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. 2019 Jul 10;26(1):135–146.e5. doi: 10.1016/j.chom.2019.05.006

Figure 3.

Figure 3

Cryptosporidium tyzzeri Infects the Small Intestine and Causes Pathology

(A) The intestinal tract from infected mice was resected and 1-cm2 segments were tested for the presence of parasite DNA by qPCR. n = 7 mice from 2 separate experiments with tissue harvested at day 10 post infection with 10,000 oocysts.

(B and C) Hematoxylin and eosin stained sections of the distal small intestine of mice. Note tall columnar villus epithelium and intact apical microvilli border with associated glycocalyx in uninfected (B) mice, in contrast to severe villus attenuation, loss of the apical glycocalyx and effacement of microvilli in infected (C) animals.

(D–H) Mice were infected with 50,000 C. tyzzeri oocysts, killed at 0, 4, 8, and 12 days post infection and histologically scored for pathological changes over the course of infection. In the small intestine of infected mice, parasite burden peaked on day 4 post infection (D). Infection resulted in a marked reduction in villus:crypt height ratio (villus blunting) (E), lymphocyte aggregation (F), epithelial dysplasia with increased mitoses (G), and villus hyperplasia (H). n = 5 mice per group, with each dot representing the score for a single mouse, data are mean ± standard deviation (SD). Significance is determined using one-way ANOVA with Dunnett multiple comparison test (p < 0.05, ∗∗p < 0.005, ∗∗∗p < 0.0005, and ∗∗∗∗p < 0.00005).