Bransfield Robert C, Wulfman Jeffrey S, Harvey William T, Usman Anju I
Department of Psychiatry, Riverview Medical Center, 225 State Route 35, Red Bank, NJ, United States.
Med Hypotheses. 2008;70(5):967-74. doi: 10.1016/j.mehy.2007.09.006. Epub 2007 Nov 5.
Chronic infectious diseases, including tick-borne infections such as Borrelia burgdorferi may have direct effects, promote other infections and create a weakened, sensitized and immunologically vulnerable state during fetal development and infancy leading to increased vulnerability for developing autism spectrum disorders. A dysfunctional synergism with other predisposing and contributing factors may contribute to autism spectrum disorders by provoking innate and adaptive immune reactions to cause and perpetuate effects in susceptible individuals that result in inflammation, molecular mimicry, kynurenine pathway changes, increased quinolinic acid and decreased serotonin, oxidative stress, mitochondrial dysfunction and excitotoxicity that impair the development of the amygdala and other neural structures and neural networks resulting in a partial Klüver-Bucy Syndrome and other deficits resulting in autism spectrum disorders and/or exacerbating autism spectrum disorders from other causes throughout life. Support for this hypothesis includes multiple cases of mothers with Lyme disease and children with autism spectrum disorders; fetal neurological abnormalities associated with tick-borne diseases; similarities between tick-borne diseases and autism spectrum disorder regarding symptoms, pathophysiology, immune reactivity, temporal lobe pathology, and brain imaging data; positive reactivity in several studies with autistic spectrum disorder patients for Borrelia burgdorferi (22%, 26% and 20-30%) and 58% for mycoplasma; similar geographic distribution and improvement in autistic symptoms from antibiotic treatment. It is imperative to research these and all possible causes of autism spectrum disorders in order to prevent every preventable case and treat every treatable case until this disease has been eliminated from humanity.
慢性传染病,包括蜱传播感染,如伯氏疏螺旋体,可能产生直接影响,引发其他感染,并在胎儿发育和婴儿期造成一种虚弱、敏感且免疫脆弱的状态,从而增加患自闭症谱系障碍的易感性。与其他诱发和促成因素的功能失调协同作用,可能通过激发先天性和适应性免疫反应,在易感个体中引发并持续产生影响,导致炎症、分子模拟、犬尿氨酸途径改变、喹啉酸增加和血清素减少、氧化应激、线粒体功能障碍和兴奋性毒性,进而损害杏仁核及其他神经结构和神经网络的发育,导致部分克吕弗-布西综合征及其他缺陷,引发自闭症谱系障碍和/或在一生中加重由其他原因导致的自闭症谱系障碍。对这一假说的支持包括多例患有莱姆病的母亲和患有自闭症谱系障碍的孩子;与蜱传播疾病相关的胎儿神经异常;蜱传播疾病与自闭症谱系障碍在症状、病理生理学、免疫反应性、颞叶病理学和脑成像数据方面的相似性;多项研究中自闭症谱系障碍患者对伯氏疏螺旋体的阳性反应(22%、26%和20 - 30%)以及对支原体的阳性反应为58%;相似的地理分布以及抗生素治疗后自闭症症状的改善。必须对自闭症谱系障碍的这些及所有可能病因进行研究,以便预防每一例可预防的病例,并治疗每一例可治疗的病例,直到这种疾病从人类中消除。