SBA Answers and Explanations
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury in SBAs for the MRCS Part A, 2018
The intermediate host (humans) – Hepatic stage: Human infection begins when sporozoites are introduced into an individual’s bloodstream as an infected mosquito takes a blood meal. Within 30 minutes, they disappear from the blood as they infect hepatocytes. Here they undergo the first round of asexual reproduction (exoerythrocytic schizogony) and develop into exoerythrocytic schizonts. These exoerythrocytic schizonts may contain many thousands of merozoites. On invasion of the hepatocyte by Plasmodium vivax and P. ovale, the development of the schizont is retarded, and a ‘dormant’ stage of the parasite, the hypnozoite, is formed. This is responsible for disease relapse months to years after supposed chemotherapeutic cure and clearance of bloodstream forms of the parasite.
Malabsorption and microsporidia
Ronald R. Watson in NUTRIENTS and FOODS in AIDS, 2017
The life cycle of microsporidia include three distinct phases. After the spore is released into the environment, it is, in the case of intestinal microsporidia, probably transmitted by the fecal-oral route. Upon ingestion by the host, the spore is stimulated in the small intestine by changes in the pH and ionic concentrations to evert its coiled tubule. Thereafter, the tubule penetrates the host cells and injects the sporoplasm which initiates a proliferative meragonic or binary fission and schizonic or multiple fission phase. When meronts develop into sporonts, sporogeny is initiated and completed when sporoblasts mature into spores. Microsporidia have great reproductive potential, being capable of multiplying within cells and spreading from cell to cell, filling the enterocytes with their progeny.
Objections to the Basic Moral Status of Human Embryos
Christopher Kaczor in The Ethics of Abortion, 2023
A questionable premise of Stretton's argument is that the single-celled zygote fissions into two duplicate, identical cells, as takes place with amoebae. The first cell division in the zygote gives rise to two cells, one of which will give rise to the embryo proper; the other of which will give rise to the trophoblast (George & Tollefsen 2011, pp. 154–155). These different developmental paths may be due to differences already present in each cell rather than to external influences. It is also questionable whether this division is properly described as fission:The main reason is that when a zygote divides a very important item is retained. Both at the initial stage and at the resulting two-cell stage there is not only a complete, connected external boundary, but, more precisely, a membrane or a physical covering—the zona pellucida—surrounding the cells. This membrane does not divide or disappear. The division takes place within its boundaries .… [T]he division of an amoeba by fission is not an adequate analogue to the division of a one-cell zygote. Amoebas do not retain a common external boundary or membrane after they divide, nor do they start to specialize into amoebas with different, yet coordinated functions.(Damschen, Gómez-Lobo, & Schönecker 2006, pp. 169, 171)
Functional genetic evaluation of DNA house-cleaning enzymes in the malaria parasite: dUTPase and Ap4AH are essential in Plasmodium berghei but ITPase and NDH are dispensable
Published in Expert Opinion on Therapeutic Targets, 2019
Hirdesh Kumar, Jessica Kehrer, Mirko Singer, Miriam Reinig, Jorge M. Santos, Gunnar R. Mair, Friedrich Frischknecht
Malaria is a devastating parasitic disease killing around 400,000 people every year, mostly young children. The occurrence of drug resistance and the absence of an efficient vaccine demand a better understanding of the parasite’s biology to aid the identification of suitable and novel drug and vaccine targets [1–4]. Plasmodium, the causative agent of the disease, is haploid throughout most of its life cycle. This protozoan uses multiple rounds of endomitosis followed by cellular morphogenesis to produce unicellular progeny in a process called schizogony [5]. This strategy is employed by the parasite to increase the population at specific time points during its life cycle: in the red blood cell a single P. falciparum merozoite produces up to 32 daughter cells [6]; following transmission to the mosquito an oocyst can generate hundreds of sporozoites [7] while in the liver thousands of merozoites emerge from a hepatocyte infected with a single sporozoite [8]. During sexual development, the male gametocyte produces eight motile gametes in a matter of minutes following transmission to the mosquito vector [9].
Can Plasmodium’s tricks for enhancing its transmission be turned against the parasite? New hopes for vector control
Published in Pathogens and Global Health, 2019
S. Noushin Emami, Melika Hajkazemian, Raimondas Mozūraitis
All malaria parasites require two hosts, the vertebrate host where schizogony occurs within the erythrocytes (human blood stages of parasite), and the mosquito vector where sporogony (mosquito stages of parasite) occurs in the mosquito midgut wall [22]. In the vertebrate host, an infection is initiated when sporozoites are injected with the saliva of an infected mosquito, and parasites replicate asexually, first in the liver, and then in the erythrocytes (reviewed in [23]). Whilst the majority of parasites invading erythrocytes are destined to continue through the asexual cycle, a small fraction can develop into gametocytes, the first sexual stage of the life cycle. In Plasmodium falciparum, the presence of gametocytes in the peripheral blood appears 7–15 days after the initial asexual wave which is long compared to the other human malaria species 1–3 days. The ratio of gametocytes to asexual stages in P. falciparum is usually found at very low levels [24]. Only people carrying gametocytes can be infectious to mosquitoes. Recent studies showed that microscopy is insufficiently sensitive to detect low densities of asexual parasites and gametocyte [25,26]. In most endemic settings, a small proportion of infecting parasites are gametocytes [27].
Imaging the in vivo growth patterns of bacteria in human gut Microbiota
Published in Gut Microbes, 2021
Liyuan Lin, Jia Song, Jian Li, Xiaolei Zuo, Hong Wei, Chaoyong Yang, Wei Wang
We further investigated whether the morphology and FDAA labeling pattern of the same species were the same in different hosts. Clostridium hathewayi, C. symbiosum, Flavonifractor plautii, Blautia producta, and Clostridiales bacterium 1-7-47FAA in both HMA and mouse native microbiotas were identified by FISH staining. Very similar labeling patterns and morphogenesis of the bacteria stained by the same FISH probe were observed in the mouse gut microbiota (Figure S9). Despite the very different cell lengths, the FDAA labeling patterns of each species were essentially the same (Figure 5(a)). For example, C. hathewayi and F. plautii divided in binary fission in both hosts, with clear red-labeled septums in the middle. When the mother cells of B. producta in both hosts prepared their septa for division, the daughter cells also began to synthesize new septa at the midcells. However, the cellular lengths of all five species were all significantly longer in the mouse native microbiota (Figure 5(b)).
Related Knowledge Centers
- Archaea
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- Cell Division
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- Prokaryote
- Organelle
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- Mitochondrion
- Chromosome