ライフサイエンスコーパス: toxoplasmosis

1 nd Toxoplasma gondii (the causative agent of toxoplasmosis).

2 s against Pneumocystis carinii pneumonia and toxoplasmosis).

3 ely fifteen million of these have congenital toxoplasmosis.

4 atent disease during later phases of chronic toxoplasmosis.

5 r for protection against cerebral and ocular toxoplasmosis.

6 designing immunotherapeutics against chronic toxoplasmosis.

7 response of mice to the parasite that causes toxoplasmosis.

8 ight contribute to the development of ocular toxoplasmosis.

9 8 differentiation is impaired during chronic toxoplasmosis.

10 g a more critical role for NAS-TLRs in human toxoplasmosis.

11 ted activity in murine models of malaria and toxoplasmosis.

12 yst stage is the underlying cause of chronic toxoplasmosis.

13 the 3d susceptible phenotype to experimental toxoplasmosis.

14 s are considered to be at increased risk for toxoplasmosis.

15 ys a central role in the pathology of ocular toxoplasmosis.

16 portant human diseases including malaria and toxoplasmosis.

17 when administered orally to mice with acute toxoplasmosis.

18 p therapies aimed at defending against human toxoplasmosis.

19 control of parasitemia during early-chronic toxoplasmosis.

20 urs in several chronic infections, including toxoplasmosis.

21 ortant human diseases, including malaria and toxoplasmosis.

22 was enhanced during chronic, but not acute, toxoplasmosis.

23 role of this enzyme in the chronic phase of toxoplasmosis.

24 racterize subsets of murine DCs during acute toxoplasmosis.

25 ficient mice, which were more susceptible to toxoplasmosis.

26 ch were otherwise highly susceptible to oral toxoplasmosis.

27 rges such as malaria, cryptosporidiosis, and toxoplasmosis.

28 is jirovecii pneumonia and Toxoplasma gondii toxoplasmosis.

29 he initial activation of CD8+ T cells during toxoplasmosis.

30 me as a valid target for the chemotherapy of toxoplasmosis.

31 espread parasites and the causative agent of toxoplasmosis.

32 ss of blood samples for genotyping in ocular toxoplasmosis.

33 on of T. gondii in the chick embryo model of toxoplasmosis.

34 y from blood samples of patients with ocular toxoplasmosis.

35 f new drugs for the treatment of malaria and toxoplasmosis.

36 a promising method for genotypic analysis of toxoplasmosis.

37 a critical protective function during acute toxoplasmosis.

38 unlikely to be efficacious for treatment of toxoplasmosis.

39 pts a reduction in WSX-1 levels during acute toxoplasmosis.

40 ing the contribution of parasite genotype to toxoplasmosis.

41 stem to study CD4(+)-T-cell responses during toxoplasmosis.

42 chemotherapeutic target for the treatment of toxoplasmosis.

43 play a critical role in the pathogenesis of toxoplasmosis.

44 f sera sampling) suggests a cause other than toxoplasmosis.

45 d a novel chicken embryo model of congenital toxoplasmosis.

46 tis carinii pneumonia, and Toxoplasma gondii toxoplasmosis.

47 gulation of inflammation during acute ocular toxoplasmosis.

48 IFN-gamma receptor 1 are not susceptible to toxoplasmosis.

49 ice induces long-term protective immunity to toxoplasmosis.

50 diagnosis of Toxoplasma gondii infection and toxoplasmosis.

51 ral candidiasis, Pneumocystis pneumonia, and toxoplasmosis.

52 endent pathway of IL-12p40 production during toxoplasmosis.

53 parasite populations from 32 cases of human toxoplasmosis.

54 urse and tissue distribution of experimental toxoplasmosis.

55 mechanisms regulate T cell responses during toxoplasmosis.

56 emiology and efficacious treatment of ocular toxoplasmosis.

57 to be involved in the pathogenesis of ocular toxoplasmosis.

58 protection is an important feature of acute toxoplasmosis.

59 unistic infectious diseases tuberculosis and toxoplasmosis.

60 ration of protective T-cell responses during toxoplasmosis.

61 lindamycin, another widely used drug against toxoplasmosis.

62 al symptoms and disability due to congenital toxoplasmosis.

63 e considered critical for control of chronic toxoplasmosis.

64 and 2012, 9260 patients had ICD-9 codes for toxoplasmosis.

65 concerning US incidence and distribution of toxoplasmosis.

66 esis generation about the pathophysiology of toxoplasmosis.

67 s, including causative agents of malaria and toxoplasmosis.

68 hyzoite life stage, is responsible for acute toxoplasmosis.

69 ule inhibitors of CDPK1 for treatment of CNS toxoplasmosis.

70 ses including malaria, cryptosporidiosis and toxoplasmosis.

71 were found to be highly susceptible to acute toxoplasmosis.

72 l tool to reduce the incidence of congenital toxoplasmosis.

73 wn whether this finding is relevant in human toxoplasmosis.

74 example concerning the spread and control of toxoplasmosis.

75 ific differences in the clinical spectrum of toxoplasmosis.

76 ing inflammation in many settings, including toxoplasmosis.

77 ites, including those that cause malaria and toxoplasmosis.

78 ence in samples from 12 patients with ocular toxoplasmosis, 1 sample from a patient with congenital t

79 ses, 95% UI 8.29-22.0 million) and foodborne toxoplasmosis (10.3 million cases, 95% UI 7.40-14.9 mill

80 y, and 1.0 per 10 000 infants had congenital toxoplasmosis (13% mean transmission rate).

81 sis, 1 sample from a patient with congenital toxoplasmosis, 22 samples from soldiers operating in the

82 This apicomplexan is the causative agent of toxoplasmosis, a leading cause of central nervous system

83 outcomes of adult patients with disseminated toxoplasmosis admitted to the intensive care unit (ICU)

84 racellular matrix, were resistant to chronic toxoplasmosis after oral infection with T. gondii.

85 famethoxazole (TMP/SMX) in the prevention of toxoplasmosis after orthotopic cardiac transplantation h

86 of certain forms of uveitis (such as ocular toxoplasmosis) after surgery, suggesting that perioperat

87 After a cluster of fatal toxoplasmosis among stem cell transplant recipients at 2

88 n, Clinical Modification codes 130-130.9 for toxoplasmosis and 042-044/795.8/795.71/V08 for HIV infec

89 aries widely, but prophylaxis against PCP or toxoplasmosis and against MAC delivers the greatest comp

90 The subsequent diagnoses were ocular toxoplasmosis and cytomegalovirus retinitis.

91 ht the importance of Flt3L for resistance to toxoplasmosis and demonstrate the existence of Flt3L-ind

92 current prevention strategies of congenital toxoplasmosis and evaluate options to improve protection

93 46 serum specimens from patients with ocular toxoplasmosis and in 28 serum specimens from patients wi

94 en is associated with severity of congenital toxoplasmosis and indicate that serological testing prov

95 (iMO) are critical for host defense against toxoplasmosis and malaria but their role in leishmaniasi

96 rasites and required for the pathogenesis of toxoplasmosis and malaria.

97 lling of pregnant women diagnosed with acute toxoplasmosis and may guide individual decisions on inve

98 008 and assessed how the risks of congenital toxoplasmosis and of clinical signs at age 3 years vary

99 h central nervous system (CNS) lymphoma from toxoplasmosis and other nonmalignant CNS lesions in pati

100 CD4 T-cell-mediated immune damage in ocular toxoplasmosis and other types of retinal immune response

101 ocumented prenatal exposure to influenza and toxoplasmosis and performance on the Wisconsin Card Sort

102 of more effective compounds for treatment of toxoplasmosis and perhaps related parasitic diseases.

103 ous parasitic infections, including malaria, toxoplasmosis and Pneumocystis pneumonia.

104 g peptide that can confer protection against toxoplasmosis and provide an important tool for the stud

105 recruited Ly6C(high) monocytes upon cerebral toxoplasmosis and reveal the behavior of further differe

106 e recipients are at high risk for developing toxoplasmosis and should be given prophylaxis and receiv

107 ry effector cells in the resistance to acute toxoplasmosis and suggests that the CCR2-dependent recru

108 retion is an important host cell response to toxoplasmosis and that the release of IL-1alpha and othe

109 um includes the causative agents of malaria, toxoplasmosis and theileriosis-diseases with a huge econ

110 development of vaccine protocols to control toxoplasmosis and/or neosporosis.

111 malaria, trypanosomiasis, leishmaniasis, and toxoplasmosis) and provides visions into the main issues

112 eba), Toxoplasma gondii (the agent for human toxoplasmosis), and other protists, Skp1 is regulated by

113 tunistic infections and no signs of cerebral toxoplasmosis, and 18 immunocompetent patients with neur

114 high impact human diseases such as malaria, toxoplasmosis, and cryptosporidiosis.

115 important human diseases including malaria, toxoplasmosis, and cryptosporidiosis.

116 hat include the causative agents of malaria, toxoplasmosis, and cryptosporidiosis.

117 -BM5 challenge prevented the reactivation of toxoplasmosis, and mice continued to live.

118 ntation anti- serology, development of acute toxoplasmosis, and the occurrence of other infections.

119 been described in diseases such as malaria, toxoplasmosis, and trypanosomiasis.

120 at mediate protective immunity during murine toxoplasmosis, and yet their effector development remain

121 59 cases of POT and 4 cases of active ocular toxoplasmosis (AOT).

122 hat regulate IL-12 production during chronic toxoplasmosis are incompletely defined.

123 le for triggering the local host response to toxoplasmosis are not fully understood.

124 mining the pathogenesis and course of ocular toxoplasmosis are poorly understood.

125 Recurrence rates of ocular toxoplasmosis are probably not higher during pregnancy,

126 The drugs currently available to treat toxoplasmosis are unable to clear the cyst form of the p

127 ristics of disease due to Toxoplasma gondii (toxoplasmosis) are dependent on the infecting strain, we

128 e tissues demonstrated signs of disseminated toxoplasmosis as a result of reactivation of infection.

129 eutic implications in combating recrudescent toxoplasmosis as well other chronic infections.

130 etic cells and can cause cerebral and ocular toxoplasmosis, as a result of either congenital or postn

131 In CNS toxoplasmosis, astrocytes are critical to controlling pa

132 or Toxoplasma gondii, responsible for human toxoplasmosis, Babesia belongs to the Apicomplexa family

133 equences from Colombian patients with ocular toxoplasmosis belonged to the group of mouse-virulent st

134 iosis was lower than those due to congenital toxoplasmosis but accords with those due to echinococcos

135 CD4 not only become exhausted during chronic toxoplasmosis but this dysfunction is more pronounced th

136 L-23, plays a dominant role in resistance to toxoplasmosis but, in the absence of IL-12, IL-23 can pr

137 o derive estimates of the risk of congenital toxoplasmosis by exact duration of gestation at maternal

138 Toxoplasmosis can be due to congenital infection or acqu

139 Diagnosis of toxoplasmosis can be established by direct detection of

140 Usually asymptomatic, toxoplasmosis can be severe and even fatal to many hosts

141 rth America (NA) and Europe, the majority of toxoplasmosis cases are benign and generally asymptomati

142 cerebrospinal fluid samples from congenital toxoplasmosis cases in Poland.

143 Toxoplasmosis causes morbidity and mortality in the Unit

144 Toxoplasmosis causes significant morbidity and mortality

145 We reported earlier that during chronic toxoplasmosis CD8(+) T cells become functionally exhaust

146 sequences (83.3%) from patients with ocular toxoplasmosis clustered with those of mouse-virulent str

147 of 51 serum cytokines from acute and chronic toxoplasmosis cohorts of pregnant women from the United

148 Nevertheless, prevention of toxoplasmosis commonly targets mainly pregnant women.

149 12/15-LOX-deficient mice died during chronic toxoplasmosis, compared to no deaths in wild-type contro

150 The susceptibility of STAT4-/- mice to toxoplasmosis correlated with a defect in their ability

151 uman and animal diseases, including malaria, toxoplasmosis, cryptosporidiosis, coccidiosis and babesi

152 Congenital toxoplasmosis (CT) and cytomegalovirus infection (cCMV)

153 ly identification of infants with congenital toxoplasmosis (CT).

154 -Schiff staining for fungi, PCR analysis for toxoplasmosis, cytomegalovirus, Epstein-Barr virus (EBV)

155 In this cohort, acute toxoplasmosis developed after transplantation in one cas

156 emonstrated that screening and treatment for toxoplasmosis during gestation result in a decrease of v

157 There were 128 episodes of ocular toxoplasmosis during the study period (6 during pregnanc

158 in patients without classic presentation of toxoplasmosis encephalitis.

159 for IL-10 in the immunopathogenesis of acute toxoplasmosis following peroral infection was examined i

160 Twenty patients (17%) with ocular toxoplasmosis had a localized RNFL defect associated wit

161 Eleven of the 12 patients with confirmed toxoplasmosis had positive PCR results in either blood o

162 ctive therapeutics for cryptosporidiosis and toxoplasmosis has led to the discovery of novel inhibito

163 The rate of HIV-associated toxoplasmosis hospitalizations among all HIV-related hos

164 HIV-associated toxoplasmosis hospitalizations dropped markedly after 19

165 Non-HIV-associated toxoplasmosis hospitalizations have been more stable.

166 Estimated HIV-associated toxoplasmosis hospitalizations increased from 9395 in 19

167 he rates of both HIV- and non-HIV-associated toxoplasmosis hospitalizations were higher in Hispanic p

168 Estimated non-HIV-associated toxoplasmosis hospitalizations were less variable from 1

169 CD-9) codes, including treatment specific to toxoplasmosis, identified patients with this disease.

170 e of IL-2 in the expansion of T cells during toxoplasmosis, IL-2(-/-) mice were infected with T. gond

171 er analysis of host-pathogen interactions in toxoplasmosis in a secondary host.

172 clinical agent for the treatment of cerebral toxoplasmosis in AIDS patients.

173 ctions with Toxoplasma gondii and congenital toxoplasmosis in Austria, a country with a nationwide pr

174 Toxoplasma gondii is the causative agent of toxoplasmosis in human and animals.

175 tinochoroiditis in the setting of congenital toxoplasmosis in human infants.

176 that causes the severe opportunistic disease toxoplasmosis in humans.

177 In addition, toxoplasmosis in immune-compromised individuals usually

178 A major challenge in treating toxoplasmosis in immunocompromised patients is lack of t

179 tion in risk of clinical signs of congenital toxoplasmosis in infected children born from mothers dia

180 h dexamethasone, we detected reactivation of toxoplasmosis in mice infected with S23-luc7 and S22-luc

181 ro and is effective against acute and latent toxoplasmosis in mice.

182 olved in the pathogenesis of acquired ocular toxoplasmosis in mice.

183 mining susceptibility to experimental ocular toxoplasmosis in murine models.

184 Type II and NE-II parasites cause congenital toxoplasmosis in North America.

185 Family clusters and epidemics of toxoplasmosis in North, Central, and South America led u

186 entified susceptibility genes for congenital toxoplasmosis in our cohort of infected humans and found

187 Although uncommon, toxoplasmosis in SOT patients causes substantial morbidi

188 factors, clinical features, and outcomes of toxoplasmosis in SOT recipients.

189 s plays an important role in pathogenesis of toxoplasmosis in the mouse model.

190 trophils are important for controlling acute toxoplasmosis in the mouse model.

191 ecific inhibitor of ABA synthesis to prevent toxoplasmosis in the mouse model.

192 ound 24 was also effective at treating acute toxoplasmosis in the mouse, reducing dissemination to th

193 howed a significant delay in producing acute toxoplasmosis in vivo.

194 or sulfonamide use, particularly in cases of toxoplasmosis in which the initial response to drug trea

195 N-gamma), a cytokine known to control latent toxoplasmosis, in chronically infected prerecrudescent m

196 raction in a murine model of acquired ocular toxoplasmosis induced by intracameral inoculation of Tox

197 T-regulatory cells is an important factor in toxoplasmosis-induced retinal damage.

198 te Toxoplasma gondii, the causative agent of toxoplasmosis, induces a protective CD8 T-cell response

199 he implementation of universal screening for toxoplasmosis infection during gestation.

200 Women who acquire toxoplasmosis infection during pregnancy (in most cases

201 nd paediatric data on 603 confirmed maternal toxoplasmosis infections.

202 Toxoplasmosis is a disease of prominent health concern t

203 in bacterial or fungal endophthalmitis, and toxoplasmosis is a major cause of ocular morbidity and p

204 Ocular toxoplasmosis is a potentially blinding intraocular infl

205 Ocular toxoplasmosis is a prominent and severe condition of hig

206 Congenital toxoplasmosis is a serious condition but little is known

207 Congenital toxoplasmosis is a severe, life-altering disease in the

208 Because congenital toxoplasmosis is almost solely the result of maternal in

209 Toxoplasmosis is an infection caused by the protozoan pa

210 asymptomatic, whereas in South America (SA) toxoplasmosis is associated with much more severe sympto

211 The diagnosis of ocular toxoplasmosis is based most often on the presence of cha

212 Although congenital toxoplasmosis is generally considered to contribute most

213 Protection from toxoplasmosis is mediated by CD8(+) T cells, but the T.

214 Toxoplasmosis is the clinical and pathological consequen

215 Toxoplasmosis is the most common cause of posterior uvei

216 Toxoplasma gondii, the causative agent of toxoplasmosis, is an intracellular parasite that demonst

217 Toxoplasma gondii, the causative agent of toxoplasmosis, is an obligate intracellular protozoan pa

218 Severe disseminated toxoplasmosis leading to ICU admission has a poor progno

219 IDO inhibition during murine toxoplasmosis led to 100% mortality, with increased para

220 in the contralateral regions) throughout the toxoplasmosis lesions and in the surrounding edema of bo

221 Reduced rCBV i toxoplasmosis lesions is probably due to a lack of vascu

222 The initially active toxoplasmosis lesions were successfully treated in all c

223 that are effective against acute and latent toxoplasmosis, likely acting as inhibitors of the Q(i) s

224 eserine presents interesting anti-parasitic (toxoplasmosis, malaria) potential.

225 table for the diseases they cause, including toxoplasmosis, malaria, and cryptosporidiosis.

226 impact on improving outcomes for those with toxoplasmosis, malaria, and ~2 billion persons chronical

227 th both typical and atypical forms of ocular toxoplasmosis may be good.

228 A murine toxoplasmosis model has been developed that results in c

229 tients with Behcet uveitis (n = 259), ocular toxoplasmosis (n = 120), and multiple sclerosis (MS)-ass

230 r brain biopsy were diagnosis unlikely to be toxoplasmosis (n=8, 42.1%), focal brain lesion (n=5, 26.

231 First episodes of ocular toxoplasmosis occurred between ages 9.6 and 38.5 years.

232 ion was the only independent risk factor for toxoplasmosis (odds ratio, 15.12 [95% confidence interva

233 Professor Silvia Moreno studies toxoplasmosis, one of the most common parasitic infectio

234 lesions (six with active lymphoma, five with toxoplasmosis, one with treated lymphoma in remission, a

235 Worldwide, ocular toxoplasmosis (OT) is the principal cause of posterior u

236 d to refer to congenital infections, such as toxoplasmosis, other infections (such as syphillis, vari

237 mester maternal infection, chorioamnionitis, toxoplasmosis, other infections, rubella, cytomegaloviru

238 e neurological and muscular pathologies that toxoplasmosis patients present with.

239 treated lymphoma in remission, and one with toxoplasmosis plus lymphomatoid granulomatosis).

240 d of patients with severe or atypical ocular toxoplasmosis, polymerase chain reaction (PCR) restricti

241 and 89 parent/case trios of presumed ocular toxoplasmosis (POT) to evaluate associations with polymo

242 In a mouse model of toxoplasmosis, pyrazolopyrimidine inhibitors of Toxoplas

243 analysis of data from women referred to the toxoplasmosis reference laboratory, Lyon, France, betwee

244 The Austrian Toxoplasmosis Register included 2147 pregnant women with

245 nalyzed retrospective data from the Austrian Toxoplasmosis Register of pregnant women with Toxoplasma

246 Results from the Austrian Toxoplasmosis Register show the efficiency of the prenat

247 d Utilization Project, we examined trends in toxoplasmosis-related hospitalizations by HIV infection

248 Toxoplasmosis-related hospitalizations often occur in pe

249 The rates of toxoplasmosis-related hospitalizations varied markedly a

250 gondii (the causative agents of malaria and toxoplasmosis, respectively), are responsible for consid

251 iological agents of severe human malaria and toxoplasmosis, respectively.

252 anifestations include punctate outer retinal toxoplasmosis, retinal vasculitis, retinal vascular occl

253 The primary outcome was recurrent toxoplasmosis retinochoroiditis within 1 year, and the s

254 The incidence of recurrent toxoplasmosis retinochoroiditis within 12 months was 0 o

255 susceptibility alleles for human congenital toxoplasmosis (rs6502997 [P, <0.000309], rs312462 [P, <0

256 tiation of this condition from pseudo-TORCH (toxoplasmosis, rubella, cytomegalovirus, and herpes simp

257 The differential diagnosis included toxoplasmosis, rubella, cytomegalovirus, herpes simplex

258 Serologic testing ruled out toxoplasmosis, rubella, cytomegalovirus, syphilis, and h

259 Toxoplasmosis, rubella, cytomegalovirus, syphilis, and h

260 including amebiasis, malaria, leishmaniasis, toxoplasmosis, schistosomiasis, and paracoccidioidomycos

261 tested all samples from patients with ocular toxoplasmosis sent to the Palo Alto Medical Foundation T

262 ional Collaborative Chicago-Based Congenital Toxoplasmosis Study (NCCCTS) have a high incidence of To

263 ional Collaborative Chicago-based Congenital Toxoplasmosis Study (NCCCTS), 1981-2009.

264 ional Collaborative Chicago-based Congenital Toxoplasmosis Study.

265 n disease burden of 10 helminth diseases and toxoplasmosis that may be attributed to contaminated foo

266 lesion formation in infants with congenital toxoplasmosis that may be relevant in the establishment

267 Together these studies suggest that during toxoplasmosis the major role of STAT1 is not in the deve

268 structure-based drug design studies against toxoplasmosis, the crystal structures of the T.gondii ap

269 lines and represent promising candidates as toxoplasmosis therapeutics.

270 asmodium spp.) and the causative organism of Toxoplasmosis, Toxoplasma gondii, possess a remnant plas

271 , including the causative agents of malaria, toxoplasmosis, trypanosomiasis, and leishmaniasis, conta

272 reviewed: infection with hepatitis viruses, toxoplasmosis, tuberculosis, bacteremia, and endogenous

273 one episode of rejection, the risk of acute toxoplasmosis was 5% (1 of 22 patients).

274 Susceptibility to toxoplasmosis was associated with an inability to up-reg

275 ility of 12/15-LOX-deficient mice to chronic toxoplasmosis was associated with reduced production of

276 Disseminated toxoplasmosis was defined as microbiological or histolog

277 CD4(+) T cells in the pathogenesis of ocular toxoplasmosis was investigated in murine models utilizin

278 the role of apoptosis in the pathogenesis of toxoplasmosis was investigated.

279 Toxoplasmosis was statistically associated with substant

280 A murine model of toxoplasmosis was thus used to examine the importance of

281 a prospective clinical study of acute ocular toxoplasmosis, we assessed the cytokine pattern in aqueo

282 the role of interleukin-10 (IL-10) in ocular toxoplasmosis, we compared C57BL/6 (B6) and BALB/c backg

283 o understand the basis of acute virulence in toxoplasmosis, we compared low and high doses of the RH

284 f strains of T. gondii associated with human toxoplasmosis, we have developed a set of four highly se

285 In an experimental model of toxoplasmosis, we have identified the presence of a nonl

286 tionality during the later phases of chronic toxoplasmosis, we next examined if adoptive transfer of

287 Nineteen confirmed congenital cases of toxoplasmosis were analyzed, including both severe and a

288 Although in the past most cases of ocular toxoplasmosis were considered to result from reactivatio

289 Isolated cases of cerebral toxoplasmosis were excluded.

290 Twenty-two cases (0.14%) of toxoplasmosis were identified among 15 800 SOTs performe

291 susceptibility alleles for human congenital toxoplasmosis were identified in the NALP1 gene.

292 c role for IL-22 was, however, identified in toxoplasmosis when infections were established by the na

293 rding all pregnancies and episodes of ocular toxoplasmosis, whether or not episodes were observed at

294 ew therapies are needed for the treatment of toxoplasmosis, which is a disease caused by the protozoa

295 aled that p40(-/-) mice rapidly succumbed to toxoplasmosis, while p35(-/-) mice displayed enhanced re

296 us-infected patients with suspected cerebral toxoplasmosis who had neither CDC diagnostic criteria no

297 consecutive adult patients with disseminated toxoplasmosis who were admitted from January 2002 throug

298 LYs (95% UI 1.65-2.48 million) and foodborne toxoplasmosis with 825,000 DALYs (95% UI 561,000-1.26 mi

299 type I, suggesting an association of ocular toxoplasmosis with this type.

300 n and livestock diseases such as malaria and toxoplasmosis, yet most of their genes remain uncharacte