T. gondii is Real

T_-gondii-Life-Cycle

What Does Cats and T. gondii Have to do with it?

An amazing fact! The common parasite, T. gondii needs cats. The feline digestive tract is the only environment for T. gondii sexual reproduction; however T. gondii can be carried by warm and cold blooded (anchovies, mussels & etc.) hosts. The rat host is particularly affected by the parasite. Once produced, T. gondii has the innate power to change the behavior of their rodent host. T. gondii causes rats to not only to lose all fear of their predators, but to seek them out. True! The how of this has long puzzled scientists. Now it has been discovered this true fact also effects humans… T. gondii changes human behaviors!

E. Coli DNA Manipulated
To demonstrate how easy it is for dedicated individuals and/or organizations with no accountability can manipulate others, E. Coli is used as an example. Twenty years ago E. Coli was made from bovine products (cows). Some people are allergic to bovine products. Scientist was able to use a ‘bad’ bug, E. Coli – most of us have already in our digestive tract – within our body defined limits to be ‘healthy’ – and hijacked the E. Coli cell’s DNA to modify to produce human insulin! E. Coli DNA is an excellent vehicle (virus) to insert and modify many existing DNA’s.

Most of get it from under-cooked meat. Most of us are infected with the parasite. It changes our behaviors and entire cultures. There is no cure. As in E. coli, 20 years ago, a “E. coli, a bad bug” was altered to provide human insulin to eliminate the use of pigs to create human insulin, a single T. gondii gene has been identified causing human behavioral changes. Who decides what behaviors are needed? Who decides the “risk vs. benefits?”

WHAT DOES CATS HAVE TO DO WITH THIS BOOK?

Half of the World is Infected with Parasite T. gondii – There is No Cure – it Changes Our Behaviors (Fox News)

Your Behaviors May Be Modified by Others to do Their “right thing” — Who is Accountable? The government who controls the human mind, control everything.

Military Applications– The U. S. military knows about Toxoplasmosis (T. gondii) and its effect on human behavior. They are interested in T. gondii. They are officially intrigued. USAF General has located his Top Secret DNA research lab in plain sight in Mojave Air and Space Port. The entrance to his Deep Underground Military Base (DUMB) is in the rear of a civilian hangar.

Wars of the future might be decided through manipulation of people’s minds, concludes a report from the UK’s Royal Society. It warns that the potential military applications of neuroscience breakthroughs need to be regulated more closely.

Mind control, or behavior control provides leadership opportunities and challenges. The mind control challenges can make good leaders turn bad. The T. gondii parasite makes humans and mammals do things that everything in their fiber normally tells them not to because it’s dangerous and ridiculous and stupid and don’t do it. With this parasite on board, humans and mammals are more likely to do things they would not have done… no one would know. They may be hidden in plain sight.

T. gondii  –  Toxoplasmosis Gondii Time Line

1908 – Nicolle and Manceaux first described the organism, after they observed the parasites in the blood, spleen, and liver of a North African rodent, Ctenodactylus gondii. The parasite was named Toxoplasma (arclike form) gondii (after the rodent) in 1909.

1908 – Splendore discovered the same parasite in a rabbit in Brazil, also erroneously identifying it as Leishmania, but he did not name it.

1910 – Mello in Turin, Italy first reported fatal toxoplasmosis in a domestic animal (a 4-mo-old dog) that died of acute visceral toxoplasmosis.

1923 – Janku reported parasitic cysts in the retina of an infant who had hydrocephalus, seizures, encephalitis, and unilateral microphthalmia.

1932 – Identified as an agent of infectious disease.

1937 – The first viable T. gondii was isolated by Albert Sabin from laboratory mice and identical to human T. gondii.

1937-1939 –  Wolf, Cowan, and Paige determined that these findings represented the syndrome of severe congenital T gondii infection.

1938 – The first case of T.gondii infecting a human host was found in an infant girl who was delivered full-term by Caesarean section on May 23, 1938 at Babies Hospital, New York. The brain, spinal cord and the right eye were removed and examined to find T. gondii.

1939 – Its medical importance was discovered when T. gondii was identified in tissues of a congenitally infected infant.

1940  – The first adult case not discovered until 1940.

1941 – Acquired toxoplasmosis. Sabin  reported toxoplasmosis in a 6-year old boy from Cincinnati, OH.

1942 – The first case of cat infected with toxoplasmosis was reported (Olafson and Monlux).

1948 –  A serological dye test was created by Sabin & Feldman, which is now the standard basis for diagnostic tests. This led to the recognition that T. gondii is a common parasite of warm-blooded hosts with a worldwide distribution.

1952 – Wilder first identified T. gondii in histological sections of eyes that had been enucleated. A group of ophthalmologists from southern Brazil initially discovered ocular toxoplasmosis in siblings.

1954 – The possibility of transmission via undercooked meat was proposed by Weinman and Chandler

1957 – Hartley and Marshall finally isolated T. gondii from aborted sheep fetuses. A major cause of abortion in sheep.

1965 – This hypothesis was tested in Paris by Desmonts, and it was found that 80% of the adults who ate undercooked meat tested positive for T. gondii antibodies, meaning the undercooked meat contained live T. gondii capable of infection compared to the fully cooked meat.

1965 – During the same year, it was discovered by Hutchison that T. gondii can be spread via the fecal–oral route via cat to a warm-blooded host.

1960’s – The discovery of the cat as the definitive host was a very important finding as it helped to complete our understanding of the parasite’s life cycle, and the oocyst stage of T. gondii shed in the feces of infected cats was found to be an important source of infection for many intermediate hosts and helped to explain infection in herbivorous animals and people with a vegetarian diet.

1968 – T. gondii became recognized as a severe and potentially fatal disease of (AIDS) adults.

1970 – The congenital mechanism of transmission of T. gondii life cycle was discovered.

1970 – Its life cycle was discovered when it was found that felids (cats – both wild, domesticated, cougars etc) are its definitive host and an environmentally resistant stage (oocyst) is excreted in feces of infected cats.

1980s and 1990s a number of scientists reported that T. gondii changed the behavior of mice and rats.

1983 –  Luft et al reported acute toxoplasmosis-induced encephalitis that was fatal for AIDS patients.

1992 – Jaroslav Flegr (SMRI grantee) and his colleagues at Charles University in Prague have, , been studying the effects of T. gondii  infection on human personality traits and behavior. Infected men were shown to be more expedient, suspicious, jealous, and dogmatic, whereas infected women had more warmth and superego strength. Thus, sex differences of the effect of T. gondii  in humans have been shown, just as they have been in rodents.

2000 – Cole et a. isolated viable T. gondii from sea otters. Indicates contamination of our seas with T. gondii oocysts washed from land.

2001 – Flegr et al. found infected individuals performed significantly more poorly and appeared to lose their concentration more quickly (Havlicek J, Gasova Z, Smith AP, et al. Decrease in psychomotor performance in subjects with latent ‘asymptomatic’ toxoplasmosis. Parasitology. 2001;122:515–520).

2002 – Flegr et al. also found humans infected with parasite T. gondii  had more than twice the risk of having caused a motor vehicle accident (Flegr J, Havlicek J, Kodym P, et al).

2005 – Mapping of T. gondii genes was achieved recently (Khan et al) .

2009 – The effects of T. gondii on cognitive measures in (Yolken RH, Dickerson FB, Torrey EF) in humans with Toxoplasma infection had significantly worse performance in measures of delayed memory (p<0.002) and immediate memory (p<0.05) and trends toward worse performance in other domains.

2012 – Danish study reported that women who were infected with T.gondii  were significantly more likely to be suicidal and twice as likely to successfully commit suicide, compared to women not infected (Pedersen MG, Mortensen PB, Norgaard-Pedersen B, Postolache TT. Toxoplasma gondii  infection and self-directed violence in mothers. Arch Gen Psychiatry. (2012; doi:10.1001/ archgenpsychiatry.2012.668).

2012 – Although at least 15 distinct strains of T. gondii  are known, most isolates of T. gondii  in Europe and North America belong to one of three strains: I, II, or III. (Hill RD, Gouffon JS Saxton)

 Sources of Human T. gondii Infection:

  • Unpasteurized dairy products also may contain the parasite T. gondii.
  • There have been rare cases of transmission through unpasteurized goat’s milk and through accidental sticks.
  • Use of contaminated knives, cutting boards or other utensils subject to T. gondii infection.
  • T. gondii infection may come from an infected organ transplant or transfused blood.
  • Epidemiological studies found a significant association between toxoplasmosis (T. gondii) and consumption of meat by human, (Bobic et al., 1998; Baril et al., 1999)
  • T. gondii oocysts (capsule, with a hardy shell) can survive in soil for up to 18 months.
  • A high prevalence of T. gondii infection was found in pet dogs.
  • Ingestion of oocysts from the environment eg, through contact with soil containing sporulated oocysts. This can also occur indirectly through eating contaminated fruit or vegetables.
  • Ingestion of meat containing tissue cysts. Fresh meat is most risky since freezing meat for several days will kill most tissue cysts.
  • Ingestion of sporulated oocysts through contact with contaminated water.
  • Coastal freshwater runoff is a risk factor for Toxoplasma gondii infection of southern sea otters (Enhydra lutris nereis) – International Journal for Parasitology 32 (2002) 997–1006
  • Chickens are considered one of the most important hosts in the epidemiology of Toxoplasma gondii infection because may become infected with this parasite after eating under cooked infected chicken meat. The prevalence of T. gondii in backyard chickens and chickens from organic farms reached up to 100%.
  • Geese infected with T. gondii may be a source of T. gondii infection for humans and cats. – Zoonoses and Public Health Volume 58, Issue 4, pages 299–302, June 2011
  • Toxoplasmosis is now also recognized to be a water-borne zoonosis. This method of transmission occurs where water treatment is ineffective or non-existent and there is a sizeable local felid population that contaminates surface water with oocysts. (DUBEY J.P. (2004).
  • Linked to this there is now also an appreciation that sea mammals are becoming infected by waters from contaminated land and from untreated urban sewage. (DUBEY J.P. (2004). Toxoplasmosis – a waterborne zoonosis. Vet. Parasitol., 126, 57–72.
  • T. gondii have been detected in body fluids, including saliva, sputum, urine, tears, semen and milk of several intermediate hosts, including sheep, goats, cows and camels (Tenter et al. 2000). An early study reported that T. gondii tachyzoites may be isolated from raw chicken eggs laid by hens with experimentally induced infection (Jacobs & Melton 1966).

T. gondii Infection from Rural Drinking Water
Occurrence of Toxoplasma gondii in water from wells located on farms. Toxoplasma gondii and Cyclospora cayetanensis are two coccidian protozoan parasites that are increasingly recognized as having potential for waterborne transmission to humans. The environmental stage for both organisms is an oocyst, shed in the faeces of the infected host and capable of surviving in the environment for months or longer, more than enough time to be transported into a drinking water supply. The infectious dose is believed to be low for both parasites, suggesting that despite massive dilution in water there is still the possibility for people to be exposed and become infected. Similar to another coccidian, Cryptosporidium spp., the oocysts of T. gondii and C. cayetanensis are resistant to disinfection by chlorination. All these life history traits are favourable for waterborne transmission, presenting the drinking water profession with yet another set of emerging pathogens with which to contend. Journal of Applied Microbiology ISSN 1364-5072 

T. gondii Infection is in the Ocean!risk areas are places that have lots of freezing, high altitude, a dry climate, really good hygiene, or very few cats. (Kevin Lafferty, Ecological Parasitology Laboratory, Department of Ecology, Evolution, and Marine Biology, University of California, Santa Barbara) Human toxoplasmosis acquired through the consumption of infective Toxoplasma gondii oocysts in contaminated drinking water is an increasing public health risk worldwide.

Currently, there are no specific recommendations or approved methods to inactivate T. gondii in public water supplies, and limited research indicates that oocysts may be difficult to destroy in water by conventional disinfection methods . Although T. gondii oocysts can be inactivated by exposure to boiling, freezing, and gamma irradiation the effect of UV radiation on these oocysts has not been evaluated.

Central California cities are dumping sewer water into the drinking water of 23 million people in Los Angeles area. See: http://dallas93444.hubpages.com/hub/Why-Is-California-State-Water-Project-Dumping-Parasite-Infection-Into-Water

Sewage Treatment Plants: These plants traditionally treat sewage to kill harmful bacteria, remove the waste solids, and pump the resultant “safe” effluent directly into a freshwater source that eventually drains into ocean bays. Unfortunately present means of sewage treatment do not kill the T. Gondii parasite. Cat owners using flushable litters, may be unwittingly contributing to the ultimate deaths of sea otters.

Storm Drain Runoff: Rain, lawn and garden surface water, and anything you manually put into that storm drain in the street near your house eventually runs off into a creek or river which flows directly into an ocean bay.

Scientists and researchers have recently discovered a correlation between Toxoplasma gondii and the decrease in the sea otter population off the California Coast. Since cats are the only creatures that shed the T. gondii parasite, through their feces, there seems to be a direct link.

The recent recognition of numerous fatal Toxoplasma gondii brain infections in southern sea otters from California has prompted concerns about the emergence of Toxoplasma gondii as a significant marine pathogen.

“Toxoplasma infection has appeared in a variety of sea mammals including beluga whales, dolphins, sea lions and seals. It has also become a major cause of death in Californian sea otters living. It is estimated that approximately 17 percent of sea otter deaths can be attributed to toxoplasma.

While many believe fresh water runoff contaminated with cat feces is to blame, there is no definitive evidence on the source of infection.” says Gloeta Massie, a graduate student who conducted the research with Associate Professor Michael Black.

“The question that drives our research is how are marine mammals from the Arctic Circle to Australia infected by a parasite that is spread primarily through the consumption of infectious cat feces and infected meat? Based on the global prevalence of T. gondii infections, we hypothesize that migratory filter feeders, specifically northern anchovies, are serving to spread T. gondii throughout the ocean,” says Gloeta Massie, a graduate student who conducted the research with Associate Professor Michael Black.

Results show natural exposure of European harbor and grey seals to T. gondii oocysts in the Atlantic Ocean. To the best of our knowledge, this is the first serological survey of T. gondii in European grey and harbor seals. US National Library of Medicine National Institutes of Health – Vet Parasitol. 2011 Jun 30;179(1-3):253-6. Epub 2011 Feb 2.

Toxoplasma gondii infection in marine mammals is intriguing and indicative of contamination of the ocean environment and coastal waters with oocysts. In previous serological surveys, 90% of bottlenose dolphins (Tursiops truncatus) from the coasts of Florida, South Carolina, and California had antibodies to T. gondii. – J. P. Dubey, P. A. Fair, N. Sundar, G. Velmurugan, O. C. H. Kwok, W. E. McFee, D. Majumdar, and C. Su, Animal Parasitic Diseases Laboratory, Animal and Natural Resources Institute, Beltsville Agricultural Research Center, United States, Department of Agriculture, Beltsville, Maryland 20705. e-mail: jitender.dubey@ars.usda.gov

T. gondii was identified in a Hawaiian monk seal (Monachus schauinslandi) – American Society of Parasitologists Recent research by Drs. Marina Collins and David Lindsay, Virginia Tech, Blackburg Campus, has expanded the understanding of the interaction between Toxoplasma gondii and oysters in the marine environment. T. gondii is prevalent in the marine environment, and it has previously been determined that Eastern oysters (Crassostrea virginica) can remove sporulated T. gondii oocysts from seawater and that the oocysts retain their infectivity for some time.

T. gondii Facts
Is your cat maybe making you crazy? Take non-scientific quiz!
1. Are you talking to more strangers than usual? For example, do you find yourself meeting ten or more new people every day?

Answer: Toxoplasmic symptom is hyper-sociability. Women with Taxoplasma exhibited more outgoing, trusting, image-conscious, and rule-abiding behavior than uninfected women.

 2. Do you find yourself suddenly taking unconventional risks? For instance, have you recently decided to take up base-jumping? Are you easily convinced to cross the street in the middle of traffic?

 Answer: significant Toxoplasmic symptom is the lack of a fear response.

 3. Does the smell of skunk no longer repel you?
Toxoplasmic patients experience hypersensitivity toward strange smells

 4. Have you had more than one fender bender in the ten minutes?
Subjects who tested positive for the parasite had significantly delayed reaction times. Toxoplasma might have an adverse impact on driving, where constant vigilance and fast reflexes are critical.

 5. Are you a man whose social calendar suddenly and unexpectedly cleared up?

6. Males who had the parasite were more introverted, suspicious, oblivious to other people’s opinions of them, and inclined to disregard social cues.

Why have I Never Heard of T. gondii?
celled protozoan organism causes a disease known as toxoplasmosis and is arguably the most successful protozoan parasite on Earth.

Between 15 and 95% of the world adult human population is chronically infected with Toxoplasma gondii depending on geographical location. Why have you never heard of the parasite T. gondii and toxoplasmosis? One major reason is that most people who are infected with the parasite do not have obvious symptoms. And when symptoms of a new infection do occur, they are usually flu-like and are often misdiagnosed.

In any event, the symptoms of the acute infection generally clear up within several weeks, without the infected person’s even knowing what caused them.

Signs and symptoms of the disease: People often do not notice they have contracted T. gondii although some do notice symptoms much like those of the flu. These include body aches, sore throat, fever, headache, fatigue, and swollen lymph nodes. Immune compromised individuals and those with severer chronic infection may develop neurological dysfunctions associated with schizophrenia.

Immune compromised individuals may also notice lung problems and blurred vision. In congenital toxoplasmosis still birth, seizures, enlarged livers and spleens, jaundice, and severer eye infections can occur. New bornes often times do not show signs of infection and a latent infection can lead to hearing loss, mental retardation, and serious eye infections.

Recent studies have suggested that Toxoplasma gondii is able to effect behavioral change in humans

This parasite influences human culture when parasitizing the brain. According to Kevin Lafferty, a USGS scientist at the University of California, Santa Barbara, people infected with T. gondii experience a wide range of long term personality changes.

A more detailed look provides my thesis, my concern of the danger of leadership with no accountability. Consider, the personalities of T. gondii infected men showed lower superego strength (rule consciousness) and higher vigilance (factors G and L on Cattell’s 16PF). Thus, the men were more likely to disregard rules and were more expedient, suspicious, jealous, and dogmatic. The personality of infected women, by contrast, showed higher warmth and higher superego strength (factors A and G on Cattell’s 16PF), suggesting that they were more warm-hearted, outgoing, conscientious, persistent, and moralistic. Both men and women had significantly higher apprehension (factor O) compared with the uninfected controls.

Humans with latent infections of the common protozoan parasite Toxoplasma gondii appear to experience a variety of long-term personality changes (Webster 2001). For instance, in infected women, intelligence, superego strength (rule-conscious, dutiful, conscientious, conforming, moralistic, staid and rule-bound) and affectothymia (warm, outgoing, attentive to others, kindly, easy-going, participating and likes people) are higher, while infected men have lower intelligence, superego strength and novelty-seeking (low novelty-seeking indicates rigid, loyal, stoic, slow-tempered and frugal personalities); both infected men and women have higher levels of guilt-proneness (they tend to be more apprehensive, self-doubting, worried, guilt prone, insecure, worrying and self-blaming; Flegr & Hrdy 1994; Flegr et al. 1996, 2000, 2003).

The seroprevalence (percentage of people with antibodies to latent infections) of T. gondii varies geographically nearly from 0 to 100% (Tenter et al. 2000), suggesting that T. gondii could lead to variation in aggregate personality among populations (Lafferty 2005). I

In other words, the average personality of a population might be shifted if a higher proportion of individuals are infected with T. gondii. The ability to detect statistically an effect of T. gondii on aggregate personalities of populations will depend on how strongly the parasite affects individual personality, the extent of variation in prevalence among populations and the consistency of the personality change between men and women.

This begs the question: could aspects of human culture result from a parasite selected to predispose its host to predation by cats (Lafferty 2005)? The report indicates associations between the prevalence of T. gondii infection and aggregate personality that could explain some of the variation in cultural dimensions among human populations.

Scientists estimate that the parasite has infected about 3 billion people, or about half of the human population. Studies by researchers in the Czech Republic have suggested T. gondii might have subtle but long-term effects on its human hosts. The parasite is thought to have different, and often opposite effects in men versus women, but both genders appear to develop a form of neuroticism called “guilt proneness.”

Flegr, an evolutionary biologist and parasitologist, has studied the effects of Toxoplasma gondii in humans. After noticing some strange patterns in his own behaviour — not perceiving danger in dangerous situations, which can be a hallmark of the manipulation — Flegr was tested to see if he was infected. He was. According to Flegr, the presence of the Toxoplasma parasite can cause a variety of behavioral changes in humans that are exposed, including changes in the way those individuals trust and interact with others and even their preference for certain scents.

Flegr also asserts that the effects of Toxoplasma can even contribute to behaviors that lead to car crashes, even suicide and other mental disorders.
Facts about T. Gondii (Toxoplosmosis)

There is no CURE! No Vaccine!
The T. gondii parasite was discovered in 1908. In 1939 T. gondii was identified in tissues of a congenitally infected infant, and veterinary importance became known when it was found to cause abortion storms in sheep in 1957.

In 1948 the recognition that T. gondii is a common parasite of warm-blooded hosts with a worldwide distribution. 1970 was when it was found that felids (cats) are the definitive host and an environmentally resistant stage (oocyst – eggs) is excreted in feces of infected cats.

The recent discovery of its common infection in certain marine wildlife (sea otters) indicates contamination of our seas with T. gondii oocysts washed from land. Hygiene remains the best preventive measure because currently there is no vaccine to prevent toxoplasmosis in humans.

The recent origin and widespread distribution of the clonal lineages is attributed to the circumvention of the sexual cycle by a new mode of transmission-asexual transmission between intermediate hosts (Khan et al., 2006).

Diagnosis
The diagnosis of toxoplasmosis is usually made by a blood test. The most common test used in the clinical setting is the polymerase chain reaction (PCR) test. This test can detect T. gondii DNA (genetic material of the parasite).

A test that measures antibodies to T. gondii is used to determine if someone has been infected recently or in the past. The diagnosis can also be made by looking for the parasite in stained tissue samples, cerebrospinal fluid (CSF—fluid that circulates around the brain and spinal column), or other material taken by biopsy. (Edvinsson B, Lundquist J, Ljungman P, Ringdén O, Evengård B. A prospective study of diagnosis of Toxoplasma gondii infection after bone marrow transplantation. APMIS. 2008 May;116(5):345-51).

In pregnant women, a sample of amniotic fluid can be obtained to test for the parasite.

Computed tomography (CT) scan or magnetic resonance imaging can be used to look for an abscess in the brain. Abscesses caused by T. gondii typically have the appearance of a dark spot in the brain tissue with a ring around it.

Reactivation of latent infection
People who are infected with T. gondii and who later develop a weakened immune system (from conditions such as HIV/AIDS, cancer, or organ transplantation), can experience severe symptoms from reactivation of latent toxoplasmosis. Symptoms of toxoplasmosis depend on where the latent infection has reactivated in the body.

In people with HIV/AIDS, reactivation typically occurs in the brain leading to toxoplasma encephalitis. Symptoms can include severe headache, lethargy, trouble thinking, confusion, seizures, weakness in the arms or legs, coma, and death. Other symptoms may occur depending upon which organs are involved in the infection.

The seroprevalence (percentage of people with antibodies to latent infections) of T. gondii varies geographically nearly from 0 to 100% (Tenter et al. 2000), suggesting that T. gondii could lead to variation in aggregate personality among populations (Lafferty 2005). In other words, the average personality of a population might be shifted if a higher proportion of individuals are infected with T. gondii.

The ability to detect statistically an effect of T. gondii on aggregate personalities of populations will depend on how strongly the parasite affects individual personality, the extent of variation in prevalence among populations and the consistency of the personality change between men and women.

This begs the question: could aspects of human culture result from a parasite selected to predispose its host to predation by cats (Lafferty 2005)? The report indicates associations between the prevalence of T. gondii infection and aggregate personality that could explain some of the variation in cultural dimensions among human populations.

Scientists estimate that the parasite has infected about 3 billion people, or about half of the human population. Studies by researchers in the Czech Republic have suggested T. gondii might have subtle but long-term effects on its human hosts. The parasite is thought to have different, and often opposite effects in men versus women, but both genders appear to develop a form of neuroticism called “guilt proneness.”
T. Gondii behavioral changes in humans.

Professor Jaroslav Flegr of Charles University in Prague has discovered evidence that infection by intracellular protozoan parasite toxoplasma gondii (T. gondii) causes changes in human personalities.

Further, consider T. gondii can alter individual personality, and modal personality can shape culture, then T. gondii may be one of the factors that shape culture. (Look what the cat dragged in: do parasites contribute to human cultural diversity. (Kevin D. Lafferty, K.D. Lafferty / Behavioral Processes 68 (2005) 279–282)

T. gondii orchestrates a significant increase in dopamine metabolism in neural cells. The observed effects on dopamine metabolism could also be relevant in interpreting reports of psycho-behavioral changes in toxoplasmosis-infected humans. (Dubey JP (2010) Toxoplasmosis of animals and humans. Boca Raton,, Florida: CRC Press. 313 p.)

Behavioral Changes Such as:

  • Women infected with toxoplasma spent more money on clothes and were consistently rated as more attractive. “We found they were more easy-going, more warm-hearted, had more friends and cared more about how they looked,” he said. “However, they were also less trustworthy and had more relationships with men.”
  • Infected men appeared to suffer from the “alley cat” effect: becoming less well groomed undesirable loners who were more willing to fight. They were more likely to be suspicious and jealous. “They tended to dislike following rules,” Flegr said.
  • The pathogen is a leading cause of neurological birth defects in children born to mothers who contract the disease during pregnancy and can cause fatal toxoplasmosis encephalitis in immunosuppressed patients.

T. gondii Factors:

  • Toxoplasma-infected men have a higher level of testosterone.
  • Slowed reaction times resulting in an increase in traffic accidents.
  • Slowed reaction times resulting in an increase in traffic accidents.
  • Men who are infected with T. Gondii tend to gain antisocial tendencies.
  • They become more aggressive, jealous, and suspicious.
  • Also their desirability to women decreases.
  • Women who are infected become more intelligent, and more promiscuous. Unsurprisingly this increases their desirability to men.
  • Toxoplasmosis also results in a higher risk of developing schizophrenia or a bipolar disorder. Epidemiologic studies indicate that infectious agents may contribute to some cases of schizophrenia.
  • In animals, infection with Toxoplasma gondii can alter behavior and neurotransmitter function.
  • In humans, acute infection with T. gondii can produce psychotic symptoms similar to those displayed by persons with schizophrenia.
  • T. Gondii is a parasitic protozoan.
  • T. Gondii causes the disease toxoplasmosis.
  • Toxoplasmosis is linked to slowed reaction time, 2.5 times increased chance of auto accidents, anti-social behavior in men, promiscuity in women, schizophrenia and bipolar disorder.
  • 30-85% of the human population is infected with T. Gondii depending on geographical location.
  • Toxoplasmosis is a potentially fatal disease of the developing human fetus and immunocompromised (e.g., AIDS and transplant) patients and can cause severe ocular disease in otherwise healthy individuals.
  • The third most common source of food borne infection in the USA.
  • Most infections remain asymptomatic and treatment is not prescribed, however, toxoplasmosis is strongly linked with development of psychosis, depression, and anxiety disorders, reckless behavior and impulsivity in youth.
  • Infected rats and mice exhibit hyperactivity, fearlessness toward cat urine odor, and novelty seeking behavior – types of conduct that most likely make them victims of cat predation. It is speculated that the pathogen targets brain of an intermediate host to increase its exposure and vulnerability to its natural predators.
  • T. gondii is listed as a category B Biodefense Agent by National Institute of Allergy and Infectious Diseases (NIAID).
  • How can the risk of transmission of toxoplasma from other sources be reduced?

These measures are essential in all ‘high risk’ groups of people and are also sensible routine hygiene precautions:

  • Gloves should be worn when gardening and hands thoroughly washed after contact with soil which may contain sporulated (infectious) oocysts.
  • Gloves should be worn when handling food to prevent exposure to oocysts and tissue cysts.
  • Hands should always be washed thoroughly afterwards.
  • Fruit and vegetables should be thoroughly washed before eating to remove any oocysts present on their surface.
  • All food preparation surfaces and utensils should be cleaned with detergent in warm water before and after use to inactivate any tissue cysts.
  • Meat should be cooked to a minimum of 58°C for 10 minutes or 61°C for four minutes to kill the tissue cysts (Dubey et al 1990).
  • Microwaving is not a safe way to kill tissue cysts as the heating is uneven. T gondii oocysts can remain infectious when stored in a refrigerator (4°C) for up to 54 months (Dubey 1998).
  • Freezing meat at –12°C to -20°C for three days kills tissue cysts as does curing or smoking (Dubey 1988, Lunden and Uggla 1992).
  • Gamma irradiated food is free from any risk of infection.

If drinking a non-mains water supply, boil or filter before drinking to remove oocysts.

More Brief facts

  • Toxoplasma gondii is an obligate intracellular parasite classified in the phylumApicomplexa, which includes numerous important human and animal pathogens such as Plasmodium species, Cryptosporidium species, Neospora caninum, etc. (click here for more examples).
  • Toxoplasma gondii is capable of infecting a wide variety of mammals and birds. This single-celled protozoan organism might cause a disease known astoxoplasmosis and is arguably the most successful protozoan parasite on Earth. Between 15 and 85% of the world adult human population is chronically infected with Toxoplasma gondii depending on geographical location.
  • The invasive stages of apicomplexans are characterized by the presence of an apical complex composed of specialized cytoskeletal and secretory organelles: micronemes (involved in attachement and penetration),rhoptries (required for creation of a transient structure, moving junction, and the establishment of parasitophorous vacuole (PV)), and dense granules (secrete proteins throughout most of parasite stages).Parasitophorous vacuole (PV) is a unique compartment delimited from the host cell cytoplasm by PV membrane (PVM), which prevents T. gondiidegradation by the host cell endocytic machinery and enables parasite intracellular propagation.
  • Cats (Felis catus, domestic cat at GeoChemBio: taxonomy, brief facts, digestive system, development) are primary hosts of Toxoplasma gondii. About sexual cycle of the parasite and its distribution by cats’ feces please see section Developmental stages below.
  • Toxoplasmosis is a potentially fatal disease of the developing human fetus and immunocompromised (e.g., AIDS and transplant) patients and can cause severe ocular disease in otherwise healthy individuals.
  • Most infections remain asymptomatic and treatment is not prescribed, however, toxoplasmosis is strongly linked with development of psychosis, depression, and anxiety disorders, reckless behavior and impulsivity in youth. Unfortunately, all above mentioned disorders are quite common and their etiology often is not explored fully.
  • Experiments on rats and mice, natural prey of cats, had shown that infected rats and mice exhibit hyperactivity, fearlessness toward cat urine ordor, and novelty seeking behavior – types of conduct that most likely make them victims of cat predation. It is speculated that the pathogen targets brain of an intermediate host to increase its exposure and vulnerability to its natural predators. Although some hosts, such as humans, cannot be considered to become a prey of a cat, it can be postulated that all hosts can be affected by similar pathways.
  • A functional immune system of the host suppresses T. gondii and makes it to encyst in various tissues including brain. Therefore, healthy host is a key condition for persistence of T. gondii. In an immunodeficient host, tachyzoite growth causes tissue damage, and persistent infection is not established. Furthermore, when healthy but chronically infected host becomes immunocompromized, bradyzoites transform into tachyzoites, causing cerebral injuries. There is no available drug that can reach the parasite encysted in the brain tissue.
  • According to most recent studies, it seems that these pathogens can secrete protein kinases into host cells to subvert host-cell signalling pathways and that this explains many of the differences in virulence among the three dominant clonal lineages.
  • Recent population genetic studies have identified a remarkably limited number of Toxoplasma gondii genotypes in nature, the vast majority of which fall into one of only three distinct lineages. They can be associated with different types of toxoplasmosis as a disease (ocular, brain, muscle, necrosis, etc.).
  • Genetic analysis of strains indicates that Toxoplasma gondii sexual recombination between different strains of the parasite is very rare in natural populations of the host (felines).

Infection pathways

  • from mother to fetus during pregnancy
  • inhaling oocysts (from litter boxes of domestic cats, from soil)
  • contamination of hands with feline feces while gardening, playing in sandboxes, etc.
  • ingestion of toxoplasma cysts contained in contaminated undercooked meat

Predominant genotypes of T. gondii

  • Type I is highly virulent in mice and, perhaps, in human.
  • Type II predominates in infections of immunocompromised patients; relatively avirulent in mouse. Type II strains are most often associated with human toxoplasmosis, especially in Europe.
  • Type III is not highly virulent in mouse, and causes chronic infections in humans.

 Developmental stages

  • Sexual      This part of the life cycle takes place only in members of theFelidae family (domestic and wild cats), after ingestion of flesh of infected animal (any warm-blooded animal including birds).
    • Enteroepithelial stage After ingestion of tissue cysts, the parasites invade the cat enterocytes, undergo several rounds of division and differentiate into microgametocytes and macrogametocytes.
      • Division Proliferation of the parasites in the cat enterocytes.
      • Differentiation Parasites differentiate into sexual structures,microgametocytes and macrogametocytes.
      • Zygote The gametocytes fuse to form a zygote or oocyst that is shed into the environment with the cat feces.
    • Fecal stage
      • Meiosis The oocyst undergoes meiosis, producing an octet of highly infectious sporozoites that are resistant to environmental damage and may persist for years in a moist environment.
  • Asexual      Asexual reproduction begins after ingestion of the cat feces by a secondary host such as a mouse.
    • Acute infection stage Sporozoites differentiate into the rapidly dividing tachyzoite form, which establishes and sustains the acute infection.
    • Chronic infection stage A chronic phase of the disease ensues, as the tachyzoite changes into a slowly dividing form known as the bradyzoite.
    • Resting stage Latent bradyzoite tissue cysts persist for the life of the host mainly within the muscles and brain. The cysts are very difficult to eradicate entirely because they rest inside the host cells.

Tissues

  •  Cyst – A small thick-walled sac that encloses dormant bradyzoites; usually resides in muscle or brain tissues (resting stage).
  •  Oocyst – Zygote produced by gametocytes fusion. Mature oocyst consists of wall surrounding two sporocysts, each of which is comprised of a sporocyst wall surrounding four sporozoites (fecal stage)
  •  Unsporulated oocyst
  •  Sporulated oocyst – Mature oocyst containing sporozoites.
  •  Sporozoite – Highly infectious form of T. gondii produced by meiosis of the oocyst; resistant to environmental damage and may persist for years in a moist environment.
  •  Tachyzoite – Sporozoites differentiate into tachyzoites – motile haploid, asexually reproducing form of the parasite – that establish and sustain the acute infection; upon host cell penetration tachyzoites form the parasitophorous vacuole (PV). PV membrane (PVM) surrounds dividing parasites and protects them from acidification by host’s endocytic vesicles; T. gondii presents three organelles that are involved in host’s cells invasion, formation of PV, nutrient acquisition, and, above all, subversion of host’s defenses, including suppression of apoptosis: microneme proteins (MICs), rhoptry proteins (ROPs), and dense granules.
  •  Bradyzoite – A slowly dividing form of the parasites; latent bradyzoite tissue cysts persist for the life of the host, re-emerging occasionally, thus sustaining chronic infection.

References

Hermes G, Ajioka JW, Kelly KA, Mui E, Roberts F, Kasza K, Mayr T, Kirisits MJ, Wollmann R, Ferguson DJ, Roberts CW, Hwang JH, Trendler T, Kennan RP, Suzuki Y, Reardon C, Hickey WF, Chen L, McLeod R.
Neurological and behavioral abnormalities, ventricular dilatation, altered cellular functions, inflammation, and neuronal injury in brains of mice due to common, persistent, parasitic infection. J Neuroinflammation. 2008 Oct 23;5:48.

T. gondii rat infection

Appearance of eleven-month-old Specific Pathogen Free (SPF) mice that are uninfected and chronically infected with T. gondii.
(A) Eleven month old uninfected Swiss Webster mouse.
(B) Eleven month old infected female mouse from the same SPF colony ten months after acquisition of T. gondii infection. Note hunched body position, poor grooming, piloerection, reduced body mass, and tail wounding.
(C) Chronically infected SPF mouse with abnormal body position.

T. gondii Cell Division

T. gondii Cell Division

Apicomplexa Are Intracellular Parasites (A) Highly simplified apicomplexan life cycle. Apicomplexans are haplonts, and meiosis (sporogony) immediately follows fertilization. Fertilization might occur within a host cell or extracellularly, giving rise to an oocyst or, less frequently, an invasive stage zygote (ookinete).
(B) Schematic representation of a zoite (not all structures are present in all apicomplexans). AP, apicoplast; AR, apical rings; CC, centrocone; CE, centrosome; CO, conoid; DG, dense granule; ER, endoplasmic reticulum; G, Golgi; IMC, inner membrane complex; MI, mitochondrion; MN, microneme; MT, subpellicular microtubule; NU, nucleus; RH, rhoptry.
(C) Zoites actively invade the cells of their hosts, establishing a specialized parasitophorous vacuole (PV) (in some species the parasite lyses the vacuole and develops freely in the cytoplasm).

Hu K, Johnson J, Florens L, Fraunholz M, Suravajjala S, DiLullo C, Yates J, Roos DS, Murray JM. Cytoskeletal components of an invasion machine–the apical complex of Toxoplasma gondii. PLoS Pathog. 2006 Feb;2(2):e13.

baby girl infected T. gondii

Baby girl with hydrocephalus due to congenital toxoplasmosis

Drawings of T. gondii. Left: a longitudinal section of a dividing cell. Lobes of the dividing nucleus bordered by ER, Golgi (yellow), and developing rhoptry (mauve) are surrounded by the developing daughters’ scaffolds (red). Maternal and daughter conoids are shown in green, secretory organelles (rhoptries) in purple. T. gondii has three membranes: aplasma membrane (black) and two additional layers (IMC, red) formed from a patchwork of flattened vesicles. Right: semitransparent view showing subpellicular MT (green).