Intestinal parasites may be associated with later behavioral problems in internationally adopted children.

AIM: At arrival in new home country, internationally adopted children often have intestinal parasites. International adoptees also exhibit more behavioral problems than their biological peers. We examined whether intestinal parasite infections in international adoptees on arrival in Finland are associated with their later behavioral and emotional problems. METHODS: Data for this study were sourced from the Finnish Adoption Study (FinAdo) based on parental questionnaires for all internationally adopted children under 18 years (n = 1450) who arrived in Finland from 1985 to 2007. A total of 1293 families provided sufficient information on the adoptee's background, parasitic status on arrival, and behavioral symptoms at the median time of 5 years after arrival (mean age = 7.8 years). Behavioral and emotional disorders were evaluated with the Child Behavior Checklist (CBCL). Statistical analyses were conducted using linear regression. RESULTS: Of the 1293 families, parents of 206 adoptive children reported intestinal parasites in their adopted children on arrival. Parasite-infected children had subsequently higher CBCL problem scores than the children without parasites (p < 0.001). The association between intestinal parasites and later behavioral problems was stronger than that between intestinal parasites and any other factors measured in this study, except disability. LIMITATIONS: The control group was naturally provided by the adopted children without parasite infections, but we could not compare the adopted children to non-adopted children without a defined parasite infection. We were unable to specify the effects associated with a specific parasite type. It was not possible either to include multiple environmental factors that could have been associated with behavioral problems in the models, which indicated only modest explanatory values. CONCLUSIONS: In this study, intestinal parasite infections in early childhood may be associated with children's later psychological wellbeing, even in children who move to a country with a low prevalence of parasites. Our findings may support further developments pertaining to the gut-brain theory.

[Behavioural Changes Caused by Parasites: The Parasite Manipulation Hypothesis]. / Wie beeinflussen Parasiten das Verhalten ihres Wirts? Die parasitäre Manipulationshypothese.

Bacteria, archaeae, fungi and viruses of the intestinal microbiome play an important role as symbionts in the complex human ecosystem. Parasites, which account for about 40 % of the earth's biodiversity, depend on hosts to complete their life cycle. This article explains how they use them and which signalling pathways play a role in this, using toxoplasmosis and malaria as examples. The parasitic manipulation hypothesis is based on impressive observations in the wild and under laboratory conditions, especially in invertebrates. For the assumption of an adaptive manipulation, every step from the genotype, the translated messenger, and its source via the used signalling pathways to the altered host behaviour must be proven. The assumption of an adaptive manipulation of humans by T. gondii in the sense of a cause-effect relationship is not proven. Alternative explanations include the inflammatory and immunological processes on the host side, which change the neuronal signal transduction as concomitant symptoms of an infection. Even without confirmation of parasitic manipulation in humans, it could be worthwhile to further investigate the observed associations in order to develop new possibilities for diagnosis and therapy, e. g. for schizophrenia.

Noradrenergic Signaling and Neuroinflammation Crosstalk Regulate Toxoplasma gondii-Induced Behavioral Changes.

Infections of the nervous system elicit neuroimmune responses and alter neurotransmission, affecting host neurological functions. Chronic infection with the apicomplexan parasite Toxoplasma correlates with certain neurological disorders in humans and alters behavior in rodents. Here, we propose that the crosstalk between neurotransmission and neuroinflammation may underlie some of these cognitive changes. We discuss how T. gondii infection suppresses noradrenergic signaling and how the restoration of this pathway improves behavioral aberrations, suggesting that altered neurotransmission and neuroimmune responses may act in concert to perturb behavior. This interaction might apply to other infectious agents, such as viruses, that elicit cognitive changes. We hypothesize that neurotransmitter signaling in immune cells can contribute to behavioral changes associated with brain infection, offering opportunities for potential therapeutic targeting.

Toxoplasmosis, behaviour and personality.

The clinical sequelae of acute and congenital toxoplasmosis are well established, but that of chronic toxoplasma infection remains uncertain. In rodents, chronic toxoplasma infection is associated with altered behaviour leading to an enhanced risk of feline predation and a putative selective advantage to the parasite. It is proposed that neurotropic cysts of toxoplasma exert an effect on animal behaviour, either directly or via the release of metabolic products. Long-standing toxoplasma infection in humans has been linked to cerebral tumour formation and personality shift. In view of the vast population with chronic toxoplasma infection, further studies of the clinical sequelae of this condition are required.