Tailored communication methods as key to implementation of evidence-based solutions in primary child health care.

Background: Evidence-based policies should underpin successful implementation of innovations within child health care. The EU-funded Models of Child Health Appraised project enabled research into effective methods to communicate research evidence. The objective of this study was to identify and categorize methods to communicate evidence-based research recommendations and means to tailor this to stakeholder audiences. Methods: We conducted an online survey among national stakeholders in child health. Analysis of the most effective strategies to communicate research evidence and reach the target audience was carried out in order to ensure implementation of optimal child health care models at a national level. Results: Representatives of stakeholders from 21 of the then 30 EU MS and EEA countries responded to the questionnaire. Three main approaches in defining the strategies for effective communication of research recommendations were observed, namely: dissemination of information, involvement of stakeholders and active attitude towards change expressed in actions. The target audience for communicating recommendations was divided int

The marsupial trypanosome Trypanosoma copemani is not an obligate intracellular parasite, although it adversely affects cell health

Background Trypanosoma cruzi invades and replicates inside mammalian cells, which can lead to chronic Chagas disease in humans. Trypanosoma copemani infects Australian marsupials and recent investigations indicate it may be able to invade mammalian cells in vitro, similar to T. cruzi. Here, T. cruzi 10R26 strain (TcIIa) and two strains of T. copemani [genotype 1 (G1) and genotype 2 (G2)] were incubated with marsupial cells in vitro. Live-cell time-lapse and fluorescent microscopy, combined with high-resolution microscopy (transmission and scanning electron microscopy) were used to investigate surface interactions between parasites and mammalian cells. Results The number of parasites invading cells was significantly higher in T. cruzi compared to either genotype of T. copemani, between which there was no significant difference. While capable of cellular invasion, T. copemani did not multiply in host cells in vitro as there was no increase in intracellular amastigotes over time and no release of new trypomastigotes from host cells, as observed in T. cruzi. Exposure of host cells to G2 trypomastigotes resulted in increased host cell membrane permeability within 24 h of infection, and host cell death/blebbing was also observed. G2 parasites also became embedded in the host cell membrane. Conclusions Trypanosoma copemani is unlikely to have an obligate intracellular life-cycle like T. cruzi. However, T. copemani adversely affects cell health in vitro and should be investigated in vivo in infected host tissues to better understand this host-parasite relationship. Future research should focus on increasing understanding of the T. copemani life history and the genetic, physiological and ecological differences between different genotypes