ABSTRACT
Cryptosporidiosis has been identified as a significant underlying cause of morbidity and mortality worldwide. Studies in high and low income countries have recognized the importance of Cryptosporidium as a cause of diarrhea. The objectives of the current study were to determine the prevalence rate and genotypes of Cryptosporidiumin in diarrheic children in Makkah Region. A total of 1,380 fecal samples were collected from children aged up to 14 years attending 3 major hospitals of Makkah between March 2015 and March 2016. Stool collected were subjected to direct microscopic examination and crypto antigen detection using ImmunoCard STAT, Cryptosporidium/Giardia rapid test. Part of each positive stool sample was kept frozen at -20ºC for molecular characterization. Initial screening by immunochromatographic detection kit revealed 23 positive cases. PCR was performed for positive cases by amplification of a piece of the gene encoding the small (18S) subunit of rRNA producing a 435-438 bp product. Cryptosporidium genotyping was performed by RFLP analysis of PCR products. Genotyping revealed 18 cases C. hominis genotype, 4 cases C. parvaum genotype and one sample failed to be amplified. The data revealed a higher incidence of the common human species C. hominis (81.8%). The detection of both C. hominis and C. parvaum genotypes point to the possibility of both anthroponotic and zoonotic transmission routes occurring in Makkah region. Further studies are needed to verify the subgenotypes of Cryptosporidium to elucidate the real transmission modes and hence plan for effective control strategies.
ABSTRACT
Infection with Schistosoma mansoni, a portal vein-residing helminth, is well known to generate life cycle-dependent, systemic immune responses in the host, type 1 deviation during the prepatent period, and type 2 polarization after oviposition. Here we investigated local immunological changes in the liver after infection. Unlike splenocytes, hepatic lymphocytes from infected mice during the prepatent period already produced a higher amount of IL-4 and a lesser amount of IFN-gamma than those from uninfected mice. Hepatic lymphocytes, particularly conventional T cells, but not NK1.1+ T cells, promptly produced IL-4 in response to worm products, soluble worm Ag preparation (SWAP), whenever presented by Kupffer cells from infected mice. The hepatic lymphocytes that had been stimulated with SWAP presented by infected mice-derived Kupffer cells produced a huge amount of IL-4, IL-13, and IL-5 as well as little IFN-gamma in response to immobilized anti-CD3 mAb. Kupffer cells from uninfected mice produced IL-6 and IL-10, but not IL-12 or IL-18, in response to SWAP stimulation and gained the potential to additionally produce IL-4 and IL-13 after the infection. These results suggested that prompt type 2 deviation in the liver after the infection might be due to the alteration of Kupffer cells that induces SWAP-mediated type 2-development of hepatic T cells.
