據(jù)報(bào)道，捷克科學(xué)家近日指出,，精神分裂癥可能與一種叫做弓漿蟲的寄生蟲有很大的關(guān)系。弓漿蟲是一種人畜共有的寄生蟲,，存在于貓的糞便中,，目前全世界有一半左右的人口已經(jīng)感染了弓漿蟲。這種寄生蟲以貓為最終宿主,，所以差不多有10%的貓帶有弓漿蟲病,，而人、豬,、牛,、羊、狗,、鳥和鼠類等都是弓漿蟲的中間宿主,。自從19世紀(jì)20年代以來(lái)，醫(yī)生已經(jīng)確認(rèn)在懷孕期間被感染的婦女會(huì)將疾病傳染給胎兒,，從而導(dǎo)致胎兒的嚴(yán)重大腦損壞,，甚至死亡。而在成年人中,，這種感染會(huì)引發(fā)類似感冒的癥狀,，對(duì)于那些免疫系統(tǒng)低下的人群來(lái)說(shuō)，會(huì)導(dǎo)致類似腦炎這種嚴(yán)重的并發(fā)癥,，這種感染大多是潛伏的,，并沒有明顯病癥。
這位63歲的捷克科學(xué)家普實(shí)克—弗萊格爾（Jaroslav Flegr）稱自己就是活生生的例子,，據(jù)他所述,，自己已被弓漿蟲感染,，在過去的20年里，他的性格改變了,，導(dǎo)致行為怪異,，且常有自虐行為發(fā)生。他在接受大西洋月刊采訪時(shí)表示,，約在30年前,，他在讀了英國(guó)牛津大學(xué)動(dòng)物學(xué)家理查德道金斯的一本書后，就開始禪思自己的推理,。書中描述了扁形蟲通過借用螞蟻身體,，感染他們的神經(jīng)系統(tǒng)來(lái)延續(xù)生命周期。這種感染改變了螞蟻的行為,，例如,，當(dāng)遇到溫度下降時(shí)，昆蟲一般會(huì)呆在地下,，但相反的是,，這些螞蟻卻爬上草葉，將草葉壓彎,，最后它們就被牧羊群吃掉,，從而扁形蟲就會(huì)在動(dòng)物腸道里繼續(xù)生命周期。弗萊格爾說(shuō)：“這是我了解到的第一例寄生蟲操縱行為案例,，對(duì)我影響深刻,，之后我便開始注意自身行為與螞蟻之間的相似處。”
據(jù)利茲大學(xué)首席研究員—格倫麥肯基龍（Glenn McConkey）醫(yī)生研究證明,，寄生蟲會(huì)影響多巴胺的產(chǎn)量,，攜帶信息的化學(xué)品在大腦里控制運(yùn)動(dòng)方向、行為認(rèn)知,，由此引發(fā)精神分裂癥和躁郁癥,，寄生蟲通過在細(xì)胞中形成囊腫，分泌絡(luò)氨酸羥基化酶來(lái)影響大腦,。研究顯示,，大部分精神分裂癥患者都有弓形體病的臨床史記錄，由于導(dǎo)致該病情的原因包含很多因素,，因此找到根治精神分裂癥的療法非常困難,，科學(xué)家目前也仍不十分清楚，寄生蟲為何選擇人類作為寄主,。而且對(duì)于老鼠來(lái)說(shuō),，效果也同樣很明顯，科學(xué)家在研究中發(fā)現(xiàn),，被感染的嚙齒動(dòng)物相比那些未被感染的更加活躍,，這就表示被感染的老鼠對(duì)于貓來(lái)說(shuō)就是更具吸引力且明顯的目標(biāo)了,。來(lái)自倫敦大學(xué)的寄生蟲學(xué)家對(duì)此解釋道，由于寄生蟲只能在貓?bào)w內(nèi)存活,，因此老鼠就成為這些寄生蟲操縱的目標(biāo),。她還發(fā)現(xiàn)，正如研究人員曾經(jīng)所展示的研究結(jié)果,，被感染的老鼠行為表現(xiàn)更活躍,，對(duì)于潛伏著的“敵人”也失去了一定的警惕性。(生物谷 Bioon.com)
doi:10.1371/journal.pone.0028925
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The Distribution of Toxoplasma gondii Cysts in the Brain of a Mouse with Latent Toxoplasmosis: Implications for the Behavioral Manipulation Hypothesis
Miroslava Berenreiterová, Jaroslav Flegr, Aleš A. Kuběna, Pavel Němec
Background
The highly prevalent parasite Toxoplasma gondii reportedly manipulates rodent behavior to enhance the likelihood of transmission to its definitive cat host. The proximate mechanisms underlying this adaptive manipulation remain largely unclear, though a growing body of evidence suggests that the parasite-entrained dysregulation of dopamine metabolism plays a central role. Paradoxically, the distribution of the parasite in the brain has received only scant attention.
Methodology/Principal Findings
The distributions of T. gondii cysts and histopathological lesions in the brains of CD1 mice with latent toxoplasmosis were analyzed using standard histological techniques. Mice were infected per orally with 10 tissue cysts of the avirulent HIF strain of T. gondii at six months of age and examined 18 weeks later. The cysts were distributed throughout the brain and selective tropism of the parasite toward a particular functional system was not observed. Importantly, the cysts were not preferentially associated with the dopaminergic system and absent from the hypothalamic defensive system. The striking interindividual differences in the total parasite load and cyst distribution indicate a probabilistic nature of brain infestation. Still, some brain regions were consistently more infected than others. These included the olfactory bulb, the entorhinal, somatosensory, motor and orbital, frontal association and visual cortices, and, importantly, the hippocampus and the amygdala. By contrast, a consistently low incidence of tissue cysts was recorded in the cerebellum, the pontine nuclei, the caudate putamen and virtually all compact masses of myelinated axons. Numerous perivascular and leptomeningeal infiltrations of inflammatory cells were observed, but they were not associated with intracellular cysts.
Conclusion/Significance
The observed pattern of T. gondii distribution stems from uneven brain colonization during acute infection and explains numerous behavioral abnormalities observed in the chronically infected rodents. Thus, the parasite can effectively change behavioral phenotype of infected hosts despite the absence of well targeted tropism.
