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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Oocysts

 
 
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Disease relevance of Oocysts

  • In terms of body weight gain, no significant difference due to toxic interaction between duokvin and any dose of lasalocid or semduramicin was detected in chickens experimentally infected with oocysts of Eimeria tenella and E. mitis [1].
  • The role of adaptive and innate immune responses in control of parasites was explored by infecting BALB/c, IFN-gamma knockout (GKO), and severe combined immune deficient (SCID) mice with S. neurona (10(4) sporocysts/mouse) [2].
  • With the exception of groups given 200mg/kg ponazuril on day 7 or 14 pi, mice in groups that got sporocysts developed abnormal neurologic signs [3].
  • These findings indicate that sulfadimethoxine did not significantly reduce the number of days or severity of diarrhea, or the number of oocysts or patent period, nor did it improve weight gains [4].
  • Piglets were each orally inoculated daily for 4 consecutive days, with 10(4)-10(5) nalidixic acid-resistant Salmonella typhimurium and, starting 1 day after inoculation, with 50 000 Isospora suis sporulated oocysts [5].
 

High impact information on Oocysts

  • Complete sporulation occurred within 5 to 13 days in oocysts maintained in potassium dichromate at 25 or 32 degrees C. Complete excystation resulted in the liberation of two sporozoites from the two sporocysts within each oocyst (cryptosporidia have four naked sporozoites within each oocyst) [6].
  • The disease can be diagnosed by identification of oocysts in faecal samples that have undergone formalin-ether concentration [7].
  • Using exogenous chitinase, we also found that the PM does not limit the number of parasites that develop into oocysts, suggesting that the parasite produces sufficient quantities of chitinase to penetrate this potential barrier [8].
  • The subcellular distribution of MAEBL, a sporozoite surface protein, is developmentally regulated from presumed storage organelles in day 15 oocysts to uniform distribution on the surface in day 22 oocysts [9].
  • Kinetic studies carried out on the enzyme derived from E. tenella oocysts demonstrated substrate inhibition by NAD and mycophenolic acid inhibition similar to that found for mammalian enzymes, but different from that for bacterial enzymes [10].
 

Chemical compound and disease context of Oocysts

 

Biological context of Oocysts

 

Anatomical context of Oocysts

  • With arginyl-6-amino-2-styrylquinoline as a substrate, aminopeptidase activity was observed in permeabilized oocysts and freshly excysted sporozoites but not on intact oocysts or empty oocyst membranes after excystation [21].
  • The electrophoretic mobility of oocysts purified on a cold Percoll-sucrose gradient after the feces was defatted with ethyl acetate (EAPS method) varied linearly with pH from 0.0 m2 V-1 s-1 at pH 2.4 to -3.2 x 10(-8) m2 V-1 s-1 at pH 10 (sigma = 0.52), thus displaying the negative surface charge at neutral pH observed by other researchers [22].
  • Of 10 mice given oocysts exposed to formaldehyde, 6 had a few developmental stages of cryptosporidium in the ileum [23].
  • We show here that Pbs25 was detectable in preparations of gametes 30 min post-gametocyte activation, expression continued on zygotes, ookinetes and oocysts indicating there is a significant overlap of expression of the two immunogenic zygote-ookinete proteins belonging to the P25/28 protein family of sexual stage antigens [24].
  • Central nervous systems were incubated with either an acetic acid or a methanolic extract of larval stages of Trichobilharzia ocellata (miracidia, mother sporocysts, cercariae) [25].
 

Associations of Oocysts with chemical compounds

  • Studies of a glycoprotein in the oocysts of Eimeria tenella [26].
  • (The fifteenth evaluable patient had a CD4 count 235 x 10(6)/l.) Of these 14 patients, five showed a major response (symptomatic improvement and eradication of Cryptosporidial oocysts from the stool), two had a minor response (symptomatic improvement with persistence of oocysts in stool), and seven had no response to therapy with letrazuril [27].
  • Lasalocid and nigericin demonstrated less activity against sporozoites but reduced the infectivity of oocysts [28].
  • They were medicated with 0, 30, 60, or 120 micrograms of halofuginone lactate per kg from days 2 to 8 postinfection (p.i.). Unmedicated calves passed large numbers of oocysts between 3 and 14 days p.i. Treatment with 30 micrograms/kg did not completely inhibit oocyst output during medication, whereas 60 and 120 micrograms/kg did [29].
  • Commonly, oocysts are exposed to a strong solution of L-cysteine [30].
 

Gene context of Oocysts

  • Groups of interferon-gamma gene knockout (IFN-gamma-KO) mice, inducible nitric oxide synthase gene knockout (iNOS-KO) mice, endothelial nitric oxide synthase gene knockout (eNOS-KO) and appropriate genetic background mice (BALB/c or C57BL/6) were orally fed sporocysts or Hanks balanced salt solution [31].
  • Overall, 14/15 volunteers who did not shed oocysts expressed either IFN-gamma or IL-15 [32].
  • Reduction in shedding of oocysts observed in the Lactobacillus supplemented mice during deminished IL-2 and IFN-gamma production may be mediated by factors released into the intestinal lumen by the Lactobacillus and possibly other host cellular mechanisms [33].
  • Excretion of oocysts by IFN- gamma -deficient mice was unaffected by treatment with anti-IL-4, indicating that IL-4 stimulated IFN- gamma activity [34].
  • During secondary infections, only perforin knockout mice produced significantly more oocysts compared to control mice [35].
 

Analytical, diagnostic and therapeutic context of Oocysts

References

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