Browsing by Autor "Carine Truyens"

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AMNIOTIC FLUID IS NOT USEFUL FOR DIAGNOSIS OF CONGENITAL TRYPANOSOMA CRUZI INFECTION
(American Society of Tropical Medicine and Hygiene, 2006) Myrna Virreira; Sabrina Sales Martínez; Cristina Alonso‐Vega; Faustino Torrico; Marco Solano; Mary Cruz Torrico; Rudy Parrado; Carine Truyens; Yves Carlier; Michal Svoboda
Although Trypanosoma cruzi can be transmitted transplacentally and induce congenital infection, no data are available about the presence of this parasite in human amniotic fluid. We examined 8, 19, and 4 amniotic fluid samples (collected at delivery or by aspiration of gastric content of neonates) from control uninfected mothers (M−B−), infected mothers delivering uninfected newborns (M+B−), and mothers of confirmed congenital cases (M+B+), respectively. Polymerase chain reaction (PCR), using nuclear and kinetoplastic DNA primers (Tcz1-Tcz2 and 121–122), were negative for all control M−B− samples, but positive for 5 of 19 M+B− and 2 of 4 M+B+ samples. To determine the number of parasites in the positive samples, real-time PCR using S35/S36 kinetoplastic DNA was performed. Only one M+B+ sample presented a high parasitic DNA amount, whereas the other six PCR-positive samples displayed traces of T. cruzi DNA. In conclusion, the release of parasites in amniotic fluid is probably a rare event that cannot be helpful for the routine diagnosis of congenital Chagas disease.
Are maternal re‐infections with Trypanosoma cruzi associated with higher morbidity and mortality of congenital Chagas disease?
(Wiley, 2006) Faustino Torrico; Cristina Alonso Vega; Eduardo Suárez; Tatiana Tellez; Laurent Brutus; Patricia Rodríguez; Mary‐Cruz Torrico; Dominique Schneider; Carine Truyens; Yves Carlier
Frequent bites of blood sucking Reduvidae during pregnancy do not induce maternal anaemia, but, likely through multiple maternal re-infections with T. cruzi, increase maternal parasitemia and worsen congenital Chagas disease. Maternal dwelling in areas of high VD is associated with a serious increased risk of severe and mortal congenital Chagas disease.
COMPARISON OF POLYMERASE CHAIN REACTION METHODS FOR RELIABLE AND EASY DETECTION OF CONGENITAL TRYPANOSOMA CRUZI INFECTION
(American Society of Tropical Medicine and Hygiene, 2003) Myrna Virreira; Faustino Torrico; Carine Truyens; Cristina Alonso‐Vega; Marco Solano; Yves Carlier; Michal Svoboda
The polymerase chain reaction (PCR) is a potentially interesting diagnostic tool for detecting congenital Trypanosoma cruzi infection at birth. We have compared the sensitivity and capacity of a group of T. cruzi PCR primers in detecting the complete spectrum of known T. cruzi lineages, and to improve and simplify the detection of infection in neonatal blood. We found that the two primers, Tcz1/Tcz2 and Diaz1/Diaz2, which target the 195-basepair satellite repeat, detected all parasitic lineages with the same sensitivity. However, the intensity of the amplicon was somewhat higher with Tcz1/Tcz2. For other tested primers (nuclear DNA primers BP1/BP2, O1/O2, Pon1/Pon2, and Tca1/Tca2 and kinetoplast DNA primers S35'/S36' and 121/122), either the intensity of amplicons varied according to T. cruzi lineages or the PCR assay was less sensitive. The use of the Tcz1/Tcz2 primers, which target a tandem repetitive sequence, requires a careful determination of the appropriate amount of Taq polymerase to avoid the formation of smears and multiple amplicon bands. The Tcz1/Tcz2 primers resulted in an intense 200-basepair amplicon with DNA extracted from blood equivalent to 0.02 parasites per assay when used with a simple DNA extraction method and of a low amount of Taq polymerase from a standard PCR kit. To better assess such PCR protocol, we assayed 311 samples of neonatal blood previously tested by parasitologic methods. The reliability of our PCR test was demonstrated, since all the 18 blood samples from newborns with congenital T. cruzi infection were positive, whereas the remaining samples (30 from control newborns of uninfected mothers and 262 of 263 from babies born to infected mothers) were negative. Since our PCR method is simple, reliable, robust, and inexpensive, it appears suitable for the detection of T. cruzi infection in neonatal blood, even in laboratories that are not equipped for performing the PCR.
CONGENITAL CHAGAS DISEASE IN BOLIVIA IS NOT ASSOCIATED WITH DNA POLYMORPHISM OF TRYPANOSOMA CRUZI
(American Society of Tropical Medicine and Hygiene, 2006) Myrna Virreira; Cristina Alonso‐Vega; Marco Solano; Juan Jijena; Laurent Brutus; Zulema Bustamante; Carine Truyens; Dominique Schneider; Faustino Torrico; Yves Carlier
This study aims to typify the Trypanosoma cruzi (sub)lineage(s) in umbilical cord blood of congenitally infected Bolivian newborns, using PCR amplifications of "Region Markers", mini-exon or kDNA fragments followed by hybridization or sequencing. New probes were also designed to distinguish three variants within the TcIId sublineage. The IIb, IId, or IIe T. cruzi sublineages, as well as different variants of the IId sublineage, were detected in infected neonates, whereas mixed infections were not found. The frequencies of the IId sublineage were similar in neonates (95.1%) and adults of the same area (94.1%). The IId-infected newborns displayed either asymptomatic, or severe and fatal clinical forms of congenital Chagas disease, as well as low or high parasitemia. Altogether these data show that T. cruzi DNA polymorphism, based on the presently available markers, is not associated with the occurrence of congenital infection or the development of severe clinical forms of congenital Chagas disease.
Congenital Transmission ofTrypanosoma cruziIs Associated with Maternal Enhanced Parasitemia and Decreased Production of Interferon‐γ in Response to Parasite Antigens
(Oxford University Press, 2004) Emmanuel Hermann; Carine Truyens; Cristina Alonso‐Vega; Patricia Rodríguez; Aurélie Berthe; Faustino Torrico; Yves Carlier
The conditions and mechanisms of congenital transmission of Trypanosoma cruzi remain largely unknown. In the present study, we compared the parasitic loads and the immune responses of pregnant T. cruzi-infected women who transmitted parasites to their fetus ("M+B+ mothers") with those of such women who did not transmit parasites to their fetus ("M+B- mothers"). M+B+ mothers had a higher frequency of positive results of hemoculture for T. cruzi than did M+B- mothers, in association with depressed production of parasite-specific interferon- gamma by blood cells that persisted after delivery. In contrast, the production of interleukin (IL)-2, IL-4, and IL-10 and transforming growth factor- beta 1 was similar between both groups of infected mothers, after stimulation with T. cruzi lysate. Flow cytometric analysis showed that T cells and monocytes of M+B+ mothers were less activated than were those of M+B- mothers. Altogether, these results indicate that congenital transmission of T. cruzi is associated with high parasitic loads and peripheral deficient immunological responses in mothers.
[Effects of maternal infection with Trypanosoma cruzi in pregnancy development and in the newborn infant].
(National Institutes of Health, 2005) Faustino Torrico; Mildred Castro; Marco Solano; Patricia Rodríguez; Mary‐Cruz Torrico; Carine Truyens; Yves Carlier
In the endemic regions of Bolivia the infection of the feminine population in fertile age by T. cruzi is frequent (20 to 50 % of the women in fertile age) and the rate of fetal maternal transmission is of approximately 5%. A great percentage of infected women do not transmit the infection to the fetus. The intention of the present study carried out at the Maternal-Infantile Hospital Germán Urquidi of Cochabamba (Bolivia) is to contribute to the knowledge regarding the pregnancy and birth of a newborn of Chagas infected women who do not transmit the infection to the fetus. 2124 mothers and 2,155 newborns were studied. The prevalence of infection by T. cruzi among these pregnant women is of 26,3%. Two groups of mothers were studied: 554 that presented infection by T. cruzi (group M+B-) and 1520 not infected (group control M-B-). Both groups of mothers are comparable in their anthropometric and obstetrical antecedents. The mothers (M+B+) are in average older than those not infected (p<0.05), which will probably have an influence on the number of gestations and abortion antecedents, which were of p<0.05 and p=0.01 respectively. Among the different anthropometric and biological parameters studied in newborns of groups M+B- and M-B -, no statistically significant differences between both groups were found. It can be inferred that the chronic maternal infection by T. cruzi seems to have no clinical influence, neither on the course of the pregnancy nor during birth, if a group of T. cruzi infected mothers is compared to a non infected group.
[Endemic level of congenital Trypanosoma cruzi infection in the areas of maternal residence and the development of congenital Chagas disease in Bolivia].
(National Institutes of Health, 2005) Faustino Torrico; Cristina Alonso‐Vega; Eduardo Suárez; Patricia Rodríguez; Mary‐Cruz Torrico; M. Dramaix; Carine Truyens; Yves Carlier
In Bolivia, the prevalence of infection by T. cruzi in women in fertile age can vary between 20 and 60%. The present study made in the Maternity Germin Urquidi of Cochabamba - Bolivia, it has demonstrated, that 19.9% of the mothers who go to this hospitable center to be taken care of in the childbirth, they are carrying of the infection and that 4,6% of them, they are going to transmit, by transplacentaria route, the infection to its babies. Of the 71 children born with congenital Chagas, only 47,8 % present/display some type of alteration or of development(Apgar to 1 minute low, BPN, prematuridad, pathological dismadurez) or signs (SDR, hepatomegalia, esplenomegalia, neurological signs, cardiomegalia, anasarca, petequias). When investigating the effect of the differences in the vectorial density (low, medium and high) of the zone of maternal residence, on the transmission of the infection of the mother infected to the fetus, we concluded that the rate of transmission of the congenital infection of T. cruzi is not modified by the level of endemicidad of the zone of maternal residence. By another infected new born sides whose mothers reside in zones of high endemicidad present/display, most frequently and of significant way, Apgar to 1 minute < to 7, low weight when being born and prematuridad or an association of these alterations with respiratory syndrome of distress or anasarca, when one compares them with new born of resident mothers in the zones of loss or medium endemicidad, mortality in this group is greater. These results suggest calls to account it of the mothers, in areas of high endemicidad, she is associate with a serious increase in the risk of Disease of newborn severe and mortal congenital Chagas in.
Estatus inmunológico de las madres infectadas por T. cruzi.
(Université Libre de Bruxelles, 2005) Cristina Alonso‐Vega; Emmanuel Hermann; Carine Truyens; Patricia Rodríguez; Mary Cruz Torrico; Faustino Torrico; Yves Carlier
The mechanisms of congenital transmission of Chagas disease remain largely unknown. To better understand the role of maternal immunology during pregnancy in congenital Chagas transmission, we studied the cytokine production and the parasitic load in three groups of mothers: infected mothers who transmitted the disease to their babies (M+B+-), infected mothers who did not transmit the disease to their babies (M+B-) and not infected mothers as a control group (M-B-). M+B+ mothers produced less IFNgamma and more IL-10 than the M+B- mothers, and they are not able to produce IL-2. M+B+ mothers showed a higher parasitic load. These results, indicated that the congenital Chagas transmission is associated with an immunological imbalance and a high parasitic load in the M+B+ mothers.
[Estimation of the parasitemia in Trypanosoma cruzi human infection: high parasitemias are associated with severe and fatal congenital Chagas disease].
(National Institutes of Health, 2005) Mary Cruz Torrico; Marco Solano; José Miguel Guzmán; Rudy Parrado; Eduardo Suárez; Cristina Alonzo-Vega; Carine Truyens; Yves Carlier; Faustino Torrico
The aim of this study was to validate the method of microhematocrit tube, as a rapid method to estimate the parasitemia in blood and to associate the parasites concentration with the morbidity and mortality of new born children with congenital Chagas diseases. Our results were determined experimentally and shown that the detection limit of the microhematocrit tube method is 40 parasites/ml when at least one of the four observed tubes is positive. Besides, it was also established that when the four examined tubes are positive the parasitemia in blood reaches more than 100 parasites/ml. It is important to highlight the modification made by our laboratory in the microscopic observation of the microhematocrit tubes with respect to the methodology used by previous investigators. A positive association exists between a high number of parasites in blood and the morbi-mortality of the newly born children with congenital chagas. The results of positive association between the parasitic load and the morbility and mortality could constitute an argument to understand the possible role of the parasite in the pathology of the disease.
Human Congenital Infection With Trypanosoma cruzi Induces Phenotypic and Functional Modifications of Cord Blood NK Cells
(Springer Nature, 2006) Emmanuel Hermann; Cristina Alonso‐Vega; Aurélie Berthe; Carine Truyens; Amilcar Flores; Marisol Córdova; Lorenzo Moretta; Faustino Torrico; Véronique M. Braud; Yves Carlier
[Immunological status of mothers infected with Trypanosoma cruzi].
(National Institutes of Health, 2005) Cristina Alonso‐Vega; Emmanuel Hermann; Carine Truyens; Patricia Rodríguez; Mary Cruz Torrico; Faustino Torrico; Yves Carlier
The mechanisms of congenital transmission of Chagas disease remain largely unknown. To better understand the role of maternal immunology during pregnancy in congenital Chagas transmission, we studied the cytokine production and the parasitic load in three groups of mothers: infected mothers who transmitted the disease to their babies (M+B+-), infected mothers who did not transmit the disease to their babies (M+B-) and not infected mothers as a control group (M-B-). M+B+ mothers produced less IFNgamma and more IL-10 than the M+B- mothers, and they are not able to produce IL-2. M+B+ mothers showed a higher parasitic load. These results, indicated that the congenital Chagas transmission is associated with an immunological imbalance and a high parasitic load in the M+B+ mothers.
Killer cell immunoglobulin‐like receptor expression induction on neonatal CD8+ T cells in vitro and following congenital infection with Trypanosoma cruzi
(Wiley, 2009) Emmanuel Hermann; Aurélie Berthe; Carine Truyens; Cristina Alonso‐Vega; Rudy Parrado; Faustino Torrico; Yves Carlier; Véronique M. Braud
Major histocompatibility complex (MHC) class I-specific inhibitory natural killer receptors (iNKRs) are expressed by subsets of T cells but the mechanisms inducing their expression are poorly understood, particularly for killer-cell immunoglobulin-like receptors (KIRs). The iNKRs are virtually absent from the surface of cord blood T cells but we found that KIR expression could be induced upon interleukin-2 stimulation in vitro. In addition, KIR expression was enhanced after treatment with 5-aza-2'-deoxycytidine, suggesting a role for DNA methylation. In vivo induction of KIR expression on cord blood T cells was also observed during a human congenital infection with Trypanosoma cruzi which triggers activation of fetal CD8(+) T cells. These KIR(+) T cells had an effector and effector/memory phenotype suggesting that KIR expression was consecutive to the antigenic stimulation; however, KIR was not preferentially found on parasite-specific CD8(+) T cells secreting interferon-gamma upon in vitro restimulation with live T. cruzi. These findings show that KIR expression is likely regulated by epigenetic mechanisms that occur during the maturation process of cord blood T cells. Our data provide a molecular basis for the appearance of KIRs on T cells with age and they have implications for T-cell homeostasis and the regulation of T-cell-mediated immune responses.
Maternal Infection with Trypanosoma cruzi and Congenital Chagas Disease Induce a Trend to a Type 1 Polarization of Infant Immune Responses to Vaccines
(Public Library of Science, 2009) Nicolás Dauby; Cristina Alonso‐Vega; Eduardo Suárez; Amilcar Flores; Emmanuel Hermann; Marisol Córdova; Tatiana Tellez; Faustino Torrico; Carine Truyens; Yves Carlier
These results show that: i) both maternal infection with T. cruzi and congenital Chagas disease do not interfere with responses to BCG, hepatitis B, diphtheria and tetanus vaccines in the neonatal period, and ii) the overcoming of immunological immaturity by T. cruzi infection in early life is not limited to the development of parasite-specific immune responses, but also tends to favour type 1 immune responses to vaccinal antigens.
MATERNAL TRYPANOSOMA CRUZI INFECTION, PREGNANCY OUTCOME, MORBIDITY, AND MORTALITY OF CONGENITALLY INFECTED AND NON-INFECTED NEWBORNS IN BOLIVIA
(American Society of Tropical Medicine and Hygiene, 2004) Faustino Torrico; Cristina Alonso‐Vega; Eduardo Suárez; Patricia J Rodriguez; Mary‐Cruz Torrico; Michèle Dramaix; Carine Truyens; Yves Carlier
This work compares the results of two epidemiologic and clinical surveys on the consequences of maternal chronic Trypanosoma cruzi infection. They were conducted in 1992-1994 and 1999-2001 in the same maternity clinic in Bolivia, a country highly endemic for infection with this parasite. In both surveys, the materno-fetal transmission of parasites occurred in 5-6% of the infected mothers. Maternal chronic T. cruzi infection had no effect on pregnancy outcome and health of newborns when there was no materno-fetal transmission of parasites. Comparisons between the older and the more recent surveys highlighted significant reductions in frequencies of symptomatic cases (from 54% to 45%), Apgar scores < 7, and low birth weights and prematurity (from 32-50% to 6-16%) among congenitally infected babies. Neonatal mortality related to congenital Chagas disease also decreased from 13% to 2% in the interval between both studies. These results suggest that the decrease in poverty that has occurred in Bolivia between both surveys might have contributed to reduce the morbidity and mortality, but not the transmission rate of T. cruzi congenital infection, which remains a serious public health problem in this country.
MaternalTrypanosoma cruziInfection Upregulates Capacity of Uninfected Neonate Cells To Produce Pro- and Anti-Inflammatory Cytokines
(American Society for Microbiology, 2000) Johan Vekemans; Carine Truyens; Faustino Torrico; Marco Solano; Mary‐Cruz Torrico; Patricia Rodríguez; Cristina Alonso‐Vega; Yves Carlier
The possibility of maternal in utero modulation of the innate and/or adaptive immune responses of uninfected newborns from Trypanosoma cruzi-infected mothers was investigated by studying the capacity of their whole blood cells to produce cytokines in response to T. cruzi lysate or lipopolysaccharide-plus-phytohemagglutinin (LPS-PHA) stimulation. Cells of such newborns occasionally released gamma interferon (IFN-gamma) and no interleukin-2 (IL-2) and IL-4 upon specific stimulation, while their mothers responded by the production of IFN-gamma, IL-2, and IL-4. Infection in mothers was also associated with a hyperactivation of maternal cells and also, strikingly, of cells of their uninfected neonates, since their release of proinflammatory (IL-1beta, IL-6, and tumor necrosis factor alpha [TNF-alpha]) as well as of anti-inflammatory (IL-10 and soluble TNF receptor) cytokines or factors was upregulated in the presence of LPS-PHA and/or parasite lysate. These results show that T. cruzi infection in mothers induces profound perturbations in the cytokine response of their uninfected neonates. Such maternal influence on neonatal innate immunity might contribute to limit the occurrence and severity of congenital infection.
Monocytes from Uninfected Neonates Born to Trypanosoma cruzi-Infected Mothers Display Upregulated Capacity to Produce TNF-α and to Control Infection in Association with Maternally Transferred Antibodies
(Multidisciplinary Digital Publishing Institute, 2023) Amilcar Flores; Cristina Alonso‐Vega; Emmanuel Hermann; Mary‐Cruz Torrico; Nair Alaide Montaño Villarroel; Faustino Torrico; Yves Carlier; Carine Truyens
Activated monocytes/macrophages that produce inflammatory cytokines and nitric oxide are crucial for controlling Trypanosoma cruzi infection. We previously showed that uninfected newborns from T. cruzi infected mothers (M+B- newborns) were sensitized to produce higher levels of inflammatory cytokines than newborns from uninfected mothers (M-B- newborns), suggesting that their monocytes were more activated. Thus, we wondered whether these cells might help limit congenital infection. We investigated this possibility by studying the activation status of M+B- cord blood monocytes and their ability to control T. cruzi in vitro infection. We showed that M+B- monocytes have an upregulated capacity to produce the inflammatory cytokine TNF-α and a better ability to control T. cruzi infection than M-B- monocytes. Our study also showed that T. cruzi-specific Abs transferred from the mother play a dual role by favoring trypomastigote entry into M+B- monocytes and inhibiting intracellular amastigote multiplication. These results support the possibility that some M+B- fetuses may eliminate the parasite transmitted in utero from their mothers, thus being uninfected at birth.
[Serum levels for IgM and IgA antibodies to anti-trypanosoma cruzi in samples of blood from newborns from mothers with positive serology for Chagas disease].
(National Institutes of Health, 2005) Patricia Rodríguez; Carine Truyens; Cristina Alonso‐Vega; Amilcar Flores; Marisol Córdova; Eduardo Suárez; Faustino Torrico; Yves Carlier
This study compares the levels of specific antibodies IgM and IgA for Chagas in samples of blood from newborns. Three groups of cord blood samples have been analysed: a group of 42 samples from newborns, displaying positive parasitemia, of seropositive mothers (M+B+), 68 samples from newborns with negative parasitemia whose mothers were seropositive (M+B-) and a group of 45 control newborns coming from mothers with negative serology for Chagas. From the 42 M+B+ samples with congenital Chagas disease, 81 and 82.9% displayed detectable levels of IgM and IgA antibodies, respectively In the M+B- group, 70.6 and 33.8% presented antibodies of IgM and IgA classes, respectively, whereas in the control group M-B-, we detected 6% and 11.1% of IgM and IgA antibodies, respectively. The calculated sensitivity of detection of congenital cases using IgM or IgA antibodies was of 82.9% and 80.9% respectively, whereas the specificity of detection was of 29.4% for IgM antibodies and of 66.1% for IgA antibodies.
The cachexia associated with Trypanosoma cruzi acute infection in mice is attenuated by anti‐TNF‐a, but not by anti‐IL‐6 or anti‐IFN‐7 antibodies
(Wiley, 1995) Carine Truyens; Faustino Torrico; ALCIRA ANGELO‐BARRIOS; Rudolf Lucas; Hubertine Heremans; Patrick De Baetselier; Yves Carlier
SUMMARY BALB/c male mice acutely infected with Trypanosoma cruzi underwent a severe weight loss (around 20%, from day 18 to 31 post‐infection), when compared to age‐matched uninfected animals. Though mice regained weight later, when blood parasites were hardly detectable, wasting extended over the chronic phase of infection. The onset and the magnitude of weight loss were related to the mouse susceptibility to infection, since they were respectively earlier and higher in male mice which will die than in surviving ones, in males than in females, and in BALB/c than in B6D2 [(C57B1/6 × DBA/2)F1], a mouse strain more resistant to infection. Fat weight of infected mice (male BALB/c) was reduced by 60 to 80%, whereas lean mass was unaffected and water content rose by 6 to 10% in acute and chronic infection. Haematocrit was also decreased by 15–16% in acute infection. Animals failed to compensate their energetic loss since their food intake remained similar to that of uninfected animals. Injections of neutralizing anti‐TNF‐α monoclonal antibody into infected male mice, during the first two weeks but not later in infection, significantly attenuated the weight loss. Early administration of anti‐IL‐6 or anti‐IFN‐γ MoAbs did not improve the mouse wasting. Taken together, these data show that TNFis a key agent of cachexia occurring in the acute T. cruzi infection in mice.