ライフサイエンスコーパス: oocyst

1 osquito midgut interactions as it becomes an oocyst.

2 essential for sporogonic development in the oocyst.

3 oked infected meat, or by uptake of cat-shed oocysts.

4 in decreased infection relative to untreated oocysts.

5 ome amplification (WGA) of DNA from purified oocysts.

6 ment, oocysts attached onto already attached oocysts.

7 that observed in mice infected with unfrozen oocysts.

8 ection of the mosquito midgut in the form of oocysts.

9 nd were infected with Cryptosporidium parvum oocysts.

10 trafficking mechanism to deliver PbSR to the oocysts.

11 les artificially spiked with Cryptosporidium oocysts.

12 to induce the excystation of Cryptosporidium oocysts.

13 d limiting the access of cattle to infective oocysts.

14 otective wall develops, forming unsporulated oocysts.

15 guts containing invading ookinetes and early oocysts.

16 ility to invade the mosquito midgut and form oocysts.

17 in, is expressed only in ookinetes and early oocysts.

18 possibility of distinguishing dead from live oocysts.

19 gives rise to haploid sporozoites within the oocysts.

20 raverse the mosquito midgut and transform to oocysts.

21 hilst also detecting damaged and/or excysted oocysts.

22 e and after a challenge with Cryptosporidium oocysts.

23 zoites, bradyzoites, and sporozoites but not oocysts.

24 irds were challenged with live E. acervulina oocysts 14 days posthatch, and fecal-oocyst shedding and

25 Escherichia coli and Cryptosporidium parvum oocysts account for most of the cases of diarrhea in the

26 Upon oocyst acquisition, these walls lose their integrity to

27 neity on transport of Cryptosporidium parvum oocyst and carboxylate microsphere in 2-dimensional micr

28 The robust oocyst and sporocyst walls protect the infective sporozo

29 ver they are severely deficient in ookinete, oocyst and sporozoite formation inside the mosquito vect

30 However, when analyzing oocyst and sporozoite infection rates separately, the re

31 ased by 30% and 24% after infection with the oocyst and sporozoite stages of Plasmodium falciparum, r

32 or differential attraction and biting at the oocyst and sporozoite stages.

33 development, fertilization, and ookinete-to-oocyst and sporozoite-to-liver stage transitions.

34 as secreted into the sporocyst cavity of the oocysts and after excystation, secretion was detected in

35 yptosporidium is transmitted by ingestion of oocysts and completes its life cycle in a single host.

36 asites lacking TRP1 failed to migrate within oocysts and did not egress, suggesting that TRP1 is a vi

37 RAW macrophages could interact rapidly with oocysts and engulfed them by remodelling of their actin

38 nt involves transformation of ookinetes into oocysts and formation of infective sporozoites.

39 or not DOC inhibits or promotes transport of oocysts and microspheres in agricultural soils and by ho

40 Transport of Cryptosporidium parvum oocysts and microspheres in two disparate (a clay- and F

41 enes, protein expression is only reported in oocysts and sporozoites indicating that repressed transc

42 , which restored fertility and production of oocysts and sporozoites, which demonstrates that mitocho

43 e var gene is selected for expression in the oocyst, and transcription of this gene increases dramati

44 iglets were orally challenged with C hominis oocysts, and oral treatment with MMV665917 was commenced

45 tidious nature, the passing of non-infective oocysts, and the short duration of oocyst shedding, dire

46 s in its feces and, after sporulation, these oocysts are infectious to cattle.

47 Oocysts are meiotic spores and the product of parasite s

48 undantly expressed at a time when developing oocysts are observed, roughly 48 to 72 h after inoculati

49 Unsporulated oocysts are shed in the faeces of cats and meiosis gives

50 ) patches for microspheres at pH 4.4 and for oocysts at pH 5.8 and 8.1, where the DLVO energy barrier

51 Sporozoites are formed within oocysts at the mosquito midgut wall and are released int

52 After initial attachment, oocysts attached onto already attached oocysts.

53 In the micromodel, oocysts attached to the forward portion of clean collect

54 hat surface charge heterogeneity allowed for oocyst attachment.

55 The Brazilian datasets were consistent with oocysts being the predominant transmission route in thes

56 lood from DP-treated children (P = .06); the oocyst burden among mosquitoes was lower among those tha

57 The annual oocyst burden measured in community surveys is 3 to 434

58 le oocyst can possibly cause infection, this oocyst burden represents a major potential public health

59 eas of children might potentially reduce the oocyst burden.

60 e host and thus the only source of infective oocysts, but other mammals and birds can develop tissue

61 nth eggs, Giardia cysts, and Cryptosporidium oocysts, but the UASB reactor system discharges higher c

62 e and chemistry of the wall of the T. gondii oocyst by combining wall surface treatments, fluorescenc

63 Effective removal of Cryptosporidium parvum oocysts by granular filtration requires the knowledge of

64 targets derived from Cryptosporidium parvum oocysts by the use of oligonucleotide-gold nanoparticles

65 described for cryopreservation of C. parvum oocysts by vitrification using custom high aspect ratio

66 While cryopreservation of Cryptosporidium oocysts by vitrification was recently achieved, the meth

67 Because a single oocyst can possibly cause infection, this oocyst burden

68 of transmission processes that amplified the oocyst concentration in the drinking-water effluent.

69 coprotein-coated microspheres best resembled oocyst concentration, despite having zeta similar to NH(

70 btain a 3-log inactivation of C. parvum Iowa oocysts, contact times of 105 and 128 min for a solution

71 These, now infectious, sporulated oocysts contaminate the environment as a source of infec

72 usually become infected through ingestion of oocyst-contaminated soil and water, tissue cysts in unde

73 The first was that oocyst contamination of the drinking-water influent, cou

74 on were assessed by calculating the mosquito oocyst count as a marker for infectivity, using standard

75 Oocysts cryopreserved using the described protocol exhib

76 pment and precipitation independently raised oocyst delivery to the ocean (average increases of 44% a

77 In contrast, NF166 and NF165 oocyst densities were strongly reduced in refractory mos

78 s and TEP1 silencing significantly increased oocyst densities.

79 genotyping, two loci significantly affecting oocyst density were identified: one on chromosome 2 betw

80 tes but did increase quality, as measured by oocyst density, by 2.4-fold.

81 doubling prevalence of infected midguts and oocyst density.

82 tor for attachment efficiencies of C. parvum oocyst deposition in porous media for a variety of envir

83 of suspended illite clay drastically enhance oocyst deposition.

84 s a method for confirming putative T. gondii oocysts detected in snail faeces and tissues by microsco

85 asexual blood forms, gametocytes, and in the oocysts developing inside mosquito mid-gut.

86 ctors of the complement-like system restores oocyst development and disease transmission to rodent ho

87 itoes that confer refractoriness (failure of oocyst development in mosquito midguts) to natural Plasm

88 mia that subsequently translated into higher oocyst development in mosquitoes.

89 ciparum, ookinete development in P. berghei, oocyst development in P. berghei and P. falciparum, and

90 D: +/- 1.80 nM) and dose-dependently blocked oocyst development in the mosquito with a 50% inhibitory

91 An antienolase antibody inhibits oocyst development of both Plasmodium berghei and Plasmo

92 tibodies against PfCelTOS strongly inhibited oocyst development of P. falciparum and Plasmodium bergh

93 Mosquito infection ensues upon oocyst development that follows ookinete invasion and tr

94 s RBC binding and plays an important role in oocyst development, a critical step in malaria transmiss

95 nts of the mosquito immune system that limit oocyst development, and provide insight into their possi

96 he mosquito midgut epithelium or ookinete-to-oocyst differentiation but mediates a late-phase immune

97 ntify SOAP as a key molecule for ookinete-to-oocyst differentiation in mosquitoes.

98 d Anopheles stephensi genes expressed during oocyst differentiation on the midgut.

99 asexual stage genes was up-regulated during oocyst differentiation.

100 model was recorded to determine the attached oocyst distributions in transversal and longitudinal dir

101 reexisting indole levels in the gut join the oocyst dose and immune status as important factors that

102 Because of its oocyst durability Cryptosporidium parvum is a significan

103 rozoites, pointing to a role for PbSR in the oocyst during sporogony.

104 n-releated protein 1 (TRP1) is important for oocyst egress and salivary gland invasion, and hence for

105 ays chlorine inactivation of Cryptosporidium oocysts, emphasizing the need for additional pool remedi

106 nt across temperatures, counterbalancing the oocyst enhancement at 24 degrees C.

107 The genotype of the oocysts excreted in feces and the relative distribution

108 Oocyst excretion and diarrhea severity were observed dai

109 engineered parasite strain totally prevented oocyst excretion following infection with wild-type T. g

110 GloWPa-Crypto L1 is most sensitive to oocyst excretion rates, due to large variation reported

111 MMV665917 significantly reduced fecal oocyst excretion, parasite colonization and damage to th

112 ent per villus and significantly exacerbated oocyst excretion.

113 lts in intensified epithelial parasitism and oocyst excretion.

114 d be a cost-effective new tool for assessing oocyst filtration in porous media, for example, to evalu

115 ce were infected with Cryptosporidium parvum oocysts for 6-13 days and compared with uninfected contr

116 o WT parasites as reflected by impairment of oocyst formation and sporogonic development in the mosqu

117 Oocyst formation and sporozoite production, necessary fo

118 st gametocytes in vitro), completely blocked oocyst formation in a mouse model of transmission.

119 le gamete formation and completely prevented oocyst formation in female Anopheles stephensi mosquitoe

120 h kinetics compared to WT parasites; however oocyst formation in mosquitoes was reduced by 50 to 80%.

121 n of PfPATPL1 also reduces the efficiency of oocyst formation in mosquitoes.

122 For successful oocyst formation newly formed ookinetes in the midgut lu

123 nd define the genes that orchestrate sex and oocyst formation through mRNA sequencing of sorted cells

124 ant WT plasminogen to depleted serum rescues oocyst formation, recombinant inactive plasminogen does

125 en depletion leads to a strong inhibition of oocyst formation.

126 o gametocytes but have drastic impairment of oocyst formation.

127 Plasmodium sporozoites mature in oocysts formed in the mosquito gut wall and then invade

128 d to be at least about 10 oocysts/g (about 1 oocyst/g for a pica child) for Cryptosporidium, about 5

129 ), levels would need to be at least about 10 oocysts/g (about 1 oocyst/g for a pica child) for Crypto

130 s of only 4 mg L(-1) SRHA and SDBS decreased oocyst hydrophobicity from 66% to 20% and from 66% to 5%

131 nsport of surface-treated, sterile C. parvum oocyst in porous media.

132 humans and animals, which is transmitted via oocysts in cat faeces or tissue cysts in contaminated me

133 n T. gondii forms cysts in vitro that induce oocysts in cats, the gold standard criterion for cysts.

134 rospheres may not be suitable surrogates for oocysts in certain types of soils.

135 exposure (as assessed by the mean number of oocysts in control mosquitoes) and antibody titers.

136 By concentrating oocysts in faecal pellets, snails may facilitate entry o

137 udies in which genotyping of Cryptospiridium oocysts in feces of dogs and cats have been successful a

138 unexcysted (in vivo) Cryptosporidium parvum oocysts in human colonic adenocarcinoma (HCT-8) cells an

139 The domestic dog excretes oocysts in its feces and, after sporulation, these oocys

140 Vitrification of C. parvum oocysts in larger volumes will expedite progress of rese

141 ocytes, PNP-deficient parasites did not form oocysts in mosquito midguts and were not transmitted fro

142 We imaged the release of sporozoites from oocysts in situ, which was preceded by active motility.

143 results in significantly elevated numbers of oocysts in susceptible and resistant mosquitoes.

144 ence of infected mosquitos at different mean oocysts in the control.

145 n maintaining the integrity of the T. gondii oocysts in the environment or after exposure to disinfec

146 Real time transport of oocysts in the micromodel was recorded to determine the

147 ilencing reduces the number of P. falciparum oocysts in the mosquito midgut by over 70% compared with

148 Plasmodium sporozoites develop within oocysts in the mosquito midgut wall and then migrate to

149 as measured by the number of Cryptosporidium oocysts in the stools) and also with the IL-1alpha conce

150 yotes (Canis latrans) can excrete N. caninum oocysts in their feces and that white-tailed deer (Odoco

151 vailable, and control focuses on eliminating oocysts in water supplies.

152 icrospheres achieved a superior match to the oocysts in zeta, concentration, mass recovery, and colli

153 of phagocytic cells in processing T. gondii oocysts, in line with non-classical routes of infection,

154 tro male gamete formation assays and reduced oocyst infection and prevalence in Anopheles mosquitoes.

155 Oocyst infection can be distinguished from bradyzoite in

156 train) gametocyte cultures slightly enhanced oocyst infection.

157 y addressed the effects of ClO2 on C. parvum oocyst infectivity in chlorinated recreational water ven

158 ly expressed as percent inhibition in either oocyst intensity (% transmission reducing activity, %TRA

159 ted the relationship between % inhibition in oocyst intensity and % inhibition of prevalence of infec

160 pooled mosquitoes accurately quantifies mean oocyst intensity and generates comparable TRA estimates.

161 AlbB reduced malaria parasite prevalence and oocyst intensity at 28 degrees C.

162 er-assay variability of % inhibition of mean oocyst intensity at each concentration of 4B7 (lower con

163 l three IgGs showed 97 to 100% inhibition in oocyst intensity compared to control IgG.

164 anti-Pfs230, and anti-PfHAP2 IgGs inhibited oocyst intensity in a dose-dependent manner.

165 Luminescence-based estimates of oocyst intensity in individual mosquitoes should be inte

166 ffect on prevalence but a marked increase in oocyst intensity.

167 supporting sporozoite excystation following oocyst internalisation.

168 and measures that decrease spread of viable oocysts into the environment.

169 f the U.S. ranging from ca. 0.005 to ca. 0.5 oocysts/L.

170 itted by contamination of food or water with oocyst-laden feces from an infected animal.

171 er account for nearly a quarter of the total oocyst load, meaning that the developing world accounts

172 he effect of manure storage and treatment on oocyst loads using scenario analysis.

173 We find that although manure storage halves oocyst loads, manure treatment, especially of cattle man

174 development (day 1 after the blood meal) and oocyst maturation (day 7 after the blood meal) but not d

175 To date, only one apicomplexan oocyst membrane protein has been identified, Cryptospori

176 identification of parasite species using egg/oocyst morphology, which could overestimate parasite sha

177 l component of the events that precede intra-oocyst motility and subsequently sporozoite egress and s

178 In a C. parvum infection with 1 x 10(6) oocysts/mouse in SCID beige (SCIDbg) mice (SCID mice lac

179 ria protein expressed in ookinetes and young oocysts, named secreted ookinete adhesive protein (SOAP)

180 nexons resulted in an increase in Plasmodium oocyst number and infection prevalence.

181 , but not AGAP006241, caused an induction in oocyst number.

182 pact Plasmodium infection outcomes, reducing oocyst numbers and the potential for malaria transmissio

183 s mosquitoes (approximately 90% reduction in oocyst numbers in the midgut).

184 ediated positive correlation between egg and oocyst numbers; impairing oogenesis by multiple 20E mani

185 ged gnotobiotic piglets with equal number of oocysts of type 1 and type 2, given either simultaneousl

186 in-binding proteins and then develop into an oocyst on the midgut basal lamina.

187 develops and differentiates within parasite oocysts on the Anopheles mosquito midgut.

188 the ookinetes into the sporozoite-producing oocysts on the mosquito midgut wall.

189 urs primarily via ingestion of environmental oocysts or consumption of undercooked/raw meat containin

190 viable in the mosquito midgut and never made oocysts or sporozoites, thereby abrogating transmission

191 ough targeted propagation in mice of progeny oocysts originating from populations lacking one parenta

192 io cholerae, and <9 x 10(-6) Cryptosporidium oocysts per 100 mL.

193 As few as 10 oocysts per 300 microl of stools could be detected with

194 nsitivity was determined to be as low as 200 oocysts per gram of feces processed, equivalent to 2 ooc

195 per gram of feces processed, equivalent to 2 oocysts per PCR.

196 en measured in community surveys is 3 to 434 oocysts per square foot and is greater in areas where ca

197 . load from livestock manure of 3.2 x 10(23) oocysts per year.

198 fect, they are unable to progress beyond the oocyst phase of the parasite mosquito stage.

199 tein is a major type of surface protein that oocysts possess.

200 Oocyst prevalence on mosquito midguts and sporozoite pre

201 Oocyst production and mosquito infectivity is also signi

202 tly, triacsin C effectively reduced parasite oocyst production up to 88.1% with no apparent toxicity

203 in 1 minus parasites were fed to a mosquito, oocyst production was reduced by 70-90%, suggesting an i

204 DNA were achieved by a combination of three oocyst purification steps and whole-genome amplification

205 Oocyst rates were 6.8% and 4.2% among resistant and susc

206 gly restricted the development of Plasmodium oocysts, reducing their number by 90%.

207 y restores ookinete-to-oocyst transition but oocysts remain small in size and produce a very small nu

208 ites were observed in macrophages containing oocyst remnants or in new macrophages, giving rise to di

209 nate-capped silver-nanoparticle treatment of oocysts resulted in morphological modifications and decr

210 abelling of viable sporozoites excysted from oocysts reveals a complex admixture of surface proteins

211 w that watersheds with the highest levels of oocyst runoff align closely with regions of increased se

212 n of food or water that is contaminated with oocysts shed by cats or by eating undercooked or raw mea

213 have focused attention on the importance of oocysts shed in the feces of infected cats.

214 rvulina oocysts 14 days posthatch, and fecal-oocyst shedding and body weight gain were determined as

215 chickens evidenced by significantly reduced oocyst shedding and disruption of the intestinal blood b

216 Fecal oocyst shedding and intestinal parasite burden were sign

217 with 3-1E protein showed significantly lower oocyst shedding and normal body weight gain than nonvacc

218 17, or -18 or IFN-gamma gene further reduced oocyst shedding compared with that achieved with 3-1E al

219 of 3-1E resulted in significantly decreased oocyst shedding compared with that in nonvaccinated chic

220 icant reduction in merozoite replication and oocyst shedding in E. tenella in vitro and in vivo.

221 ice (SCID mice lacking functional NK cells), oocyst shedding was first demonstrated 18 days after inf

222 ing parameters, including diarrhea severity, oocyst shedding, and overall health.

223 Fecal oocyst shedding, as well as intestinal parasite burden,

224 unocompromised mice and dramatically reduces oocyst shedding, diarrhea, and dehydration in neonatal c

225 infective oocysts, and the short duration of oocyst shedding, direct contact with cats is not thought

226 Eimeria spp. genes related to gamete fusion, oocyst shedding, mitosis and spermiogenesis.

227 infection was monitored by quantifying fecal oocyst shedding.

228 Genes significantly overexpressed in oocysts show evidence of specialized functions not found

229 Analysis of RNA-Seq data from replicate oocyst, sporozoite and intracellular samples revealed si

230 nses only in malaria-infected mosquitoes (at oocyst, sporozoite or both stages).

231 asites suggesting a role for this protein in oocyst/sporozoite transmission to susceptible hosts.

232 e mRNAs and proteins that are upregulated in oocyst sporozoites (UOS) or upregulated in infectious sp

233 ulation of at least 47 genes (upregulated in oocyst sporozoites [UOS genes]) before they infect the s

234 dynamic transcriptomes and proteomes of both oocyst sporozoites and salivary gland sporozoites in bot

235 n, resulting in parasites capable of forming oocyst sporozoites but blocked in the salivary gland tra

236 Conversely, oocyst sporozoites show upregulation of at least 47 gene

237 he sporozoite secretory organelles, rendered oocyst sporozoites unable to infect the mosquito salivar

238 ed that SSP3 is expressed in mosquito midgut oocyst sporozoites, exhibiting an intracellular localiza

239 r microarray analysis shows that compared to oocyst sporozoites, salivary gland sporozoites upregulat

240 rts into gametocytes that produce infectious oocysts (sporozoites) that are expelled into the environ

241 e analyzed the transcriptome of C. parvum in oocysts, sporozoites and infected cell monolayers 2-48 h

242 While oocyst sporulation rates of PbSR knockout parasites are

243 owever, progression from the ookinete to the oocyst stage and sporozoite formation were completely ab

244 reas TgROM2 and TgROM3 were expressed in the oocyst stage involved in transmission.

245 us protozoan parasite Toxoplasma gondii, the oocyst stage possesses a bilayered wall that protects th

246 ved organelle of the Plasmodium ookinete and oocyst stage required for sporogony-is dependent on the

247 also reveal an increased sugar uptake at the oocyst stage that decreased at the sporozoite stage of i

248 cidian parasites are transmitted via a fecal oocyst stage that is exceptionally resistant to environm

249 idase production that limit the ookinete and oocyst stages of malaria parasite development, respectiv

250 to the mosquito-specific ookinete and young oocyst stages of the parasite.

251 eric repulsion and possibly other changes in oocyst surface properties.

252 e mosquito late-phase immune response limits oocyst survival are less understood.

253 a late-phase immune response that decreases oocyst survival.

254 nt immune mechanisms regulating ookinete and oocyst survival.

255 ite expansion > 100-fold and generate viable oocysts that are transmissible in vitro and to mice, cau

256 knockout parasites produce normal numbers of oocysts that fail to form sporozoites, pointing to a rol

257 ilisation, decreased fecundity and generates oocysts that fail to produce sporozoites.

258 richia coli cells and Cryptosporidium parvum oocysts that have been embedded in ground meat.

259 ur column data confirm for freshly harvested oocysts that the presence of iron coatings on the sand m

260 Oocysts, the extremely hardy free-living environmental s

261 ite transmission occurs through ingestion of oocysts, through either direct contact or consumption of

262 wall to digestive enzymes and the ability of oocysts to cause parenteral infections, the present stud

263 ith freshly harvested Cryptosporidium parvum oocysts to evaluate the effects of solution chemistry, s

264 es and discusses the inability of UV-exposed oocysts to regain infectivity.

265 Attachment of oocysts to silica surface in a radial stagnation point f

266 d as the sporozoites transit from the midgut oocysts to the salivary glands.

267 he transcriptome found in the host cell, the oocyst transcriptome is less diverse.

268 em through RNAi largely restores ookinete-to-oocyst transition but oocysts remain small in size and p

269 After invasion ookinete-to-oocyst transition must occur, a process believed to requ

270 ia ookinetes and disappear after ookinete-to-oocyst transition.

271 ranular filtration requires the knowledge of oocyst transport and deposition mechanisms, which can be

272 ased on real time microscopic observation of oocyst transport in porous media.

273 hrough the temperate soil 5-fold, whereas no oocyst transport was detected in tropical soil.

274 SRHA had only a nominal effect in increasing oocysts transport in tropical soil, but caused a 6-fold

275 SDBS also increased oocysts transport through the temperate soil 5-fold, whe

276 the dissolved organic carbon (DOC), whereas oocysts transport was more affected by soil mineralogy.

277 sion of HSP70 mRNA in Cryptosporidium parvum oocysts via a simple heat shock process provides nonenzy

278 ffective in killing the parasite because the oocyst wall acts as a primary barrier to physical and ch

279 es to identify chemical factors that lead to oocyst wall disruption under physiological conditions.

280 ndings suggest a key biological role for the oocyst wall mechanics in maintaining the integrity of th

281 protein has been identified, Cryptosporidium oocyst wall protein 1 (COWP1).

282 polymorphism analysis of the Cryptosporidium oocyst wall protein gene for 134 of 136 (98.5%) samples

283 analysis of the 18S rRNA and Cryptosporidium oocyst wall protein genes.

284 indentation measurements indicated that the oocyst wall resembles common plastic materials, based on

285 hesis that multiple COWPs play a role in the oocyst wall structure.

286 Given the resistance of the oocyst wall to digestive enzymes and the ability of oocy

287 OWP8 specifically localized to the C. parvum oocyst wall, supporting the hypothesis that multiple COW

288 fication of mRNA from as few as 30 C. parvum oocysts was demonstrated directly on-chip and compared t

289 infected with P. gallinaceum, the number of oocysts was dramatically reduced in midguts, and no spor

290 from as few as 5 x 10(3) purified C. parvum oocysts was successfully detected.

291 Internalised oocysts were associated to macrophage acidic compartment

292 g exposure to T. gondii-containing seawater, oocysts were detected by microscopy in snail faeces and

293 l and sexual stages and the formation of new oocysts were observed during the course of infection.

294 Moreover, the majority of oocysts were retarded in their growth and were smaller i

295 d the same log reduction in concentration as oocysts, whereas results from unmodified microspheres de

296 al infection or abortion and by ingestion of oocysts, which, if it occurs during gestation, can also

297 used to identify live and inactive C. parvum oocysts with over 90% certainty, whilst also detecting d

298 (mouse) model, we observed that treatment of oocysts with silver nitrate and proteinate-capped silver

299 t experiments determine the number of mature oocysts, without considering that different immune mecha

300 ch includes clays, and SRHA, both caused the oocysts zeta potential (zeta) to become more negative, b