definitive host of the parisite. The host must be any form of feline, for toxoplasma gondii to reproduce. Felines can become infected through ingestion of food or water that is contaminated with oocysts, or through parasitemia, which is the spreading the parasite from the mother to the fetus; if she becomes infected during pregnancy (Dubey, 2005). After the parasite sexually reproduction in the felines intestinal tract, it takes a minimum of 18 days for the oocysts to be excreted in their stool (Dubey, 2005). Over a period of only a few days, cats can shed millions of oocysts (Dubey, 2005). Sporulated oocysts can survive in a moderate climate for long periods of time (Dubey, 2005). In moist soil an oocyst can survive for months to years. With the colossal amount of oocysts produced in only a few days, even though only <1% of cats carry toxoplasma gondii, it is extremely easy for the oocysts to infect other animals. It can be spread on animals that have rolled over in infected cat feces, or on fruits and vegetables that are contaminated (Dubey, 2005).
The transfer of toxoplasma gondii to humans does not have a definitive origin, because of the numerous ways that it can be transferred from felines to humans, but the forms in which it is most likely to infect humans is through ingestion or handling of undercooked meat (generally pork) infected with tissue cysts, unfiltered water containing oocysts, and organ transplants (Montoya, 2004). Toxoplasma gondii infection can also be spread congenially, but only when the mother becomes infected during the pregnancy, or a maximum of three months before.
Toxoplasmosis in humans is generally asymptomatic, depending on the immune system of the infected person (Montoya, 2004). In a person with a normal immune system, the symptoms may be as small as swollen lymph nodes for a few weeks (Montoya, 2004). In Immunocompromised patients, toxoplasmosis can be life threatening, as the symptoms include “CNS lymphoma, progressive multifocal leukoencephalopathy, cytomegalovirus ventriculitis and encephalitis, focal lesions caused by other organisms including Cryptococcus neoformans, Aspergillus spp, Mycobacterium tuberculosis, and Nocardia spp, or bacterial brain abscess,” (Montoya, 2004).
Recently there has been a flux of information citing the abnormal behaviors of rats that are infected with toxoplasmosis. When put into a circler arena where bobcat urine was placed in an opposing quadrant to rabbit urine, non-infected rats had a fear response to the bobcat urine, and almost all of them went to the side that contained the rabbit urine (Sapolsky, 2007). These rats reacted quite normally, and showed a normal predatorily fear response (Sapolsky, 2007). But when the toxoplasmosis-infected rats were put into the same situation, more of them went into the corner with the bobcat urine than the rabbit (Sapolsky, 2007). Completely going against what seems to be an important fear for the rat’s survival. Obviously there is a large change in rat behavior from the infection of toxoplasmosis, and it would be easy to think that the rats would behave with no fear or anxiety in other situations. This is not the case, and the toxoplasmosis-infected rats show the same fear of open spaces, bright lights, and other learned fears (Sapolsky, 2007). There were no other noticeable changes within the rats behavior, they ate and weighted the same amount as the non-infected, but showed no fear to cat pheromones (Sapolsky, 2007). All of this data has made a team of researchers from Stanford University hypothesize something they termed “behavioral manipulation hypothesis.” The main theory of which is that parasites can specifically alter its host’s behavior to increase its own transfer efficiency. Thus providing a case for why these rats would only lose their fear for cat pheromones. The main concentration of parasitic cysts in the rats brain were in the amygdalar structures, which is the main brain region that deals with learned fear, anxiety-like behaviors, olfaction, and nonaversive learning (Sapolsky, 2007). The infection did not influence their fear conditioning or the extinction of fears, in the rats (Sapolsky, 2007). The infection did not affect the hippocampal-dependent learning, which are generally spatial learning skills (Sapolsky, 2007). Infection did not affect the social behaviors of the rats (Sapolsky, 2007). Yet the parasite seems able to rewire the brains of the rats, from a learned fear, into a sexual attraction (Sapolsky, 2007).
The implications of a rat’s behavior being manipulated by toxoplasmosis to such a degree that they become sexually attracted to something that will kill them are astounding, but if such mind control can be done on rats, what happens to humans infected by the same parasite? What change really happens in the human brain is not completely known, but there are some implications from a few different studies that span from, toxoplasmosis infection linking to schizophrenia, some behavioral changes from becoming infected with toxoplasmosis, and a major increase in car accident among infected individuals.
The findings of automobile accidents correlating with toxoplasmosis infection were very high, when a team from Prague studied a cohort group and a control comparing the rate of accidents between the two (Flegr, 2009). There are some flaws with the as they only studied men, and as implied by a different study on the behavior affects of toxoplasmosis on humans showed, there is a large difference between the affect on male and female subjects (Flegr, 2007). So the real measurement is on male subjects who are infected, and seeing if the rate of automobile accidents increase. When compared the infected men have a 2.6 times higher risk of being in an accident, than those who are not infected (Flegr, 2009). The explanation proposed was relating to a slower reaction time found from testing infected individuals (Flegr, 2009). Even though humans are “dead-end hosts” for the toxoplasma gondii, the infection could be similar to the findings within rats, but having a more general lack of anxiety (Flegr, 2009). They also proposed the alternative answer, that people who lead a general lifestyle are more likely to become infected, as well as having a higher risk of getting into car accidents, and the two being merely a correlation (Flegr, 2009).
The link between toxoplasmosis and schizophrenia has been observed since 1953 (Torrey, 2003). The majority of conclusions have been of a correlative nature (Torrey, 2003). In one study a substantial amount of patients diagnosed with toxoplasmosis, reported having psychiatric disturbances quite like symptoms of schizophrenia, and ranged from jumbled words to visual hallucinations. A study comparing the average toxoplasmosis infection rate in schizophrenic patients, whom resided in a clinic, to people that were not schizophrenic, showed a positive correlation between schizophrenia and toxoplasmosis infection (Torrey, 2003). Toxoplasma gondii has also been shown to affect levels of the neurotransmitters dopamine, norepinephrine and other neurotransmitters generally associated with schizophrenia (Torrey, 2003). There is no proof of causation between the two, but the importance of the symptoms associated with both, means that researching one will help solve the puzzle of the other. As shown by a different study, which found, “loss of fear to predator odor in infected rats can be reversed by treatment with the antipsychotic drugs haloperidol and valproic acid. This study provides one example of the value of integrating behavioral effects of Toxoplasma in models of emotional and psychiatric conditions, “(Sapolsky, 2007).
Toxoplasmosis is a globally prevalent disease, which previously has been thought of as asymptomatic, but now can be seen as having behavioral changes in humans. Toxoplasma gondii is an extremely evolved parasite, and is able to replicate itself, even though it is only to sexually reproduce in one form of definitive host. It can rewire the brains of its rat hosts, to easily find its way back into the stomach of a cat. With the current information about neurology, we cannot fully understand what happens within the human brain affected by toxoplasmosis, but the implications of what might be happening can lead to amazing knowledge about just how our brains work. This parasite can somehow lead itself to a specific neuropathway within the rat’s brain, and hijack it to produce a sexual response instead of fear.
If interested in Toxoplasmosis, please take a look at this interview given by Robert Sopolsky,
http://www.edge.org/3rd_culture/sapolsky09/sapolsky09_index.html
Papers cited in this post,
Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. Ajai Vyas, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky, 2007
http://hsc.sca.nsw.gov.au/biology/terms-and-definitions
Increased incidence of traffic accidents in Toxoplasma-infected military drivers and protective effect RhD molecule revealed by a large-scale prospective cohort study Jaroslav Flegr, Jiří Klose, Martina Novotná, Miroslava Berenreitterová, and Jan Havlíček
BMC Infect Dis. 2009; 9: 72. Published online 2009 May 26. doi: 10.1186/1471-2334-9-72.
PMCID: PMC2692860
Effects of Toxoplasma on Human Behavior
Jaroslav Flegr
Schizophr Bull. 2007 May; 33(3): 757–760.
Published online 2007 January 11. doi: 10.1093/schbul/sbl074.
Toxoplasmosis
J G Montoya, O Liesenfeld
THE LANCET • Vol 363 • June 12, 2004
Torrey EF, Yolken RH. Toxoplasma gondii and schizophrenia. Emerg Infect Dis Nov 2003 Available from: URL: http://www.cdc.gov/ncidod/EID/vol9no11/03-0143.htm
The Life Cycle of Toxoplasma gondii
J.P. Dubey, 2005
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