Differences in the occurrence and epidemiology of cryptosporidiosis in Aboriginal and non-Aboriginal people in Western Australia (2002-2012).

Cryptosporidiosis is a diarrhoeal illness caused by the protozoan parasite Cryptosporidium. In Australia, very little is known about the epidemiology of cryptosporidiosis in Aboriginal peoples. The present study analysed long-term cryptosporidiosis patterns across Western Australia (WA) (2001-2012), combined with genotyping and subtyping data at the 18S and glycoprotein 60 (gp60) loci respectively.

Metabolomic profiling of faecal extracts from Cryptosporidium parvum infection in experimental mouse models.

Cryptosporidiosis is a gastrointestinal disease in humans and animals caused by infection with the protozoan parasite Cryptosporidium. In healthy individuals, the disease manifests mainly as acute self-limiting diarrhoea, but may be chronic and life threatening for those with compromised immune systems. Control and treatment of the disease is challenged by the lack of sensitive diagnostic tools and broad-spectrum chemotherapy.

Human cryptosporidiosis diagnosed in Western Australia: a mixed infection with Cryptosporidium meleagridis, the Cryptosporidium mink genotype, and an unknown Cryptosporidium species.

This report describes a case of cryptosporidiosis from an immunocompetent patient from Perth, Western Australia, suffering from diarrhea and a spectrum of other symptoms. Molecular identification revealed that this patient was infected with three Cryptosporidium species-Cryptosporidium meleagridis, the Cryptosporidium mink genotype, and an unknown Cryptosporidium species.

Molecular characterization of Cryptosporidium spp. from wild rats and mice from rural communities in the Philippines.

In order to examine the prevalence of Cryptosporidium in wild rodents in the Philippines and understand the role wild rodents play in the transmission of this parasite to humans and livestock, 194 fecal samples from wild rats and mice from Luzon and Mindoro islands were examined. Molecular screening at the 18S and actin gene loci identified an overall prevalence of 25.8% (95%CI: 19.