Academic literature on the topic 'Eosinophic parasite'
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Journal articles on the topic "Eosinophic parasite"
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Bates, Alan W. H. "Diagnosing Eosinophilic Colitis: Histopathological Pattern or Nosological Entity?" Scientifica 2012 (2012): 1–9. http://dx.doi.org/10.6064/2012/682576.
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Reports of “eosinophilic colitis”—raised colonic mucosal eosinophil density in patients with lower gastrointestinal symptoms—have increased markedly over the last fifteen years, though it remains a rarity. There is no consensus over its diagnosis and management, and uncertainty is compounded by the use of the same term to describe an idiopathic increase in colonic eosinophils and an eosinophilic inflammatory reaction to known aetiological agents such as parasites or drugs. In patients with histologically proven colonic eosinophilia, it is important to seek out underlying causes and careful clinicopathological correlation is advised. Because of the variability of eosinophil density in the normal colon, it is recommended that histological reports of colonic eosinophilia include a quantitative morphometric assessment of eosinophil density, preferably across several sites. Few reported cases of “eosinophilic colitis” meet these criteria. As no correlation has been shown between colonic eosinophil density and symptoms in older children or adults, it is suggested that treatment should be directed towards alleviation of symptoms and response to treatment assessed clinically rather than by histological estimates of intramucosal eosinophils.
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Sturm, Eva Maria, Eva Knuplez, and Gunther Marsche. "Role of Short Chain Fatty Acids and Apolipoproteins in the Regulation of Eosinophilia-Associated Diseases." International Journal of Molecular Sciences 22, no. 9 (April 22, 2021): 4377. http://dx.doi.org/10.3390/ijms22094377.
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Eosinophils are key components of our host defense and potent effectors in allergic and inflammatory diseases. Once recruited to the inflammatory site, eosinophils release their cytotoxic granule proteins as well as cytokines and lipid mediators, contributing to parasite clearance but also to exacerbation of inflammation and tissue damage. However, eosinophils have recently been shown to play an important homeostatic role in different tissues under steady state. Despite the tremendous progress in the treatment of eosinophilic disorders with the implementation of biologics, there is an unmet need for novel therapies that specifically target the cytotoxic effector functions of eosinophils without completely depleting this multifunctional immune cell type. Recent studies have uncovered several endogenous molecules that decrease eosinophil migration and activation. These include short chain fatty acids (SCFAs) such as butyrate, which are produced in large quantities in the gastrointestinal tract by commensal bacteria and enter the systemic circulation. In addition, high-density lipoprotein-associated anti-inflammatory apolipoproteins have recently been shown to attenuate eosinophil migration and activation. Here, we focus on the anti-pathogenic properties of SCFAs and apolipoproteins on eosinophil effector function and provide insights into the potential use of SCFAs and apolipoproteins (and their mimetics) as effective agents to combat eosinophilic inflammation.
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Folkard, S. G., P. J. Hogarth, M. J. Taylor, and A. E. Bianco. "Eosinophils are the major effector cells of immunity to microfilariae in a mouse model of onchocerciasis." Parasitology 112, no. 3 (March 1996): 323–29. http://dx.doi.org/10.1017/s0031182000065847.
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SUMMARYMice inoculated with microfilariae of the filarial nematode Onchocerca lienalis clear their parasites over a period of 3–4 months and are highly resistant to re-infection. We have investigated the comparative roles of the eosinophil, macrophage and neutrophil in effecting this parasite clearance, employing agents specifically to perturb cell function in vivo. Using the anti-IL-5 monoclonal antibody TRFK-5, we show that eosinophils are of primary importance in effecting resistance to re-infection. Ablation of macrophages (with carbon) and neutrophils (with the monoclonal antibody NIMP-R14) had no effect on parasite clearance following re-infection. Neutralization of these 3 cell types during a primary infection showed that while the removal of both eosinophils and macrophages caused a small but significant delay in parasite clearance, the depletion of neutrophils had no effect. This report describes the first direct evidence for eosinophil-mediated killing of microfilariae in vivo, and is consistent with Th-2 cell responses previously described in this model.
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Kierszenbaum, F., F. Villalta, and P. C. Tai. "Role of inflammatory cells in Chagas' disease. III. Kinetics of human eosinophil activation upon interaction with parasites (Trypanosoma cruzi)." Journal of Immunology 136, no. 2 (January 15, 1986): 662–66. http://dx.doi.org/10.4049/jimmunol.136.2.662.
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Abstract The kinetics of human eosinophil activation and granule secretion initiated by interaction with Trypanosoma cruzi amastigotes was studied by using a monoclonal IgG1 antibody (termed EG2) that is specific for an epitope present only in the secreted forms of both eosinophil cationic protein (ECP) and the eosinophil protein X (EP-X), and hence not detectable in unstimulated resting eosinophils. Studies were carried out by using electron microscopy and indirect immunofluorescence. In the electron microscopy studies, deposits of protein A-gold particles in parasite-containing eosinophils that had been incubated previously with EG2 antibody were first detected 4 hr after initiation of the eosinophil-amastigote interaction. Control tests performed with a monoclonal IgG1 unreactive with eosinophils showed no deposition of protein A-gold particles. EG2 antibody binding was confined to the crystalloid granule matrix, where ECP and EP-X are known to be stored. A similar kinetic pattern of ECP/EP-X solubilization and secretion was confirmed by the results of the indirect immunofluorescence experiments also showing the binding of EG2 antibody after 4 hr of cell-parasite interaction. The kinetics of ECP/EP-X solubilization and secretion paralleled the kinetics of destruction of internalized amastigotes, suggesting a role for these basic proteins in parasite killing. Consistent with this notion was the detection of ECP/EP-X in the fluid of phagocytic vacuoles containing amastigotes and associated with the ingested organisms at the same time as the parasites began to show structural alterations. These results outlined the kinetics of eosinophil activation in terms of the time required for mobilization of two basic proteins associated with eosinophil secretion that are known to be biologically active.
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Yamaguchi, Y., Y. Hayashi, Y. Sugama, Y. Miura, T. Kasahara, S. Kitamura, M. Torisu, S. Mita, A. Tominaga, and K. Takatsu. "Highly purified murine interleukin 5 (IL-5) stimulates eosinophil function and prolongs in vitro survival. IL-5 as an eosinophil chemotactic factor." Journal of Experimental Medicine 167, no. 5 (May 1, 1988): 1737–42. http://dx.doi.org/10.1084/jem.167.5.1737.
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The recent molecular cloning of the complementary DNA encoding T cell--replacing factor (TRF) has demonstrated that a single molecule is responsible for B cell growth factor II (BCGF-II) activity and eosinophil differentiation activity. It has been proposed that this molecule be called interleukin 5 (IL-5). We previously reported that purified rIL-5 supports the terminal differentiation and proliferation of eosinophilic precursors. In this study, we examined the effects of IL-5 on functional activities of mature eosinophils. IL-5 maintained the viability of mature eosinophils obtained from peritoneal exudate cells of mice infected with parasites. It also induced superoxide anion production in a dose-dependent manner. The Boyden's chamber Millipore assay revealed that IL-5 had a marked chemokinetic effect on eosinophils in a dose-dependent manner. Moreover, IL-5 was found to be an eosinophil chemotactic factor by the checkerboard assay. In conclusion, IL-5 is suggested to play an important role in increasing the functional activities of eosinophils as well as their production in allergic and parasitic diseases.
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Macapagal, Daphne, Jane Connor, Tomas Mikael Mustelin, Thirumalai Ramalingam, Thomas Wynn, and Todd Davidson. "Necrotic liver induces pyroptosis through caspase-1 in eosinophils." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 221.8. http://dx.doi.org/10.4049/jimmunol.198.supp.221.8.
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Abstract During sterile inflammatory reactions, damage associated molecular patterns (DAMPS) are released from necrotic cells and recruit immune cells to the sites of tissue injury. We found that necrotic liver homogenates, when injected intraperitoneally, can recruit large numbers of immune cells. Among these immune cells were activated eosinophils. While eosinophils are well known to accumulate in the lungs of asthmatics or in response to helminths and parasites, several studies have shown the presence of eosinophils in liver biopsies of drug-induced liver injury, primary biliary cirrhosis, chronic hepatitis C, hepatic allograft rejection, and liver fibrosis. The prevalence of eosinophilic infiltrates in the liver points to a correlation between infiltration and disease outcome. Our results demonstrated eosinophil activation upon exposure to necrotic liver components. Exposure to necrotic liver cells induced eosinophil degranulation as measured by expression of CD107a and eosinophil peroxidase release into the supernatant as measured by ELISA. Further study of eosinophil activation during necrotic liver exposure showed IL-1β and IL-18 release as well as cell death. All of these responses were dependent upon caspase-1 activation. Caspase-1 mediated cell death accompanied by IL-1β and IL-18 release are hallmarks of pyroptosis, an inflammatory cell death pathway. We verified eosinophil pyroptosis in vivo using a liver fibrosis model involving Schistosoma mansoni infected mice. Eosinophils extracted from S. mansoni infected livers showed caspase-1 activation and cytokine release indicating that these cells undergo pyroptosis in vivo in response to hepatocyte injury.
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Macapagal, Daphne, Jane Connor, Thirumalai R. Ramalingam, Thomas A. Wynn, Tomas Mikael Mustelin, and Todd S. Davidson. "Necrotic liver induces pyroptosis through Caspase-1 in eosinophils." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 56.1. http://dx.doi.org/10.4049/jimmunol.196.supp.56.1.
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Abstract During sterile inflammatory reactions damage associated molecular patterns (DAMPS) are released from necrotic cells and recruit immune cells to the sites of tissue injury. We found that necrotic liver homogenates, when injected intraperitoneally, can recruit large numbers of immune cells. Among these immune cells were activated eosinophils. Eosinophils are polymorphonuclear leukocytes typically found within tissues of the gastrointestinal and respiratory tracts. While eosinophils are well known to accumulate in the lungs of asthmatics or in response to helminths and parasites, several studies have shown the presence of eosinophils in liver biopsies of drug-induced liver injury, chronic hepatitis C and liver fibrosis. The prevalence of eosinophilic infiltrates in the liver points to a correlation between infiltration and disease outcome. Our results demonstrated eosinophil activation upon exposure to necrotic liver components. Exposure to necrotic liver cells induced eosinophil degranulation as measured by expression of CD107a and eosinophil peroxidase release as measured by ELISA. Further study of eosinophil activation during necrotic liver exposure showed IL-1β and IL-18 release as well as cell death. All of these responses were dependent upon caspase-1 activation. Caspase-1 mediated cell death accompanied by IL-1β and IL-18 release are hallmarks of pyroptosis, an inflammatory cell death pathway. We verified eosinophil pyroptosis in vivo using a liver fibrosis model involving Schistosoma mansoni infected mice. Eosinophils extracted from S. mansoni infected livers showed caspase-1 activation and cytokine release indicating that these cells undergo pyroptosis in vivo in response to hepatocyte injury.
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Patnode, Michael L., Jennifer K. Bando, Matthew F. Krummel, Richard M. Locksley, and Steven D. Rosen. "Leukotriene B4 amplifies eosinophil accumulation in response to nematodes." Journal of Experimental Medicine 211, no. 7 (June 2, 2014): 1281–88. http://dx.doi.org/10.1084/jem.20132336.
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Eosinophil accumulation is a defining feature of the immune response to parasitic worm infection. Tissue-resident cells, such as epithelial cells, are thought to initiate eosinophil recruitment. However, direct recognition of worms by eosinophils has not been explored as a mechanism for amplifying eosinophil accumulation. Here, we report that eosinophils rapidly migrate toward diverse nematode species in three-dimensional culture. These include the mammalian parasite Nippostrongylus brasiliensis and the free-living nematode Caenorhabditis elegans. Surprisingly, collective migration toward worms requires paracrine leukotriene B4 signaling between eosinophils. In contrast, neutrophils show a minimal response to nematodes, yet are able to undergo robust leukotriene-dependent migration toward IgG-coated beads. We further demonstrate that eosinophils accumulate around C. elegans in the lungs of mice. This response is not dependent on bacterial products, CCR3, or complement activation. However, mice deficient in leukotriene signaling show markedly attenuated eosinophil accumulation after injection of C. elegans or N. brasiliensis. Our findings establish that nematode-derived signals can directly induce leukotriene production by eosinophils and that leukotriene signaling is a major contributor to nematode-induced eosinophil accumulation in the lung. The similarity of the eosinophil responses to diverse nematode species suggests that conserved features of nematodes are recognized during parasite infection.
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Tsarev, Sergey V. "Eosinophilic pneumonia in allergological practice." Russian Journal of Allergy 18, no. 1 (March 15, 2021): 32–40. http://dx.doi.org/10.36691/rja1413.
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In this article, current data on pulmonary eosinophilia are presented. Pulmonary eosinophilia is defined as the infiltration of eosinophils into the airways, interstitia, and alveoli. There are diverse processes in etiology, the common feature of which is the presence of pulmonary eosinophilic infiltrates, and as a rule, peripheral blood eosinophilia. Causes of pulmonary eosinophilia include various infections, medications, parasites, autoimmune processes, malignancies, and presence of obstructive pulmonary diseases. A unified classification of pulmonary eosinophilia is lacking, and instead, various versions of classifications have been presented. The most convenient classification option for use is also distinguished. This article discusses the historical transformation of the term eosinophilic pneumonia in the field of allergology, showing the lack of unambiguity in the concept of eosinophilic pneumonia, as well as the location of eosinophilic pneumonia in the pulmonary eosinophilia section. Eosinophilic pneumonia is defined as a disease characterized by an increase in the eosinophil content in the pulmonary tissue or bronchoalveolar lavage fluid. Most eosinophilic pneumonias are associated with peripheral blood eosinophilia. Two main variants of the disease are acute and chronic eosinophilic pneumonias. Thus, various ways to formulate diagnoses in various cases of eosinophilic pneumonia have been proposed.
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Park, Sunghee, Jiwon Jung, Yong Pil Chong, Sung-Han Kim, Sang-Oh Lee, Sang-Ho Choi, Yang Soo Kim, and Min Jae Kim. "Infectious Causes of Eosinophilic Meningitis in Korean Patients: A Single-Institution Retrospective Chart Review from 2004 to 2018." Korean Journal of Parasitology 59, no. 3 (June 21, 2021): 227–33. http://dx.doi.org/10.3347/kjp.2021.59.3.227.
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Eosinophilic meningitis is defined as the presence of more than 10 eosinophils per μl in the cerebrospinal fluid (CSF), or eosinophils accounting for more than 10% of CSF leukocytes in patients with acute meningitis. Parasites are the most common cause of eosinophilic meningitis worldwide, but there is limited research on patients in Korea. Patients diagnosed with eosinophilic meningitis between January 2004 and June 2018 at a tertiary hospital in Seoul, Korea were retrospectively reviewed. The etiology and clinical characteristics of each patient were identified. Of the 22 patients included in the study, 11 (50%) had parasitic causes, of whom 8 (36%) were diagnosed as neurocysticercosis and 3 (14%) as Toxocara meningitis. Four (18%) patients were diagnosed with fungal meningitis, and underlying immunodeficiency was found in 2 of these patients. The etiology of another 4 (18%) patients was suspected to be tuberculosis, which is endemic in Korea. Viral and bacterial meningitis were relatively rare causes of eosinophilic meningitis, accounting for 2 (9%) and 1 (5%) patients, respectively. One patient with neurocysticercosis and 1 patient with fungal meningitis died, and 5 (23%) had neurologic sequelae. Parasite infections, especially neurocysticercosis and toxocariasis, were the most common cause of eosinophilic meningitis in Korean patients. Fungal meningitis, while relatively rare, is often aggressive and must be considered when searching for the cause of eosinophilic meningitis.
Dissertations / Theses on the topic "Eosinophic parasite"
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Stevenson, Lesley Margaret. "Studies on the role of the eosinophil leukocyte in ovine nematode infections." Thesis, Edinburgh Napier University, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386225.
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Issouf, Mohamed. "Etude du rôle des P-glycoprotéines dans le dialogue moléculaire entre Haemonchus contortus et Heligmosomoides polygyrus bakeri et leurs hôtes." Thesis, Tours, 2013. http://www.theses.fr/2013TOUR4035/document.
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Le parasitisme est un des principaux problèmes dans les élevages des ruminants. Les nématodes parasites du tractus digestif des ovins et caprins sont responsables d’importantes baisses de rendement. La maîtrise de ces parasitoses a été longtemps basée sur l’utilisation de molécules anthelminthiques. Cependant, l’efficacité des traitements est fréquemment remise en cause par l’émergence d’isolats résistants à une ou plusieurs de ces molécules. Dans ce contexte, une meilleure connaissance des mécanismes impliqués dans l’installation et la survie des parasites dans leur hôte est essentielle pour le développement de méthodes de lutte efficaces. Les P-glycoprotéines sont des pompes membranaires de la superfamille des transporteurs ABC. Ces pompes transportent des molécules très variées qui ont en commun leur caractère hydrophobe. Nous avons émis l’hypothèse de l’implication de ces transporteurs dans l’interaction hôte-parasite. Dans le contexte de ce travail nous avons identifié des séquences partielles ou complètes d’ADNc de 9 Pgps du nématode parasite Haemonchus contortus. Une forte activation des Pgps des nématodes en présence des produits de dégranulation des éosinophiles de l’hôte a été observée, démontrant ainsi l’interaction entre les Pgps des nématodes et les produits issus de l’hôte. De plus, l’exposition in vitro des nématodes parasites aux produits de l’hôte montrent après analyse par PCR quantitative une induction significative de l’expression de deux Pgps (Hco-pgp-3, et Hco-pgp-16). Chez le nématode murin Heligmosomoides polygyrus bakeri 5 Pgps ont été identifiés. D’autre part, l’analyse du niveau d’expression des Pgps d’H. bakeri a permis de montrer que le gène Hba-pgp-2 est exprimé uniquement chez les stades en contact avec les produits de l’hôte (oeufs, L4 et adultes). De plus, une induction spécifique d’Hba-pgp-2 par le cholestérol a été observée suggérant ainsi l’implication d’Hba-pgp-2 dans la capture et/ou la distribution des stérols des cellules de l’hôte indispensable aux nématodes. Ce travail constitue la première mise en évidence de l’interaction entre les Pgps des nématodes parasites et des produits issus de leur hôte. Ces résultats constituent une base solide pour le développement d’une méthode efficace permettant de bloquer ces transporteurs et d’éliminer les nématodes parasitesGastrointestinal nematodes cause significant economic loses in goat and sheep livestocks. Control of these parasites is mainly based on anthelmintic treatments. However, the efficacy of these molecules is questioned by the emergence of isolates resistant to one or several antiparasitic drugs. In this context, a better understanding of the mechanisms involved in the nematode parasites establishment and survival in the host is essential for the development of an effective control methods. P-glycoproteins are membrane pumps belonging to the ABC transporter family. These pumps transport a wide range of hydrophobic molecules. In the present study, we hypothesized that in addition to their critical role in xenobiotic resistance, helminth ABC transporters such as P-glycoproteins (Pgps) may also be involved in the transport of host products. Using the sheep parasitic nematode Haemonchus contortus, we investigated the modulation and expression of parasite Pgps activity in response to host eosinophil granule products. These works allowed to identify nine partial or complete H. contortus Pgps. Using a rhodamine efflux assay, we provided functional evidence that host eosinophil granule products can activate Pgps from the parasite suggesting that granule products could act as potential modulators of the ABC transporters activity. We showed by quantitative RT-PCR that among nine different H. contortus Pgp genes; Hco-pgp-3, Hco-pgp-9.2, Hco-pgp-11 and, Hco-pgp-16 were specifically up-regulated in parasitical life stages suggesting a potential involvement of these Pgps during the host-parasite interaction. Using exsheated L3 larvae, we demonstrated that eosinophil granules induced in a dose response manner an overexpression of Hco-pgp-3 and the closely related Hco-pgp-16 gene highlighting the possible involvement of these Pgps in host product transport. . The mice parasitic nematode Heligmosomoides polygyrus bakeri was used for studying the involvement of Pgps in the cholesterol transport. These works allowed identifying five Pgps in H. bakeri. The analysis of the mRNA expression level of H. bakeri Pgps has shown that Hba-pgp-2 gene is expressed only in stages in contact with host products. In addition, a specific induction of Hba-pgp-2 by cholesterol was observed suggesting the involvement of Hba-pgp-2 in the capture and / or distribution of cholesterol from host cells. Taken together, our results provide the first evidence that a subset of helminth Pgps could be involved in the transport of host products. This opens the way for further studies aiming to explore the function of helminth Pgps in host-parasite interactions including host immune response evasion
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Gama, Danielle Correia. "Aspectos epidemiológicos e laboratoriais (Eosinófilos e IgE total) em portadores de Schistosoma mansoni e Geohelmintos." Universidade Federal de Alagoas, 2010. http://repositorio.ufal.br/handle/riufal/921.
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This study aimed to evaluate laboratory aspects (total IgE and eosinophils) in
patients with Schistosoma mansoni and geohelminths in three localities in Rio Largo,
Alagoas. Coprological survey was conducted in 3030 subjects and examined two
slides for each stool sample by the Kato-Katz technique, blood count to determine
the absolute and relative number of eosinophilic and quantification of serum total IgE
using the automated chemiluminescence system (Automated Chemiluminescence
Systems) ACS: 180 SIEMENS, adapted to the System II and MAGIC LITE using
commercial kits in 547 individuals from three localities infested by the snail
Biomphalaria glabrata, close to the river Mundaú and environmental similarities. The
subjects were divided into four groups, G1 (co-infected with S. mansoni and
geohelminths): n = 115 (21.02%) with mean age 21.18 ± 13.08 years, G2 (infected
only by S. mansoni): n = 127 (23.22%) with mean age 29.59 ± 16.54 years; G3
(infected only by geohelminths): n = 149 (27.24%) with mean age 23.99 ± 15.52
years and G4 (negative for S. mansoni and geohelminths, the control group): n = 156
(28.52%) with mean age 25.44 ± 14.60 years. The parasitic load of S. mansoni was
quantified and classified according to intensity of infection by the number of eggs per
gram of feces detected. The study was approved by the Ethics Committee of the
Federal University of Alagoas and implemented in accordance with the resolution
MS-CNS 196/96. For processing and data analysis used the software SPSS 11.5.
In all analysis was considered the 5% level of significance. The descriptive statistical
analysis of qualitative and quantitative variables were performed by the distribution of
relative frequencies and absolute position measurements (mean) and dispersion
(standard deviation). He applied the normality test, t test, analysis of variance oneway
(ANOVA), chi-square test, Fisher exact test, Pearson and Spearman correlation
and linear regression. Of the 3030 samples, 1,209 (39.90%) were positive for any
helminth, and 679 (22.41%) positive for A. lumbricoides, 546 (18.02%) for T.
Trichiura, 220 (7.26%) to Ancyostomatidae and 242 (8.0%) for S. mansoni. There
was no statistically significant difference (p>0.05) of individuals positive for S.
mansoni separated by gender, age and locality, the mean parasite burden was
moderate and 111 epg (minimum 24 and maximum of 4,080 epg). Eosinophils
increased significantly with increasing parasite load (p<0.05). The absolute and
relative eosinophilia appear to have greater significance in relation to group coinfected,
because presented more frequently than the other groups. There were no
significant differences (p>0.05) between worm burden of S. mansoni and total IgE
levels, nor between serum total IgE and age. Thus the total IgE test was not
considered relevant to the diagnosis of Schistosomiasis mansoni. There was no
correlation between markers of total IgE and geohelminth infections, whether they
are co-infected with S. mansoni. The results suggest the importance of including
eosinophil counts in epidemiological surveys, the complementation of the findings
and parasitological diagnosis of schistosomiasis, contributing to more precise
investigations focused on the control of schistosomiasis in endemic areas.Este estudo objetivou avaliar aspectos laboratoriais (IgE total e eosinófilos) em portadores de Schistosoma mansoni e geohelmintos em três localidades no município de Rio Largo, Alagoas. Foi realizado inquérito coprológico em 3.030 indivíduos e analisadas duas lâminas para cada amostra de fezes pela técnica de Kato-katz, hemograma para determinar o número absoluto e relativo de eosinífilos e quantificação sérica de IgE total utilizando o sistema de quimioluminescência automatizado (Automated Chemiluminescence Systems) ACS: 180 da SIEMENS, adaptado ao Sistema MAGIC LITE II e usando kits comerciais em 547 indivíduos de três localidades infestadas pelo molusco Biomphalaria glabrata, próximas ao rio Mundaú e com semelhanças ambientais. Os indivíduos foram divididos em 4 grupos, G1 (co-infectados por S. mansoni e geohelmintos): n=115 (21,02%) com média de idade 21,18 ± 13,08 anos; G2 (infectados apenas por S. mansoni): n=127 (23,22%) com média de idade 29,59 ± 16,54 anos; G3 (infectados exclusivamente por geohelmintos): n=149 (27,24%) com média de idade 23,99 ± 15,52 anos e G4 (negativos para S. mansoni e geohelmintos, considerado grupo controle): n=156 (28,52%) com média de idade 25,44 ± 14,60 anos. A carga parasitária do S. mansoni foi quantificada e classificada de acordo com a intensidade da infecção pelo número de ovos por grama de fezes detectados. O estudo foi aprovado pelo Comitê de Ética em Pesquisa da Universidade Federal de Alagoas e executado de acordo com a resolução CNS-MS 196/96. Para o processamento e análise dos dados utilizou-se o software SPSS 11.5. Em todas as análises foi considerado o nível de 5% de significância. A análise estatística descritiva das variáveis qualitativas e quantitativas foram realizadas através da distribuição de freqüências relativas e absolutas, medidas de posição (média aritmética) e dispersão (desvio padrão). Aplicou-se teste de normalidade, teste t, análise de variância one-way (ANOVA), teste do quiquadrado de Pearson, teste exato de Fisher, correlação de Pearson e Spearman e regressão linear simples. Das 3.030 amostras, 1.209 (39,90%) estavam positivas para algum helminto, sendo 679 (22,41%) positivas para A. lumbricoides , 546 (18,02%) para T. Trichiura, 220 (7,26%) para Ancyostomatidae e 242 (8,0%) para S. mansoni. Não houve diferença estatisticamente significante (p>0,05) dos indivíduos positivos para S. mansoni separados por gênero, faixa etária e localidades, a média da carga parasitária foi moderada e de 111 opg (mínimo de 24 e máximo de 4.080 opg). Os eosinófilos aumentavam significantemente conforme o aumento da carga parasitária (p<0,05). As eosinofilias absoluta e relativa parecem ter maior significado em relação ao grupo de co-infectados, pois apresentram maior frequência em relação aos demais grupos. Não foram observadas diferenças significantes (p>0,05) entre carga parasitária de S. mansoni e níveis de IgE total, nem entre níveis séricos de IgE total e faixa etária. Desta forma o teste de IgE total não foi considerado relevante para o diagnóstico de esquistossomose mansoni. Não houve correlação entre os marcadores de IgE total e as infecções geohelmínticas, independente de estarem co-infectados por S. mansoni. Os resultados sugerem a importância da inclusão de contagem de eosinófilos em inquéritos epidemiológicos, na complementação dos achados parasitológicos e no diagnóstico da esquistossomose, contribuindo para investigações mais precisas voltadas para o controle da esquistossomose mansônica nas áreas endêmicas.
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Knott, Michelle Louise. "Host-parasite interactions in primary and secondary infections with Nippostrongylus brasiliensis and Heligmosomoides bakeri." Thesis, 2010. http://hdl.handle.net/2440/67240.
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Parasitic helminth infections are a significant problem worldwide. Some helminth species are becoming resistant to current therapies and new forms of treatment and/or vaccines are required. Nippostrongylus brasiliensis is a tissue-invasive parasitic helminth that infects rodents, and the lifecycle of this parasite is similar to that of the human hookworms. The aims of this study were to investigate primary and secondary immune responses to N. brasiliensis, focusing on the pre-lung phase of infection. The roles of cytokines, chemokines, signalling pathways and leukocytes such as eosinophils were investigated in the skin, lungs and small intestine. The roles of eosinophils were also investigated in primary infections with the intestinal nematode Heligmosomoides bakeri. Interleukin (IL)-5 is important for eosinophil development and maturation and for protection during some helminth infections. Over-expression of IL-5 provides potent protection in primary infections with N. brasiliensis in the pre-lung phase of infections. Although mice deficient in IL-5 or eosinophils might therefore be predicted to be more susceptible to N. brasiliensis, IL-5-deficient (IL-5⁻/⁻) and eosinophil-deficient (ΔdblGATA) mice showed similar infection patterns as wildtype (WT) mice during primary N. brasiliensis infections. Intestinal worm and/or egg numbers however were elevated in mice with defective eosinophilopoiesis compared with WT animals. In secondary infections, despite skin inflammatory responses (4 hours p.i.) being similar in WT, IL-5⁻/⁻ and ΔdblGATA animals, at day 2 p.i., lung larval burdens in the two latter hosts were significantly higher than in the resistant WT controls. However, parasites were expelled from intestines of all mice by day 7 of secondary infections. These data suggest that in the pre-gut phase of secondary infection, IL-5 and eosinophils play an important role in resistance to N. brasiliensis. Despite this, eosinophils do not appear to be essential for protection mediated within the gut during secondary infections, even though IL-5 and eosinophils do appear to confer some protection in the gut during primary infections. Complement is required for the recruitment of eosinophils into the skin in the first 150 minutes of primary infection with N. brasiliensis (Giacomin et al., 2008a), however other chemotactic factors appear to be involved after this time. Although eotaxin is chemotactic for eosinophils in some tissues, the importance of eotaxin and signalling pathways involved in expression of this chemokine has not been previously characterized in N. brasiliensis infections. Signal transducer and activator of
transcription (STAT)6 is a key transcription factor in the IL-4/IL-13 signalling pathway and these cytokines can induce expression of eotaxin in some tissues. Expulsion of N. brasiliensis adult worms during primary infections is profoundly impaired in STAT6- deficient (STAT6⁻/⁻) mice. IL-5 Tg mice are highly resistant to primary infections with N. brasiliensis and in the current study, it was shown that ablation of eotaxin-1 or STAT6 in IL-5 Tg mice did not impair the strong innate resistance typically seen in the pre-lung phase of N. brasiliensis infections. While recruitment of eosinophils to the skin (4 hours p.i.) was reduced in these mice compared with IL-5 transgenic (Tg) mice, protective capacity was preserved in both primary and secondary infections. Further, eotaxin-1⁻/⁻ single mutant mice were strongly resistant to secondary N. brasiliensis infections, with few larvae migrating to the lungs on day 2 p.i. In contrast, STAT6⁻/⁻, IL-13⁻/⁻, IL-4Rα⁻/⁻ and IL-13⁻/⁻/IL-4Rα⁻/⁻-double deficient mice had significantly higher secondary lung larval burdens than WT mice and parasite egg production was prolonged in all of these strains. These data suggest a role for this signalling pathway in protection during the early stages of secondary infections with this parasite. In both primary and
secondary infections, eosinophils were recruited to the skin in all gene knock out strains in comparable numbers to those seen in WT mice, and this suggests that alternative eosinophil recruitment pathways may compensate for the absence of these factors. Adding to the extensive work on the intestinal phase of N. brasiliensis, this work clearly indicates for the first time that early pre-lung events are crucial in determining the outcome of infection, and should be the focus of future studies with N. brasiliensis. In contrast, when STAT6- and eotaxin-1-deficient mice were infected with another intestinal nematode, H. bakeri, the mutant strains were as susceptible as WT mice, with parasite eggs present in similar numbers on all days examined. Resistance mechanisms that operate in the intestine during N. brasiliensis infections do not therefore appear to extend to a parasite that can infect naïve hosts for many months. The FVB/N mouse strain was introduced into this study whilst exploring the potential roles of eosinophils in the intestinal phase of N. brasiliensis infections. The impact of intestine-specific expression of transgenes encoding IL-5 and eotaxin-1 were examined and although both lines of Tg mice were highly resistant to N. brasiliensis, naïve WT FVB/N mice also showed very potent innate resistance. Very few worms were observed in the small intestine of WT FVB/N animals on day 7 p.i., whereas skin larval and leukocyte numbers (4 hours p.i.) and lung larval burdens (day 2 p.i.) were similar in WT FVB/N and WT CBA/Ca mice. Interestingly, lung larvae recovered from WT FVB/N animals were significantly smaller in size (days 1-2 p.i.) and less motile than lung larvae recovered from WT CBA/Ca mice. Further, there were significantly fewer eggs (day 6 p.i.) and worms (day 7 p.i.) in the former. However, WT FVB/N mice were no more resistant to infections with H. bakeri than WT CBA/Ca mice, with parasite eggs detected in comparable numbers until day 116 p.i. Resistance mechanisms operating against N. brasiliensis in WT FVB/N mice would not therefore appear to extend to H. bakeri infections. Eosinophils can provide potent protection in some helminth infections and this study builds on our previous work and that of other groups. We have now shown that early pre-lung events may be critical in determining host resistance against N. brasiliensis. In secondary N. brasiliensis infections, cytokine signalling pathways that protect against adult worms in the late intestinal phase of infection also play a role in resistance during the early pre-lung phase, when the parasite is still at the larval stage. Eosinophils are also of importance for protection against this parasite, and future studies should focus on the early events to further characterize resistance mechanisms. This information may prove useful for the development of successful vaccines against hookworms and other nematodes.Thesis (Ph.D.) -- University of Adelaide, School of Molecular and Biomedical Science, 2010
Books on the topic "Eosinophic parasite"
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Fadiel, Mahmoud Mahdy. Mast cells, eosinophils and ion transport in the small intestine from experimental animals infected with 'fasciola hepatica'. Dublin: University College Dublin, 1996.
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Barsoum, Rashad S. Schistosomiasis. Edited by Neil Sheerin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0181_update_001.
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AbstractSchistosomes are blood flukes that parasitize humans, apes, cattle, and other animals. In these definitive hosts they are bisexual, and lay eggs which are shed to fresh water where they complete an asexual cycle in different snails, ending in the release of cercariae which infect the definitive hosts to complete the life cycle.Seven of over 100 species of schistosomes are human pathogens, causing disease in different organs depending on the parasite species. Racial and genetic factors are involved in susceptibility, severity, and sequelae of infection.Morbidity is induced by the host’s immune response to schistosomal antigens. The latter include tegument, microsomal, gut, and oval antigens. The former are important in the process of invasion and establishment of infection, oval antigens in formation of granulomata which lead to fibrosis in different sites, and the gut antigens constitute the main circulating antigens in established infection, leading to immune-complex disease, particularly in the kidneys. The host immunological response includes innate and adaptive mechanisms, the former being the front line responsible for removing 90% of the infecting cercarial load. Adaptive immunity includes a Th1 phase, dominated by activation of an acute inflammatory response, followed by a prolonged Th2 phase which is responsible for immunity to re-infection as well as progression of tissue injury. Switching from Th1 to Th2 phases is controlled by functional and morphological change in the antigen-presenting cells, which is achieved by molecules of host as well as parasitic origin.Many cells participate in parasite killing, but also in the induction of tissue injury. The most potent of these is the eosinophil, which by binding antibodies to the parasite, particularly immunoglobulin E, facilitates parasite elimination. However, this process is complex, including agonist as well as antagonist pathways, which provide escape mechanisms for the parasite to survive, thereby achieving a delicate balance that permits schistosomes to live for decades in the infected host.
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Potter, Kathleen A. Eosinophil chemotactic and chemokinetic activity associated with Taenia Taeniaeformis infection in the rat. 1985.
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Wang, Qiao-Ping, and Zhao-Rong Lun. Angiostrongylus cantonensis and Human angiostrongylosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0066.
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Angiostrongylus cantonensis was first discovered in rats in Guangzhou (Canton), China in 1935 (Chen 1935). A. cantonensis is a zoonotic pathogen, which causes human angiostrongylosis with the main clinical manifestation of eosinophilic meningitis. The first case of human angiostrongylosis was reported in Taiwan in 1945. Subsequently several outbreaks of this disease occurred in Pacific Islands (Rosen et al. 1961; Kliks and Palumbo 1992). In the past decade, a number of outbreaks of human angiostrongylosis have emerged in some endemic regions, especially in China (Wang et al. 2008). Additionally, increasing numbers of travellers are diagnosed with eosinophilic meningitis caused by A. cantonensis after returning from endemic regions (Lo et al. 2001; Slom et al. 2002; Bartschi et al. 2004; Podwall et al. 2004; Kumar et al. 2005; Leone et al. 2007; Ali et al. 2008). The parasite continues to threaten human beings, especially people living in the Pacific Islands and Asia. So far, at least 2,825 cases have been recorded; of them, 1,337 were reported in Thailand, 769 in China (Hong Kong and Taiwan), 256 in Tahiti, 116 in the USA (Hawaii and Samoa) and 114 cases in Cuba (Wang et al. 2008).
Book chapters on the topic "Eosinophic parasite"
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Kliks, Michael M., William K. K. Lau, and Nicholas E. Palumbo. "Neurologic Angiostrongyliasis: Parasitic Eosinophilic Menigoencephalitis." In Laboratory Diagnosis of Infectious Diseases, 754–67. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3898-0_78.
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Korenaga, Masataka, and Fabrizio Bruschi. "Qualitative and Quantitative Studies of Eosinophils in Parasitic Infections." In Methods in Molecular Biology, 203–13. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1016-8_18.
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Nawa, Y., M. Owhashi, and H. Maruyama. "Mechanism of Eosinophilia in Parasitic Infection with Special Emphasis on the Eosinophil Chemotactic Lymphokines Directed Against Different Maturation Stages of Eosinophils." In Intestinal Anisakiasis in Japan, 225–38. Tokyo: Springer Japan, 1990. http://dx.doi.org/10.1007/978-4-431-68299-8_29.
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Bourke, S. J., and G. P. Spickett. "Eosinophilic pneumonia." In Oxford Textbook of Medicine, edited by Pallav L. Shah, 4238–41. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0422.
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Eosinophilic pneumonia is characterized by eosinophilic inflammation of the alveoli, usually with an accompanying eosinophilia of peripheral blood. The diagnosis should be considered when infiltrates on a chest radiograph are associated with blood eosinophilia, and is confirmed by demonstrating an excess of eosinophils in bronchoalveolar lavage fluid. Before concluding that the cause is ‘idiopathic’, the following must be considered: parasitic infestation with blood-borne parasites such as (in tropical eosinophilia) filarial worms; adverse drug reaction; asthma; allergic bronchopulmonary mycosis; vasculitis, notably eosinophilic granulomatosis with polyangiitis (previously known as Churg–Strauss syndrome); hypereosinophilic syndrome, a rare haematological disorder; and other disorders known to be associated with eosinophilic pneumonia. Causal factors need to be treated, but eosinophilic pneumonia otherwise often responds well to corticosteroid medication.
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Weller, Peter F. "Eosinophilia." In Oxford Textbook of Medicine, edited by Chris Hatton and Deborah Hay, 5254–58. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0520.
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Eosinophilia (eosinophil count >0.45 × 109/litre) is associated with some infections, some allergic diseases, and a variety of other conditions, sometimes neoplastic. Parasitic diseases—eosinophilia is a characteristic feature of infection by multicellular helminth parasites (e.g. Strongyloides stercoralis) with diagnosis typically based on geographical/dietary history, serological tests, and examination of stool or tissues for parasite forms. Other diseases—eosinophilia can be caused by the fungal disease coccidioidomycosis, and modest eosinophilia may accompany retroviral infections such as HIV and HTLV-1. Common allergic diseases—asthma, rhinitis, and atopic dermatitis are associated with modest eosinophilia. Drug reactions—these are a frequent cause of eosinophilia, at times in reactions characterized by rashes and pyrexia. More severe reactions may also manifest with (1) pulmonary eosinophilia and lung infiltrates; (2) interstitial nephritis; (3) hepatitis; (4) myocarditis; (5) drug-induced hypersensitivity vasculitis; (6) gastroenterocolitis; and (7) DRESS syndrome. Other conditions—these include (1) eosinophilic granulomatosis with polyangiitis; (2) hyper-IgE syndromes; (3) chronic myeloid leukaemia, acute myeloid leukaemia, and lymphoma; (4) a variety of pulmonary, skin, gastrointestinal, and endocrine diseases. Hypereosinophilic syndromes are defined by (1) eosinophilia (>1.5 × 109/litre) sustained over a month, (2) lack of an identifiable cause precipitating a secondary eosinophilia, and (3) symptoms and signs of organ involvement. About 30% of patients will have either a myeloproliferative condition (chronic eosinophilic leukaemia) or hypereosinophilia mediated by clonal expansion of specific T cells producing interleukin-5 (IL-5). Treatment—patients without organ damage do not require treatment. Aside from supportive care, chronic eosinophilic leukaemia may respond to tyrosine kinase inhibitors (e.g. imatinib), and nonmyeloproliferative hypereosinophilic syndrome may respond to high-dose corticosteroids, with hydroxyurea, interferon-α or anti-IL-5 monoclonal antibody used in refractory cases.
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Weller, Peter F. "Eosinophilia." In Oxford Textbook of Medicine, 4356–61. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.220406.
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Eosinophilia (eosinophil count >0.45 × 109/litre) is associated with some infections, some allergic diseases, and a variety of other conditions, often neoplastic. Parasitic diseases—eosinophilia is a characteristic feature of infection by multicellular helminth parasites, e.g. Strongyloides stercoralis, with diagnosis typically based on geographical/dietary history and examination of stool for ova and larvae....
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Martínez-Jiménez, Santiago. "Eosinophilic Lung Diseases." In Chest Imaging, 367–70. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780199858064.003.0063.
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Eosinophilic lung disease (ELD) comprises a group of disorders that affect the lungs and manifest with blood and/or tissue eosinophilia. ELD may be secondary to a variety of conditions such as infection by parasites (e.g. ascariasis, strongyloidiasis, paragonimiasis, etc.), drug reaction, bronchopulmonary aspergillosis (ABPA) and malignancy. ELD may also be a primary process either limited to the lung (e.g. acute and chronic eosinophilic disease) or as part of a systemic disorder (e.g. allergic granulomatosis with polyangiitis or hypereosinophilic syndrome). On imaging ABPA is characterized by tubular branching opacities that may exhibit the finger-in-glove sign (i.e. inspissated mucus within dilated central bronchi). Strongyloidiasis often manifests with multifocal pulmonary opacities affecting all pulmonary lobes. AEP may simulate cardiogenic pulmonary edema on imaging. Chronic eosinophilic pneumonia (CEP) may have varied imaging manifestations, including the so-called “photographic negative of pulmonary edema”.
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Wolfe, Martin S. "The Eosinophilic Patient with Suspected Parasitic Infection." In The Travel and Tropical Medicine Manual, 637–49. Elsevier, 2008. http://dx.doi.org/10.1016/b978-141602613-6.10045-x.
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Wolfe, Martin S. "The Eosinophilic Patient with Suspected Parasitic Infection." In The Travel and Tropical Medicine Manual, 598–609. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-323-37506-1.00049-0.
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Mutyambizi, Kudakwashe, and Philip Bolduc. "Dermatologic Complications of HIV." In Fundamentals of HIV Medicine 2021, 355–67. Oxford University PressNew York, 2021. http://dx.doi.org/10.1093/med/9780197576595.003.0037.
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Abstract This chapter describes the dermatologic complications of HIV infection and treatment. The chapter includes information about the incidence, presentation, and management of inflammatory dermatoses in HIV, including seborrheic dermatitis, psoriasis, atopic dermatitis and xerosis, papular pruritic eruption of AIDS, and HIV-associated eosinophilic pustular folliculitis. In addition, common and important cutaneous adverse drug reactions among people with HIV and management factors are presented for antiretroviral drug classes. Lastly, learners are presented with information on the diagnosis and management of viral, fungal, bacterial, and parasitic opportunistic infections occurring in HIV patients and presentation and treatment of cancers associated with HIV and aging.
Conference papers on the topic "Eosinophic parasite"
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Prasad, V. Pratibh, Jai Mullerpattan, Radhika Banka, Avinash Gandhare, and Lancelot Pinto. "Blood eosinophil count as a predictor of obstructive airway disease (OAD) in a high parasite burden setting." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa3434.
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Cushen, B., R. Stead, S. Malley, D. Armstrong-James, and J. Hull. "S52 Development of a dedicated protocol for screening for occult parasitic infection prior to initiation of anti-IL5 therapy in patients with severe eosinophilic asthma." In British Thoracic Society Winter Meeting 2019, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 4 to 6 December 2019, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2019. http://dx.doi.org/10.1136/thorax-2019-btsabstracts2019.58.
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