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      Eosinophilia and cystic echinococcosis: what is the relationship?

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          Abstract

          Background

          Cystic echinococcosis (CE) is a chronic, complex and neglected zoonotic disease caused by Echinococcus granulosus. Eosinophilia in CE is a classic analytic alteration, although its presentation and importance is very variable and not well established.

          Methods

          We performed a retrospective observational study of inpatients diagnosed with CE and eosinophilia from January 1998 to December 2017 in the Complejo Asistencial Universitario de Salamanca in western Spain.

          Results

          During the study period, 475 patients with a CE diagnosis underwent a haemogram and 118 (24.8%) patients had eosinophilia. Eighty-two (69.5%) were male and the mean age was 52.1±20.8 y, which was younger in the group with eosinophilia (p<0.001). The patients with eosinophilia had less comorbidity (33.1% vs 52.9%; p<0.001) and they were diagnosed with more complications (60.2% vs 39.8% asymptomatic; p<0.001). Clinical manifestations appeared in 71 cases (60.2%). The eosinophilia was related to the presence of pre-surgical fistulas (p=0.005). We observed significant differences when considering whether eosinophilia is a marker of the type of treatment (p<0.001).

          Conclusions

          Eosinophilia can be an indicator for an active search in CE because as much as 40% of cases are asymptomatic at diagnosis. In patients with eosinophilia, management is usually more aggressive and is usually a combined treatment. Our work shows the importance of eosinophilia in our patients with CE and raises unresolved questions.

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          Most cited references 21

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          Expert consensus for the diagnosis and treatment of cystic and alveolar echinococcosis in humans.

          The earlier recommendations of the WHO-Informal Working Group on Echinococcosis (WHO-IWGE) for the treatment of human echinococcosis have had considerable impact in different settings worldwide, but the last major revision was published more than 10 years ago. Advances in classification and treatment of echinococcosis prompted experts from different continents to review the current literature, discuss recent achievements and provide a consensus on diagnosis, treatment and follow-up. Among the recognized species, two are of medical importance -Echinococcus granulosus and Echinococcus multilocularis - causing cystic echinococcosis (CE) and alveolar echinococcosis (AE), respectively. For CE, consensus has been obtained on an image-based, stage-specific approach, which is helpful for choosing one of the following options: (1) percutaneous treatment, (2) surgery, (3) anti-infective drug treatment or (4) watch and wait. Clinical decision-making depends also on setting-specific aspects. The usage of an imaging-based classification system is highly recommended. For AE, early diagnosis and radical (tumour-like) surgery followed by anti-infective prophylaxis with albendazole remains one of the key elements. However, most patients with AE are diagnosed at a later stage, when radical surgery (distance of larval to liver tissue of >2cm) cannot be achieved. The backbone of AE treatment remains the continuous medical treatment with albendazole, and if necessary, individualized interventional measures. With this approach, the prognosis can be improved for the majority of patients with AE. The consensus of experts under the aegis of the WHO-IWGE will help promote studies that provide missing evidence to be included in the next update. Copyright 2009 Elsevier B.V. All rights reserved.
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            Worldwide epidemiology of liver hydatidosis including the Mediterranean area.

            The worldwide incidence and prevalence of cystic echinococcosis have fallen dramatically over the past several decades. Nonetheless, infection with Echinococcus granulosus (E. granulosus) remains a major public health issue in several countries and regions, even in places where it was previously at low levels, as a result of a reduction of control programmes due to economic problems and lack of resources. Geographic distribution differs by country and region depending on the presence in that country of large numbers of nomadic or semi-nomadic sheep and goat flocks that represent the intermediate host of the parasite, and their close contact with the final host, the dog, which mostly provides the transmission of infection to humans. The greatest prevalence of cystic echinococcosis in human and animal hosts is found in countries of the temperate zones, including several parts of Eurasia (the Mediterranean regions, southern and central parts of Russia, central Asia, China), Australia, some parts of America (especially South America) and north and east Africa. Echinococcosis is currently considered an endemic zoonotic disease in the Mediterranean region. The most frequent strain associated with human cystic echinococcosis appears to be the common sheep strain (G1). This strain appears to be widely distributed in all continents. The purpose of this review is to examine the distribution of E. granulosus and the epidemiology of a re-emerging disease such as cystic echinococcosis.
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              Echinococcus granulosus antigen B impairs human dendritic cell differentiation and polarizes immature dendritic cell maturation towards a Th2 cell response.

              Despite inducing a strong host cellular and humoral immune response, the helminth Echinococcus granulosus is a highly successful parasite that develops, progresses, and ultimately causes chronic disease. Although surgery remains the preferred therapeutic option, pharmacological research now envisages antihelminthic strategies. To understand the mechanisms that E. granulosus uses to escape host immunosurveillance and promote chronic infection, we investigated how two hydatid cyst components, purified antigen B (AgB) and sheep hydatid fluid (SHF), act on host dendritic cell (DC) differentiation from monocyte precursors and how they influence maturation of DC that have already differentiated. We evaluated the immunomodulatory potential of these antigens by performing immunochemical and cytofluorimetric analyses of monocyte-derived DCs from healthy human donors. During monocyte differentiation, AgB and SHF downmodulated CD1a expression and upregulated CD86 expression. Compared with immature DCs differentiated in medium alone (iDCs), AgB- and SHF-differentiated cells stimulated with lipopolysaccharide included a significantly lower percentage of CD83(+) cells (P < 10(-4)) and had weaker costimulatory molecule expression. When stimulated with AgB and SHF, iDCs matured and primed lymphocytes towards the Th2 response typical of E. granulosus infection. SHF and particularly AgB reduced the production of interleukin-12p70 (IL-12p70) and tumor necrosis factor alpha in lipopolysaccharide-stimulated iDCs. Anti-IL-10 antibodies increased the levels of IL-12p70 secretion in AgB- and SHF-matured DCs. AgB and SHF induced interleukin-1 receptor-associated kinase phosphorylation and activated nuclear factor-kappaB, suggesting that Toll-like receptors could participate in E. granulosus-stimulated DC maturation. These results suggest that E. granulosus escapes host immunosurveillance in two ways: by interfering with monocyte differentiation and by modulating DC maturation.
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                Author and article information

                Journal
                Transactions of The Royal Society of Tropical Medicine and Hygiene
                Oxford University Press (OUP)
                0035-9203
                1878-3503
                November 14 2019
                November 14 2019
                Affiliations
                [1 ]Servicio de Medicina Interna, Complejo Asistencial Universitario de Salamanca, Salamanca, Spain
                [2 ]Servicio de Medicina Interna, Complejo Asistencial Universitario de Salamanca, Instituto de investigación Biomédica de Salamanca, Centro de Investigación de Enfermedades Tropicales de la Universidad de Salamanca, Universidad de Salamanca, Salamanca, Spain
                [3 ]Área de Medicina Preventiva y Salud Pública, Instituto de investigación Biomédica de Salamanca, Centro de Investigación de Enfermedades Tropicales de la Universidad de Salamanca, Universidad de Salamanca, Salamanca, Spain
                [4 ]Servicio de Medicina Interna, Sección de Enfermedades Infecciosas, Complejo Asistencial Universitario de Salamanca, Instituto de investigación Biomédica de Salamanca, Centro de Investigación de Enfermedades Tropicales de la Universidad de Salamanca, Universidad de Salamanca, Salamanca, Spain
                [5 ]Centro de Atención Primaria, Puente San Miguel, Cantabria, Santander, Spain
                [6 ]Laboratorio de Inmunología Parasitaria y Molecular, Instituto de investigación Biomédica de Salamanca, Centro de Investigación de Enfermedades Tropicales de la Universidad de Salamanca, Facultad de Farmacia, Universidad de Salamanca, Salamanca, Spain
                [7 ]Servicio de Dermatología, Complejo Asistencial Universitario de Salamanca, Instituto de investigación Biomédica de Salamanca, Centro de Investigación de Enfermedades Tropicales de la Universidad de Salamanca, Universidad de Salamanca, Salamanca, Spain
                [8 ]Servicio de Microbiologia, Complejo Asistencial Universitario de Salamanca, Instituto de investigación Biomédica de Salamanca, Centro de Investigación de Enfermedades Tropicales de la Universidad de Salamanca, Universidad de Salamanca, Salamanca, Spain
                [9 ]Servicio de Medicina Interna, Sección de Enfermedades Infecciosas, Complejo Asistencial Universitario de Salamanca, Instituto de investigación Biomédica de Salamanca, Centro de Investigación de Enfermedades Tropicales de la Universidad de Salamanca, Universidad de Salamanca, Paseo San Vicente 58-182, 37007, Salamanca, Spain
                [10 ]Servicio de Medicina Interna, Centro de Investigación de Enfermedades Tropicales de la Universidad de Salamanca, IDIVAL, Instituto de Investigación Marqués de Valdecilla, Hospital Marques de Valdecilla, Avenida Valdecilla S/N, Santander, Spain
                Article
                10.1093/trstmh/trz105
                © 2019

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