Category Archives: Cryptosporidium

AEM 

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ABSTRACT

Cryptosporidiosis, a leading cause of diarrhea among infants, is caused by apicomplexan parasites classified in the genus Cryptosporidium. The lack of effective drugs is motivating research to develop alternative treatments. With this aim, the impact of probiotics on the course of cryptosporidiosis was investigated. The native intestinal microbiota of specific pathogen-free immunosuppressed mice was initially depleted with orally administered antibiotics. A commercially available probiotic product intended for human consumption was subsequently added to the drinking water. Mice were infected with Cryptosporidium parvum oocysts. On average, mice treated with the probiotic product developed more severe infections. The probiotics significantly altered the fecal microbiota, but no direct association between ingestion of probiotic bacteria and their abundance in fecal microbiota was observed. These results suggest that probiotics indirectly altered the intestinal microenvironment or the intestinal epithelium in a way that favored proliferation of C. parvum.

IMPORTANCE The results of our study show that C. parvum responded to changes in the intestinal microenvironment induced by a nutritional supplement. This outcome paves the way for research to identify nutritional interventions aimed at limiting the impact of cryptosporidiosis.

Cambridge Press 

Image CDC

Cryptosporidium is a protozoan parasite that causes the diarrhoeal disease, cryptosporidiosis. Although many species have been identified, the majority of human disease worldwide is caused by two species; Cryptosporidium parvum and Cryptosporidium hominis. In Australia, data from the National Notifiable Diseases Surveillance System (NNDSS) show that cryptosporidiosis outbreaks occur every few years. To better understand the transmission, trends and nature of cryptosporidiosis outbreaks in Western Australia, epidemiological and genomic data from three cryptosporidiosis outbreaks in 2003, 2007 and 2011 were reviewed. The 2007 outbreak was the largest (n = 607) compared with the outbreaks in 2003 (n = 404) and 2011 (n = 355). All three outbreaks appeared to have occurred predominantly in the urban metropolitan area (Perth), which reported the highest number of case notifications; increases in case notifications were also observed in rural and remote areas. Children aged 0–4 years and non-Aboriginal people comprised the majority of notifications in all outbreaks. However, in the 2003 and 2007 outbreaks, a higher proportion of cases from Aboriginal people was observed in the remote areas. Molecular data were only available for the 2007 (n = 126) and 2011 (n = 42) outbreaks, with C. hominis the main species identified in both outbreaks. Subtyping at the glycoprotein 60 (gp60) locus identified subtype IbA10G2 in 46.3% and 89.5% of C. hominis isolates typed, respectively, in the 2007 and 2011 outbreaks, with the IdA15G1 subtype was identified in 33.3% of C. hominis isolates typed in the 2007 outbreak. The clustering of cases with the IdA15G1 subtype in the remote areas suggests the occurrence of a concurrent outbreak in remote areas during the 2007 outbreak, which primarily affected Aboriginal people. Both the C. hominis IbA10G2 and IdA15G1 subtypes have been implicated in cryptosporidiosis outbreaks worldwide; its occurrence indicates that the mode of transmission in both the 2007 and 2011 outbreaks was anthroponotic. To better understand the epidemiology, sources and transmission of cryptosporidiosis in Australia, genotyping data should routinely be incorporated into national surveillance programmes.