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Fig. 7. a in Anti-cryptosporidial activity of Camellia sinensis (green tea extract) in experimentally infected immunocompromised mice

Fig. 7. a) A section of the small intestine in GV revealed normal villous architecture with a normal brush border (H&E stain, X200); b) Sections examined from the liver in this group showed preserved hepatic lobular architecture (H&E stain, X200).

Fig. 6. a in Anti-cryptosporidial activity of Camellia sinensis (green tea extract) in experimentally infected immunocompromised mice

Fig. 6. a) A section of the small intestine in GIV revealed marked villous broadening (red line) with decreased villous height to crypt length ratio. There was dense infiltration by mononuclear inflammatory cells within the villous core (green arrows), degeneration of the villous tip-regions (black arrows), and increased mucin production (H&E stain, X200). b) Sections from the small intestine revealed many adherents (red arrows) and separate (black arrows) Cryptosporium stages, probably oocyst (H&E stain, X1000). c)Sections examined from the liver in this group showed hepatocellular degeneration (black arrow) and focal mononuclear cellular infiltration (red arrows) (H&E stain, X200)

Fig. 5. a in Anti-cryptosporidial activity of Camellia sinensis (green tea extract) in experimentally infected immunocompromised mice

Fig. 5. a) A section of the small intestine in GIII revealed moderate villous broadening, infiltration by mononuclear inflammatory cells within the villous core (red arrow), focal degeneration of the villous tip regions (black arrow), and increased mucin production (H&E stain, X200). b) Sections examined from the liver in this group showed focal mononuclear cellular infiltration (red arrow) (H&E stain, X200).

Fig. 3. a in Anti-cryptosporidial activity of Camellia sinensis (green tea extract) in experimentally infected immunocompromised mice

Fig. 3. a) A section of the small intestine in GI revealed villous broadening (red line) with an expansion of the villous core by mononuclear inflammatory cells (black arrow) (H&E stain, X200); b) Sections examined from the liver in this group showed preserved hepatic lobular architecture and cloudy swelling of hepatocytes (H&E stain, X200).

Fig. 1. a in Anti-cryptosporidial activity of Camellia sinensis (green tea extract) in experimentally infected immunocompromised mice

Fig. 1. a) Cryptosporidium oocyst (stained red to deep purple with the modified Ziehl–Neelsen method); b) immunofluorescence staining of Cryptosporidium oocyst (ovoid or spherical brilliant apple/ green structure)

Fig. 2 in Anti-cryptosporidial activity of Camellia sinensis (green tea extract) in experimentally infected immunocompromised mice

Fig. 2. Agarose gel electrophoresis showing: Lane 1: 50 bp DNA molecular weight marker, Lane 2: Positive control, Lane 3: Negative control, Lane 4: Positive sample of nested PCR products targeting COWP gene of Cryptosporidium at 553 bp, Lane 5: 50 bp DNA molecular weight marker, and Lane 6: RFLP products of the sample after digestion with RsaI endonuclease (C. parvum genotype 2 digestion products at 410, 106, and 34 (too small to be detected) bp.

Fig. 4. a in Anti-cryptosporidial activity of Camellia sinensis (green tea extract) in experimentally infected immunocompromised mice

Fig. 4. a) A section of the small intestine in GII revealed returning of the normal villous pattern, normal mucosa, and goblet cells (H&E stain, X200). b) Sections examined from the liver in this group showed preserved hepatic lobular architecture (H&E stain, X200).

opencc-by-4.0Dec 2013View details →

Figures 1–20 in Trypanosoma (Megatrypanum) lainsoni n. sp. from Mesomys hispidus (Rodentia: Echimyidae) in Brazil: trypomastigotes described from experimentally infected laboratory mice

Figures 1–20. Trypanosoma (Megatrypanum) lainsoni n. sp., parasites found in peripheral blood of experimentally infected mice; Figure 1: Epimastigote with signs of nuclear division; Figures 2–20: Trypomastigotes. Scale in Figure 20.

opencc-by-4.0Aug 2017View details →

Fig. 1 in Apparent effect of chronic Plasmodium infections on disease severity caused by experimental infections with Mycoplasma gallisepticum in house finches

Fig. 1. Mean severity of eye lesions ± SE (circles), and M. gallisepticum-load (log (qPCR+1)) (triangles) of birds infected through horizontal transmission with the CA2015 strain of M. gallisepticum. Birds in which Plasmodium was detected by PCR (grey symbols) developed more severe disease than birds in which Plasmodium was not found (white symbol). As there is no significant interaction between M. gallisepticum ‾strain and Plasmodium infection (Table 2) the results for the other M. gallisepticum strains are qualitatively similar and therefore not shown.

Fig. 1 in Pathology, clinical signs, and tissue distribution of Toxoplasma gondii in experimentally infected reindeer (Rangifer tarandus)

Fig. 1. Brain squash picture of T. gondii tissue cyst of reindeer 2 brain visualized on compound microscopy (60×).

Fig. 2 in Pathology, clinical signs, and tissue distribution of Toxoplasma gondii in experimentally infected reindeer (Rangifer tarandus)

Fig. 2. Histological section of reindeer 3 diaphragm containing a T. gondii cyst visualized at 100× with oil immersion after immunohistochemical stain.

Fig. 3 in Using experimental de-worming to measure the immunological and pathological impacts of lungworm infection in cane toads

Fig. 3. The effects of lungworm (Rhabdias pseudosphaerocephala infection level on lung pathology of 15 cane toads. (A) number of areas of inflammation predominated by lymphocytes, (B) number of areas of regional septal fibrosis, and (C) areas of inflammation predominated by neutrophils and macrophages. The size of the symbols represents sample size of each count.

Fig. 2 in Using experimental de-worming to measure the immunological and pathological impacts of lungworm infection in cane toads

Fig. 2. Effects of anthelmintic injection (Ivermectin) on the viability of adult lungworms (Rhabdias pseudosphaerocephala inside the lungs of cane toads (n = 10) hosts over a 7-day period following anthelmintic injection. Lungworm viability scores (see text for definitions) decreased with time since injection. The size of the symbols represents sample size of each score. Two toads had not been treated with anthelmintic when euthanized and were given scores of 0 days post injection.

Fig. 6 in Using experimental de-worming to measure the immunological and pathological impacts of lungworm infection in cane toads

Fig. 6. (A) The effects of anthelmintic treatment on relative liver mass of 5 de-wormed (open bars) vs. 6 not de-wormed (grey bars) free-ranging toads. (B) Effect of experimental treatment on relative liver mass of 49 captive cane toads. ID = infected, dewormed (n = 11), IC = infected, control (n = 13), ND = non-infected, de-wormed

Fig. 4 in Using experimental de-worming to measure the immunological and pathological impacts of lungworm infection in cane toads

Fig. 4. The effects of lungworm (Rhabdias pseudosphaerocephala) abundance on leukocyte concentrations in cane toads. Captive toads (n = 19) exhibited high leukocyte concentrations that were independent of the level of Rhabdias infection. In contrast, leukocyte concentrations in free-ranging toads (n = 11) increased with Rhabdias infection level.

opencc-by-4.0Apr 2021View details →

Fig. 2 in Workflow of Lotmaria passim isolation: Experimental infection with a low-passage strain causes higher honeybee mortality rates than the PRA-403 reference strain

Fig. 2. Kaplan-Meier survival curves for the experimental groups (C1, control and PRA-403), showing the cumulative mortality over time. Vertical ticks indicate censored observations.

opencc-by-4.0Apr 2021View details →

Fig. 1 in Workflow of Lotmaria passim isolation: Experimental infection with a low-passage strain causes higher honeybee mortality rates than the PRA-403 reference strain

Fig. 1. Workflow for the isolation of bee-infecting trypanosomatid parasites from honeybee guts. A. Dissection and tissue processing (steps 1–4), and trypanosomatid culture and expansion (step 5) in liquid or Solid Cultures. B. Growth curve of L. passim PRA-403 strain in decreasing concentrations of 5-Fluorocytosine (1 × 106 μg/ mL-100 μg/mL) to determine the maximum dose for parasite survival. C. Giemsa staining of L. passim C1 (CCP 1). D. Hoescht DNA staining of live L. passim C1 (CCP 1): N, Nucleus; K, Kinetoplast; E, Scanning Electron Microscopy of L. passim C1 (CCP 1) grown in Agar Solid cultures 20 days post-inoculation.

opencc-by-4.0Dec 2023View details →

Fig. 2 in Experimental evaluation of pathogenicity and acquired immunity of Eimeria species, E. uekii and E. raichoi, infecting Japanese rock ptarmigans in a subspecies of the birds

Fig. 2. The number of oocysts per gram of feces (OPG) after inoculation with E. uekii and E. raichoi oocysts. Panels A and B show E. uekii and E. raichoi OPG, respectively. Chicks Nos. 1–3 were inoculated depending on the manner of oocysts E. uekii and E. raichoi as described at the bottom of Figure, and mouse no. 4 was inoculated with oocysts of E. raichoi.