An Outbreak of Cryptosporidium sp. Associated with a Public Swimming Pool
Meera Chand, John Holton in Case Studies in Infection Control, 2018
Cryptosporidium has a monoxenous life cycle completed within the gastrointestinal tract of a single host. Infection follows ingestion of the oocyst life-cycle stage, which is shed in faeces. Under conditions triggered in the intestine, the oocysts each release four motile infectious sporozoites in a process known as excystation. These actively probe, attach, invade, and become engulfed by host epithelial cells at the luminal surface. An asexual cycle follows, involving differentiation and, sequentially, trophozoites, Type I meront, and merozoite production. The parasite proliferates as six or eight merozoites are released to invade neighbouring epithelial cells, and they either develop into trophozoites, repeating the asexual cycle, or into Type II meronts. The sexual cycle is initiated following production of four merozoites by Type II meronts, which are then released to invade neighbouring host cells and differentiate into either macrogamonts (ova) or microgamonts. Microgamonts release microgametes (sperm) into the intestinal lumen. The microgametes attach and penetrate infected epithelial cells to fertilize the macrogamete, producing a zygote. Following meiosis, the zygote differentiates into four sporozoites as the oocyst matures and is released into the intestinal lumen. Sporulated oocysts are shed in the faeces, often in large numbers, and are immediately infectious for the next susceptible host. Autoinfection of the host can occur as sporozoites may be released directly into the intestinal lumen, and the life cycle continues.
The Parasite's Way of life
Eric S. Loker, Bruce V. Hofkin in Parasitology, 2015
Cats acquire an infection when they consume a prey animal infected with tissue cysts (Figure 3.15). Each cyst contains up to a thousand or more bradyzoites. This slowly growing, encysted life-cycle stage (brady, from the Greek for slow) is responsible for chronic toxoplasmosis. Bradyzoites are released in the cat’s intestine, whereupon they invade intestinal epithelial cells. Here they undergo a form of asexual reproduction called merogony. Unlike binary fission, merogony is a type of multiple fission in which the nucleus and other organelles of the bradyzoite divide several times before cell division, resulting in the simultaneous production of many merozoites. The merozoites are released from infected cells, whereupon they invade new cells. They may then commence a new cycle of merogony or they may enter gametogony, the sexual stage of the life cycle during which gametes are produced. As in many other apicomplexans, two types of gametes, the smaller microgamete and the larger macrogamete, are produced. After they are released from epithelial cells, microgametes enter a different host cell containing a macrogamete. Fertilization occurs and the newly formed zygote gives rise to the cystlike oocyst, which is passed with the cat’s feces. A second round of asexual multiple fission known as sporogony takes place within the oocyst. After a few days, the now mature oocyst contains two sporocysts, each containing four sporozoites, which are the infective stage for the intermediate host.
Malaria
F. Y. Liew in Vaccination Strategies of Tropical Diseases, 2017
The paired rhoptry organelles of merozoites contain a number of proteins synthesized during schizogony.6 Since invasion is associated with the discharge of rhoptry contents onto the erythrocyte membrane, there is interest in the possible use of rhoptry antigens as vaccine components. Immunization with a P. falciparum, 41-kDa rhoptry antigen in FCA partially protected Saimiri monkeys against challenge.52 An affinity-purified, 140-kDa rhoptry antigen partially protected one out of three Aotus monkeys against challenge.47 Immunization of mice with an affinity-purified P. yoelii, 235-kDa rhoptry antigen protected them against challenge.46 The Mab against this protein was also protective on passive transfer, indicating that the protective response was at least partially antibody mediated. Further characterization of rhoptry antigens will be necessary before their potential efficacy in a vaccine can be assessed.
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).
Antimalarial drugs: what’s new in the patents?
Published in Expert Opinion on Therapeutic Patents, 2023
Elizabeth A. Lopes, Maria M. M. Santos, Mattia Mori
Remarkable efforts have been spent in the prevention of malaria transmission and infection using vaccines. Four types of vaccines have been developed so far: 1) pre-erythrocytic vaccines, 2) asexual blood-stage vaccines, 3) transmission blocking vaccines, and 4) multistage combination vaccines [82]. The pre-erythrocytic stage vaccines, also named circumsporozoite protein-based strategies, target sporozoites and/or schizont-infected hepatocytes. Targeting this stage confers immunity and prevents latent malaria infection. The asexual blood-stage vaccines act against the infected red blood cells or the merozoite. As this infection stage is responsible for the disease symptoms, these vaccines are designed to minimize clinical severity and/or prevent merozoites from invading erythrocytes [83]. Transmission blocking vaccines prevent the mosquitoes to become infected when feeding from malaria infected hosts. This strategy avoids the parasite to mature in the mosquito through antibodies [84]. The multistage combination malaria vaccines target multiple stages of the parasite life cycle [85].
Correlates of malaria vaccine efficacy
Published in Expert Review of Vaccines, 2021
Danielle I. Stanisic, Matthew B. B. McCall
Functional antibodies against merozoites and pRBCs can directly inhibit parasite growth (i.e., invasion and replication) or act via engagement with immune cells and/or complement. Opsonization of merozoites and pRBCs can facilitate Fc-R mediated phagocytosis or phagocytosis via complement fixation and clearance through the complement receptor (reviewed in [53]). Similar to sporozoites, antibody-dependent complement fixation on merozoites can also result in direct lysis of the parasite [54]. Opsonized parasites interacting with phagocytes can also trigger the release of soluble factors e.g. tumor necrosis factor (TNF) and free radicals that inhibit parasite growth in vitro through antibody-dependent cellular inhibition (ADCI) and antibody-dependent respiratory burst (ADRB) [55,56]. Antibodies that target antigens on pRBCs can prevent schizont egress [57] and prevent adhesion to tissue receptors, facilitating clearance by the spleen.
Related Knowledge Centers
- Biochemistry
- Morphology
- Multinucleate
- Cell Nucleus
- Cytokinesis
- Organelle
- Intracellular Parasite
- Biological Life Cycle
- Fission
- Theileria