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Fig. 7 in Host-parasite interactions during a biological invasion: The fate of lungworms (Rhabdias spp.) inside native and novel anuran hosts

Fig. 7. Histological investigation of lungworm infection in anurans. Graphs show the proportion of (a) metamorph native frogs (Cyclorana australis) and (b) metamorph cane toads (Rhinella marina) infected with lungworms, not infected with lungworms, or with inflammatory 'foci' (probable cases of a lungworm larva penetrating the anuran's body but failing to survive).

Fig. 2 in Host-parasite interactions during a biological invasion: The fate of lungworms (Rhabdias spp.) inside native and novel anuran hosts

Fig. 2. The distribution of lungworm larvae in cane toad metamorphs. (a) Toad metamorphs infected with Rhabdias hylae (native frog lungworm) and (b) toad metamorphs infected with Rhabdias pseudosphaerocephala (cane toad lungworm). Data in panel (b) are from Pizzatto et al. (2010), with permission. LUNG refers to adult lungworms found within the lung, SKIN/MUSCLE refers to larvae found in the skeletal muscle or subcutaneous tissue, HEAD refers to larvae detected in the head or neck region (excluding those found in eye tissue), EYE indicates larvae found in the eye or periocular tissue, and COELOM denotes larvae within the coelom or coelomic membranes.

Fig. 1. Histological image depicting a in Host-parasite interactions during a biological invasion: The fate of lungworms (Rhabdias spp.) inside native and novel anuran hosts

Fig. 1. Histological image depicting a transverse section of (a) R. hylae larva in the connective tissue of the head of a cane toad and (b) the inflammatory response composed primarily of macrophages and multinucleated giant cells surrounding the parasite. Haematoxylin and eosin stain, 400× magnification, scale bar equals 30 μm.

Fig. 4 in Host-parasite interactions during a biological invasion: The fate of lungworms (Rhabdias spp.) inside native and novel anuran hosts

Fig. 4. Effect of time since exposure to Rhabdias hylae larvae on cane toad metamorphs: (a) shows the number of larvae found in toads and (b) shows the number of foci (areas of inflammation with no visible larvae) in toads, as determined by histological methods.

Fig. 9 in Host-parasite interactions during a biological invasion: The fate of lungworms (Rhabdias spp.) inside native and novel anuran hosts

Fig. 9. Change in the average number of inflammatory foci (probable cases of larval parasites breaking down) observed in all anurans over time. Graph shows average values ± 1 S.E.M.

Fig. 6 in Host-parasite interactions during a biological invasion: The fate of lungworms (Rhabdias spp.) inside native and novel anuran hosts

Fig. 6. Effects of Rhabdias hylae infection on cane toad metamorphs: (a) the average percentage of neutrophils and (b) lymphocytes around inflammation sites over time in cane toads infected with Rhabdias hylae. Graphs show average values ±1 S.E.M.

Fig. 3 in Host-parasite interactions during a biological invasion: The fate of lungworms (Rhabdias spp.) inside native and novel anuran hosts

Fig. 3. The state of Rhabdias hylae larvae in cane toads as a function of days-post treatment. The graph shows larval numbers as the percentage of total larvae that were seen at each time period.

Fig. 5 in Host-parasite interactions during a biological invasion: The fate of lungworms (Rhabdias spp.) inside native and novel anuran hosts

Fig. 5. Average inflammation severity surrounding Rhabdias hylae larvae and foci (probable larvae being broken down by the host's immune system) within infected cane toads at different numbers of days post-infection. Graph shows average values ±1 S.E.M.

Fig. 8 in Host-parasite interactions during a biological invasion: The fate of lungworms (Rhabdias spp.) inside native and novel anuran hosts

Fig. 8. Changes through time (days post-infection) on the relative numbers of anurans that were infected with lungworms, and that contained adult versus juvenile stages of the parasites involved. Data are shown for two lungworm species (Rhabdias hylae from native frogs, and Rhabdias pseudosphaerocephala from invasive cane toads) and for two types of host: the native frog, Cyclorana australis, and the cane toad, Rhinella marina. The panels show data for (a) C. australis infected with R. pseudosphaerocephala, (b) C. australis infected with R. hylae, (c) cane toads infected with R. pseudosphaerocephala and (d) cane toads infected with R. hylae.

Fig. 1 in Observation of a novel Babesia spp. in Eastern Grey Kangaroos (Macropus giganteus) in Australia

Fig. 1. Photomicrograph of a blood smear from an Eastern Grey kangaroo stained with Giemsa and showing the presence of Babesia species merozoites. Bar = 10 µm.

Fig. 3 in Observation of a novel Babesia spp. in Eastern Grey Kangaroos (Macropus giganteus) in Australia

Fig. 3. Electron micrographs of Babesia spp. (Case 2) within an erythrocyte. Nucleus (N); host cytoplasm (HC); endoplasmic reticulum (ER); ribosome (RI); mitochondria (MC), and invagination (I). Bar = 0.5 µm.

Fig. 2 in Observation of a novel Babesia spp. in Eastern Grey Kangaroos (Macropus giganteus) in Australia

Fig. 2. Photomicrograph of blood smears stained with Diff-Quik (A) and Giemsa (B–F) from eastern grey kangaroos (Cases 2 and 3) showing diverse forms of Babesia including paired merozoites (2A), multiple ring-shaped trophozoites with a chromatin dot (2B), a large ring-shaped trophozoite with three chromatin dots (2C), ring-shaped trophozoite with a pair of buds in early dividing stage (2D), two dividing trophozoites with a cytoplasmic bridge (2E), and a clump of diverse forms of extraerythrocytic Babesia (3F). Bar = 10 µm.

Fig. 4 in Observation of a novel Babesia spp. in Eastern Grey Kangaroos (Macropus giganteus) in Australia

Fig. 4. Minimum evolution phylogenetic tree based on a 1560 bp 18S rRNA alignment for representatives of the genus Babesia including the new kangaroo-infecting species (in bold and underlined) originating from Cases 1 and 2. Also underlined and in bold are other species sequenced as part of this study. Branch support is shown with a ‡ where all tree building methods (parsimony, distance and likelihood) had at least 70% bootstrap and Bayesian support.

Fig. 2 in Identification of novel Theileria genotypes from Grant's gazelle

Fig. 2. Phylogenetic analysis of Theileria genotypes isolated from Grant's gazelles (Nanger granti) in Kenya. Bayesian analysis of a 400 nucleotide fragment of the 18S ribosomal RNA gene from 1 sequence of Toxoplasma gondii, 33 Theileria sequences from GenBank, and 3 representative Theileria sequences from Grant's gazelles (GG1, GG2, GG3) in this study (bold font). The tree is rooted on the lineage of T.gondii. Numbers above the branches indicate bootstrap support based on 1000 replicates. Host species, geographic location of isolation, and GenBank accession numbers of the sequences are provided where known. Numbered sequences are listed in Table 1.

Fig. 1 in Identification of novel Theileria genotypes from Grant's gazelle

Fig. 1. Light microscopy of a blood smear stained with Giemsa showing single and paired hemoparasites (highlighted by arrows).

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Fig. 2. Maximum parsimony tree inferred from 18S in Novel piroplasmid and Hepatozoon organisms infecting the wildlife of two regions of the Brazilian Amazon

Fig. 2. Maximum parsimony tree inferred from 18S rRNA gene sequences of Hepatozoon spp., with Babesia sp. as outgroup (488 characters; 52 parsimony-informative sites). Numbers at nodes are the support values for the major branches (bootstrap over 500 replicates). The sequences obtained in this study are in bold. Numbers in brackets are GenBank accession numbers.

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Fig. 1. Maximum parsimony tree inferred from 18S in Novel piroplasmid and Hepatozoon organisms infecting the wildlife of two regions of the Brazilian Amazon

Fig. 1. Maximum parsimony tree inferred from 18S rRNA gene sequences of piroplasmids (Babesia spp., Theileria spp., Cytauxzoon spp.), with Plasmodium ovale as outgroup (316 characters; 65 parsimony-informative sites). Numbers at nodes are the support values for the major branches (bootstrap over 500 replicates). The sequences obtained in this study are in bold. Numbers in brackets are GenBank accession numbers.

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Fig. 1. A in A novel quantitative real-time PCR diagnostic assay for seal heartworm (Acanthocheilonema spirocauda) provides evidence for possible infection in the grey seal (Halichoerus grypus)

Fig. 1. A: graphical representation of cluster 20 (C20). B: representation of the selected contig and the sequence used to design the C20 quantitative real-time PCR assay. The forward primer is in bold, the reverse primer is indicated by a dotted underline, and the double-quenched probe is underlined.

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Fig. 2. Standard curve generated using the log10 in A novel quantitative real-time PCR diagnostic assay for seal heartworm (Acanthocheilonema spirocauda) provides evidence for possible infection in the grey seal (Halichoerus grypus)

Fig. 2. Standard curve generated using the log10 of the ng of input A. spirocauda DNA plotted against Ct value. Unknown values are displayed as stars. For unknown samples, the total input DNA was 1 ng, which contains a mixture of seal DNA from the blood and A. spirocauda DNA. R2 = 0.985 for linear fit of standards. Curve is described by the equation y = −5.63x + 17.16, where y is the log (ng) and x is the Ct value. 95% confidence intervals are denoted by the dotted lines.