cryptosporidiosis/carbohydrate

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Serum mannose-binding lectin deficiency is associated with cryptosporidiosis in young Haitian children.

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BACKGROUND Mannose-binding lectin (MBL) is a component of the innate immune response and binds microbial surfaces through carbohydrate recognition domains. MBL deficiency may contribute to susceptibility to a variety of infectious diseases, particularly in young children. MBL binds to the

Developmentally regulated biosynthesis of carbohydrate and storage polysaccharide during differentiation and tissue cyst formation in Toxoplasma gondii.

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Toxoplasma gondii belongs to the Apicomplexa phylum, which comprises protozoan parasites of medical and veterinary significance, responsible for a wide variety of diseases in human and animals, including malaria, toxoplasmosis, coccidiosis and cryptosporidiosis. During infection in the intermediate

Variability among Cryptosporidium parvum genotype 1 and 2 immunodominant surface glycoproteins.

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Published genomic differences between Cryptosporidium parvum genotype 1 (human-derived) and genotype 2 (animal and human-derived) isolates suggest that these may belong to two distinct species. This is of significant interest since genotype 1 isolates are associated with sporadic cases of human

[Identification and molecular characterization of a Toxoplasma gondii microneme].

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Protozoan of the phylum Apicomplexa are of high medical and veterinary importance, causing diseases such as malaria, toxoplasmosis and cryptosporidiosis. Invasive stages of apicomplexans possess organelles named micronemes, which are involved in the invasion process. We have recently characterized a

Differential metabolic response in AIDS-related chronic protozoal diarrhoea.

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OBJECTIVE As the pro-inflammatory cytokine tumour necrosis factor-alpha is greater in microsporidiosis than cryptosporidiosis, there may be a distinct metabolic response between the two organisms. METHODS Male HIV seropositive subjects with an untreated AIDS-defining diagnosis of microsporidiosis or

Interaction of Cryptosporidium hominis and Cryptosporidium parvum with primary human and bovine intestinal cells.

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Cryptosporidiosis in humans is caused by the zoonotic pathogen Cryptosporidium parvum and the anthroponotic pathogen Cryptosporidium hominis. To what extent the recently recognized C. hominis species differs from C. parvum is unknown. In this study we compared the mechanisms of C. parvum and C.

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

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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

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