Cryptosporidiosis in Other Vertebrates

Kváč, Martin; McEvoy, John; Stenger, Brianna; Clark, Mark E.

doi:10.1007/978-3-7091-1562-6_5

Cited by 29 publications

(33 citation statements)

References 314 publications

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“…It is therefore unsurprising that the host range of C. avium overlaps that of other avian-adapted Cryptosporidium, including the closely related avian genotype II (Abe and Makino 2010). In contrast to C. meleagridis , which has been reported in calves, pigs, rabbits, rats, mice, and humans (Akiyoshi et al 2003; Cama et al 2003; Darabus and Olariu 2003; Elwin et al 2012; Huang et al 2003; O'Donoghue 1995; Xiao and Ryan 2004) there is no evidence that C. avium infects non-avian hosts (present study; Kváč et al 2014b). …”

Section: Discussioncontrasting

confidence: 75%

Cryptosporidium avium n. sp. (Apicomplexa: Cryptosporidiidae) in birds

et al. 2016

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The morphological, biological, and molecular characteristics of Cryptosporidium avian genotype V are described, and the species name Cryptosporidium avium is proposed to reflect its specificity for birds under natural and experimental conditions. Oocysts of C. avium measured 5.30–6.90 μm (mean = 6.26 μm) × 4.30–5.50 μm (mean = 4.86 μm) with a length to width ratio of 1.29 (1.14–1.47). Oocysts of C. avium obtained from four naturally infected red-crowned parakeets (Cyanoramphus novaezealandiae) were infectious for 6-month-old budgerigars (Melopsittacus undulatus) and hens (Gallus gallus f. domestica). The prepatent periods in both susceptible bird species was 11 days post infection (DPI). The infection intensity of C. avium in budgerigars and hens was low, with a maximum intensity of 5,000 oocysts per gram of faeces. Oocysts of C. avium were microscopically detected at only 12–16 DPI in hens and 12 DPI in budgerigars, while PCR analyses revealed the presence of specific DNA in faecal samples from 11 to 30 DPI (the conclusion of the experiment). Cryptosporidium avium was not infectious for 8-week-old SCID and BALB/c mice (Mus musculus). Naturally or experimentally infected birds showed no clinical signs of cryptosporidiosis and no pathology was detected. Developmental stages of C. avium were detected in the ileum and caecum using scanning electron microscopy. Phylogenetic analyses based on small subunit rRNA, actin, and heat shock protein 70 gene sequences revealed that C. avium is genetically distinct from previously described Cryptosporidium species.

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Section: Discussioncontrasting

confidence: 75%

Cryptosporidium avium n. sp. (Apicomplexa: Cryptosporidiidae) in birds

et al. 2016

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“…So far, 30 species and over 100 genotypes of Cryptosporidium have been described in various vertebrate hosts and environmental sources (Kváč et al 2014). Among them, Cryptosporidium hominis and Cryptosporidium parvum are responsible for over 90 % of human cryptosporidiosis cases (Rossle and Latif 2013).…”

Section: Introductionmentioning

confidence: 99%

Cryptosporidium spp. and Enterocytozoon bieneusi in introduced raccoons (Procyon lotor)—first evidence from Poland and Germany

et al. 2016

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The raccoon (Procyon lotor) carnivore native to North America is a fast spreading, invasive species in the Europe now. At the moment, the highest population occupies areas near the German-Polish border. The data on the occurrence of Cryptosporidium spp. and microsporidia in raccoons is limited to North America’s territory and is totally lacking in the case of their introduction to Europe. Therefore, the objective of this study was to investigate the occurrence of microparasites, i.e., Cryptosporidium spp. and microsporidia in the introduced raccoons obtained from localities in Poland and Germany. A PCR-based approach that permitted genetic characterization via sequence analysis was applied to raccoon fecal samples (n = 49), collected during 2012–2014. All fecal samples were simultaneously tested with the use of genetic markers, and DNA of microsporidia and Cryptosporidium spp. was detected among the examined raccoons. The results of our research confirmed the presence of Cryptosporidium skunk genotype and Enterocytozoon bieneusi NCF2 genotype. The results suggest a possible role of raccoons in the contamination of the environment, including urban areas, with pathogens of zoonotic significance as well as their role in the transmission and introduction of new genotypes of microparasites in the areas where P. lotor has not been observed yet. To our knowledge, there has been no literature data on the above genotypes detected previously in humans or animals from the examined study sites so far.

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“…The apicomplexan Cryptosporidium parasitizes the major vertebrate groups (Kváč et al, 2014) and is a major cause of diarrheal disease in humans and livestock. Twenty-six species are currently recognized (Ryan et al, 2014), but these represent just a fraction of Cryptosporidium diversity.…”

Section: Introductionmentioning

confidence: 99%

Highly divergent 18S rRNA gene paralogs in a Cryptosporidium genotype from eastern chipmunks (Tamias striatus)

Stenger

Clark

Kváč

et al. 2015

Infection, Genetics and Evolution

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Cryptosporidium is an apicomplexan parasite that causes the disease cryptosporidiosis in humans, livestock, and other vertebrates. Much of the knowledge on Cryptosporidium diversity is derived from 18S rRNA gene (18S rDNA) phylogenies. Eukaryote genomes generally have multiple 18S rDNA copies that evolve in concert, which is necessary for the accurate inference of phylogenetic relationships. However, 18S rDNA copies in some genomes evolve by a birth-and-death process that can result in sequence divergence among copies. Most notably, divergent 18S rDNA paralogs in the apicomplexan Plasmodium share only 89–95% sequence similarity, encode structurally distinct rRNA molecules, and are expressed at different life cycle stages. In the present study, Cryptosporidium 18S rDNA was amplified from 28/72 (38.9%) eastern chipmunks (Tamias striatus). Phylogenetic analyses showed the co-occurrence of two 18S rDNA types, Type A and Type B, in 26 chipmunks, and Type B clustered with a sequence previously identified as Cryptosporidium chipmunk genotype II. Types A and B had a sister group relationship but shared less than 93% sequence similarity. In contrast, actin and heat shock protein 70 gene sequences were homogeneous in samples with both Types A and B present. It was therefore concluded that Types A and B are divergent 18S rDNA paralogs in Cryptosporidium chipmunk genotype II. Substitution patterns in Types A and B were consistent with functionally constrained evolution; however, Type B evolved more rapidly than Type A and had a higher G+C content (46.3% versus 41.0%). Oocysts of Cryptosporidium chipmunk genotype II measured 4.17 μm (3.73–5.04 μm) × 3.94 μm (3.50–4.98 μm) with a length-to-width ratio of 1.06 ± 0.06 μm, and infection occurred naturally in the jejunum, cecum, and colon of eastern chipmunks. The findings of this study have implications for the use of 18S rDNA sequences to infer phylogenetic relationships.

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Cryptosporidiosis in Other Vertebrates

Cited by 29 publications

References 314 publications

Cryptosporidium avium n. sp. (Apicomplexa: Cryptosporidiidae) in birds

Cryptosporidium avium n. sp. (Apicomplexa: Cryptosporidiidae) in birds

Cryptosporidium spp. and Enterocytozoon bieneusi in introduced raccoons (Procyon lotor)—first evidence from Poland and Germany

Highly divergent 18S rRNA gene paralogs in a Cryptosporidium genotype from eastern chipmunks (Tamias striatus)

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