Microsporidiosis is a common disease in animals and humans around the world. Enterocytozoon bieneusi is the most common microsporidian species in humans. Many animal species may be a potential source of human microsporidiosis. However, information concerning prevalence and genotypes of E. bieneusi infection in farmed foxes (Vulpes lagopus) is scarce. Therefore, the present study examined prevalence, risk factors and genotypes of E. bieneusi in farmed foxes in northern China using a genetic approach. Of 302 fecal samples from farmed foxes, 37 (12.25 %, 95 % CI 8.55–15.95) were PCR-positive for E. bieneusi, and the prevalence was highly associated with the farming mode in that foxes raised outdoors (26.03 % positive, 95 % CI 18.91–33.15) had a significantly higher E. bieneusi prevalence than those raised indoors. Eleven internal transcribed spacer (ITS) genotypes were identified among the positive samples: four known E. bieneusi genotypes (Peru 8, Types IV, CHN-DC1 and D) and seven novel genotypes (NCF1-NCF7). Genotype NCF2 was the commonest (n = 13) and was found in five farms across three provinces (Jilin, Heilongjiang and Hebei). All genotypes belonged to phylogenetic group 1. Multilocus sequence typing (MLST) analyses revealed additional diversity. These findings indicate the presence of zoonotic E. bieneusi infection in farmed foxes in northern China. This is also the first report of genotypes Peru8, CHN-DC1 and Type IV, and seven novel genotypes (NCF1-NCF7) in farmed foxes by ITS combining with microsatellite and minisatellite markers for the first time. The results will provide baseline data for preventing and controlling E. bieneusi infection in farmed foxes, other animals and humans.

Significant progress has been made in the prevention, control, and elimination of human parasitic diseases in China in the past 60 years. However, parasitic diseases of poverty remain major causes of morbidity and mortality, and inflict enormous economic costs on societies. In this article, we review the prevalence rates, geographical distributions, epidemic characteristics, risk factors, and clinical manifestations of parasitic diseases of poverty listed in the first issue of the journal Infectious Diseases of Poverty on 25 October 2012. We also address the challenges facing control of parasitic diseases of poverty and provide suggestions for better control.

Brain microRNAs (miRNAs) change in abundance in response to Toxoplasma gondii infection. However, their precise role in the pathogenesis of cerebral infection with T. gondii oocyst remains unclear. We studied the abundance of miRNAs in the brain of mice on days 11 and 33 post-infection (dpi) in order to identify miRNA pattern specific to early (11 dpi) and late (33 dpi) T. gondii infection. Mice were challenged with T. gondii oocysts (Type II strain) and on 11 and 33 dpi, the expression of miRNAs in mouse brain was investigated using small RNA (sRNA) sequencing. miRNA expression was confirmed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed to identify the biological processes, molecular functions, and cellular components, as well as pathways involved in infection. More than 1,500 miRNAs (1,352 known and 150 novel miRNAs) were detected in the infected and control mice. The expression of miRNAs varied across time after infection; 3, 38, and 108 differentially expressed miRNAs (P < 0.05) were detected during acute infection, chronic infection and chronic vs. acute infection, respectively. GO analysis showed that chronically infected mice had more predicted targets of dysregulated miRNAs than acutely infected mice. KEGG analysis indicated that most predicted targets were involved in immune- or disease-related pathways. Our data indicate that T. gondii infection alters the abundance of miRNAs in mouse brain particularly at the chronic stage, probably to fine-tune conditions required for the establishment of a latent brain infection.