SOME BIOLOGICAL REQUIREMENTS AND HOST–PARASITE RELATIONS OF ENTAMOEBA INVADENS

1958 ◽  
Vol 36 (4) ◽  
pp. 513-523 ◽  
Author(s):  
Eugene Meerovitch

A hypothesis explaining the processes leading to the encystation of E. invadens is presented. It is suggested that E. invadens can live in turtles as a harmless commensal because the conditions necessary for its encystation and the completion of its life cycle are available in the intestinal lumen of turtles. As these conditions are not present in snakes, the amoebae feed on the mucous secretion of the snakes' intestinal epithelium, and invade the tissues.

2021 ◽  
pp. 270-284
Author(s):  
Regina M. D. G. Carneiro ◽  
Marcilene F. A. Santos ◽  
José Mauro C. Castro

Abstract The following review of the nematodes from cultivated guava is limited to the major problem caused by M. enterolobii, its idenfication and its management strategies. The synonymization of Meloidogyne enterolobii with Meloidogyne mayaguensis and the different methods of identifying Meloidogyne species are discussed. The life cycle, host-parasite relationships, symptoms, damage and dissemination of M. enterolobii are described. The host status of cover crops, maize and fruit plants for M. enterolobii is discussed, as well as the resistance in Psidium spp. to root-knot nematodes. New prospects using genetic resistance in Brazil and some control strategies that can be used in an integrated way are presented.


2011 ◽  
Vol 208 (11) ◽  
pp. 2263-2277 ◽  
Author(s):  
Georgios Nikitas ◽  
Chantal Deschamps ◽  
Olivier Disson ◽  
Théodora Niault ◽  
Pascale Cossart ◽  
...  

Listeria monocytogenes (Lm) is a foodborne pathogen that crosses the intestinal barrier upon interaction between its surface protein InlA and its species-specific host receptor E-cadherin (Ecad). Ecad, the key constituent of adherens junctions, is typically situated below tight junctions and therefore considered inaccessible from the intestinal lumen. In this study, we investigated how Lm specifically targets its receptor on intestinal villi and crosses the intestinal epithelium to disseminate systemically. We demonstrate that Ecad is luminally accessible around mucus-expelling goblet cells (GCs), around extruding enterocytes at the tip and lateral sides of villi, and in villus epithelial folds. We show that upon preferential adherence to accessible Ecad on GCs, Lm is internalized, rapidly transcytosed across the intestinal epithelium, and released in the lamina propria by exocytosis from where it disseminates systemically. Together, these results show that Lm exploits intrinsic tissue heterogeneity to access its receptor and reveal transcytosis as a novel and unanticipated pathway that is hijacked by Lm to breach the intestinal epithelium and cause systemic infection.


1989 ◽  
Vol 26 (3) ◽  
pp. 260-264 ◽  
Author(s):  
S. McOrist ◽  
G. H. K. Lawson ◽  
A. C. Rowland ◽  
N. MacIntyre

Gnotobiotic pigs and conventional hamsters were given suspensions of intestinal mucosa from a pig with proliferative hemorrhagic enteropathy and killed 10 or 21 days later. Affected animals had evidence of marked proliferation of immature enterocytes in the intestinal crypts. Numerous Campylobacter-like organisms were in the cytoplasm of enterocytes, and in some instances, bacteria were closely associated with enter-ocytes. Some intracellular bacteria lying below the microvillous border were within membrane-bound structures. Immunofluorescence and electron immunogold staining with specific antibodies indicated that these organisms were antigenically different from curved bacteria in the crypt lumen of early lesions. This study indicates that the life cycle of the intracellular organisms may involve entry into crypt enterocytes from the intestinal lumen with subsequent intracellular multiplication.


Parasitology ◽  
1998 ◽  
Vol 116 (S1) ◽  
pp. S47-S55 ◽  
Author(s):  
J. C. Koella ◽  
P. Agnew ◽  
Y. Michalakis

SummarySeveral recent studies have discussed the interaction of host life-history traits and parasite life cycles. It has been observed that the life-history of a host often changes after infection by a parasite. In some cases, changes of host life-history traits reduce the costs of parasitism and can be interpreted as a form of resistance against the parasite. In other cases, changes of host life-history traits increase the parasite's transmission and can be interpreted as manipulation by the parasite. Alternatively, changes of host's life-history traits can also induce responses in the parasite's life cycle traits. After a brief review of recent studies, we treat in more detail the interaction between the microsporidian parasite Edhazardia aedis and its host, the mosquito Aedes aegypti. We consider the interactions between the host's life-history and parasite's life cycle that help shape the evolutionary ecology of their relationship. In particular, these interactions determine whether the parasite is benign and transmits vertically or is virulent and transmits horizontally.Key words: host-parasite interaction, life-history, life cycle, coevolution.


Parasitology ◽  
1987 ◽  
Vol 95 (3) ◽  
pp. 507-516 ◽  
Author(s):  
H. M. Murare ◽  
M. J. Doenhoff

SUMMARYA laboratory life-cycle ofSchistosoma boviswas established in order to study the host-parasite relationship in immunologically intact and T-cell deprived mice. Normal mice were found to have ‘self-cured’ theirS. bovisinfections almost completely by 10 weeks after cercarial administration, and there was no evidence of self-cure by day 79 in T-cell deprived animals, Thus, groups of deprived mice autopsied between 9 and 11 weeks after infection were invariably found to have greater worm burdens and a greater total number of eggs in the liver than comparably-infected normal mice. However, liver egg counts/worm pair were similar in the two types of host, and differences between normal and deprived mice with respect to totalS. bovisegg counts in the intestine were also not consistently in the same direction in all experiments. Faecal egg counts were always less in deprived mice than in normal mice, even in an experiment in which the deprived mice had a significantly higher intestinal tissue egg count than the normal control group. The results are discussed in relation to the better knownS. mansoni/mouse host-parasite relationship.


1982 ◽  
Vol 60 (12) ◽  
pp. 3370-3376 ◽  
Author(s):  
W. M. Hominick ◽  
S. L. Croft ◽  
F. A. S. Kuzoe

Parasitic stages of Hexamermis glossinae from Glossina palpalis s. 1. and G. pallicera, which were collected immediately prior to the rainy season near Bouaflé, Ivory Coast, are described and illustrated. Specimens have an onchiostylet and were similar to Coccinellimermis coccinellae exochomi (Rubtzov, 1971) Rubtzov, 1978. Adults of Coccinellimermis are unknown. Possession of an onchiostylet is probably a specific rather than a generic character and Coccinellimermis is therefore a subjective junior synonym of Hexamermis. Results from 200 G. palpalis collected in a localized area showed that 5% of the flies were infected and that 12.3% of the males were parasitized compared with 2.1% of the females. Four of the 10 flies harbouring nematodes also harboured trypanosomes. Such concurrent infections were more frequent than expected since fewer than 10% of the 200 flies harboured trypanosomes. No correlation exists between age of the female flies, estimated by ovarian ageing, and length of the parasites. Infected females had fed and ovulated, and two carried a developing larva in the uterus. The life cycle of this mermithid is unknown, but all stages of the life cycle may occur where female flies larviposit.


2021 ◽  
Vol 11 ◽  
Author(s):  
Xinyu Yu ◽  
Gaoqian Feng ◽  
Qingfeng Zhang ◽  
Jun Cao

Advances in research over the past few decades have greatly improved metabolomics-based approaches in studying parasite biology and disease etiology. This improves the investigation of varied metabolic requirements during life stages or when following transmission to their hosts, and fulfills the demand for improved diagnostics and precise therapeutics. Therefore, this review highlights the progress of metabolomics in malaria research, including metabolic mapping of Plasmodium vertebrate life cycle stages to investigate antimalarials mode of actions and underlying complex host-parasite interactions. Also, we discuss current limitations as well as make several practical suggestions for methodological improvements which could drive metabolomics progress for malaria from a comprehensive perspective.


2019 ◽  
Author(s):  
Chikako Arai ◽  
Aki Suyama ◽  
Shigeyuki Arai ◽  
Norie Arai ◽  
Chiyo Yoshizane ◽  
...  

Abstract Background: Trehalose is a functional disaccharide that has anti-metabolic activities such as suppression of adipocyte hypertrophy in mice and alleviation of impaired glucose tolerance in humans. Trehalase hydrolyzes trehalose in the small intestine into two glucose molecules. In this study, we investigated whether trehalose can suppress adipocyte hypertrophy in mice in the presence or absence of trehalase. Methods: Trehalase knockout (KO) mice and wild-type (WT) mice were fed a high fat diet (HFD) and administered water with 0.3% (w/v) or without trehalose for 8 weeks. At the end of the experimental period, mesenteric adipose tissues and the small intestine were collected and the adipocyte size and proportion of cytoplasmic lipid droplets (CLDs, %) in jejunum epithelium were measured by image analysis. Results: Trehalose treatment was associated with suppressed adipocyte hypertrophy in both trehalase KO and WT mice. The rate of CLDs in the jejunal epithelium was increased in both trehalase KO and WT mice given water containing trehalose relative to untreated control mice. Since there was a negative correlation between jejunal epithelial lipid droplet volume and mesenteric adipocyte size, together with these results, trehalose treatment would suppress adipocyte hypertrophy. Because of jejunal epithelium containing lipid droplets falled into the intestinal lumen, triglyceride (TG) levels in feces tended to be higher in the KO/HFD/Tre group than in the KO/HFD/Water group. Whereas feces from trehalose-treated trehalase KO and WT mice tended to have more free fatty acids (FFA) than the untreated groups. Chylomicron-TG tended to be decreased in both trehalose-treated trehalase KO and WT mice. In vitro , addition of trehalose to differentiated Caco-2 cells increased intracytoplasmic lipid droplets and decreased secretion of the chylomicron marker ApoB48. Conclusions: The suppression of adipocyte hypertrophy in the presence and absence of trehalase indicates that trehalose mediates effects prior to being hydrolyzed into glucose. In both trehalase KO and WT mice, trehalose treatment increased the rate of CLDs in jejunal epithelium, reduced chylomicron migration from the intestinal epithelium to the periphery, and suppressed adipocyte hypertrophy. Thus, trehalose ingestion could prevent metabolic syndrome by trapping fat droplets in the intestinal epithelium and suppressing rapid increases in chylomicrons.


2019 ◽  
Vol 49 (12) ◽  
pp. 975-984 ◽  
Author(s):  
Axl S. Cepeda ◽  
Ingrid A. Lotta-Arévalo ◽  
David F. Pinto-Osorio ◽  
Jhon Macías-Zacipa ◽  
Gediminas Valkiūnas ◽  
...  

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