|Toxoplasma gondii (Nicolle et Manceaux, 1908) Nicolle et Manceaux, 1909|
宿主の細胞に侵入すると寄生体胞 (parasitophorous vacuole) を作ってその内部で内生二分裂 (endodyogeny) を行い増殖する。これは、母虫体の細胞内に2つの娘虫体が生じ、それが母虫体を破壊するという特殊な分裂様式である。原虫の増殖にともない寄生体胞は肥大化していき、宿主細胞が耐えきれなくなると破裂して、ふたたび原虫が周囲の細胞に侵入することを繰り返す。この時期の原虫のことを急増虫体 (tachyzoite) と呼ぶ。急増虫体は通常は宿主の免疫系の作用によって排除されていくが、免疫系の作用が及びにくい筋肉や脳ではシスト (cyst) を作ってその中で緩やかに増殖を続ける。シスト中の原虫を緩増虫体 (bradyzoite) と呼ぶ。以上が無性生殖期であり、アピコンプレックス門一般で言うメロゴニーに相当する。
一方、終宿主に初感染した場合には、腸の粘膜上皮細胞の中で有性生殖（ガメトゴニー）を行う。上皮細胞に侵入した原虫は雌雄どちらかの生殖母体となり、配偶体を生じる。雌雄の配偶体が受精すると、オーシスト (oocyst) を生じてその中でスポロゴニーが始まる。オーシストは12×10μmの大きさで、未成熟なままで糞便内に排出される。外界で2個のスポロシスト (sporocyst) ができ、成熟するとその中にそれぞれ4個計8個のスポロゾイト（sporozoite、種虫）が無性的に生じる。オーシストの排出は数週間でおさまる。排出されたオーシストは生体外の環境で1年は生存することが確認されている。
1908年にアトラスグンディ Ctenodactylus gundi の寄生虫として発見され、当初は Leishmania gondii と命名され、翌年に Toxoplasma gondii と新属が与えられた。
ノーマン・D・レヴィン Norman D. Levine は、トキソプラズマ属 Toxoplasma には7種があるとしているが、T. gondii 以外は爬虫類や両生類から見出されたものが多く、その後詳しい研究はされていない。通常は T. gondii のみが認められている。
トキソプラズマ科（トキソプラズマ亜科）には、ネコ科を終宿主とする Hammondia hammondi と Besnoitia 属、イヌ科を終宿主とする H. heydorni と Neospora caninum などが知られている。このうちネコ科を終宿主とする H. hammondi は、トキソプラズマと極めて近縁である。
|T. gondii tachyzoites under 100x magnification with oil|
(Nicolle & Manceaux, 1908)
Toxoplasma gondii (tŏk'sə-plāz'mə gŏn'dē-ī') is an obligate, intracellular, parasitic protozoan that causes the disease toxoplasmosis.
Found worldwide, T. gondii is capable of infecting virtually all warm-blooded animals. In humans, it is one of the most common parasites; serological studies estimate that 30–50% of the global population has been exposed to and may be chronically infected with T. gondii, although infection rates differ significantly from country to country. For example, previous estimates have shown the highest prevalence of persons infected with T. gondii to be in France, at 84%. Although mild, flu-like symptoms occasionally occur during the first few weeks following exposure, infection with T. gondii produces no readily observable symptoms in healthy human adults. This asymptomatic state of infection is referred to as a latent infection and has recently been associated with numerous subtle adverse or pathological behavioral alterations in humans. In infants, HIV/AIDS patients, and others with weakened immunity, infection can cause serious and occasionally fatal illness (toxoplasmosis).
T. gondii has been shown to alter the behavior of infected rodents in ways thought to increase the rodents' chances of being preyed upon by cats. Support for this “Manipulation Hypothesis” stems from studies showing T. gondii infected rats have a decreased aversion to cat urine and increased reaction time. Because cats are the only hosts within which T. gondii can sexually reproduce to complete and begin its lifecycle, such behavioral manipulations are thought to be evolutionary adaptations to increase the parasite's reproductive success, in one of the manifestations the evolutionary biologist Richard Dawkins attributes to the "extended phenotype". The primary mechanisms of T. gondii–induced behavioral changes in rodents is now known to occur through epigenetic remodeling in neurons which govern the associated behaviors; for example, it modifies epigenetic methylation to cause hypomethylation of arginine vasopressin-related genes in the medial amygdala to greatly decrease predator aversion. Widespread histone-lysine acetylation in cortical astrocytes appears to be another epigenetic mechanism employed by T. gondii. Differences in aversion to cat urine are observed between non-infected and infected humans and sex differences within these groups were apparent as well.
A number of studies have suggested subtle behavioral or personality changes may occur in infected humans, and infection with the parasite has recently been associated with a number of neurological disorders, particularly schizophrenia. A 2015 study also found cognitive deficits in adults to be associated with joint infection by both toxoplasma gondii and helicobacter pylori in a regression model with controls for race-ethnicity and educational attainment. However, although a causal relationship between latent toxoplasmosis with these neurological phenomena has not yet been established, preliminary evidence suggests that T. gondii infection can induce some of the same alterations in the human brain as those observed in mice.
The lifecycle of T. gondii can be broadly summarized into two components: 1) a sexual component that occurs only within cats (felids, wild or domestic), and 2) an asexual component that can occur within virtually all warm-blooded animals, including humans, cats, and birds. Because T. gondii can sexually reproduce only within cats, they are defined as the definitive host of T. gondii. All other hosts – hosts in which only asexual reproduction can occur – are defined as intermediate hosts.
When a member of the cat family is infected with T. gondii (e.g. by consuming an infected mouse laden with the parasite's tissue cysts), the parasite survives passage through the stomach, eventually infecting epithelial cells of the cat's small intestine. Inside these intestinal cells, the parasites undergo sexual development and reproduction, producing millions of thick-walled, zygote-containing cysts known as oocysts.
Infected epithelial cells eventually rupture and release oocysts into the intestinal lumen, whereupon they are shed in the cat's feces. Oocysts can then spread to soil, water, food, or anything potentially contaminated with the feces. Highly resilient, oocysts can survive and remain infective for many months in cold and dry climates.
Ingestion of oocysts by humans or other warm-blooded animals is one of the common routes of infection. Humans can be exposed to oocysts by, for example, consuming unwashed vegetables or contaminated water, or by handling the feces (litter) of an infected cat. Although cats can also be infected by ingesting oocysts, they are much less sensitive to oocyst infection than are intermediate hosts.
T. gondii is considered to have three stages of infection; the tachyzoite stage of rapid division, the bradyzoite stage of slow division within tissue cysts, and the oocyst environmental stage. When an oocyst or tissue cyst is ingested by a human or other warm-blooded animal, the resilient cyst wall is dissolved by proteolytic enzymes in the stomach and small intestine, freeing sporozoites from within the oocyst. The parasites first invade cells in and surrounding the intestinal epithelium, and inside these cells, the parasites differentiate into tachyzoites, the motile and quickly multiplying cellular stage of T. gondii. Tissue cysts in tissues such as brain and muscle tissue, form approximately 7–10 days after initial infection.
Inside host cells, the tachyzoites replicate inside specialized vacuoles (called the parasitophorous vacuoles) created during parasitic entry into the cell. Tachyzoites multiply inside this vacuole until the host cell dies and ruptures, releasing and spreading the tachyzoites via the bloodstream to all organs and tissues of the body, including the brain.
Following the initial period of infection characterized by tachyzoite proliferation throughout the body, pressure from the host's immune system causes T. gondii tachyzoites to convert into bradyzoites, the semidormant, slowly dividing cellular stage of the parasite. Inside host cells, clusters of these bradyzoites are known as tissue cysts. The cyst wall is formed by the parasitophorous vacuole membrane. Although bradyzoite-containing tissue cysts can form in virtually any organ, tissue cysts predominantly form and persist in the brain, the eyes, and striated muscle (including the heart). However, specific tissue tropisms can vary between species; in pigs, the majority of tissue cysts are found in muscle tissue, whereas in mice, the majority of cysts are found in the brain.
Cysts usually range in size between five and 50 µm in diameter, (with 50 µm being about two-thirds the width of the average human hair).
Consumption of tissue cysts in meat is one of the primary means of T. gondii infection, both for humans and for meat-eating, warm-blooded animals. Humans consume tissue cysts when eating raw or undercooked meat (particularly pork and lamb). Tissue cyst consumption is also the primary means by which cats are infected.
Tissue cysts can be maintained in host tissue for the lifetime of the animal. However, the perpetual presence of cysts appears to be due to a periodic process of cyst rupturing and re-encysting, rather than a perpetual lifespan of individual cysts or bradyzoites. At any given time in a chronically infected host, a very small percentage of cysts are rupturing, although the exact cause of this tissue cysts rupture is, as of 2010, not yet known.
Theoretically, T. gondii can be passed between intermediate hosts indefinitely via a cycle of consumption of tissue cysts in meat. However, the parasite's lifecycle begins and completes only when the parasite is passed to a feline host, the only host within which the parasite can again undergo sexual development and reproduction.
Khan et al. reviewed evidence that despite the occurrence of a sexual phase in its life cycle, T. gondii has an unusual population structure dominated by three clonal lineages (Types I, II and III) that occur in North America and Europe. They estimated that a common ancestor founded these clonal lineages about 10,000 years ago. In a further and larger study (with 196 isolates from diverse sources including T. gondii found in the bald eagle, gray wolves, Arctic foxes and sea otters), Dubey et al. also found that T. gondii strains infecting North American wildlife have limited genetic diversity with the occurrence of only a few major clonal types. They found that 85% of strains in North America were of one of three widespread genotypes (Types II, III and Type 12). Thus T. gondii has retained the capability for sex in North America over many generations, producing largely clonal populations, and matings have generated little genetic diversity.
During different periods of its life cycle, individual parasites convert into various cellular stages, with each stage characterized by a distinct cellular morphology, biochemistry, and behavior. These stages include the tachyzoites, merozoites, bradyzoites (found in tissue cysts), and sporozoites (found in oocysts).
Motile, and quickly multiplying, tachyzoites are responsible for expanding the population of the parasite in the host. When a host consumes a tissue cyst (containing bradyzoites) or an oocyst (containing sporozoites), the bradyzoites or sporozoites stage-convert into tachyzoites upon infecting the intestinal epithelium of the host. During the initial, acute period of infection, tachyzoites spread throughout the body via the blood stream. During the later, latent (chronic) stages of infection, tachyzoites stage-convert to bradyzoites to form tissue cysts.
Like tachyzoites, merozoites divide quickly, and are responsible for expanding the population of the parasite inside the cat intestine prior to sexual reproduction. When a feline definitive host consumes a tissue cyst (containing bradyzoites), bradyzoites convert into merozoites inside intestinal epithelial cells. Following a brief period of rapid population growth in the intestinal epithelium, merozoites convert into the noninfectious sexual stages of the parasite to undergo sexual reproduction, eventually resulting in the formation of zygote-containing oocysts.
Bradyzoites are the slowly dividing stage of the parasite that make up tissue cysts. When an uninfected host consumes a tissue cyst, bradyzoites released from the cyst infect intestinal epithelial cells before converting to the proliferative tachyzoite stage. Following the initial period of proliferation throughout the host body, tachyzoites then convert back to bradyzoites, which reproduce inside host cells to form tissue cysts in the new host.
Sporozoites are the stage of the parasite residing within oocysts. When a human or other warm-blooded host consumes an oocyst, sporozoites are released from it, infecting epithelial cells before converting to the proliferative tachyzoite stage.
The following have been identified as being risk factors for T. gondii infection:
Infection in humans and other warm-blooded animals can occur:
In warm-blooded animals, such as brown rats, sheep, and dogs, T. gondii has also been shown to be sexually transmitted, and it is hypothesized that it may be sexually transmitted in humans, although not yet proven. Although T. gondii can infect, be transmitted by, and asexually reproduce within humans and virtually all other warm-blooded animals, the parasite can sexually reproduce only within the intestines of members of the cat family (felids). Felids are therefore defined as the definitive hosts of T. gondii, with all other hosts defined as intermediate hosts like human or other mammals.
Sewage has been identified as a carriage medium for the organism.
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The following precautions are recommended to prevent or greatly reduce the chances of becoming infected with T. gondii. This information has been adapted from the websites of United States Centers for Disease Control and Prevention and the Mayo Clinic.
In 1908, while working at the Pasteur Institute in Tunis, Charles Nicolle and Louis Manceaux discovered a protozoan organism in the tissues of a hamster-like rodent known as the gundi, Ctenodactylus gundi. Although Nicolle and Manceaux initially believed the organism to be a member of the genus Leishmania that they described as "Leishmania gondii", they soon realized they had discovered a new organism entirely. They named it Toxoplasma gondii, a reference to its morphology (Toxo, from Greek τόξον (toxon); arc, bow, and πλάσμα (plasma); i.e., anything shaped or molded) and the host in which it was discovered, the gundi (gondii). The same year Nicolle and Mancaeux discovered T. gondii, Alfonso Splendore identified the same organism in a rabbit in Brazil. However, he did not give it a name.
The first conclusive identification of T. gondii in humans was in an infant girl delivered full term by Caesarean section on May 23, 1938, at Babies' Hospital in New York City. The girl began having seizures at three days of age, and doctors identified lesions in the maculae of both of her eyes. When she died at one month of age, an autopsy was performed. Lesions discovered in her brain and eye tissue were found to have both free and intracellular T. gondii'. Infected tissue from the girl was homogenized and inoculated intracerebrally into rabbits and mice; the animals subsequently developed encephalitis. Later, congenital transmission was found to occur in numerous other species, particularly in sheep and rodents.
The possibility of T. gondii transmission via consumption of undercooked meat was first proposed by D. Weinman and A.H Chandler in 1954. In 1960, the cyst wall of tissue cysts was shown to dissolve in the proteolytic enzymes found in the stomach, releasing infectious bradyzoites into the stomach (and subsequently into the intestine). The hypothesis of transmission via consumption of undercooked meat was tested in an orphanage in Paris in 1965; yearly acquisition rates of T. gondii rose from 10% to 50% after adding two portions of barely cooked beef or horse meat to the orphans' daily diets, and to 100% after adding barely cooked lamb chops.
In 1959, a study in Bombay found the prevalence of T. gondii in strict vegetarians to be similar to that found in nonvegetarians. This raised the possibility of a third major route of infection, beyond congenital and carnivorous transmission. In 1970, the existence of oocysts was discovered in cat feces, and the fecal-oral route of infection via oocysts was demonstrated.
Throughout the 1970s and 1980s, a vast number of species were tested for the ability to shed oocysts upon infection. Whereas at least 17 different species of felids have been confirmed to shed oocysts, no nonfelid has been shown to be permissive for T. gondii sexual reproduction and subsequent oocyst shedding.
The differences in behavior observed in infected hosts compared to non-infected individuals have been shown to be sex dependent. In humans for example, studies using the Cattell’s 16 Personality Factor questionnaire, found that infected men scored lower on Factor G (superego strength/rule consciousness) and higher on Factor L (vigilance) while the opposite pattern was observed for infected women. In 9 out of 11 studies, sex differences within personality traits were observed using Cattell’s Personality Factor questionnaire. However, human studies have not been able to show causation as they have all been observational studies. Therefore it is possible that people who already possess certain personality traits have a higher likelihood of becoming infected, as opposed to T. gondii causing behavioral or personality changes inside of its host. Animal studies have shown that mice infected with T. gondii have motor performance worse than non-infected mice. In a human study with volunteer blood donors, reaction times and the amount of time the subject remained focused for were worse for the infected group than for the control group. However, the infection status was found to only explain less than 10% of the variability in motor performance, making this a weak correlation. A few observational studies on human subjects have also found the risk of traffic accidents to be significantly greater in infected persons than non-infected controls. One of these studies concluded this risk was 2.65 times greater for infected persons, and it is hypothesized that the patterns of decreased psychomotor performance could be responsible for the increased prevalence of traffic accidents among persons infected with T. gondii. Rhesus blood type was also found to be correlated with the prevalence of traffic accidents with Rhesus-positive infected persons having a lower risk for traffic accidents than Rhesus-negative infected persons.
Toxoplasmosis is becoming a global health hazard as it infects 30-50% of the world human population. Clinically, the life-long presence of the parasite in tissues of a majority of infected individuals is usually considered asymptomatic. However, a number of studies show that this 'asymptomatic infection' may also lead to development of other human pathologies. ... The seroprevalence of toxoplasmosis correlated with various disease burden. Statistical associations does not necessarily mean causality. The precautionary principle suggests however that possible role of toxoplasmosis as a triggering factor responsible for development of several clinical entities deserves much more attention and financial support both in everyday medical practice and future clinical research.
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