Both CE and AE have recently been

Both CE and AE have recently been included on the WHO Neglected Tropical disease list. Echinococcosis has a global estimated disease burden of 2–5×107 DALY (Disability Adjusted Life Years) highlighting the considerable medical, social and economic impacts on animal and human populations worldwide (Torgerson and Macpherson, 2011). This estimate includes livestock related as well as sylvatic strains of echinococcosis. We discuss current knowledge and knowledge gaps for future exploration with regard to the life cycles, genotypes, animal hosts, and human cases of Echinococcus canadensis (G6, G8, G10) one of the causative agents for cystic echinococcosis (CE) and Echinococcus multilocularis, the causative agent of alveolar echinococcosis (AE) in these northern countries.
Echinococcus canadensis
Echinococcus multilocularis
Current challenges and future needs for E. canadensis and E. multilocularis in the north
Conclusions Our knowledge regarding E. canadensis and E. multilocularis in wildlife in Russia, Fennoscandia and North America, is continuously growing. However, without systematic surveillance in humans, animals and environmental samples obtaining reliable data on incidence, prevalence, genetic beta-lactamase and human health burden from across the circumpolar region remains problematic. We are fortunate that E. canadensis appears to have considerably lower pathogenicity compared to E. granulosus ss. and that the “North American” E. multilocularis strains may have lower zoonotic potential than European and Asian genotypes. However this situation could be changing due to rapid climate and landscape change, anthropogenic changes in the wildlife/human interface, and globalisation of trade and travel. Increasing survey effort and more powerful molecular tools are already bringing to light a much more complicated picture of genetic diversity with Echinococcus including the presence of Asian and European type strains of E. multilocularis in animals around the circumpolar north. It may be a decade or more before we are able to assess the effects in the human populations in the region.
Acknowledgements We would like to thank Karen Gesy for her comments on the manuscript. The work carried out by A. Miller in Sweden was funded by an EU Formas grant (EMIDA-ERA NET), project “Echinococcus Multilocularis In ROdents (EMIRO)”, grant number 221-2011-2212.
Introduction Cryptosporidium has been an enigma since it was first described by Edward Tyzzer in 1907 in the gastric glands of a mouse (Tyzzer, 1907). He placed it in the coccidian family Asporocystidae reflecting the lack of sporocysts in the oocyst (i.e. naked sporozoites) and what were presumed to be the possession of similar life cycle features (Levine, 1988). It is interesting when going back to Tyzzer\'s morphological description, how atypical it is for a coccidian, in particular the possession of an organ of attachment - a structure that has only recently been given the attention it clearly warrants in terms of considering Cryptosporidium\'s true affinities. For the next 70years following Tyzzer\'s description, Cryptosporidium continued to be viewed as a curiosity. More species were described largely on the basis of host occurrence, but the parasite was always viewed as atypical. This was not only because of its oocyst and attachment organ, but also because of the ability of unshed oocyst to produce autoinfections, and the extra-cytoplasmic association with its host cell with endogenous developmental stages confined to the apical surfaces of epithelial cells, a characteristic now referred to as epicellular (Barta and Thompson, 2006; Clode et al., 2015; Thompson et al., 2005; Valigurová et al., 2007). However, these fascinating biological peculiarities were overshadowed by the serious public health consequences of opportunistic infections with Cryptosporidium that emerged in the 1980\'s, principally taking advantage of the weakened immune systems of AIDS patients (Checkley et al., 2014). This health emergency brought a sharp focus on the need for chemotherapeutics and quickly confirmed Cryptosporidium\'s complete insensitivity to anti-coccidial drugs (Tenter et al., 2002; Thompson et al., 2005).