China
Africa
Explore chapters and articles related to this topic
Cryptosporidium spp
Published in Peter D. Walzer, Robert M. Genta, Parasitic Infections in the Compromised Host, 2020
Excystation, the release of infective sporozoites from environmentally resistant oocysts, is a key event in the life cycle of every true coccidian. This infectioninitiating event usually occurs in the lumen of the gastrointestinal tract following ingestion of oocysts by a suitable host. In most coccidian species examined to date, excystation may also be triggered in vitro by exposing oocysts to conditions that simulate the gastrointestinal environment of the host (i.e., reducing conditions, CO2, host body temperature, bile salts, and trypsin). Much of our understanding of this process is based on in vitro excystation studies of coccidian species belonging to the families Eimeriidae (34,35) and Sarcocystidae (36-38) whose oocysts possess sporocysts, each containing infective sporozoites (Fig. 1B). Such investigations have suggested that there may be two major steps in excystation. The first step is alteration of oocyst wall permeability, allowing influx of proteolytic enzymes and bile salts. This can be triggered by exposure to host body temperature and CO2 and is often accomplished by a peeling away or dissolving of the micropyle, a thinning of the oocyst wall at one pole. This step can also be accomplished by removing the oocyst wall with a tissue grinder, releasing sporocysts. The second step is the release of sporozoites from sporocysts by the action of pancreatic enzymes and/or bile salts. Sporozoites of eimeriid coccidia (e.g., Eimeria spp. and some Isospora spp.) escape through an opening in one pole of the sporocysts that is formed by degradation of a plug, the Stieda body (Fig. 1B). It is believed that trypsin degrades the Stieda body and that bile salts stimulate sporozoite motility. Species of coccidia assigned to the family Sarcocystidae have sporocysts whose walls are composed of four plates joined by sutures. Trypsin and/or bile salts cause dissolution of the sutures, allowing sporozoites to escape between the collapsed plates.
Cystoisospora belli
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Chaturong Putaporntip, Somchai Jongwutiwes
Parasitic protozoa in the phylum Apicomplexa inhabit tissues, blood, or lymphoid cells of the host, and most of them, including the genus Cystoisospora, belong to the class Sporozoea. Previous taxonomic classification based on biology and characteristics of protozoa placed the formerly known mammalian Isospora species, currently classified as genus Cystoisospora, in the subclass Coccidia, suborder Eimeriina, and family Eimeriidae, whose members include the genera Eimeria and Cyclospora, with monoxenous life cycle. Although mature oocysts of mammalian Cystoisospora contain two sporocysts (diplosporocystic) and each with four sporozoites (tetrasporozoic) akin to some members of protozoa in the family Eimeriidae, the absence of a polar Stieda body in each sporocyst and recent phylogenetic inference from the small subunit ribosomal RNA sequences of several members of apicomplexan protozoa have repositioned members of mammal host species of Cystoisospora within tissue-cyst–forming coccidia to the family Sarcocystidae [6]. The members in this family include the genera Toxoplasma, Neospora, Hammondia, and Sarcocystis as a monophyletic group. Avian host species Isospora robini and I. gryphoni are clustered within another monophyletic group consisting of the genera Caryospora, Eimeria, and Cyclospora, all of which are non-tissue-cyst–forming coccidia in the family Eimeriidae (Figure 54.2) [7–9]. The presence of tissue cyst in the genus Cystoisospora favors phylogenetic rather than phenetic classification [10–12]. The genus Cystoisospora was created by Frenkel in 1977 based on the characteristics of oocysts and the presence of tissue cysts in paratenic hosts that are distinct from those of the genus Isospora [13]. Meanwhile, Isospora hominis described over seven decades ago was misclassified, which de facto belongs to the genus Sarcocystis based on the life cycle and structures of the developmental stages. Other species of Cystoisospora are parasitic in wild and domestic animals, for example, C. arctopitheci in nonhuman primates, C. canis and C. ohioensis in dogs, C. rivolta and C. felis in cats, and C. suis in pigs [14]. More than 300 species of Cystoisospora have been proposed and found to infect a wide range of animals, including amphibians, reptiles, birds, and mammals. However, some of these species may require further validation.
Anticoccidial effect of Fructus Meliae toosendan extract against Eimeria tenella
Published in Pharmaceutical Biology, 2020
Ting Yong, Meng Chen, Yunhe Li, Xu Song, Yongyuan Huang, Yaqin Chen, Renyong Jia, Yuanfeng Zou, Lixia Li, Lizi Yin, Changliang He, Cheng Lv, Xiaoxia Liang, Gang Ye, Zhongqiong Yin
Avian coccidiosis is a major intracellular parasitic disease caused by the genus Eimeria (Eimeriidae), leading to tremendous economic losses of poultry worldwide (Allen and Fetterer 2002; Dalloul and Lillehoj 2006). The life cycle of E. tenella is complex. It starts from the exogenous stage of unsporulated oocysts shedding in faeces, then sporulation and infection. In the endogenous phase, when the environmentally resistant oocysts infect chickens, the haploid sporozoites are released from sporocysts contained within each oocyst (Sharman et al. 2010), and subsequently invade intestinal epithelial cells. Eventually, the final generation of merozoites differentiates into either male or female microgametes and release from the host cells, and male gametes invade and fuse with intracellular female gametes to form zygotes. Zygotes mature into oocysts within the gut and are excreted into faeces (Kinnaird et al. 2004). Intestinal colonization can cause damage to the intestinal tract and caecum, which decreases feed conversion, leading to lower productivity and performance. Moreover, coccidiosis also causes the disbalance of intestinal microflora, such as increasing Enterobacteriaceae abundance, decreasing Bacillales and Lactobacillales abundance, and weakening the immune function, even boosting the susceptibility to secondary bacterial infections (Morris et al. 2007; Shirley et al. 2007; Tian et al. 2014; MacDonald et al. 2017).